In JB v Bailey, 2026 ABKB 243, an obstetrician admitted that she had been negligent and admitted that her negligence caused a brain injury at birth. The family still lost the central part of the case. The reason is the single hardest issue in any birth injury claim: causation. An admission that a doctor was negligent, and even an admission that the negligence caused a brain injury, does not establish that the brain injury caused the child’s lasting impairments. The plaintiff must still prove that link, and here the Court of King’s Bench of Alberta held that the family had not.
Because this is an Alberta decision, it is persuasive only in Ontario and not binding here. The causation principles it applies, however, come from the Supreme Court of Canada, so the reasoning travels well.
What the case was about
JB was born in May 2013 after a traumatic labour. Dr. Bailey was the attending obstetrician. She admitted that she owed a duty of care to both mother and baby, that she breached the standard of care by inappropriately using and managing oxytocin and by not performing a caesarean section, and that this breach caused JB to suffer hypoxic ischemic encephalopathy (HIE) during labour and a brachial plexus injury (BPI) during delivery. HIE is a brain injury caused by an inadequate supply of oxygenated blood to the brain. A BPI is an injury to the nerves that supply the shoulder, arm, and hand.
By trial, JB was twelve. His mother reported a range of difficulties: low muscle tone, fatigue, poor balance and coordination, fine motor problems, memory and attention issues, and bladder control problems. The parties agreed that if the negligence caused JB’s neurodevelopmental impairments, damages were settled. The whole trial therefore turned on whether the HIE caused those impairments.
Causation is a separate element, and the burden was the family’s
Negligence requires four things: a duty of care, a breach of the standard of care, a compensable injury, and causation (Ediger v Johnston, 2013 SCC 18). The admission disposed of duty, breach, and the existence of an injury. It did not dispose of causation. As the court put it, an admission that Dr. Bailey was negligent does not make her liable for JB’s neurodevelopmental impairments.
Causation was assessed on the familiar but-for test, applied with a robust and common-sense approach to the evidence (Clements v Clements, 2012 SCC 32; Snell v Farrell, 1990 CanLII 70 (SCC)). Factual causation in law is distinct from medical causation, and proof does not require medical or scientific certainty (Benhaim v St-Germain, 2016 SCC 48). But the burden stayed on the family throughout. This is the same architecture that governs anyone suing for medical malpractice in Ontario: breach and causation are different questions, and winning the first does not win the second.
Why the causation case failed
Several threads ran against the family, and the court treated them cumulatively.
The HIE was moderate, not severe. The contemporaneous records described mild to moderate HIE, and the court found moderate stage 2 HIE. It was critical of expert evidence that recharacterized the injury as more severe than the records supported, noting that an expert’s impartiality affects the weight of the opinion (White Burgess Langille Inman v Abbott and Haliburton Co, 2015 SCC 23).
JB recovered quickly in the neonatal period. His heart rate and breathing normalized within minutes to an hour, and by discharge the treating pediatric neurologist recorded a likely good prognosis.
His brain imaging was normal. An MRI within the optimal window after therapeutic cooling, and a repeat MRI in 2022, showed no pattern of HIE injury. The defence experts and a neuroradiologist relied on the literature to put the chance of an adverse outcome, for a child with moderate HIE and a normal MRI after cooling, at roughly one in four or lower. A normal MRI after cooling does not rule out later sequelae, but the court accepted that such outcomes are uncommon, and that nothing in JB’s presentation placed him in that minority.
There were no seizures. Apart from an unrelated febrile seizure as a toddler, JB has never had a seizure, and no treating neurologist diagnosed epilepsy. Where there was a question of a future seizure tendency, the treating neurologist thought it more likely genetic in origin than a consequence of the HIE.
There was no cerebral palsy. None of JB’s treating physicians ever diagnosed it. A cerebral palsy diagnosis offered for the first time by a litigation expert was rejected as a misdiagnosis, because it could not be reconciled with the normal neurological examinations performed by the treating neurologists and the defence developmental pediatrician.
The alternative-cause defence: heritable conditions and the genetics trap
The defence did not have to prove an alternative cause, and the family did not have to disprove one. But where causation rests on inference, a defendant may point to other explanations to undercut that inference (Clements). Here the alternatives were strong. There was a documented family history of joint hypermobility and of attention difficulties, both highly heritable, and the court accepted that JB’s own joint hypermobility plausibly accounted for his fine motor delays, pain, fatigue, and coordination problems, while heritable attention traits explained his distractibility.
