COURT OF APPEAL FOR ONTARIO

CITATION: Goodman v. Viljoen, 2012 ONCA 896

DATE: 20121220

DOCKET: C53377

Doherty, Feldman and LaForme JJ.A.

BETWEEN

Paul Goodman, Jaqueline Goodman, Calvin Goodman, a minor by his litigation guardian, the Children’s Lawyer and Daniel Goodman, a minor by his litigation guardian, the Children’s Lawyer

Plaintiffs (Respondents)

and

Johan Viljoen

Defendant (Appellant)

J. Thomas Curry, Anne Posno and Rebecca Jones, for the appellant

Donald Rogers and Anita Varjacic, for the respondents

Heard: January 17, 2012

On appeal from the judgment of Justice Linda M. Walters of the Superior Court of Justice dated February 3, 2011, with reasons reported at 2011 ONSC 821.

Doherty J.A. (Dissenting):

I

overview

[1] Calvin Goodman and Daniel Goodman are twin brothers. They were delivered prematurely on August 18, 1995. Both developed cerebral palsy (“CP”). They sued the defendant, Dr. Johan Viljoen, their mother’s obstetrician, for negligence.

[2] The plaintiffs alleged that Dr. Viljoen was negligent in his prenatal care of Mrs. Goodman. They further alleged that his negligence caused the plaintiffs to develop CP.

[3] The trial judge found that Dr. Viljoen was negligent. She further found that his negligence caused the plaintiffs’ CP. The parties had agreed on damages prior to trial. The trial judge granted judgment in favour of the plaintiffs in the amounts agreed upon.

[4] Dr. Viljoen appeals. He does not challenge the finding that he failed to meet the appropriate standard of care. He does, however, submit that the causation finding made by the trial judge cannot stand. He argues that the action should be dismissed. For the reasons that follow, I would allow the appeal, set aside the judgment below and dismiss the action.

II

dr. viljoen’s failure to meEt the standard of care

[5] Mrs. Goodman was pregnant with twins in the summer of 1995. It was her first pregnancy. Dr. Viljoen was her obstetrician. Mrs. Goodman saw Dr. Viljoen on August 9, 1995. Routine tests showed a urinary infection and Dr. Viljoen prescribed antibiotics.

[6] On August 16, 1995, Mrs. Goodman awoke to feel fluid gushing out of her. There was no sign of any blood in the fluid. Mrs. Goodman suspected that the fluid might be related to the urinary infection.

[7] Mrs. Goodman testified that she called Dr. Viljoen’s office later on August 16 and reported the fluid leakage. She spoke to his secretary who said that she would talk to Dr. Viljoen. The secretary called back later that day and told Mrs. Goodman that the leakage was related to the bladder infection and that she should continue to take the antibiotics. The secretary also told her to call the office if there were any further problems.

[8] The plaintiffs’ allegation that Dr. Viljoen failed to meet the appropriate standard of care turned on whether Mrs. Goodman called his office on August 16 as she testified. The defence acknowledged that if Mrs. Goodman called with complaints of leaking fluid, Dr. Viljoen should have seen her or told her to go to the hospital immediately. The defence contended that Ms. Goodman did not convey that information to his office on August 16.

[9] After a thorough review of the evidence, the trial judge found that Mrs. Goodman phoned Dr. Viljoen’s office and described the leaking fluid to Dr. Viljoen’s secretary. The trial judge also found that Mrs. Goodman was told that the leakage was related to the urinary infection. She was not told to come into the office or to go to the hospital. Those factual findings are not challenged on appeal. It follows from those findings that Dr. Viljoen did not meet the applicable standard of care.

III

events between august 16 and august 18, 1995

[10] After speaking with Dr. Viljoen’s secretary on August 16, Mrs. Goodman carried on with her daily routine. August 17 was uneventful.

[11] Mrs. Goodman awoke on the morning of August 18 feeling crampy. She spoke to her mother and decided to telephone Dr. Viljoen. Dr. Viljoen was out of town. Mrs. Goodman called her family doctor and saw her later that day. After taking a history, her family doctor told Mrs. Goodman to go to the hospital immediately. At the local hospital the attending physician quickly confirmed that Mrs. Goodman was in premature labour and that her membranes had ruptured.

[12] Mrs. Goodman was transferred immediately to McMaster Hospital, a tertiary care centre, in Hamilton, Ontario. The twins were born in the early evening of August 18 shortly after Mrs. Goodman arrived at McMaster Hospital. They were at 29 weeks gestation when delivered by caesarean section. They appeared to be in good condition, although they were treated as 27 week gestation babies because of their size. The premature birth of the twins was unrelated to Dr. Viljoen’s failure to meet the applicable standard of care.

IV

the medical cause of the twins’ cp

[13] The twins had developed CP by the time they were 18 months old. CP is a non-progressive nerve disorder and describes a cluster of conditions that includes motor difficulties, such as spasticity of the limbs, and sometimes includes cognitive problems. Daniel, the first born, is physically disabled but does very well in school. Calvin has more significant medical problems than Daniel. He also has some behavioural problems.

[14] CP develops in the months or even years following birth. CP is sometimes associated with medical problems that occurred during or shortly after birth. For example, some CP is associated with respiratory distress syndrome (“RDS”) experienced by some premature babies during the birth process. RDS can have a direct connection to the subsequent development of CP, or it can lead to a variety of other medical problems that in turn are associated with the later development of CP. For example, some kinds of intraventricular hemorrhaging (“IVH”) are associated with RDS and the later development of CP in premature babies.

[15] In many cases, especially in full-term pregnancies, CP cannot be attributed to any specific event or medical cause. The risk of CP is known to be much higher among premature infants than full-term babies. Premature twins are more susceptible to CP than are single premature babies.

[16] The experts all agreed that the twins’ CP was caused by a condition known as diffuse periventricular leukomalacia (“PVL”). PVL is among the many problems that premature babies face in making the adjustment to life outside of the womb.

[17] PVL involves the inadequate blood supply to an area of the premature baby’s brain referred to as the watershed zone. Arterial blood supplies to the brain meet in the watershed zone. In premature infants, the arterial membranes may not develop fully. The brain cells affected by PVL are unstable and vulnerable. The expert evidence suggested that the damage to the affected areas of the brain caused by PVL occurs during delivery or in the first few days following birth.

[18] Babies born before 34 weeks gestation are more prone to PVL than other babies. PVL is the most common cause of brain injuries suffered by premature babies.

[19] PVL is associated with the later onset of CP. The descending nerve tracts to the legs and arms pass through the area of the brain adversely affected by PVL.

[20] PVL may be caused by hypoxia, that is reduced oxygen in the blood flow circulating to the affected area of the brain, or ischemia, that is a deficiency in the blood supply to the affected area of the brain due to reduced blood pressure. Either hypoxia or ischemia results in the death of brain cells in the affected area of the brain. The twins’ PVL was likely caused by ischemia.

V

the causation question

[21] The causation issue at trial turned on whether the plaintiffs could establish a causal link between the twins’ CP and the failure to give Mrs. Goodman a full course of antenatal corticosteroids (“ACS”) prior to the twins’ delivery. The defence accepted that had Dr. Viljoen seen Mrs. Goodman on August 16 or sent her to the hospital, as the trial judge found he should have, Mrs. Goodman would have received a course of ACS consisting of at least two doses on August 16. Instead, because Mrs. Goodman was not seen by a doctor until August 18, she received only a single dose of ACS about two or three hours before delivery.

[22] Full-term babies secrete a surge of hormones immediately before birth. The hormone surge accelerates the maturation process and assists in the transition by the fetus to life outside of the womb. Premature babies do not experience this hormone surge. ACS serve as a substitute for that surge and are given as a means of artificially maturing the fetus. ACS are administered to the mother and cross the placenta into the fetus. ACS induce the production of enzymes throughout the fetus within 24 to 48 hours of administration.

[23] A course of ACS has known short-term benefits for premature babies. Mothers at risk of giving birth to premature babies are now routinely given a course of ACS because of those recognized short-term benefits.

