Concussion Litigation in Rugby – Part III: Causation
1. Introduction
This article is the third in a series of articles on the ongoing concussion litigation in rugby union, which was instigated in December 2020 by a group of former professional players against the Rugby Football Union (“RFU”), the Welsh Rugby Union (“WRU”) and World Rugby, the sport’s International Federation.
Part I introduced the series and considered the existence and scope of the duties of care owed by the sport’s governing bodies, while Part II addressed the question of whether those duties have been breached. Both parts concluded that there were good arguments in favour of the claimant players.
This Part III will analyse the issues of causation – i.e. whether, as a matter of law, the governing bodies’ (arguable) negligence could be deemed to have caused the claimant players’ probable CTE and early onset dementia. This is perhaps the most complex part of the concussion litigation, which will present significant challenges for all parties.
2. Causation in English law
Causation in English law can typically be broken down into two elements: factual causation and legal causation. Factual causation is typically expressed as the “but for” test – i.e. “but for” the defendant’s negligence, would the injury have occurred? If the answer is no, the defendant is the factual cause of the injury. Legal causation relates to the question of whether the harm falls within the scope of the defendant’s responsibility.
If a defendant has negligently breached their duty of care and is found to have caused the claimant’s loss, the defendant will, prima facie, be liable.
2.1 Factual Causation
The “but for” test applies in most cases to determine factual causation.[1] However, in certain instances, it fails to produce a satisfactory result.
For example, if there are multiple possible and/or contributing causes of a single injury, it may be impossible (as a matter of science) to prove, on a “but for” analysis, the contribution of each possible cause. As such, to mitigate unfairness to claimants, the law has developed to modify the “but for” test in certain circumstances, often in the context of industrial disease.
2.1.1 Material Contribution to the Injury
Following Bonnington Castings v Wardlaw,[2] factual causation will be established where there are multiple cumulative causes of a single injury, the inadequacies of medical science mean that the relative potency of the causes cannot be established,[3] (at least) one of those causes was tortious (i.e. the result of negligence) and the claimant can prove that this cause made a material contribution to the injury. The claimant does not have to prove that the defendant’s negligence was the sole, or even the main, cause of the damage.
A “material contribution” means a contribution to the injury that is more than de minimis.[4]
Where there are multiple tortfeasors (i.e. defendants), each of whom made a material contribution to the injury, the tortfeasors shall be jointly and severally liable. In other words, each individual tortfeasor shall be liable for the whole of the damage. Thus, if one of the tortfeasors has disappeared or has become insolvent, the claimant will not be left without a remedy. If multiple tortfeasors are still in existence, they can then seek to apportion the damages between themselves.[5]
2.1.2 “Doubling the Risk” Test
Some cases have alternatively referred to the “doubling the risk” test, as a means of establishing factual causation. For example, in Novartis Grimsby v Cookson,[6] it was held that causation was established where it was proven epidemiologically that negligent exposure to carcinogens accounted for 70% of the total risk of the claimant developing bladder cancer. Thus, the negligent exposure had more than doubled the risk of the claimant developing bladder cancer owing to non-tortious, environmental factors. As the court held, in such circumstances, “it must, as a matter of logic, be probable that the disease was caused by the former”[7] and causation could thus be inferred, on the balance of probabilities.
However, it is clear that proving that a tortious act has doubled the risk of the injury will not be necessary in material contribution cases,[8] and the Appellate courts have signalled caution in using epidemiological data in this way.[9]
2.1.3 A Two-Stage Approach
In Heneghan v Manchester Dry Docks,[10] the Court of Appeal (led by Lord Dyson MR) advocated a two-stage approach to causation in complex cases involving multiple possible causes and multiple tortfeasors.[11]
Stage 1 is the “what” question – i.e. what was the causative agent of the disease/injury? In Heneghan, the possible causative agents were asbestos, smoking or “something else”. Lord Dyson MR held:[12]
The “doubles the risk” test is one that applies epidemiological data to determining causation on the balance of probabilities where medical science does not permit determination with certainty of how an injury was caused. If statistical evidence shows that a tortfeasor more than doubled the risk that the victim would suffer the injury, it follows that it is more likely than not that the tortfeasor caused the injury. Some doubt has been expressed as to the validity of the doubling the risk test…But there can be no doubt as to the validity of applying it to answer the first question…
In Heneghan, for example, it was found that exposure to asbestos over the course of his various employments resulted in more than a fivefold increase in the risk of contracting the disease, so the case got past stage 1.