The family leaned on negative genetic testing to close off these alternatives, and this is where the decision is most instructive. A negative whole genome test does not eliminate polygenic or multifactorial conditions such as hypermobile EDS, genetic generalized epilepsy, or ADHD, and it cannot confirm that an event like intrapartum HIE was the cause of a child’s presentation. The court preferred the geneticist who explained those limits over the one who testified that the testing definitively eliminated a genetic explanation and proved HIE was the cause. That overreach is a familiar pattern in genetic defences in medical malpractice, and it cuts both ways: just as a defendant cannot use a negative test to manufacture a heritable cause, a plaintiff cannot use one to manufacture proof of an acquired one.
Two further problems compounded the family’s difficulty. The mother’s account of JB’s limitations was found to be significantly out of step with his teachers’ reports, his school performance, standardized testing, and in-home observation. And JB’s own test results were inconsistent across examiners, with two assessors noting reduced effort and non-physiological findings. Inconsistency across testing environments is the opposite of what a true neurological deficit should look like, and the court said so.
A missed source of evidence
The family did not call JB’s treating physicians, including his pediatrician and his treating pediatric neurologists. The defence asked the court to draw an adverse inference. The court declined, because the medical records were fully in evidence, the defence had been able to question two of the treating doctors before trial, and there was extensive expert evidence to resolve the issues. In doing so it rejected the broad proposition that a treating physician is always within a plaintiff’s exclusive control, citing among other cases the Alberta birth injury decision in KY v Bahler. No inference was drawn, but the practical point remains: the people best placed to speak to whether HIE caused this child’s difficulties were the doctors who had followed him for years, and the court was left to reconstruct that picture from records and retained experts.
The brachial plexus injury
The BPI was a different story. Dr. Bailey admitted causing it but argued it was de minimis and not compensable. The court disagreed. The injury was real, required focused attention and follow-up after discharge, and was not the kind of transient annoyance the de minimis principle is meant to exclude (Mustapha v Culligan of Canada Ltd, 2008 SCC 27). On the evidence the BPI resolved within JB’s first year with no residual impairment, and the mother’s evidence of ongoing left-arm weakness was found inconsistent with the records. The court awarded $22,000 in non-pecuniary damages, below the $38,000 to $66,000 the family sought, plus a subrogated health-services claim of $1,677.19 and pre-judgment interest. It refused an enhanced award for the emotional cost of the traumatic birth, and it denied an in-trust claim for the mother’s at-home exercises, finding that care had been folded into ordinary parenting rather than amounting to extraordinary care.
What it means for Ontario plaintiffs
JB v Bailey is not binding in Ontario, but the lesson is portable and sobering. In HIE and birth injury claims, causation is usually the battleground, and it is a question entirely separate from negligence. Counsel can have an admission of breach, an admission that the breach caused a brain injury, and a child with genuine difficulties, and still lose if the evidence cannot connect those difficulties to the injury on a balance of probabilities.
The features that decided this case are the ones that decide many of them: the severity of the HIE, the speed of neonatal recovery, whether the MRI after cooling shows a recognizable injury, whether there were seizures, whether there is cerebral palsy, and whether a plausible heritable explanation sits alongside the birth injury. It is the same dynamic seen in other infant brain injury claims that have foundered on causation rather than breach, such as Hanson-Tasker v Ewart. Importantly, the court did not hold that HIE could never cause impairments like JB’s. It accepted that HIE sequelae can emerge years later and that many of his reported impairments are common consequences of HIE. The family simply did not prove the link. As the court found on the evidence before it, “JB has normal intelligence, normal academic achievement and no significant disabilities.”
The takeaways for building, rather than losing, these cases are concrete: secure the treating physicians, not just the records; retain current, impartial experts whose characterizations match the chart; confront the heritable alternatives directly rather than hoping a genetic test will erase them; and align the family’s account with the objective evidence before trial, because a gap between a parent’s report and the testing will be used against the claim.
JB v Bailey, 2026 ABKB 243 (CanLII), is available at canlii.org.
JB v Bailey: Admitted Negligence Is Not Proof of Causation in a Birth Injury Case
Dr. Bailey admitted that her management of labour was negligent and that it caused a hypoxic brain injury at birth. The plaintiffs still lost, because they could not prove that the brain injury caused the child's lasting impairments. JB v Bailey is an Alberta decision, persuasive only in Ontario, but it is a clear reminder that admitted negligence and admitted injury are not the same as proven causation.