[24] There are also long-term benefits, sometimes associated with the short-term benefits. For example, a course of ACS reduces the risk of RDS during delivery. RDS is one of the most common problems faced by pre-term babies. RDS can lead to a variety of short- and long-term medical problems, including CP. To the extent that a course of ACS prevents a baby from developing RDS, it can be said that a course of ACS has both short- and long-term benefits for a premature baby.

[25] The trial judge described the causal question in these terms, at para. 47:

In order to succeed, the plaintiffs must establish that the failure to receive a full course of ACS materially affected the twins’ outcome. That is, they must establish that “but for” the failure to receive a full course of ACS, the twins would not have suffered from the conditions they now do, or that the severity of these afflictions would have been materially reduced.

[26] The trial judge also indicated, at para. 56, that although some of the evidence drew a distinction between the twins’ CP and any developmental delay experienced by them, she treated the two as one and the same for the purposes of the causation inquiry. I accept that approach.

VI

THE POSITIONS OF THE PARTIES on causation

[27] As often occurs in the medical malpractice litigation, the causation issue required the trial judge to assess the competing opinions of eminently qualified experts. All of the experts agreed that there were no clinical studies or any other form of direct scientific evidence showing a correlation between the administration of ACS to a mother prenatally and a reduction in the premature baby’s risk of developing PVL. The defence experts contended that the absence of any direct scientific proof of a cause and effect relationship was determinative. However, the plaintiffs’ experts testified that the necessary causal connection could be made on a balance of probabilities standard without the kind of evidence demanded by the scientific standard of proof.

(a) The Plaintiffs’ Experts

[28] The plaintiffs advanced their causation case primarily through the evidence of Dr. Perlman, a neonatologist and pediatrician, and Dr. Barrett, an obstetrician and maternal fetal medicine specialist. I do not propose to distinguish between the evidence of the two except to make one point. Dr. Barrett did not base his opinion on any causal connection between the failure to administer ACS and the development of PVL. In his opinion, there was a causal connection between the failure to administer ACS and the later development of CP regardless of the immediate medical cause of the CP.

[29] The plaintiffs’ experts opined that had Mrs. Goodman received a course of ACS on August 16, two days before the twins were born, it was more likely than not that the twins would not have developed CP, or alternatively, that their disabilities from CP would have been less severe. In advancing this opinion, the experts relied principally on what one of them called “biological plausibility” and on the results of a study referred to at the trial as the Cochrane analysis.

[30] The “biological plausibility” thesis is built on two accepted medical facts:

• a course of ACS has well-recognized positive short-term effects on prenatal babies, such as reducing RDS; and

• steroids have a general maturing effect on tissues and membranes in the fetus.

[31] The plaintiffs’ experts testified that from these established facts it could be inferred that a course of ACS would assist in the maturation of the membranes in the arteries located in the watershed zone of the premature baby’s brain. It was equally reasonable to infer that this enhanced maturation would eliminate, or at least materially reduce, both the risk of and the severity of PVL.

[32] The plaintiffs’ experts further testified that the data analyzed by the Cochrane analysis supported the inferences suggested by the “biological plausibility” line of reasoning. The experts testified that while the data did not reach the level of statistical significance, it did show a strong trend suggesting that a course of ACS reduced the risk of the development of CP in premature babies. The experts opined that the data added force to the inferences to be drawn from the “biological plausibility” line of reasoning.

[33] The plaintiffs’ experts found support for their “biological plausibility” thesis in the evidence showing that ACS had a maturation effect on tissues in various parts of the fetus, including the lungs and intestines. The maturation process reduced the risk of certain conditions associated with the later development of CP such as RDS. The plaintiffs’ experts reasoned that if ACS matured the membranes in the lungs and other parts of the fetus and therefore eliminated or reduced the problems associated with conditions that could lead to CP, there was no reason to think that ACS would not work in the same way in the parts of the brain adversely affected by PVL.

[34] The plaintiffs’ experts referred to various studies that, in their view, supported the “biological plausibility” approach. These included a study showing a positive effect between neonatal blood pressure and the administration of ACS. Precipitous drops in blood pressure are one of the causes of PVL. There were also studies showing a correlation between the administration of ACS and the reduction in the risk of cystic periventricular leukomalacia, a different kind of leukomalacia than that suffered by the twins. Lastly, there was an animal study showing a positive correlation between fetal brain development and the administration prenatally of ACS to the mother.

[35] The Cochrane analysis, the second basis on which the plaintiffs’ experts advance their opinion, involved a review of 21 controlled studies that examined over 3,800 women and some 4,269 pre-term infants. The five studies relevant to the effect of ACS on CP involved 904 children, 48 of whom developed CP. Of those 48, 20 mothers had received a prenatal course of ACS and 28 had not.

[36] The Cochrane analysis reported a 40 per cent reduction in the risk of CP 93.5 per cent of the time through the administration of a course of ACS. This result was not statistically significant for scientific purposes. Scientists will draw a cause and effect relationship only when a result follows at least 95 per cent of the time. The results reported in the Cochrane analysis fell just below that standard.

[37] The plaintiffs’ experts, while accepting that the results were not statistically significant, testified that because the correlation was so close to the standard of statistical significance, it supported the existence of a causal connection between the administration of a course of ACS prenatally and the reduction in the risk of the subsequent development by the baby of CP. The plaintiffs’ experts further testified that the results examined in the Cochrane analysis probably understated the beneficial effects of ACS since the data did not take into account those babies who developed CP, but suffered significantly fewer disabilities because their mothers had received a course of ACS. According to the plaintiffs’ experts, one could safely assume that in a certain number of cases in which ACS did not prevent the development of CP, it did reduce the severity of the disabilities associated with the disease.

[38] The plaintiffs’ experts also testified that if the data produced by the Cochrane analysis were analyzed using a statistical approach described as the Bayesian analysis, the result did show a statistically significant correlation between the administration of ACS and the incidence of CP. Bayesian analysis was an accepted statistical approach, although it was not typically used to determine whether a causal relationship existed between the two events. The plaintiffs’ experts maintained that the Bayesian analysis was appropriate in this case because of the acknowledged short-term beneficial effects of ACS.

(b) The defence experts

[39] The defence position on causation came primarily from Dr. Hellmann, a neonatologist, and Dr. Farine, an expert in fetal medicine. I will not distinguish between the evidence of the two in my summary of their evidence.

[40] The defence argued that as the twins’ CP was known to have been caused by PVL, a causal connection between PVL and the failure to administer ACS had to be established. The defence experts maintained that one could not demonstrate a causal relationship between the twins’ CP and the failure to administer ACS by showing a general relationship between the failure to administer ACS and the development of CP. The defence experts contended that the focus had to be on the specific medical cause of the twins’ CP.

[41] The defence experts testified that the scientific literature established a causal connection between the administration of a course of ACS prenatally and the reduction in the risk of certain medical conditions associated with the later development of CP such as RDS and IVH. However, no such evidence existed indicating that a course of ACS would reduce the risk that premature babies would develop PVL.

[42] The defence experts rejected the “biological plausibility” argument as simplistic, not plausible, and unsupported by the relevant science. They explained that steroids were powerful drugs with both positive and negative effects for those who received them. The manner in which steroids worked varied within the body and even within the same organ. The impact of steroids on brain cell development was particularly uncertain. One defence expert summarized his assessment of “biological plausibility” in this way:

We know that steroids have very different effects on different organs and we, even within the same organ they can have different effects. So, in one area they may damp down an inflammatory response and in another might inhibit growth, so it’s, it’s really, it’s, it’s hugely complex to, to, just to distil it down to one effect in one other organ system and apply it to another and say therefore this is the mechanism, I, I, I don’t find that critical.

[43] The defence experts did not accept that the data from the Cochrane analysis demonstrated any causal connection between the failure to administer a course of ACS and the development of CP in the twins. They opined that the Cochrane analysis reported a “trend” and not a correlation. In their assessment, because the data did not reach the level of statistical significance, the results contradicted rather than supported the claim that there was a causal connection between the failure to administer ACS and the incidence of CP.

