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CITATION: Boyd et al. v. Edington et al., 2014 ONSC1130
COURT FILE NO.: 29/12
DATE: 2014-02-20
ONTARIO
SUPERIOR COURT OF JUSTICE
B E T W E E N : )
)
DANIELLE EDITH BOYD, ELAINE
LUCIE FRETZ, RICHARD JAMES
BOYD, and KAIDEN RICHARD BOYD
by his Litigation Guardian, Elaine
Lucie Fretz
)
)
)
)
)
André Michael and Jill McCartney,
for the Plaintiffs
)
Plaintiffs )
)
- and - )
) )
DR. RICHARD BRUCE EDINGTON )
)
)
Andrea Plumb, Carolyn Brandow
and Sarah Martens, for the
Defendant
)
Defendant )
)
)
)
)
)
HEARD: March 11-12, September
9-13, 17-19, 30, October 1-4, 7-9, 22
and 23, 2013
REASONS FOR JUDGMENT
SPROAT J.
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TABLE OF CONTENTS
I. OVERVIEW ..................................................................................................4
II. STANDARD OF CARE .................................................................................7
A. THE LAW .................................................................................................7
B. DID DR. EDINGTON BREACH THE STANDARD OF CARE? ...................9
(a) Dr. Edington’s Evidence ............................................................................9
(b) The Expert Witnesses ............................................................................. 14
(i) Plaintiffs’ Experts ............................................................................ 14
(ii) Defence Experts ............................................................................. 15
(c) Plaintiffs’ Expert Evidence ....................................................................... 15
(d) Defence Expert Evidence........................................................................ 20
(e) Analysis and Conclusion ......................................................................... 24
III. CAUSATION .............................................................................................. 31
A. THE LAW ............................................................................................... 31
B. OVERVIEW ............................................................................................ 32
(a) Terminology and Anatomy ...................................................................... 32
(b) The Expert Witnesses ............................................................................. 34
(i) Plaintiffs’ Experts ............................................................................ 34
(ii) Defence Experts ............................................................................. 35
C. WOULD LHSC HAVE ACCEPTED IMMEDIATE TRANSFER OF MS.
BOYD?.......................................................................................................... 36
D. WAS THE STROKE THE RESULT OF A BLOOD CLOT OR ARTERY
DISSECTION? .............................................................................................. 38
(a) Introduction............................................................................................. 38
(b) The Indicia – Clot or Dissection ............................................................... 38
(i) Blood Clot Is Most Often The Cause Of Stroke ............................... 38
(ii) Circumstances Conducive To Blood Clotting................................... 39
(iii) Does Any Of The Imaging Show A Blood Clot?............................... 40
(iv) Is The Blockage At The Area Of Dissection Or Beyond It? .............. 43
(v) Could A Dissection Extend Beyond PICA Yet Not Block PICA?....... 47
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(vi) No Additional Areas of Infarction Identified...................................... 48
(vii) Step Like Progression Of Signs And Symptoms .............................. 48
(c) Analysis and Conclusion ......................................................................... 49
E. DID LOWERING BP AND DELAY IN ADMINISTERING HEPARIN CAUSE
THE STROKE? ............................................................................................. 54
(a) Introduction............................................................................................. 54
(b) Lowering of BP by Dr. Edington .............................................................. 55
(c) LHSC BP Orders .................................................................................... 55
(d) Plaintiffs’ Expert Evidence ....................................................................... 55
(i) Lowering BP ................................................................................... 55
(ii) Delay in Administering Heparin ....................................................... 58
(iii) Typical Outcomes for VAD Patients – Efficacy of Treatment ........... 60
(e) Defence Expert Evidence........................................................................ 61
(i) Lowering BP ................................................................................... 61
(ii) Delay in Administering Heparin ....................................................... 64
(iii) Typical Outcomes for VAD Patients – Efficacy of Treatment ........... 65
(f) Analysis and Conclusion ......................................................................... 66
F. DAMAGES ............................................................................................. 81
G. CONCLUSION........................................................................................ 82
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INTRODUCTION
I. OVERVIEW
[1] On December 27, 2008, Danielle Boyd, (“Ms. Boyd”) age 24, went
bowling. She was taking medication for high blood pressure (“BP”) and had
recently been suffering from severe headaches. She was feeling sick and a
friend drove her from the bowling alley to Hanover Hospital just after 22:00. On
arrival, her symptoms included left-sided numbness, unsteadiness on her feet,
speech garbled at times, involuntary eye movement and headache. Her BP was
elevated. Ms. Boyd was at Hanover Hospital from the evening of December 27
to the morning of December 28, and I will not repeat references to the date and
year.