In JB v Bailey, 2026 ABKB 243, an obstetrician admitted that she had been negligent and admitted that her negligence caused a brain injury at birth. The family still lost the central part of the case. The reason is the single hardest issue in any birth injury claim: causation. An admission that a doctor was negligent, and even an admission that the negligence caused a brain injury, does not establish that the brain injury caused the child’s lasting impairments. The plaintiff must still prove that link, and here the Court of King’s Bench of Alberta held that the family had not.
Because this is an Alberta decision, it is persuasive only in Ontario and not binding here. The causation principles it applies, however, come from the Supreme Court of Canada, so the reasoning travels well.
What the case was about
JB was born in May 2013 after a traumatic labour. Dr. Bailey was the attending obstetrician. She admitted that she owed a duty of care to both mother and baby, that she breached the standard of care by inappropriately using and managing oxytocin and by not performing a caesarean section, and that this breach caused JB to suffer hypoxic ischemic encephalopathy (HIE) during labour and a brachial plexus injury (BPI) during delivery. HIE is a brain injury caused by an inadequate supply of oxygenated blood to the brain. A BPI is an injury to the nerves that supply the shoulder, arm, and hand.
By trial, JB was twelve. His mother reported a range of difficulties: low muscle tone, fatigue, poor balance and coordination, fine motor problems, memory and attention issues, and bladder control problems. The parties agreed that if the negligence caused JB’s neurodevelopmental impairments, damages were settled. The whole trial therefore turned on whether the HIE caused those impairments.
Causation is a separate element, and the burden was the family’s
Negligence requires four things: a duty of care, a breach of the standard of care, a compensable injury, and causation (Ediger v Johnston, 2013 SCC 18). The admission disposed of duty, breach, and the existence of an injury. It did not dispose of causation. As the court put it, an admission that Dr. Bailey was negligent does not make her liable for JB’s neurodevelopmental impairments.
Causation was assessed on the familiar but-for test, applied with a robust and common-sense approach to the evidence (Clements v Clements, 2012 SCC 32; Snell v Farrell, 1990 CanLII 70 (SCC)). Factual causation in law is distinct from medical causation, and proof does not require medical or scientific certainty (Benhaim v St-Germain, 2016 SCC 48). But the burden stayed on the family throughout. This is the same architecture that governs anyone suing for medical malpractice in Ontario: breach and causation are different questions, and winning the first does not win the second.
Why the causation case failed
Several threads ran against the family, and the court treated them cumulatively.
The HIE was moderate, not severe. The contemporaneous records described mild to moderate HIE, and the court found moderate stage 2 HIE. It was critical of expert evidence that recharacterized the injury as more severe than the records supported, noting that an expert’s impartiality affects the weight of the opinion (White Burgess Langille Inman v Abbott and Haliburton Co, 2015 SCC 23).
JB recovered quickly in the neonatal period. His heart rate and breathing normalized within minutes to an hour, and by discharge the treating pediatric neurologist recorded a likely good prognosis.
His brain imaging was normal. An MRI within the optimal window after therapeutic cooling, and a repeat MRI in 2022, showed no pattern of HIE injury. The defence experts and a neuroradiologist relied on the literature to put the chance of an adverse outcome, for a child with moderate HIE and a normal MRI after cooling, at roughly one in four or lower. A normal MRI after cooling does not rule out later sequelae, but the court accepted that such outcomes are uncommon, and that nothing in JB’s presentation placed him in that minority.
There were no seizures. Apart from an unrelated febrile seizure as a toddler, JB has never had a seizure, and no treating neurologist diagnosed epilepsy. Where there was a question of a future seizure tendency, the treating neurologist thought it more likely genetic in origin than a consequence of the HIE.
There was no cerebral palsy. None of JB’s treating physicians ever diagnosed it. A cerebral palsy diagnosis offered for the first time by a litigation expert was rejected as a misdiagnosis, because it could not be reconciled with the normal neurological examinations performed by the treating neurologists and the defence developmental pediatrician.
The alternative-cause defence: heritable conditions and the genetics trap
The defence did not have to prove an alternative cause, and the family did not have to disprove one. But where causation rests on inference, a defendant may point to other explanations to undercut that inference (Clements). Here the alternatives were strong. There was a documented family history of joint hypermobility and of attention difficulties, both highly heritable, and the court accepted that JB’s own joint hypermobility plausibly accounted for his fine motor delays, pain, fatigue, and coordination problems, while heritable attention traits explained his distractibility.