[44] The defence experts also testified that whatever the data gathered by the Cochrane analysis might say about the administration of ACS and the development of CP in a general sense, it said nothing about any connection between the administration of ACS and the development of PVL. The Cochrane analysis did not look to the medical causes underlying the development of CP in the 48 babies who had developed CP in the studies reviewed by the Cochrane analysis. That data provided no insight into the connection, if any, between the administration of ACS and the risk of developing PVL.

[45] The defence experts were critical of some of the studies underlying the Cochrane analysis. They testified that the authors of the Cochrane analysis stressed that further information was needed before any conclusions could be drawn concerning the effect of the administration of ACS in twin pregnancies.

[46] The defence experts also referred to a second study (the “Foix study”) that reported the long-term outcome of some 1,781 premature babies. That study also failed to demonstrate any statistically significant correlation between the administration of a course of ACS and the development of CP. It did show a tendency toward the reduction of the risk of CP in premature babies born between 28 and 32 weeks. That reduction, about 25 per cent, was not statistically significant. Like the Cochrane analysis, this study did not distinguish among the various underlying medical causes of CP.

[47] Lastly, the defence experts observed that neither the Cochrane analysis, nor any other scientific literature offered any support for the “assumption” that even when a premature baby developed CP, a prenatal course of ACS would materially reduce the severity of that baby’s disabilities. The Cochrane analysis simply reported the diagnosis of CP in 48 cases. It made no attempt to describe the extent of the disabilities suffered by any of the 48 babies who developed CP. No comparison could be made between the degree of disability suffered by the 20 babies who developed CP even though the mothers had received a course of ACS and the degree of severity of the CP developed by the 28 babies whose mothers had not received a course of ACS.

VII

the trial judge’s analysis

[48] The trial judge began her reasons by reference to the relevant causation principles: at paras. 10-12. After reviewing the case law and some of the academic literature, the trial judge correctly identified the “but for” requirement as the appropriate test for causation: at para. 167-75. She wrote at paras. 174-75:

The present scenario involves the tortious act of one individual, Dr. Viljoen. While there may be other non tortious “causes” of the injuries to the twins, there is no proverbial second shooter, nor is there an intervening third party. Likewise although there is arguably a lack of scientific evidence as to the cause of the PVL, this lack of scientific evidence does not produce the situation of “circular causation” with regard to the tortious causes that would be required to open the door to the material contribution test.

Accordingly, in order to succeed, the plaintiffs must prove, on a balance of probabilities, that but for Dr. Viljoen’s negligence, the Goodman twins would not have suffered the injuries they did or the magnitude of those injuries would have been reduced. [Emphasis added.]

[49] Having set the legal backdrop and identified the burden of proof, the trial judge turned to the evidence and her findings of that evidence. She ultimately found that the plaintiffs had established causation in two ways. First, they had established a causal connection between PVL and the failure to administer ACS, and second, they had established a causal connection between the plaintiffs’ CP and the failure to administer ACS prenatally regardless of the immediate medical cause of the twins’ CP. Either finding was sufficient to establish legal causation.

[50] The trial judge dealt first with the plaintiffs’ assertion that the failure to provide a course of ACS caused the plaintiffs’ PVL. She described the “root cause” of PVL as premature birth: at para. 181. She next observed that there was “no direct scientific evidence” that a course of ACS would reduce the risk that a premature baby would develop PVL: at para. 182. Nor, the trial judge pointed out, was there any scientific evidence that there was no connection between the use of ACS prenatally and the incidence of PVL in premature babies: at paras. 182-83, 187.

[51] The trial judge’s finding on the causation issue as it relates to PVL is found at para. 188:

On the totality of the evidence before me, it is reasonable to infer that since PVL results from the immaturity of the pre-term infant’s brain and vascular system, and ACS have a maturational effect beyond lung function to mature these systems, that it is more likely than not that the administration of ACS would reduce the risk of PVL. Thus, but for the defendant’s negligence, the twins would not have suffered from PVL, and consequently would not have suffered from CP. [Emphasis added.]

[52] In finding a causal connection between the administration of ACS and the development of PVL, the trial judge preferred the evidence of the plaintiffs’ experts. She accepted and relied heavily on the “biological plausibility” approach advanced by the plaintiffs’ experts to support her finding that a course of ACS would have materially reduced the risk of PVL: at paras. 184-87.

[53] Having found a causal connection between the administration of ACS and the development of PVL, the trial judge turned to the alternative basis for her causation finding. She introduced that finding at para. 189:

Even if I am incorrect in my conclusion that the PVL (and therefore the CP) would not have occurred but for the failure to receive a full course of ACS, this is not fatal to the plaintiffs’ claim. I am satisfied that the evidence before me establishes on a balance of probabilities that ACS reduce the risk and severity of CP in general, that is, no matter what the cause of the CP. [Emphasis added.]

[54] In concluding that the evidence showed that a course of ACS reduced the risk and severity of CP regardless of the medical cause, the trial judge relied heavily on the interpretation of the Cochrane analysis data offered by the plaintiffs’ experts, particularly Dr. Barrett, who did not regard the presence of PVL as relevant to his analysis. The trial judge rejected the argument that she could not rely on the data because it did not reach the level of statistical significance: at paras. 192, 198. In her view, the data could support a finding of causation based on the balance of probabilities. She also accepted the evidence that the statistical significance of the data was more properly analyzed using the Bayesian approach: at paras. 199-203.

[55] The trial judge rejected the defendant’s contention that the Cochrane analysis, put at its best from the plaintiffs’ perspective, showed only a 40 per cent reduction in the risk of CP and could not establish a causal link on the balance of probabilities: at paras. 193-96. In the trial judge’s assessment, the Cochrane data underreported the beneficial effects of ACS because it did not take into account those cases in which babies whose mothers had received ACS had developed CP, but with significantly less serious disabilities than they would have had their mothers not received a course of ACS: at para. 195. After noting that the disabilities associated with CP occurred over a broad spectrum, the trial judge accepted the evidence of the plaintiffs’ experts that it only made common sense that a course of ACS would moderate the severity of CP in at least some of those cases in which it did not prevent CP: at para. 195.

[56] The trial judge also observed that the 40 per cent figure reported in the Cochrane analysis had to be placed in the context of the clinical experiences of the plaintiffs’ experts: at paras. 206-7. She held that their testimony, in particular the “biological plausibility” explanation, enhanced the causal relationship picture painted by the Cochrane analysis data: at para. 207.

[57] The trial judge concluded her analysis of the claim that there was a causal link between a course of ACS and the risk of CP without regard to the medical cause of the CP with this finding, at para. 207:

Both Drs. Barrett and Perlman, exercising their clinical judgment and expertise, considering the statistical evidence, answered unequivocally that it is more likely than not that had the twins received a full course of steroids, they would not have suffered the injuries they did, or the magnitude of those injuries would have been reduced. I agree with this conclusion. It is supported by the statistical and medical evidence and the common sense inferences that flow therefrom. I, therefore, find that the plaintiffs have established on a balance of probabilities that the defendant’s negligence caused the CP from which they now suffer.

VIII

the appellant’s submissions

[58] Mr. Curry, in his able submissions for the appellant, challenges both routes taken to causation by the trial judge. He alleges legal errors and material misapprehensions of important evidence. Counsel further submits that the trial judge’s factual findings underlying her causation determination cannot be supported on any reasonable view of the evidence.

[59] To succeed on the appeal, the appellant must show that both routes to causation taken by the trial judge are fatally flawed. I will begin with the trial judge’s alternative finding that the evidence demonstrated that a course of ACS would reduce the risk and severity of CP regardless of the underlying medical cause.

(a) Did the trial judge err in holding that ACS reduce the risk and severity of CP regardless of the immediate medical cause of the CP?

[60] Counsel for the appellant submits that the trial judge erred in law in holding that the plaintiffs could succeed without showing a causal relationship between the administration of ACS and the risk of PVL. Counsel contends that the trial judge, having found that the twins’ CP was caused by PVL, erred in law in holding that “[p]roof of [c]ausation of PVL is [n]ot [r]equired”. Counsel submits that if the administration of ACS did not prevent PVL, then the twins’ CP would not have been avoided regardless of the effect of the administration of ACS on any other underlying cause of CP. The plaintiffs were thus required to establish a causal link between the administration of ACS and the development of PVL since PVL was the immediate medical cause of the twins’ CP.