[2] Dr. Edington saw Ms. Boyd immediately. He considered possible
diagnoses of “HTN” (meaning hypertensive crisis), “migraine equivalent” and
alcohol use. He kept her in hospital for observation and administered
medication to lower her BP.
[3] The attending nurse recorded at 02:30 that Ms. Boyd was unable to move
her left arm at all, was drowsy and complained of being very dizzy with
movement. The nurse advised Dr. Edington of the change in Ms. Boyd’s
condition. Dr. Edington was resting at that time and he did not reassess her.
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[4] Dr. Edington did reassess Ms. Boyd at 05:30. By 06:45, Ms. Boyd’s signs
had worsened and her left leg was now less mobile. At 07:00, Dr. Edington
contacted the neurology department at London Heath Services Centre (“LHSC”)
and arrangements were made to transfer her.
[5] Ms. Boyd arrived at LHSC at 09:40 on December 28. By 12:30, imaging
revealed that she had a dissection of her right vertebral artery (“RVA”). The
dissection extended from near the top of her spinal cord into her cranium. A
“dissection” means that the arterial layers have separated and blood enters or
bleeding occurs between the layers. The artery wall expands and it can narrow
or block the artery. Dissections often result in blood clots which can block
arteries. At 13:13, Ms. Boyd was administered heparin, an anticoagulant used
to try to prevent the formation of blood clots.
[6] Ms. Boyd’s condition was stable until approximately midnight on
December 29. At that time, her condition deteriorated abruptly. She suffered a
stroke, which killed the tissue in her upper spinal cord and lower brain stem.
When I refer in these reasons to Ms. Boyd’s “stroke”, I am referring to this major
stroke.
[7] Ms. Boyd submits that:
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(a) Dr. Edington was negligent in failing to recognize the signs of stroke,
and in failing to contact LHSC and arrange for her transfer eight
hours earlier;
(b) Dr. Edington’s lowering of her BP exacerbated what were minor
transient symptoms, and created conditions conducive to blood clot
formation;
(c) the immediate cause of the stroke was a blockage caused by a blood
clot; and
(d) but for the lowering of her BP, and the approximate eight hour delay
in administering heparin, she would not have suffered a debilitating
stroke.
[8] Dr. Edington submits that:
(a) he met the standard of care by treating Ms. Boyd for high BP and
observing her overnight;
(b) in any event, an extension of the dissection of the artery wall caused
the blockage and not a blood clot. (It is agreed that heparin is not
effective to treat a dissection and that lowering BP would not cause a
dissection to extend. As such, if the stroke was caused by the
dissection, this action must be dismissed);
(c) even assuming the stroke was caused by a blood clot, the reduction
in Ms. Boyd’s BP in Hanover did not cause or contribute to the
formation of blood clots; and
(d) even assuming the stroke was caused by a blood clot, the weight of
scientific opinion is that heparin is not recommended for treating
vertebral artery dissection (“VAD”) and should not be administered. As such, any delay in administering non-recommended treatment
cannot cause damage.
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II. STANDARD OF CARE
A. THE LAW
[9] There was no dispute as to the applicable law which I will summarize
briefly.
[10] Both sides cited Crits v. Sylvester, [1956] O.R. 132-151, at p. 143
(C.A.) as follows:
Every medical practitioner must bring to his task a reasonable degree of skill and knowledge and must exercise a reasonable degree of skill and
knowledge and must exercise a reasonable degree of care. He is bound to
exercise that degree of care and skill which could reasonably be expected
of a normal, prudent practitioner of the same experience and standing.
[11] The plaintiffs made reference to Justice Picard and Professor
Robertson’s treatise, Legal Liability of Doctors and Hospitals in Canada (4th ed.
2007), respecting diagnosis:
A number of cases have commented on the care, skill and judgment to be
exercised by a doctor when formulating a diagnosis. In Wade v.
Nayernouri, a patient suffering from severe headache, nausea, dizziness, numbness and photophobia was diagnosed in 15 minutes by a doctor
employed in an emergency ward as having “migrainous headaches plus
nervous overtone.” In fact he was in the early stages of a subarachnoid
haemorrhage, and some days later, a recurrence caused his death. The
Court found liability for a misdiagnosis, concluding that:
In my opinion the cases have established that an erroneous
diagnosis does not alone determine the physician’s liability. But if the
physician, as an aid to diagnosis, does not avail himself of the
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scientific means and facilities open to him for the collection of the
best factual data upon which to arrive at his diagnosis, does not
accurately obtain the patient’s history, does not avail himself in this
particular case of the need for referral to a neurologist, does not
perform the stiff neck tests and the lumbar puncture test, the net
result is not an error in judgment but constitutes negligence.
