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 Childrens Lawyer and Daniel Goodman, a
    minor by his litigation guardian, the Childrens 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 mothers
    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. viljoens 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. Viljoens 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. Viljoens office and described the leaking fluid to Dr.
    Viljoens 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. Viljoens 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.
    Viljoens 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 babys 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 babys 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 babys 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 its, its really, its, its 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 dont 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 babys 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 judges 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. Viljoens
    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 judges 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 infants 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
    defendants 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 failure to administer ACS prenatally 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 defendants 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 judges 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 defendants
    negligence caused the CP from which they now suffer.

VIII

the appellants 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
    judges 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
    judges 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 judges 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 judges 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
    defendants 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. Barretts 80 per cent figure.  She also applied it to
    premature babies despite Dr. Barretts evidence that he could not say it had
    any such application.  The trial judge was clearly entitled to accept Dr.
    Barretts evidence.  She was not, however, entitled to treat it as applicable
    to premature babies such as the twins.  The trial judges misapprehension of
    Dr. Barretts 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 judges 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 judges 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 judges 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
    appellants contention does not, however, find support in the case law from the
    Supreme Court of Canada or this court: see
Snell v. Farrell
, [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), 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
    Mansfields 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
    defendants negligence caused her loss.  Scientific proof of causation is not
    required.

[75]

Nothing
    in the Chief Justices 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. Viljoens 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 judges 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 judges 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 judges 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
Laferriè
re
    v. Lawson
, [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 judges 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 judges 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 judges 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), 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 infants 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
    defendants 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 judges 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 judges 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. Barretts
    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 judges 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 judges 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 judges 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 courts
    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 colleagues 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 appellants
    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. Viljoens
    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 defendants
    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 judges 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 infants 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 defendants 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 plaintiffs
    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 judges 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 respondents 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 theres infection, whether theres
    asphyxia, whatever, whatever the cause is, steroids stabilize membranes and
    its those membranes in the brain which break, which can breakdown and cause
    cerebral palsy. So, we know theres a biological plausibility; we know theres
    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, Im 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 thats what the, the statistical
    probability is of the long term studies, its about 85 and for me thats 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. Barretts 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. Barretts
    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 thats why I think its, I dont know
    if its 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 infectionyou
    start getting further and further away from the truth either because of small
    sample sizes or because youre 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. Barretts 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.
    Perlmans 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. Perlmans 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
    defendants 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, its determined to err on the side of
    exactness. However, Im 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.
    Barretts 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 colleagues
    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)
, [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).


COURT OF APPEAL FOR ONTARIO

CITATION:
Habib v. Mucaj, 2012
    ONCA 880

DATE: 20121214

DOCKET: C55652

LaForme and Watt JJ.A. and Lederman J. (
ad
    hoc
)

BETWEEN

Salman Habib

Plaintiff (Appellant)

and

Kloreta Mucaj and Leviq Tunaj

Defendants (Respondents)

Ken Singh, for the appellant

Josephine Stark, for the respondents

Heard: December 10, 2012

On appeal from the orders of Justice Brian P. OMarra of
    the Superior Court of Justice, dated May 29, 2012 and June 15, 2012.

ENDORSEMENT

Overview

[1]

The Master
set aside the Registrars order of
    dismissal
of the plaintiffs action and found that: (i) plaintiffs
    counsel provided a weak explanation for the delay, but there was no intentional
    delay; (ii) the delay was inadvertent; (iii) plaintiffs counsel moved promptly
    upon learning of the dismissal; and (iv) there was no evidence of actual
    prejudice to the defendants.

[2]

However, the appeal to the Superior Court of Justice was allowed and the
    order of the Registrar was reinstated.  This is because, according to the
    appeal judge, the Master:

1.   Misapprehended
    the totality of the evidence: first, in regard to the explanation of the
    litigation delay, and second, when he characterized the missing of crucial
    deadlines by counsel for the plaintiff as mere sloppiness or inadvertence.

2.   He failed
    to factor in the significant public interest in finality of proceedings.

[3]

The appeal judge in this case rested his decision principally on the
    explanation for the delay.  He identified the Masters error in this regard as
    misapprehending the evidence on delay causing him to wrongly find it mere
    sloppiness or inadvertence.  His opinion was that the evidence of delay
    amounted to conduct that was either negligent or bordering on negligent.
    The plaintiff appeals this decision.