[61] I agree that the plaintiffs had to show a causal connection between PVL and the failure to administer a course of antenatal ACS. I also agree that parts of the trial judge’s reasons, read in isolation, suggest that her alternative basis for finding causation was made without finding a causal link between the failure to administer ACS and the twins’ PVL.

[62] I think a fair reading of the entirety of her reasons, however, supports a different interpretation. In approaching the alternative causation finding, the trial judge did not depart from her earlier finding that PVL was the medical cause of the twins’ CP. She did not, however, look for a specific causal link between PVL and ACS, but instead looked for a link between ACS and CP in premature infants. On this approach to causation, the trial judge still found that the failure to administer a course of ACS was causative of the twins’ PVL. However, she reached that conclusion on the basis of evidence which, in her view, supported the inference that the failure to administer ACS was causative of CP in premature infants regardless of the specific immediate medical cause. I see no legal error in this approach to the causation question raised in this case, assuming that the evidence supported the inference that a course of ACS would materially reduce the risk of CP, regardless of the cause.

[63] Counsel for the appellant next submits that the trial judge misapprehended the evidence in arriving at her conclusion that the failure to administer ACS was causative of CP regardless of the immediate medical cause. Counsel for the appellant refers to para. 210 of the trial judge’s reasons where she states:

It was the uncontested testimony of Dr. Barrett that 80% of CP in all gestations have no associated infection, RDS or IVH (those being conditions upon which ACS have a recognized effect). This being the case, it defies common sense that the 40% reduction of CP in its entirety (shown in the Cochrane analysis) would be attributable solely to the aforementioned causes, which account for only a small percentage of all CP cases. As such, and notwithstanding my conclusion that PVL would not have occurred but for the defendant’s negligence, I have little difficulty finding that proof of that conclusion is not required for the plaintiffs to succeed.

[64] As the trial judge indicates, Dr. Barrett, who provided the 80 per cent figure, testified that the figure applied to all babies who developed CP, not just premature babies. Dr. Barrett expressly testified that he could not say whether the 80 per cent figure had any application to premature babies or to twins. The distinction between all babies and premature babies is potentially important in the context of the medical causes of CP since premature babies are known to suffer from various conditions that have an established causative connection to the later development of CP, such as RDS.

[65] The trial judge accepted Dr. Barrett’s 80 per cent figure. She also applied it to premature babies despite Dr. Barrett’s evidence that he could not say it had any such application. The trial judge was clearly entitled to accept Dr. Barrett’s evidence. She was not, however, entitled to treat it as applicable to premature babies such as the twins. The trial judge’s misapprehension of Dr. Barrett’s evidence was central to her finding that the failure to provide a course of ACS was causative of CP regardless of the specific medical cause.

[66] Apart from the misapprehension of the evidence, as a matter of logic, I do not see how the inference can be drawn that because there is an overall 40 per cent reduction in the risk of CP, and the specific medical cause of CP is known in only 20 per cent of cases, all of which respond positively to ACS, it must follow that a course of ACS reduces the risk of CP regardless of the medical cause. Just as it defies common sense to attribute the entirety of the 40 per cent reduction of CP to those 20 per cent of cases in which the cause of CP is known, it is equally untenable to suggest that ACS must reduce the risk of CP regardless of the medical cause. To me, this data suggests only that a course of ACS has a positive effect in some cases where the medical cause of CP is unknown. As a matter of logic, it does not automatically follow that the administration of ACS will reduce the risk of CP no matter the cause. There may be unknown causes that do not respond to ACS.

[67] The trial judge’s logic is all the more untenable when one bears in mind that the 40 per cent figure comes from the Cochrane analysis’ review of 48 cases in which premature babies developed CP. That review does not address the medical cause of CP in any of the 48 cases. Nor does it indicate whether the cause was known or unknown. Without that information, an analysis of the data from those 48 cases could not support the inference that a course of ACS reduces the risk of CP regardless of the underlying medical cause. For example, it may be that none of the 48 cases involved PVL. How could any reasonable conclusion be drawn about a causal connection between a course of ACS and CP caused by PVL from a review of 48 cases, none of which involved PVL? Similarly, it may be that all 48 cases involved conditions like RDS that are known to both cause CP and to be amenable to a prenatal course of ACS. How could data from those cases tell one anything about the value of ACS in reducing the risk of CP when the immediate medical cause of the CP had not been shown to be amenable to a treatment of ACS?

[68] Ignoring the inapplicability of the 80 per cent figure to premature babies, I think the most that could be said about the figures quoted by the trial judge is that they suggest that a course of ACS has value in cases other than those cases in which a link has been established between ACS and the immediate medical cause of the CP. That finding, however, is a long way from a finding that a course of ACS reduces the risk and severity of CP regardless of the immediate medical cause of the CP. The finding is further still from a finding that the twins’ CP was caused by the failure to administer a course of ACS prenatally. The evidence at trial does not support the trial judge’s alternative finding of causation.

(b) Did the trial judge err in finding that the failure to administer a course of ACS caused the twins’ PVL?

[69] As I would hold that the trial judge’s alternative basis for finding causation cannot stand, the outcome of this appeal turns on the sustainability of her finding that the failure to administer a course of ACS was causative of the twins’ PVL and therefore causative of their later development of CP. As described above, the trial judge was satisfied that it was more likely than not that the twins would not have suffered PVL or alternatively that the disabilities related to the CP caused by the PVL would have been materially reduced had Mrs. Goodman received a prenatal course of ACS. Counsel for the appellant challenges this finding on several grounds.

(i) Did the trial judge wrongly take a “robust and pragmatic” approach to the evidence relevant to causation?

[70] Counsel for the appellant submits that because the defence led evidence to contradict the plaintiffs’ causation evidence, the trial judge erred in taking a robust and pragmatic approach to the evidence of causation. That proposition finds some support in Ediger v. Johnston, 2011 BCCA 253, 333 D.L.R. (4th) 633, at paras. 83-85, leave to appeal to S.C.C. granted, [2011] S.C.C.A. No. 371.

[71] The appellant’s contention does not, however, find support in the case law from the Supreme Court of Canada or this court: see Snell v. Farrell, 1990 CanLII 70 (SCC), [1990] 2 S.C.R. 311, at p. 330; Clements v. Clements, 2012 SCC 32, 346 D.L.R. (4th) 577, at para. 46; Fisher v. Atack, 2008 ONCA 759, 242 O.A.C. 164, at paras. 54-59, leave to appeal to S.C.C. refused, [2009] S.C.C.A. No. 14; Aristorenas v. Comcare Health Services (2006), 2006 CanLII 33850 (ON CA), 83 O.R. (3d) 282 (C.A.), at paras. 54-61, leave to appeal to S.C.C. refused, [2006] S.C.C.A. No. 487.

[72] In Snell, at p. 330, in the exact passage relied on by the appellant, Sopinka J. makes it clear that the robust and pragmatic approach to evidence of causation applies when the defence leads evidence to contradict the plaintiffs’ causation theory:

The legal or ultimate burden remains with the plaintiff, but in the absence of evidence to the contrary adduced by the defendant, an inference of causation may be drawn although positive or scientific proof of causation has not been adduced. If some evidence to the contrary is adduced by the defendant, the trial judge is entitled to take account of Lord Mansfield’s famous precept. This is, I believe, what Lord Bridge had in mind in Wilsher when he referred to a “robust and pragmatic approach to the ... facts” (p. 569). [Emphasis added.]

[73] The first sentence of the above-quoted passage speaks to the drawing of an inference of causation in the absence of positive evidence of causation from the plaintiff, and the absence of any evidence from the defendant. The second sentence speaks to the approach to be taken to the evidence when there is conflicting evidence from the defence. Sopinka J. applies the “robust and pragmatic approach” to cases in which the defence has led evidence.