[Emphasis added in original.]
Thus, a thorough history, proper examination, appropriate tests, and
consultations with colleagues and specialists where necessary, are clearly
basic to a proper diagnosis. A reasonable doctor should also heed a
patient’s complaints during treatment for they may be harbingers of change
in condition.
[12] Further reference was made to the same treatise respecting the
proper approach to differential diagnosis:
A key feature of differential diagnosis is the importance of eliminating the
most serious possibility first, rather than the most probable. This was
emphasized in an Ontario case involving the death of a patient who was
diagnosed as suffering from constipation, but who in fact had small bowel
obstruction. The trial judge was critical of the way in which the process of
differential diagnosis was undertaken. According to the trial judge:
Those who diagnosed [the patient] did not follow the systematic
process of differential diagnosis. Critically, several doctors preferred
to deal with the most likely cause, rather than the most serious. The
worst possible ailment was not eliminated from the list of differential alternatives first. The form of diagnosis used by the defendants
remained focused on probability, whereas a proper differential
diagnosis must also be informed by considerations of severity.
The trial judge added:
If doctors were to diagnose based on probability, rare and severe
ailments would regularly be ignored in favour of common, non-life
threatening alternatives. When faced with symptoms that point to
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two or more diseases, the universally acceptable system to use is a
differential diagnosis that accounts for severity.
[13] I am also in agreement with the legal principles as set out by the
defence in their closing written submissions, which I summarize briefly as
follows:
(a) an error in judgment does not amount to negligence where the
physician appropriately exercises clinical judgment;
(b) the standard is not perfection;
(c) misdiagnosis does not necessarily mean negligence;
(d) the court should avoid hindsight;
(e) a choice made where there is controversy as to the appropriate
treatment should be respected;
(f) the standard of care at the time must be applied;
(g) a bad outcome does not constitute proof of negligence;
(h) in the absence of specific recollection, a doctor’s evidence as to
his/her ordinary practice is strong evidence as to what occurred; and
(i) no assumption should be made concerning the information disclosed
by the patient.
B. DID DR. EDINGTON BREACH THE STANDARD OF CARE?
(a) Dr. Edington’s Evidence
[14] Dr. Edington graduated from medical school in 1981. He did three
years of post-graduate education which included a rotating internship which
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incorporated family medicine: one year spent at a family medicine centre in Mt.
Brydges, Ontario and three months of a family medicine residency in Cochrane,
Ontario. He passed the necessary exams and in 1984, became a member of
the Canadian College of Family Practice. He became a fellow of the College of
Family Practice by virtue of having exceeded the requisite number of hours of
continuing professional development over an extended period of time.
[15] From 1985 to 1993, he worked in Cochrane and his duties included
at least one 24-hour emergency room shift per week. Dr. Edington then moved
to Hanover and, has had a varied family practice which, from 1993 to 2004,
included one 24-hour shift in the emergency department per week. Since 2004,
he has worked four 12-hour emergency department shifts per month. In both
Cochrane and Hanover he has had experience in consulting with regional
centres to obtain specialized advice and in transferring patients to such centres.
[16] In Dr. Edington’s experience, dealing with patients presenting with
possible stroke, a patient would be accepted for transfer if it was within the time
window in which tPA (“tissue plasminogen activator” - the clot busting drug)
could be administered and if the patient had a fixed focal deficit, meaning loss
of function in one limb. The patient would also be accepted for transfer if there
was something beyond a stroke, such as evidence of a bleed or unusual
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neurological symptoms. Otherwise, a neurologist would typically refer the
patient to a neurology clinic to be seen within a few days.
[17] When Dr. Edington saw Ms. Boyd, he was part way through a 24-
hour shift that began at 07:00. He did not believe there were other patients in
the emergency department at the time.
[18] Ms. Boyd presented with left-sided numbness, headache,
unsteadiness on her feet, garbled and slurred speech, nystagmus (being an
abnormal and involuntary rapid beating of the eyes) and high BP. He noted Ms.
Boyd had an extremely high BP of 170/112. He ordered an ECG to see if there
was an irregular rhythm that might be straining her heart or causing neurological
signs. The ECG had no significant findings.
[19] Dr. Edington formulated three potential diagnoses:
(a) “HTN” meaning hypertensive crisis which could account for Ms.
Boyd’s symptoms;
(b) “migraine equivalent” which he noted with a question mark because it would account for some but not all of Ms. Boyd’s symptoms; and
(c) alcohol because it is a sedative which can affect speech, gait and
cause nystagmus.