Analysis

[4]

It is well settled that a misapprehension of evidence may involve
    a failure to take into account an item or items of evidence relevant to a
    material issue, or it may have to do with a mistake about the substance of the
    evidence.  A misapprehension of evidence may also reflect a failure to give
    proper effect to evidence:
R. v. Mahmood
, 2011 ONCA 693, at para. 46.
    The appeal judge in this case appears to suggest that the Master did not appreciate,
    or did not give proper effect to the evidence about the delay.  We disagree.

[5]

There are four well established factors to
    consider when deciding to set aside an order to dismiss an action: (i)
explanation
    of the litigation delay
 a deliberate decision not to advance the
    litigation will usually be fatal; (ii)
inadvertence in missing the deadline
 the intention always was to set the action down within the time limit; (iii)
the
    motion is brought promptly
 as soon as possible after the order came to the
    partys attention; and (iv)
no prejudice to the defendan
t
 the
    prejudice must be significant and arise out of the delay:
Reid v. Dow
    Corning Corp.

(2001), 11 C.P.C. (5
th
) 80 (Ont. Div.
    Crt.).

[6]

No one factor is necessarily decisive of the issue.  Rather, a
    contextual approach is required where the court weighs all relevant
    considerations to determine the result that is just.  Here, the Master
    specifically referenced the proper test and engaged in the weighing exercise.
    He found that, after the weighing exercise, the just result was to set aside
    the dismissal order.  The Masters order was discretionary and was made as part
    of his duty to manage the trial list.  The decision, therefore, attracts
    significant deference from a reviewing court:
Finlay v. Paassen
, 2010
    ONCA 204.

[7]

Furthermore, on a motion to set aside a dismissal order, the court
    should be concerned primarily with the rights of the litigants, not with the
    conduct of their counsel.  However, where the lawyers conduct is not
    inadvertent but deliberate, this may be different:
Marché dAlimentation
    Denis Thériault Ltée. v. Giant Tiger Stores Ltd.

(2007), 87 O.R.
    (3d) 660 (O.C.A.), at para. 28.  Here, the plaintiff lawyers conduct was
    found by the Master not to be deliberate.  Simply because the appeal judges
    view is that the conduct was negligent or bordering on negligent, does not
    mean the Master was not entitled to find the conduct not to be deliberate or
    not intentional.

[8]

In assessing the Masters findings of fact under the
Reid
factors,
    the appeal judge was required to decide whether the findings were unreasonable
    or unsupported by the evidence.  He was not entitled to replace one reasonable
    inference for another, merely because he disagreed with
    the decision under review.

[9]

The inference drawn by the Master  that the delay was mere sloppiness
    or inadvertence  is a reasonable one based on the evidence.  The fact that the
    inference of the appeal judge - that the delay was caused by negligence  is
    also reasonable does not amount to reversible error on the part of the Master.
    The Masters decision was entitled to significant deference and the appeal
    judge was in error in failing to accord it.

[10]

Finally,
    the Masters reasons reflect an understanding of the significant public
    interest in finality of proceedings factor, which he properly considered along
    with the
Reid
factors, and not as a stand-alone one.  The Master
    recognized that the dismissal of the action more than two years following the
    expiry of the limitation period gave rise to a presumption of prejudice.
    However, he found that the plaintiff had rebutted the presumption and that the
    defendants failed to show any actual prejudice to them.  The Master noted that
    the key independent witness was still available and had a clear recollection of
    the accident.  As well he observed that documentary evidence in the form of
    clinical notes, medical records, and the plaintiffs family physicians notes
    were also available.  Given this, the significant public interest factor alone
    is not a reason to interfere with the Masters decision.

[11]

In
    the end, the Master considered and balanced all the appropriate factors.  His
    conclusion based on the evidence was reasonable and there is no basis to
    interfere with it.

Disposition

[12]

For these reasons, the appeal is allowed and the decision of the
    Master is ordered reinstated.  The appellant is awarded his costs of the appeal
    fixed in the amount of $10,000 inclusive of disbursements and HST.  He is also
    awarded his costs in the Superior Court of Justice fixed at $7,500, also
    inclusive of disbursements and HST.

H.S. LaForme J.A.

David
    Watt J.A.

S.
    Lederman J. (
ad hoc
)