[74] Whatever controversy there may have been in the case law was put to rest in Clements. The Chief Justice, in the course of summarizing the present law of causation in Canada, stated, at para. 46:

As a general rule, a plaintiff cannot succeed unless she shows as a matter of fact that she would not have suffered the loss “but for” the negligent act or acts of the defendant. A trial judge is to take a robust and pragmatic approach to determining if a plaintiff has established that the defendant’s negligence caused her loss. Scientific proof of causation is not required.

[75] Nothing in the Chief Justice’s summary suggests that a different approach is to be taken to the evidence when the defence calls evidence relevant to causation.

[76] The robust and pragmatic approach describes the manner in which evidence is to be evaluated, not some special burden of proof: see Aristorenas, at para. 56. The robust and pragmatic approach takes into account the nature of the factual issues underlying the causation question and the kind of evidence that the parties are reasonably capable of producing on those issues. The approach acknowledges that the causation inquiry is essentially a practical one based on the entirety of the evidence and made with a view to determining whether the plaintiff has established causation on the balance of probabilities and not to a scientific certainty. Clearly, as counsel for the appellant urges, the robust and pragmatic approach does not countenance speculation or resort to common sense to determine issues that require expert knowledge. To resort to speculation or the misuse of common sense is to misapply the robust and pragmatic approach.

[77] The trial judge made no error in taking a robust and pragmatic approach in her evaluation of the evidence relevant to causation.

(ii) Did the trial judge reverse the burden of proof?

[78] The trial judge on several occasions in her reasons indicated that the plaintiffs carried the burden of proof. For example, at para. 175 she stated:

Accordingly, in order to succeed, the plaintiffs must prove, on a balance of probabilities, that but for Dr. Viljoen’s negligence, the Goodman twins would not have suffered the injuries they did or the magnitude of those injuries would have been reduced.

[79] The trial judge’s analysis of the evidence and her factual findings flowing from that analysis do not suggest any reversal of the burden of proof. The two references in her reasons relied on by the appellant do not offer support for the contention that the trial judge reversed the burden of proof.

[80] The first reference in the trial judge’s reasons, at para. 183, is merely an observation on the evidence. The trial judge noted that the defence did not lead scientific evidence to show that ACS did not affect PVL. The observation was correct and, in making that observation, the trial judge did not suggest that the defence carried any legal burden to produce that kind of evidence.

[81] The second reference in the trial judge’s reasons, at para. 198, is no more than a statement of the non-contentious proposition that a finding of legal causation based on a balance of probabilities standard is not to be equated with a finding of causation measured against a scientifically acceptable standard of proof.

[82] The trial judge did not reverse the burden of proof.

(iii) Did the trial judge err in accepting the plaintiffs’ interpretation of the Cochrane analysis data?

[83] Counsel submits that the trend evinced by the data in the Cochrane analysis could not assist the trial judge in her fact-finding because that evidence did not reach the level of statistical significance demanded by a scientific inquiry into causation. Counsel puts it this way in his factum:

Where a scientific effect is not shown to a level of statistical significance, it is not proven.

[84] I take counsel to be arguing that proof of a causal relationship between a course of ACS and a reduction in the risk of PVL amounted to a “scientific effect”, and that proof of that relationship, even in the context of attempting to establish causation on the balance of probabilities, requires proof that meets the level of statistical significance. The trial judge rejected this submission: at paras. 192, 198. So do I. Legal causation is about proof of a cause and effect relationship on the balance of probabilities. Scientific proof of causation imposes a much more exacting standard: see Laferrière v. Lawson, 1991 CanLII 87 (SCC), [1991] 1 S.C.R. 541, at pp. 606-7, 608-9.

[85] Scientific evidence is often only part of the causation picture painted at trial. Scientific evidence revealing a trend suggestive of a causal connection between fact A and fact B is not discarded at trial because it does not reach the level of scientific proof. Instead, that evidence is considered along with any other evidence that is relevant to the question of causation. The trial judge’s consideration is of course informed by and directed at the requirement that the plaintiffs prove the causal link on the balance of probabilities.

[86] The trial judge had opposing expert opinions as to the value of the data in the Cochrane analysis on the question of causation. It was her responsibility to sort through that evidence. She did so and, in my view, made no error in accepting the evidence of the plaintiffs’ experts that the data suggested a connection between ACS and CP that could assist in determining whether the plaintiffs had established causation according to the legal test for causation.

(iv) Did the trial judge err in accepting the plaintiffs’ “biological plausibility” theory?

[87] The appellant contends that the trial judge erred in accepting the “biological plausibility” theory advanced by the plaintiffs’ experts. In essence, counsel argues that the phrase “biological plausibility” described nothing more than speculation unsupported by any real scientific proof.

[88] This argument echoes the testimony given by the defence experts at trial. The trial judge, however, rejected their evidence in favour of the evidence advanced by the plaintiffs’ experts. Her reasons demonstrate that she fully appreciated the competing evidence given by the experts on this issue.

[89] I do not accept the argument that the plaintiffs’ experts went beyond the scope of their expertise in advancing the “biological plausibility” explanation. The “biological plausibility” explanation advanced so convincingly by Mr. Rogers, counsel for the plaintiffs at trial and on this appeal, involved the experts drawing inferences based on their specialized knowledge about steroids, the recognized short-term benefits to premature babies provided by a prenatal course of steroids, and the reaction of various body tissues in a fetus to a prenatal course of steroids prior to delivery. The experts pointed to support for their “biological plausibility” theory in the kinds of sources customarily referred to by medical experts to support their opinions. Clearly, the force of the “biological plausibility” explanation suffered because there were no specific studies to support the inferences that the plaintiffs’ experts drew. The absence of that kind of evidence does not, however, make the inferences drawn by the plaintiffs’ experts speculation. At most, it weakens the force of those inferences.

[90] The plaintiffs’ experts testified that, based on what they knew about steroids and how they worked in pre-term babies, certain inferences could be drawn about the operation of a course of ACS in relation to the specific part of the fetal brain affected by PVL. Accepting that the defence experts demonstrated that the inferences drawn by the plaintiffs’ experts were certainly debatable in the absence of any supporting scientific studies, I do not think that the evidence of the defence experts rendered the trial judge’s decision to accept the view of the plaintiffs’ experts on this matter unreasonable. That was a decision for the trial judge to make.

(v) Was the trial judge’s finding that it was more likely than not that the twins would not have developed PVL had Mrs. Goodman received a course of ACS unreasonable?

[91] This submission assumes that the trial judge was entitled to accept that the “biological plausibility” theory and the data from the Cochrane analysis demonstrating a trend in the reduction of CP following the administration of a prenatal course of ACS were sufficient to show a connection between the administration of ACS and a reduction in the risk of developing PVL and later CP. This submission proceeds from the premise that the evidence can be read as going so far as to indicate that the twins would have had a better chance of not developing PVL had Mrs. Goodman received a prenatal course of ACS.

[92] Counsel contends, however, that even if the evidence goes that far, it still does not establish causation in the relevant sense. Counsel argues that there is no evidence quantifying the potential reduction in the risk to the twins. He submits that absent evidence of quantification, the trial judge could not properly find that it was more likely than not that the twins would not have developed PVL and consequently CP had Mrs. Goodman received ACS. Counsel relies on the well-established authority to the effect that evidence of a possibility short of a probability, sometimes referred to as a chance, does not establish causation for the purposes of tort law: see Cottrelle v. Gerrard (2003), 2003 CanLII 50091 (ON CA), 67 O.R. (3d) 737 (C.A.), at paras. 23-26, leave to appeal to S.C.C. refused, [2003] S.C.C.A. No. 549.

[93] In the course of the part of her reasons in which the trial judge analyzed the evidence leading to her conclusion that the failure to administer a course of ACS had caused the twins to develop PVL which led to CP, the trial judge did not distinguish between a finding that ACS would reduce the risk of PVL and the finding that the failure to administer ACS had caused the PVL. I repeat her finding, at para. 188:

On the totality of the evidence before me, it is reasonable to infer that since PVL results from the immaturity of the pre-term infant’s brain and vascular system, and ACS have a maturational effect beyond lung function to mature these systems, that it is more likely than not that the administration of ACS would reduce the risk of PVL. Thus, but for the defendant’s negligence, the twins would not have suffered from PVL, and consequently would not have suffered from CP. [Emphasis added.]