[20] Dr. Edington was concerned that Ms. Boyd’s neurological symptoms
were caused by high BP so he administered medication to lower it. At 01:20,
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after writing the orders for BP medication, he went to lie down and fell asleep.
The nurse awakened him at 02:45 and reported that Ms. Boyd could not move
her left arm but could withdraw it in response to a pain stimulus. He did not
assess her further at that time because having a motor response in her left arm
meant that she would not be considered for tPA.
[21] Dr. Edington said his sleep was disturbed after 02:45 because he
was concerned about Ms. Boyd’s signs and symptoms. He did reassess Ms.
Boyd at 05:30. At that time he became aware of the nurse’s note from 02:45,
which also referred to Ms. Boyd being drowsy and very dizzy with movement,
and the note from 03:45, referring to Ms. Boyd still having no movement in her
left arm.
[22] Dr. Edington reassessed Ms. Boyd again at 06:45. The nurse’s note
records that Ms. Boyd continued to be unable to move her left arm and her left
leg was now less mobile. Dr. Edington’s 07:00 note refers to Ms. Boyd
experiencing a spinning sensation, not being able to move her left side, having
difficulty opening her eyes and experiencing nausea with movement. Dr.
Edington revised his differential diagnosis to include a brain tumor or a sub-
arachnoid hemorrhage (“SAH”) which is a bleed in the brain. Dr. Edington
called LHSC, spoke to a neurologist and then made arrangements for an
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ambulance to transfer Ms. Boyd. Dr. Edington accompanied Ms. Boyd to
LHSC.
[23] In cross-examination, Dr. Edington agreed that the signs of stroke
include:
(a) numbness to one side of the body;
(b) difficulties with speech;
(c) sudden, severe and unusual headaches; and
(d) loss of balance.
[24] Dr. Edington agreed that at the time of his initial examination of Ms.
Boyd, he did not question Ms. Boyd’s friend, who accompanied her to the
hospital, regarding her alcohol consumption nor did he order a blood alcohol
test.
[25] Dr. Edington agreed that his differential diagnosis of HTN indicated
he believed Ms. Boyd might be having a hypertensive crisis, which is a very
uncommon condition.
[26] Dr. Edington said that he was aware of the potential harm in
lowering the BP of a patient suffering from a stroke resulting in reduced blood
flow.
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(b) The Expert Witnesses
(i) Plaintiffs’ Experts
[27] Dr. DePetrillo was the principal expert for the plaintiffs. He has
extensive experience working as an emergency room physician in rural
hospitals. He worked at the Geraldton Hospital for approximately seven years,
doing 24-hour emergency room shifts every four or five days. He has also
worked in the emergency departments of hospitals in Grimsby and Dunnville,
Ontario. Since 2007, Dr. DePetrillo has been an Assistant Professor at the
Northern Ontario School of Medicine.
[28] I also heard evidence from Dr. Sharma and Dr. Young, both highly
qualified neurologists whose qualifications I will discuss in more detail when I
come to causation. They were permitted to give evidence on the standard of
care, given that as neurologists they:
(a) were involved in the education of medical students and residents;
(b) interacted with family physicians working in emergency rooms in rural
hospitals; and
(c) accepted the transfer of patients from such family physicians, and so
had an opportunity to review the notes of their examinations and
diagnoses.
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[29] In closing submissions, counsel for both sides accepted that such
evidence was admissible and that the fact Dr. Sharma and Dr. Young were not
themselves family physicians with emergency department experience goes to
weight.
(ii) Defence Experts
[30] Dr. Antoniadis was the principal expert for the defendant. He
received his M.D. in 1989 and has extensive experience having worked in nine
rural hospitals. In those positions he has always worked a regular rotation in the
emergency room. Similar to Dr. Edington, he has worked as a general
practitioner anesthetist.
[31] I also heard evidence from Dr. Teal and Dr. Silver, both highly
qualified neurologists whose qualifications I will discuss in more detail later
when I come to causation. Dr. Teal also has 11 years experience as an
emergency room physician.
(c) Plaintiffs’ Expert Evidence
[32] With respect to Dr. Edington’s possible diagnosis of high BP, Dr.
DePetrillo pointed out that this is really a sign that was present, but not itself a
diagnosis. High BP can in fact be a symptom of a stroke, in that it can result
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from the attempt by the body to increase blood flow to the brain when it has
been compromised by a blockage or bleed. High BP is also a risk factor for
stroke.
[33] With respect to the possible diagnosis of migraine equivalent, Dr.