Stage 2 is the “who” question – i.e. which of the multiple tortfeasors (or non-tortious causes) caused the disease/injury? According to Lord Dyson MR, this is where the material contribution analysis comes into play,[13] and where it is inappropriate to rely on the “doubles the risk” test.
2.2 Legal Causation
As noted above, legal causation is the question of whether damage (factually) caused by the defendant falls within the scope of their responsibility, such that they should be liable for it. The primary test is one of reasonable foreseeability – i.e. if a reasonable person would have foreseen damage of the kind which occurred, the damage will not be too remote, and the defendant will be liable for it.[14] The extent of the harm is irrelevant,[15] and it is a general principle that you take your victim as you find them (such that it is no excuse to say that a claimant’s particular vulnerability aggravated the damage)[16].
Given that, in order to reach the causation stage of the analysis, it would already have been found that long-term brain damage was a reasonably foreseeable consequence of any established breach of duty, this causal element is unlikely to be controversial. Likewise, it would not be open to the defendants to rely on any individual player’s particular (intrinsic) vulnerability to suffering brain injuries/dementia. The “eggshell skull” principle would have an unfortunately literal application.
The remainder of this article will therefore focus on the issues of factual causation.
3. Causation in the Rugby Concussion Litigation
For the purposes of analysing the issues of factual causation in the rugby concussion litigation, this author will follow the two-stage approach set out in Heneghan (above).
Stage 1 – what is the cause of the players’ early onset dementia and probable CTE?
As noted in Part II, the latest consensus statement by the Concussion in Sport Group recognised that the potential for developing CTE (a form of dementia) after “repetitive head-impact exposure and concussions…must be a consideration” but concluded that a “cause-and-effect relationship has not yet been demonstrated between CTE and [sport-related concussions] or exposure to contact sports”.
However, an association between CTE and repetitive head trauma is well-established, and there has been evidence of a link between CTE and contact sports since the 1920s.[17] There are many experts who would disagree with the CISG’s approach, particularly in light of developments since its most recent Consensus Statement, and would say that CTE is caused by repetitive hits to the head sustained over a period of years, even if it is not possible to say exactly how many concussive and sub-concussive impacts are needed to produce such effects.[18] It is those experts’ evidence upon which the claimant rugby players will, no doubt, seek to rely.
The players may further rely upon epidemiological evidence, likely applying the Bradford Hill criteria, to establish a causal relationship between the presumed cause (i.e. exposure to repetitive head impacts) and the observed effect (i.e. early onset dementia and probable CTE).[19] The defendants, meanwhile, will seek to undermine this relationship and will likely argue that there is simply not yet sufficient scientific understanding to establish a causal relationship on the balance of probabilities.
The players’ case will likely be that CTE can only be caused by repetitive head trauma, but it may well be argued by the defendants that Early Onset Dementia can have various causes, including lifestyle factors and genetic make-up. The players may then seek to rely upon the “doubles the risk” test, to prove their case, though it is not clear whether there is sufficient data available to establish the level of risk in professional rugby, as compared against the general population. Data from other contact sports may prove useful. This may not be necessary, though, if it is found that CTE is the probable cause of their conditions and that this is only caused by repetitive head trauma.
This will be a significant hurdle for the players to overcome and the defendants would, no doubt, press the CISG line but, in this author’s view, on the balance of the medico-scientific literature (which continues to evolve), it is not a hurdle which will necessarily be insurmountable.
Stage 2 – who is the cause of the players’ early onset dementia and probable CTE?
The second stage of the factual causation analysis, assuming that the first hurdle is cleared, will be to identify who was the cause. The current litigation has been started against World Rugby, the RFU and the WRU, each of whom may have acted in breach of duty concurrently over the course of the players’ careers. Further, it might well be argued that the players’ clubs negligently contributed to the harm (for example, by failing to properly apply the protocols in place at the relevant time(s)). Breach of duty might also be alleged against league organising bodies.[20] There are thus multiple potential tortfeasors.
There may also be non-tortious (i.e. innocent) causes. Of course, it cannot reasonably be argued that rugby’s governing bodies were negligent in failing to prevent players suffering any head trauma. The risk of head trauma is intrinsic in the sport and the governing bodies could not reasonably be expected to eliminate it altogether. Thus, some of the head trauma suffered by the players will not be the result of negligence – i.e. it will be non-tortious. Likewise, it may be that some individual claimant players also suffered head injuries outside of the sport of rugby union.