[94] The above passage is the linchpin of the trial judge’s analysis of the causal connection between a course of ACS and the development of PVL. The trial judge expressly moves directly from a finding that the risk of PVL would be reduced by a course of ACS to the further finding that the twins would not have suffered from PVL that eventually caused their CP had they received a course of ACS. The latter does not follow from the former. A reduction in the risk of disease “A” brought about the administration of drug “B” does not mean that the failure to administer drug “B” caused disease “A” to occur.

[95] The trial judge’s finding that a course of ACS reduced the risk of PVL was based almost entirely on her acceptance of the plaintiffs’ “biological plausibility” theory. I agree that the “biological plausibility” theory could support an inference that a course of ACS would reduce the risk of PVL. That evidence could not, however, assist in quantifying the extent of any reduction of the risk and could not establish that the risk would be reduced to the point where it could be said that the failure to administer a course of ACS probably caused the twins’ PVL.

[96] Without evidence quantifying the reduction in the risk of PVL, the trial judge could not bridge the gap between a finding of a reduced risk and the finding that the twins would not have developed PVL had Mrs. Goodman received a course of ACS. That evidentiary gap made it impossible to reasonably conclude that the plaintiffs had established a causal connection between the failure to administer ACS and the twins’ PVL.

[97] Not only did the trial judge not refer to any evidence capable of quantifying the reduction in the risk of PVL, I do not think there was any such evidence. Dr. Barrett’s evidence could not assist on this point as he treated the twins’ PVL as irrelevant to the causation inquiry. Dr. Perlman relied on the data in the Cochrane analysis. As that data did not identify the medical causes of the CP in any of the 48 cases referred to in the analysis, I do not think it could assist in quantifying any relationship between the failure to administer ACS and the reduction in the risk of developing PVL.

[98] In my view, the absence of any evidence capable of quantifying the reduced risk of PVL flowing from a course of ACS precluded a finding that the failure to administer ACS caused the twins’ PVL which in turn caused their CP. That was the primary basis on which the trial judge found causation.

[99] The trial judge did address the quantification of the reduction of the risk of developing CP in the context of her alternative finding of causation based on her determination that the data in the Cochrane analysis established that the risk of CP would be reduced regardless of the specific medical cause of the CP. That analysis cannot remedy the trial judge’s failure to address the quantification of the risk in the context of her finding that the failure to administer a course of ACS caused the twins’ PVL. Nor can it salvage her finding that the CP was caused by the failure to administer ACS regardless of its immediate medical cause. I have already explained, at paras. 63-68, why in my view that finding is unsupported by the evidence. For the sake of completeness, however, I will address this aspect of her reasons.

[100] The trial judge accepted that the Cochrane analysis data established that a course of ACS would reduce the risk of CP in premature babies by 40 per cent. The trial judge also recognized that a 40 per cent reduction in the risk would not establish legal causation. She then went on to hold that the Cochrane analysis data did not identify those cases in which babies who had developed CP, even though their mothers had received a course of ACS, had developed significantly less severe disabilities than those babies who had developed CP and whose mothers had not received a course of ACS. In the trial judge’s assessment, this category of babies who were less seriously handicapped was sufficiently large to inflate the effect of the impact of ACS on CP beyond the 40 per cent reduction in CP. According to the trial judge, many babies who developed CP would be less seriously handicapped because of the administration of ACS to the mother prenatally. The cumulative effect of the two categories, that is babies who did not suffer CP and babies whose disabilities were significantly lessened, was sufficiently large to reach the required legal threshold of a balance of probabilities.

[101] The Cochrane analysis in fact provided no evidence that a course of ACS had any effect on the severity of the symptoms of those babies who developed CP. The Cochrane analysis did not describe the level of disability of any of the 48 babies referred to in the studies it considered. Clearly, the Cochrane analysis made no attempt to compare the level of disability among the 28 babies whose mothers had not received ACS with the level of disabilities among the 20 babies who had developed CP despite the fact that their mothers had received a course of ACS.

[102] Although the Cochrane analysis data itself could offer no support for the assertion that a course of ACS would reduce the severity of the disabilities suffered by babies who developed CP, the plaintiffs’ experts, applying I think the “biological plausibility” explanation, had testified that it only made common sense that if a course of ACS eliminated CP in 40 per cent of the cases, it would reduce the severity of the disabilities flowing from CP in some unspecified number of other cases. The plaintiffs’ experts acknowledged that the reduction in the severity of symptoms associated with CP in babies who had received a course of ACS had never been studied much less reported in the scientific literature.

[103] Although the evidence to support the reduced severity contention is far from strong, I think it was open to the trial judge to accept that evidence. In my view, however, it did not get the plaintiffs over their causation difficulties.

[104] The trial judge began her causation analysis by accepting that the Cochrane analysis data showed a 40 per cent reduction in the occurrence of CP when the mothers had received a course of ACS. She then placed on top of that 40 per cent an additional unquantified number of cases in which the severity of the disabilities suffered by the babies had been materially reduced. The two combined met the balance of probabilities standard.

[105] For reasons set out above, the Cochrane analysis data cannot reasonably support a finding that a course of ACS would reduce by 40 per cent the risk that a premature baby would develop CP regardless of the underlying medical cause of the CP. The data goes no further than to suggest that a course of ACS may reduce the risk of CP in cases other than those in which a connection has been shown between the underlying medical cause of CP and a course of ACS. The quantification of that reduction in premature babies at 40 per cent, the trial judge’s starting point in her causation calculus, has no basis in the evidence.

[106] Putting the causation case at its best for the plaintiffs, there was evidence suggesting that a course of ACS would reduce the risk that premature babies would develop CP in an unspecified number of cases. There was also evidence that in an unspecified number of cases, a course of ACS may have a positive effect on the seriousness of the disabilities suffered by babies who did develop CP. Placing these two unquantifiable amounts together could not demonstrate the requisite causal connection on the balance of probabilities. Pushing the evidence to the edge of its reasonableness limits does not provide a basis upon which the trial judge could reasonably find that it was more likely than not that the twins would not have suffered CP or that their disabilities associated with CP would have been significantly reduced had their mother received a full course of ACS prenatally.

IX

[107] For the reasons set out above, the causation finding cannot stand. I would allow the appeal, set aside the judgment below and dismiss the claim in its entirety.

[108] At the conclusion of oral argument, the parties agreed that costs of the appeal would be fixed at $40,000. Mr. Rogers, for the respondents, did indicate that some further submissions on cost-related matters may be necessary after the court’s disposition of the appeal was known. I would ask counsel to advise the Registrar within 14 days of the release of these reasons whether any further costs submissions are necessary. If no further submissions are necessary, I would award costs in the amount of $40,000, if demanded, to the appellant. If further submissions are needed, counsel should agree between themselves as to the terms of those further submissions, or, if necessary, arrange for a conference call with me.

“Doherty J.A.”

Feldman J.A.:

[109] I have had the benefit of reading the comprehensive reasons of Doherty J.A., who would allow the appeal and set aside the decision of the trial judge that found the appellant doctor liable to the respondents. I do not agree with my colleague’s conclusion. In my view, the trial judge made no reversible error of law, palpable and overriding error of fact or misapprehension of the evidence. I would defer to her decision and dismiss the appeal.

[110] As my colleague has fully set out the background, the relevant evidence and the issues, I propose to go directly to those issues and to explain why I disagree that the trial judge made any reversible error.

[111] The parties had agreed prior to trial on the quantum of damages. The trial judge having found that Mrs. Goodman, a patient of the appellant obstetrician, did call the appellant’s office on August 16, 1995 complaining of leaking fluid, it was also agreed that the appellant fell below the standard of care by failing to either see her or refer her to hospital. It was also undisputed that had she been seen by a doctor, she would have received two doses of steroids (antenatal corticosteroids or “ACS”) that day. Because she went to hospital on an emergency basis two days later when the twins were born, she only received one course of steroids, which was probably given so close to the time of the births as to be ineffective.

[112] The issue left was causation: whether “but for the failure to receive a full course of ACS, the twins would not have suffered from the conditions they now do, or that the severity of these afflictions would have been materially reduced”: Goodman v. Viljoen, 2011 ONSC 821, at para. 47.