DePetrillo testified that numbness on one side, unsteadiness and garbled
speech, would all be highly unusual in the case of a migraine. Migraine
headaches usually begin in adolescence. Migraines almost never result in
nystagmus.
[34] With respect to the possible diagnosis of alcohol use, it does not
cause numbness on only one side. Only at high levels of intoxication does
alcohol cause garbled speech and unsteadiness. It only causes nystagmus in
chronic alcoholics. Ms. Boyd’s own report of alcohol consumption and the fact
that the nurse did not note anything related to apparent alcohol impairment
would seem to exclude alcohol as the cause.
[35] Strokes can occur at any age but are more common in older people.
In the opinion of Dr. DePetrillo, a stroke was well within the realm of a
differential diagnosis for a 24-year-old with this constellation of symptoms. His
opinion is that failing to consider stroke was a breach of the standard of care.
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[36] Dr. DePetrillo testified that there was no reason to bring Ms. Boyd’s
BP down as quickly as Dr. Edington did and, given her neurological symptoms,
her BP should not have been reduced unless stroke had already been ruled
out. An emergency department physician should know that high BP has a
protective effect on the brain during a stroke.
[37] An emergency room physician should consider first the most
significant possible cause of signs and symptoms. In this case that would be a
stroke or bleed. A thorough neurological exam and a proper differential
diagnosis would have led to consulting a neurologist and obtaining CT or MRI
imaging.
[38] The additional symptoms of nausea at 00:20 and inability to move
her left arm, extreme dizziness with movement and drowsiness at 02:45, all
suggest neurological concerns and indicate clinical deterioration. Not
reassessing Ms. Boyd was a breach of the standard of care given the obvious
and alarming changes in her clinical condition.
[39] Dr. Edington was not busy that evening. While small hospitals have
challenges, one advantage is usually that there is only one patient presenting
potentially grave symptoms, so there is an opportunity to frequently assess that
patient and to have considerable time to reassess and/or consult.
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[40] In cross-examination, Dr. DePetrillo agreed that there may be
circumstances in which a patient who has had a stroke may be referred, on an
outpatient basis, to an urgent care neurology clinic. He did not think that was
acceptable given all the circumstances of Ms. Boyd.
[41] Dr. DePetrillo agreed that Dr. Edington proceeded appropriately
given his differential diagnosis. The problem is that he formed the wrong
differential diagnosis. Dr. DePetrillo agreed that in his initial August 15, 2012
report, he did not say it was an inappropriate differential diagnosis. He also
agreed he did not state, in his initial report, that the aggressive treating of BP
prior to consultation with a neurologist was a breach of the standard of care.
This was stated in his second report, dated February 10, 2013.
[42] Dr. Sharma supported the conclusion of Dr. DePetrillo, stating:
(a) the fact that Ms. Boyd’s symptoms were fluctuating means that the
blood supply to the affected area of her brain was tenuous;
(b) the fact that numbness was left-sided and that Ms. Boyd’s speech was affected points to a problem in the brain;
(c) nystagmus is referable to a focal area in the brain;
(d) alcohol use does not produce one-sided numbness or nystagmus;
(e) migraine headaches are typically recurrent and present with an aura,
which usually lasts for tens of minutes and can involve numbness
and problems with speech. Migraine is a diagnosis that should only
come after excluding more serious possible causes. Migraines do
not result in nystagmus; and
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(f) hypertension is by far the leading risk factor for stroke because it can
cause damage to blood vessels and the heart and can lead to
rupture.
[43] In the opinion of Dr. Sharma, Dr. Edington breached the standard of
care required of an emergency department physician in a rural hospital by not
consulting a neurologist at LHSC and by lowering Ms. Boyd’s BP.
[44] In cross-examination, Dr. Sharma said he has reviewed thousands
of cases and has been able to see what emergency department doctors do in
terms of diagnosis and treatment. He also sees when a stroke diagnosis is
missed, which is about ten per cent of the time. He did not agree that it was
challenging for a rural emergency department doctor to make a diagnosis of
stroke. He said when stroke is missed it is frequently because the patient is
suffering from some other condition such as being in hospital after surgery.
[45] Dr. Sharma agreed that patients with minor or non-disabling strokes
may not even be admitted and may be discharged home with timely out-patient
care. This should only be done, however, following a diagnosis and after
ensuring that the right measures have been taken to avoid additional deficits.
[46] In his testimony, Dr. Young made many of the same points as Dr.
Sharma. In his opinion, if LHSC had been consulted after Ms. Boyd’s initial
assessment, she almost certainly would have been transferred at that time.