Given the multiplicity of concurrent causes, and the indivisible nature of CTE/dementia, it will unlikely be possible to prove the precise contribution of each cause to the players’ injuries. However, if, as it appears, CTE is cumulative (i.e. more exposure to repeated head trauma increases the severity of the injury to the brain),[21] the approach in Bonnington Castings (above) ought to apply.[22] Thus, the players’ case will likely be that the governing bodies’ negligence materially contributed to their development of CTE/early onset dementia.
Proving material contribution in this case would likely involve the players establishing the effect of the governing bodies’ negligence. In other words, what difference would introducing concussion substitutes and head injury assessments sooner have made? How would introducing limits on contact training have affected the incidence of head trauma and concussion? What would have happened if the governing bodies had properly enforced the regulations that were in force at the relevant times? In this regard, much will turn on the court’s findings on breach of duty – i.e. what the court finds the defendants unreasonably failed to do. If the players successfully prove a wide array of breaches, it may be more straightforward for them to establish a material contribution (remembering that the threshold is one of de minimis.
The defendants, though will likely seek to argue that the players would have suffered from CTE in any event, given the inherent risks of the game – i.e. that any negligence on their part was of only de minimis effect. Players will bring statistical evidence and may point to the lauded success of recent measures as proof that this would have had a more than negligible effect, but such hypothetical questions are difficult to answer and will thus present a further significant hurdle.
4. Conclusion
As noted at the outset, causation is perhaps the most complex element of the rugby concussion litigation, given the scientific uncertainty and the number of potential causes of the players’ damage, both tortious and non-tortious.
The players will essentially have two main hurdles to clear:
i) Proving that repeated head trauma caused their dementia/probable CTE; and
ii) Proving that the governing bodies’ (arguable) negligence made a material contribution to their outcome.
Whilst this author hopes that the above analysis sheds some light on these issues, it is clear that much will depend upon the expert medico-scientific evidence adduced in the proceedings.
Were the case to proceed to trial, the court’s findings on the first issue could be hugely significant, not only for the present litigation, but also for future potential claims and for the future of concussion management in sport more broadly.
Part IV of this series, which will focus on the rugby governing bodies’ potential defences, will follow in due course.
Article by Ben Cisneros. Ben is a Trainee Solicitor at Morgan Sports Law, though this article reflects only the author’s personal views. Please email ben.cisneros@morgansl.com for any legal or media enquiries.
[1] Barnett v. Chelsea and Kensington Hospital Management Committee [1969] 1 QB 428
[2] [1956] AC 613. See also Bailey v Ministry of Defence [2008] EWCA Civ 883 and Williams v Bermuda Hospitals Board [2016] UKPC 4
[3] i.e. the injury is indivisible.
[4] See Bonnington Castings v Wardlaw [1956] AC 613, at 621
[5] Typically, under the Civil Liability (Contribution) Act 1978.
[7] Ibid. at para. 74
[8] Sienkiewicz v. Greif [2011] UKSC 10
[9] Ibid. at para. 170 and Williams v. Bermuda Hospitals Board [2016] UKPC 4, at para. 48
[11] Ibid. at paras. 8-9
[12] Ibid. at para. 8
[13] In Heneghan, the “material contribution to the risk” test (Fairchild v Glenhaven Funeral Services [2003] 1 AC 32) was applied. This, further, adaption of the “but for” test is not considered to have particular relevance to the rugby concussion litigation (given its narrow application) and, thus, is not considered in detail here.
[14] Wagon Mound (No. 1) [1961] AC 388
[15] Hughes v. Lord Advocate [1963] AC 837; Vacwell Engineering v BDH Chemicals [1971] 1 QB 88
[16] Smith v Leech Brain [1962] 2 QB 405
[18] Ibid.
[19] See Cuthbert S. and Rawlinson QC M., ‘CTE and Causation: The Key Medico-Legal Issues in Rugby Union’s Concussion Litigation’, LawInSport (9 July 2021).
[20] The current defendants may well seek to bring professional clubs and league organising bodies into the litigation, to offset some of their potential liability (see Part V).
[21] Clearly, this will be one of the issues on which expert evidence will be crucial.
[22] For their part, the defendants might argue that there is insufficient evidence that CTE is caused cumulatively, and that the players can only establish that the breach(es) of duty increased the risk of CTE. Whilst, the courts have been willing to find causation established on such a basis (see Fairchild v Glenhaven Funeral Services [2003] 1 AC 32 etc.), they have done so only in very limited circumstances and it would be surprising if it was applied here.