[113] After setting out the evidence in detail, the trial judge turned to the legal issue regarding the applicable test for causation and determined that this was not a case where the “material contribution” test from the decision in Resurfice Corp. v. Hanke, 2007 SCC 7, [2007] 1 S.C.R. 333 could apply. She therefore applied the “but for” test, which meant that the onus was on the plaintiffs to prove on a balance of probabilities that “but for Dr. Viljoen’s negligence, the Goodman twins would not have suffered the injuries they did or the magnitude of those injuries would have been reduced.”

[114] The trial judge observed that her decision on the causation issue “is heavily dependent on the expert evidence”. She then made the critical finding that she preferred the opinions of the plaintiffs’ experts, Dr. Perlman and Dr. Barrett, to those of the defendant’s experts, Dr. Farine and Dr. Hellmann. And she gave reasons for that important conclusion.

[115] Although all four doctors held significant credentials, Dr. Barrett had special expertise in twin pregnancies. He was steadfast in his opinion, despite a vigorous and lengthy cross-examination, and he gave his evidence in a fair and impartial manner. In the trial judge’s view, Dr. Farine and Dr. Hellmann took a very dogmatic approach to the scientific literature. They completely dismissed the results of the Cochrane analysis because it did not reach the 95% level accepted as statistically significant. They did so even though almost all of the expert witnesses agreed that its meta-analysis on the effect of steroids on CP was the best available evidence and would remain so. This was because, for ethical reasons, no similar study could now be done with a control group that did not receive steroids given the known benefits of steroid treatment. Finally, Dr. Hellmann was very argumentative in cross-examination and reluctant to concede the smallest point. He also appeared not to be familiar with some of the literature that dealt with other effects of ACS.

[116] The trial judge then addressed the causation question in two alternative forms. The first was premised on the accepted fact that the twins’ CP was caused by PVL (periventricular leukomalacia). On that premise the trial judge formulated the causation question in the following way: “would the twins have suffered from the PVL but for the failure to receive a full course of ACS?” She began by noting that there was “no direct scientific evidence on the specific effect of ACS on PVL.”

[117] ACS are steroids that are routinely administered to mothers who are about to bear premature babies. The effect of the steroids is to replace the natural secretion of hormones that occurs in the days before birth in a full-term baby. These hormones induce the production of enzymes in the body which cause the fetus to quickly mature in anticipation of the transition to life outside the womb.

[118] A number of short-term benefits of the steroids were documented in a 1994 meta-analysis of a number of studies that looked at the effects of the administration of the steroids. The benefits included significant reduction in the incidence of respiratory distress syndrome (“RDS”); reduction in the incidence of periventricular hemorrage and necrotizing entercolitis; substantial reduction of neonatal morbidity; and possible protection against neurological abnormality. The study also showed a benefit in terms of decreases in ruptured membranes. It is damaged or immature membranes in the brain, inhibiting the control of blood supply there, that causes PVL.

[119] The Cochrane analysis, another meta-analysis on the benefits of steroids for pre-term babies, was published in 2006. It was republished in 2008. Dr. Perlman referred to its results as “state-of-the-art”. That study showed a “trend” that the steroids in question reduced CP by 40%. He explained that “trend” meant that the results did not meet the statistically significant standard of 95%, but that they came very close at 93.5%. He also stated that although the study looked only at subjects who developed CP versus those who did not, “one would assume” that even in the cases where CP developed, the steroids would have decreased the severity. This is because CP is defined in terms of a broad set of symptoms that are not all or nothing, but instead operate on a continuum.

[120] Dr. Perlman and Dr. Barrett both opined, and the trial judge accepted, that “ACS has a general maturational effect on all body organs”. Dr. Barrett testified that it is biologically plausible that corticosteroids stabilize all membranes including those in the brain and that steroids reduce the incidence of CP by stabilizing those membranes and preventing their disruption.

[121] The trial judge articulated her conclusion that the steroids would have prevented or materially reduced the negative effects of the PVL, at paras. 187-88, as follows:

[187] The defendant is correct in stating that none of the literature filed specifically found a connection between the use of ACS and PVL. However, using the robust and pragmatic approach to fact finding, logical inferences may be drawn from the many recognized [e]ffects of ACS and their effect on other organs and systems in humans and animals. This, in combination with the clinical judgment and experiences of Drs. Perlman and Barrett, leads me to conclude that the plaintiffs have made the case for causation.

[188] On the totality of the evidence before me, it is reasonable to infer that since PVL results from the immaturity of the pre-term infant’s brain and vascular system, and ACS have a maturational effect beyond lung function to mature these systems, that it is more likely than not that the administration of ACS would reduce the risk of PVL. Thus, but for the defendant’s negligence, the twins would not have suffered from PVL, and consequently would not have suffered from CP.

[122] This conclusion was attacked by the appellants on a number of bases. My colleague addresses each of these bases in turn, finding no merit in any but one of them. He concludes that the trial judge made no legal error: 1) in applying the robust and pragmatic approach to evaluating the evidence on causation; 2) on the burden of proof; 3) in accepting the plaintiffs’ experts’ interpretation and application of the Cochrane analysis to the causation question, despite the fact that it did not reach statistical significance; 4) in deciding to accept the plaintiff’s experts’ “biological plausibility" theory rather than rejecting it because there were no scientific studies to support their specific inferences. Although the absence of such studies weakened the force of their inferences, it did not make their inferences merely speculation.

[123] Although Doherty J.A. is therefore willing to accept that the trial judge was entitled to find that “the twins would have had a better chance of not developing PVL had Mrs. Goodman received a prenatal course of ACS”, his issue is with the trial judge’s finding that the reduction in risk amounted to causation. In his view, in order to prove causation the respondents had to be able to quantify that chance as over 50% to amount to proof on a balance of probabilities, and the experimental evidence did not go that far. At para. 98 of his reasons, Doherty J.A. states:

In my view, the absence of any evidence capable of quantifying the reduced risk of PVL flowing from a course of ACS precluded a finding that the failure to administer ACS caused the twins’ PVL which in turn caused their CP. That was the primary basis on which the trial judge found causation.

[124] I do not agree with my colleague that it was necessary for the court to have experimental evidence that quantified the reduction in risk of PVL. The court was entitled to accept the evidence of the experts who were satisfied that had the twins been administered the ACS, they either would not have suffered from CP or the severity of their symptoms would have been materially reduced. The experts were able to fill in the gaps in the scientific studies from their clinical experience, as Dr. Perlman stated in his cross-examination.[^1]

[125] The trial judge accepted the evidence of the respondent’s expert witnesses, Dr. Barrett and Dr. Perlman. Dr. Barrett did not look at the impact of steroids on any particular cause of CP but rather his view was that the correct approach was to look at the effect of steroids on CP generally. His clear opinion was that steroids would have either reduced or removed the impact of prematurity on these twins. I quote from two passages of his evidence. At p. 105/63, lines 4-13 and p. 108/66, lines 23-28 of the record in his examination in chief he stated:

[W]e know corticosteroids stabilize membranes, all membranes, whether there’s infection, whether there’s asphyxia, whatever, whatever the cause is, steroids stabilize membranes and it’s those membranes in the brain which break, which can breakdown and cause cerebral palsy. So, we know there’s a biological plausibility; we know there’s a short term outcome plausibility and we have a long term outcome which almost treats it which leads me to the conclusion that based on this probability the outcome of these babies would have been significantly better had they had the steroids.

Well, I can tell you that, for me, when I looked at this case, my opinion was, I’m at least 85 per cent sure that the use of steroids would have either, reduced, removed the serious impact of the prematurity on these babies cause that’s what the, the statistical probability is of the long term studies, it’s about 85 and for me that’s good enough.

[126] Dr. Perlman stated at p. 130/375, lines 27-29 of the record that: “When I weighed the whole picture I still saw an advantage more likely than not for these twins had they been, had they received the optimal course of steroids.”