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[47] In cross-examination, Dr. Young agreed that aspects of his report,
related to several symptoms he said would have been evident to Dr. Edington,
were in hindsight, overstated or not fair.
[48] Dr. Young agreed it can be difficult to recognize stroke in young
adults and, in the last few years, there have been increased efforts to educate
frontline health care professionals to detect the symptoms of stroke.
[49] Dr. Young agreed that stroke was not his primary area of expertise
and he did not publish or write in that area.
[50] Dr. Young actively became involved in Ms. Boyd’s care on
December 30, 2008. He met with Ms. Boyd and her parents regarding
treatment and prognosis. This was an exceptional case with a very young
person suffering a devastating stroke. He came to know the family well and
from December 2008 to May 2009, he assessed Ms. Boyd on average every
other day.
(d) Defence Expert Evidence
[51] Dr. Antoniadis testified that he did not feel it was necessary for Dr.
Edington to call a neurologist after the initial assessment because his
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differential diagnosis would account for Ms. Boyd’s clinical signs and
symptoms, and he had a treatment plan based on that differential diagnosis.
[52] He did not agree with Dr. DePetrillo that it was necessary to consult
a neurologist before lowering BP. Dr. Edington was quite familiar with the
medications and used them appropriately. Ms. Boyd’s neurological signs had
partially resolved by the time Dr. Edington assessed her so it was reasonable to
lower her BP.
[53] Dr. Antoniadis testified that Dr. Edington did not breach the standard
of care by going to sleep at 01:20. He had a logical treatment plan and he
needed to observe Ms. Boyd further before changes in the treatment plan could
be considered.
[54] Dr. Antoniadis did not think that a neurologist should have been
called at 05:30. He said that Ms. Boyd’s condition at 05:30 was consistent with
her condition at the bowling alley. He noted that her condition had improved
after the bowling alley. It was reasonable for Dr. Edington to continue to
observe her in Hanover because he still felt his initial diagnosis was a
“possibility”.
[55] I will discuss further aspects of the cross-examination of Dr.
Antoniadis when I come to my analysis and conclusion.
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[56] Dr. Teal testified that Dr. Edington’s management in the emergency
room was appropriate. Strokes are much less common in young people, so a
stroke would be less likely to be included in the differential diagnosis of Ms.
Boyd. There are host of conditions that can mimic strokes. In a rural hospital
you see relatively few strokes. It would be even more unusual to see a young
stroke victim.
[57] If Dr. Edington believed Ms. Boyd’s symptoms were due to HTN, it
was reasonable to cautiously lower her BP. Alcohol is a common mechanism
for slurred speech, staggering or other problems with gait. Migraine headaches
can cause numbness and affect speech, and are the most common mimic of
stroke in young adults.
[58] Dr. Teal indicated that the key factors for an emergency department
doctor, in diagnosing stroke, are motor deficits, such as one-sided weakness or
significant language problems. He was then asked whether Ms. Boyd’s
recorded sign of “speech garbled at times” would not be a finding indicating a
neurological problem. Dr. Teal said there are other mechanisms that can cause
garbled speech and that in the emergency department, “the most common is
alcohol of course”.
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[59] In cross-examination, Dr. Teal agreed that there were cerebellar
signs such as nystagmus, slurred speech, problems with balance, nausea and
vertigo (meaning spinning dizziness). He said that there can be other causes of
these signs.
[60] Following re-examination, I asked Dr. Teal to explain his comment
that “alcohol is an issue which confounded her presentation”. Dr. Teal
responded that patients in an emergency department have often been drinking.
I then pointed out that his comment was directed to Ms. Boyd specifically and
not emergency patients generally. Dr. Teal responded that while he was
satisfied that Ms. Boyd’s symptoms were not related to alcohol, it was a
“confounder” and one more thing for Dr. Edington to think about.
[61] Dr. Silver testified that Dr. Edington’s observation of Ms. Boyd
walking into emergency and getting on a stretcher would indicate she had no
significant neurological deficits. Dr. Edington tested her motor ability and she
was not weak on one side. Dr. Silver graded Dr. Edington as having done a
good assessment of Ms. Boyd.
[62] Dr. Silver thinks it was appropriate to consider that a migraine might
be causing transitory symptoms and also nystagmus. He said migraine
equivalent often does account for symptoms of strokes.
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[63] Dr. Silver was asked about Dr. Sharma’s opinion that nystagmus
should steer the doctor away from migraine and towards stroke. He said
nystagmus is rarely reflective of a brain stem problem and alcohol and drugs
are the most common cause.