The family leaned on negative genetic testing to close off these alternatives, and this is where the decision is most instructive. A negative whole genome test does not eliminate polygenic or multifactorial conditions such as hypermobile EDS, genetic generalized epilepsy, or ADHD, and it cannot confirm that an event like intrapartum HIE was the cause of a child’s presentation. The court preferred the geneticist who explained those limits over the one who testified that the testing definitively eliminated a genetic explanation and proved HIE was the cause. That overreach is a familiar pattern in genetic defences in medical malpractice, and it cuts both ways: just as a defendant cannot use a negative test to manufacture a heritable cause, a plaintiff cannot use one to manufacture proof of an acquired one.
Two further problems compounded the family’s difficulty. The mother’s account of JB’s limitations was found to be significantly out of step with his teachers’ reports, his school performance, standardized testing, and in-home observation. And JB’s own test results were inconsistent across examiners, with two assessors noting reduced effort and non-physiological findings. Inconsistency across testing environments is the opposite of what a true neurological deficit should look like, and the court said so.
A missed source of evidence
The family did not call JB’s treating physicians, including his pediatrician and his treating pediatric neurologists. The defence asked the court to draw an adverse inference. The court declined, because the medical records were fully in evidence, the defence had been able to question two of the treating doctors before trial, and there was extensive expert evidence to resolve the issues. In doing so it rejected the broad proposition that a treating physician is always within a plaintiff’s exclusive control, citing among other cases the Alberta birth injury decision in KY v Bahler. No inference was drawn, but the practical point remains: the people best placed to speak to whether HIE caused this child’s difficulties were the doctors who had followed him for years, and the court was left to reconstruct that picture from records and retained experts.
The brachial plexus injury
The BPI was a different story. Dr. Bailey admitted causing it but argued it was de minimis and not compensable. The court disagreed. The injury was real, required focused attention and follow-up after discharge, and was not the kind of transient annoyance the de minimis principle is meant to exclude (Mustapha v Culligan of Canada Ltd, 2008 SCC 27). On the evidence the BPI resolved within JB’s first year with no residual impairment, and the mother’s evidence of ongoing left-arm weakness was found inconsistent with the records. The court awarded $22,000 in non-pecuniary damages, below the $38,000 to $66,000 the family sought, plus a subrogated health-services claim of $1,677.19 and pre-judgment interest. It refused an enhanced award for the emotional cost of the traumatic birth, and it denied an in-trust claim for the mother’s at-home exercises, finding that care had been folded into ordinary parenting rather than amounting to extraordinary care.
What it means for Ontario plaintiffs
JB v Bailey is not binding in Ontario, but the lesson is portable and sobering. In HIE and birth injury claims, causation is usually the battleground, and it is a question entirely separate from negligence. Counsel can have an admission of breach, an admission that the breach caused a brain injury, and a child with genuine difficulties, and still lose if the evidence cannot connect those difficulties to the injury on a balance of probabilities.
The features that decided this case are the ones that decide many of them: the severity of the HIE, the speed of neonatal recovery, whether the MRI after cooling shows a recognizable injury, whether there were seizures, whether there is cerebral palsy, and whether a plausible heritable explanation sits alongside the birth injury. It is the same dynamic seen in other infant brain injury claims that have foundered on causation rather than breach, such as Hanson-Tasker v Ewart. Importantly, the court did not hold that HIE could never cause impairments like JB’s. It accepted that HIE sequelae can emerge years later and that many of his reported impairments are common consequences of HIE. The family simply did not prove the link. As the court found on the evidence before it, “JB has normal intelligence, normal academic achievement and no significant disabilities.”
The takeaways for building, rather than losing, these cases are concrete: secure the treating physicians, not just the records; retain current, impartial experts whose characterizations match the chart; confront the heritable alternatives directly rather than hoping a genetic test will erase them; and align the family’s account with the objective evidence before trial, because a gap between a parent’s report and the testing will be used against the claim.
JB v Bailey, 2026 ABKB 243 (CanLII), is available at canlii.org.
Paul Cahill
Partner, Davidson Cahill Morrison LLP | LSO Certified Specialist in Civil Litigation
Paul represents victims of medical malpractice across Ontario, with trial experience including a $11.5M jury verdict in a birth injury case. He is recognized in Best Lawyers in Canada and serves as trial counsel to other lawyers on complex medical negligence matters.
About PaulMore on medical malpractice in Ontario.
Other articles by Paul exploring the conditions, decisions, and systems behind preventable medical harm.
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