[127] Doherty J.A. discounts the evidence of both doctors on the question whether the failure to give the ACS caused the twins to have PVL. He discounts Dr. Barrett’s evidence on the basis that it did not assist because “he treated the twins’ PVL as irrelevant to the causation inquiry.” Respectfully, this is a misapprehension of Dr. Barrett’s evidence. Dr. Barrett did not believe it was helpful to break down the studied effects of steroids on the basis of known proximal causes such as infection versus PVL, etc. This is because, in his view, to break down the numbers in this way was to unacceptably reduce the sample sizes. At pp. 139-140/97-98, lines 31-12 of his cross-examination he explained:

So, the answer to me is the PVL question is interesting, but pertinent to this matter is what are the long-term effects of steroids on cerebral palsy and that’s why I think it’s, I don’t know if it’s so relevant to, to do that kind of subgroup analysis and the problem with subgroup analysis, in other words, taking a large question like cerebral palsy and breaking it down into subgroups that are associated with infection…you start getting further and further away from the truth either because of small sample sizes or because you’re not in randomized trials anymore.

[128] For this reason, Dr. Barrett considered it more useful to look to the studied effects of the steroids on all types of CP, including those caused by PVL. It was Dr. Barrett’s opinion, using the biological plausibility theory, that he was 85% sure that these twins, who had CP caused by PVL, would have had either no symptoms or reduced symptoms of CP had they received the full dose of steroids.

[129] Doherty J.A. also discounted Dr. Perlman’s opinion because Dr. Perlman relied on the data from the Cochrane analysis which did not identify the medical causes of the CP in any of the 48 cases that were studied. Doherty J.A. concludes that the Cochrane analysis can therefore not be used to quantify the relationship between the failure to give the steroids and the development of PVL.

[130] In my view, the trial judge made no error by accepting Dr. Perlman’s evidence in her consideration of this issue. Dr. Perlman gave his opinion in this case based not only on the Cochrane analysis of 48 cases, but also on his knowledge of the earlier 2004 study and analysis, his knowledge of animal studies showing a relationship between ACS and CP, his expertise and experience, as well as the biological plausibility approach and the Bayesian probability analysis by Dr. Willan. The biological plausibility approach in particular addresses the likelihood that steroids have a maturational effect on all membranes including the brain membranes whose disruption leads to PVL.

[131] Dr. Perlman gave his evidence in this case about these twins who developed CP as a result of PVL. His entire evidence would have been irrelevant if he were not referring to the cause of these twins’ PVL.

[132] The trial judge had a second, alternative basis for finding causation on a balance of probabilities. The alternative was based on formulating the causation question in relation to CP generally as opposed to PVL in particular. Based on the testimony of the expert witnesses, the trial judge concluded that one could combine the known 40% reduction in actual CP cases from the Cochrane findings with the experts’ explanation of the mechanism of ACS and their conclusion that it was “more likely than not” that had the twins received the full course of steroids they would not have suffered the injuries or the magnitude would have been reduced.

[133] At para. 207 of her reasons, the trial judge summarized the evidence she relied on in concluding that causation had been proved on a balance of probabilities:

Both Drs. Barrett and Perlman, exercising their clinical judgment and expertise, considering the statistical evidence, answered unequivocally that it is more likely than not that had the twins received a full course of steroids, they would not have suffered the injuries they did, or the magnitude of those injuries would have been reduced. I agree with this conclusion. It is supported by the statistical and medical evidence and the common sense inferences that flow therefrom. I therefore find that the plaintiffs have established on a balance of probabilities that the defendant’s negligence caused the CP from which they now suffer.

[134] When the trial judge refers to the statistical and medical evidence as well as to the common sense inferences, she is referring to the experts’ reliance on these three components in coming to their conclusions. She was not acting as her own expert. For example, on the notion of common sense, Dr. Perlman testified in cross-examination that: “Science errs on the side of exactness, so if science is not exact in itself, then it, it’s determined to err on the side of exactness…. However, I’m talking about common sense not science” (Transcript, pp. 109-110/354-355, lines 26-4). He also testified in his examination-in-chief that, “[t]here are a whole gambit of causes that everybody knows. We would predict them mostly from common sense. We, we do the same sort of thing in medicine” (Transcript, p. 37, lines 20-23).

[135] Doherty J.A.’s objection (at para. 106) is that at its highest, the experimental evidence showed two unquantifiable effects of steroids, one on CP development from unknown causes in premature babies and the other on the severity of the CP if it did develop; adding the two unquantified effects together still gives an unquantifiable effect that cannot amount to causation in this case.

[136] I agree that it would have been an error for the trial judge to find proof on a balance of probabilities by simply adding together two unquantifiable effects based on her own analysis of the experimental data. The trial judge was, however, entitled to accept the expert evidence which interpreted the data and quantified some of the risks, based, as she said in para. 207 of her reasons, on their experience and knowledge as experts as well as on that data.

[137] The trial judge could have rejected the experts’ evidence and conducted her own analysis of the scientific data as Doherty J.A. did. But that was not what she did. She accepted their evidence and gave her reasons for doing so.

[138] After completing her analysis and concluding that causation had been proven on both bases, the trial judge went on to discuss why she believed it was sufficient to prove the second causation route only. There she essentially reasoned that because only 20% of CP cases are associated with conditions upon which ACS has a recognized effect (Dr. Barrett’s evidence was that 80% have unknown causes) “it defies common sense” that the 40% reduction of CP demonstrated in the Cochrane analysis where ACS were administered, would be attributable only to cases with these known causes.

[139] Doherty J.A. says the trial judge made two errors in this analysis. The first one, he says, is that Dr. Barrett acknowledged that he did not know specifically how the 80% statistic for CP cases with unknown causes applied to premature babies, which is all we are talking about here. Second, he objects as a matter of logic to the following reasoning: since ACS must have a positive effect on CP with some unknown cause, therefore it must have a positive effect on CP no matter what the cause.

[140] I have two responses to my colleague’s concerns. The first is that the trial judge did not use the 80% figure or the impugned logic in her analysis of either of the routes to causation. To the extent she made a logical error in reasoning that if steroids positively affect CP from some unknown causes, that means they will have that effect no matter the cause, that error does not affect the findings she had already made on causation, which were based in large part on the opinions of the experts that she accepted.

[141] The second is that although Dr. Barrett did not have an available statistic particular to premature babies or twins, this subgroup was not excluded from the overall 80% figure. More to the point, Dr. Barrett believed the 80% figure to be relevant to analyzing this particular case.

[142] The standard of review in this case is to defer to the evidentiary findings of the trial judge unless her findings have no basis in the evidence. That is not the case here. In my view, the appellants are asking this court to re-examine all the evidence and to come to different conclusions than those reached by the trial judge – i.e., to retry the case. That is not the role of an appellate court. See Stein v. Kathy K (The), 1975 CanLII 146 (SCC), [1976] 2 S.C.R. 802; Housen v. Nikolaisen, 2002 SCC 33, [2002] 2 S.C.R. 235, at paras. 15-18; and H.L. v. Canada (Attorney General), 2005 SCC 25, [2005] 1 S.C.R. 401.

[143] This was a complex medical malpractice case. The causation issue was particularly difficult because, as is not uncommon, there were no specific scientific studies on which the experts or the parties could rely for definitive answers to the specific issues before the court. The administration of steroids prenatally in the case of premature births has had such a significant positive effect, including on the incidence of CP from certain causes, that the accepted standard of care is to administer the steroids in all such cases. However, that does not mean that the failure to do so in any particular case caused the CP in that case.

[144] The trial judge well understood both the deficiencies in the available experimental evidence and the analysis she had to conduct to be satisfied of causation to the required standard.

[145] In my view, the trial judge made no error of law or palpable and overriding error in the apprehension of the evidence, including the expert opinion evidence, or in her findings of fact based on the robust and pragmatic approach.

[146] I would therefore dismiss the appeal with costs to the respondent, otherwise in accordance with para. 108 of the reasons of Doherty J.A.

RELEASED: Dec. 20, 2012 “K. Feldman J.A.”

“DD” “I agree H.S. LaForme J.A.”

[^1]: “Basic science, there are a lot of gaps. Clinical is much more complete” (Transcript, p. 292/47, lines 5-6).