[64] He said the alcohol consumption could have confounded the
diagnosis by providing an alternative explanation for nystagmus, unsteadiness
and garbled speech. In addition, once alcohol is front and center, it is easy to
assume some of the symptoms relate to alcohol. Medical residents are often
advised to multiply reported consumption by three or four.
[65] Dr. Silver would be very concerned about a patient with a BP
reading of 170/112 and going higher. He would not discharge the patient and
would monitor and consider treating the high BP. In his opinion, it was
reasonable to treat the BP as Dr. Edington did. He did not believe it was
necessary to consult a neurologist first.
(e) Analysis and Conclusion
[66] My starting point is that I find Dr. Edington should have readily
concluded that alcohol had nothing to do with Ms. Boyd’s presenting signs and
symptoms. Ms. Boyd was a young, single parent who lived with her parents
and had gone out in the early evening with friends. She reported consuming
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one to two alcoholic drinks. As a matter of common sense and experience,
exceedingly drunk individuals cannot turn garbled speech off and on. The fact
that Ms. Boyd had garbled speech when she spoke to the nurse, but not when
she spoke to Dr. Edington, was a strong indicator alcohol was not the cause.
Numbness that is only left-sided is obviously not related to alcohol.
[67] Dr. Edington was not rushed for time. Ms. Boyd was the only patient
that night with a potentially serious condition. If, despite the foregoing, he had
any thought alcohol was involved, he could and should have pursued this. It
would have taken only a few moments to have Ms. Boyd review in detail her
alcohol consumption. Dr. Edington could and should have impressed upon her
that it was critically important she provide precise and accurate information. If
Ms. Boyd’s responses did not satisfy him, the friend who accompanied her
could have been questioned. If Dr. Edington had taken these simple steps, I
find he should have been satisfied that alcohol had nothing to do with Ms.
Boyd’s condition.
[68] The evidence of the defence witnesses on the subject of Ms. Boyd’s
alcohol consumption leads me to conclude that, perhaps unintentionally, they
had crossed the line from objectivity to advocacy.
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[69] It was suggested to Dr. Antoniadis that it was unlikely that two
drinks could cause nystagmus. That is a simple question. Dr. Antoniadis gave
a non-responsive answer to the effect that there are over 400 causes of
nystagmus and that he did not know if Ms. Boyd had congenital nystagmus.
[70] Dr. Teal stated that “alcohol is an issue which confounded her
presentation”. I asked Dr. Teal to explain this, however, instead of focusing on
Ms. Boyd he referred to the general experience that patients are not accurate
reporters of alcohol consumption.
[71] Dr. Silver was asked if horizontal nystagmus should prompt a call to
a neurologist. He responded stating that Ms. Boyd had been drinking and that
alcohol can cause nystagmus. This is another example of losing focus on Ms.
Boyd. As Dr. DePetrillo and Dr. Sharma stated, nystagmus is associated with
extremely high alcohol consumption or brain deficits caused by chronic
alcoholism, which obviously had nothing to do with Ms. Boyd.
[72] Dr. Silver said alcohol could have confounded the diagnosis by
providing an alternative explanation for nystagmus, unsteadiness and garbled
speech. He then related that medical residents are often advised to multiply the
alcohol consumption patients report by three or four. Whatever merit there is to
this involving clearly intoxicated patients, it had nothing to do with Ms. Boyd.
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[73] Dr. Silver said that most doctors who observed nystagmus and
unsteadiness would relate it to alcohol. He commented that it was unfortunate
to assume the most common explanation, but it is part of human nature to do
so.
[74] In summary, I found the efforts of the defence witnesses to justify Dr.
Edington’s inclusion of alcohol in his differential diagnosis completely
unreasonable. I further find that the defence experts exhibited partiality and
advocacy in their evidence in this regard.
[75] Dr. DePetrillo testified that Ms. Boyd’s signs and symptoms,
including left-sided numbness, headache, unsteadiness on her feet, garbled
speech and nystagmus, should have indicated the possibility of a serious
neurological emergency. In his opinion, stroke should have been part of any
differential diagnosis. As such, Dr. Edington should have consulted a
neurologist at LHSC following his initial assessment. In his opinion, it was a
breach of the standard of care required of an emergency department physician
in a rural hospital to not do so.
[76] The defence submitted that I should discount the evidence of Dr.
DePetrillo because:
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(a) his first report did not criticize the differential diagnosis made by Dr.
Edington after his initial assessment;
(b) his first two reports did not state it was necessary to call a neurologist
after the initial assessment of Ms. Boyd; and
(c) it was only in his second report that he stated it was necessary to call
a neurologist before lowering Ms. Boyd’s BP.
[77] The defence suggested that Dr. DePetrillo was effectively changing
his opinion over time. On a fair reading of his reports I do not agree. Dr.
DePetrillo’s initial report was four pages, two of which recited Ms. Boyd’s history
and treatment. Dr. DePetrillo framed his analysis by suggesting that the breach
of the standard of care related to not conducting a more thorough neurological
examination. He stated that a focused neurological assessment would likely
have alerted Dr. Edington to a “central or peripheral neurological disorder”.
Further, he stated that if Dr. Edington had met the standard of care it could
have resulted in “an earlier change in management, timely diagnostic testing
and potentially earlier treatment possibilities”. The last substantive paragraph in
the report indicates meeting the standard of care may have led to “expedited
transfer to a tertiary care centre”.
[78] In terms of assessing Dr. DePetrillo’s credibility and reliability, it is
not concerning that he did not mention until his second report that Ms. Boyd’s
BP should not have been lowered prior to consulting a neurologist. The first
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report made clear that a neurologist should have been consulted after the initial
assessment. Dr. Edington himself agreed that BP should not be lowered if
stroke is suspected. All the experts agreed stroke could only be definitely
diagnosed at a facility like LHSC with imaging capability. To summarize, there
was nothing in the content of Dr. DePetrillo’s reports, or his evidence, that
suggested to me that he was not being professional and objective in stating his
opinion.
[79] There are a number of other aspects of the evidence of Dr.
Antoniadis that do cause me to discount the weight I give to his evidence.
[80] When asked to agree with the straightforward proposition that some
strokes are hemorrhagic and some ischemic, Dr. Antoniadis went on to refer to
the rare incidence of VAD which occurs in less than 1 in 100,000 cases.
[81] When later asked essentially the same question, whether strokes
cause damage by hemorrhage or ischemia, Dr. Antoniadis responded there can
also be strokes caused by trauma to the brain. He was then simply asked to
agree that “would still be called a stroke or categorized as a traumatic stroke?”
He said “yes” and then in a non-responsive manner went on to state that, “the
unfortunate history of Danielle Boyd is that she suffered a VAD, which once
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again is a very rare event, less than 1 in 100,000, and this led to reduced blood
flow”.
[82] Dr. Antoniadis was asked if an emergency department physician
should consult a specialist if a patient exhibits the signs of a stroke. This was a
straightforward question. He gave a generally non-responsive rambling answer
that occupied a full page of transcript. Dr. Antoniadis referred to the fact that
Ms. Boyd had a very rare presentation: she had a rare VAD, she did not have
an embolic stroke (caused by a clot) and she was outside the window to use
tPA.
[83] Dr. Antoniadis was asked a series of questions concerning whether
various signs such as weakness and difficulty speaking can be a sign of stroke.
In a non-responsive manner Dr. Antoniadis added, in responding to every
question, that there can be many other causes of the signs.
[84] The fact that VAD is a rare condition was a key point the defence
was emphasizing. The fact that Dr. Antoniadis repeatedly interjected this point
in non-responsive answers demonstrated to me that he was exhibiting partiality
and acting as more of an advocate than an expert. The evidence of Dr.
Antoniadis was also in conflict with Dr. Teal, who was unequivocal in his
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opinion that Dr. Edington did breach the standard of care by reassessing Ms.
Boyd, and calling LHSC when she deteriorated at 02:45.
[85] For the reasons I have explained, I much prefer the evidence of Dr.
DePetrillo in particular, and the plaintiffs’ witnesses in general, to the
defendant’s witnesses. I accept the evidence of Dr. DePetrillo and find as a
fact that, Dr. Edington breached the standard of care required of an emergency
department physician in a rural hospital, by not recognizing the possibility of
stroke, by reducing Ms. Boyd’s BP while stroke was a possibility and by failing
to consult LHSC after his initial assessment of Ms. Boyd.
III. CAUSATION
A. THE LAW
[86] The parties agreed that the onus is on the plaintiff to establish “but
for” causation. In Clements v. Clements, 2012 SCC 32, [2012] 2 S.C.R. 181, at
paras. 8-9, Chief Justice McLachlin described this test as follows:
The test for showing causation is the “but for” test. The plaintiff must
show on a balance of probabilities that “but for” the defendant’s
negligent act, the injury would not have occurred. Inherent in the
phrase “but for” is the requirement that the defendant’s negligence
was necessary to bring about the injury - - in other words that the
injury would not have occurred without the defendant’s negligence.
This is a factual inquiry. If the plaintiff does not establish this on a
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balance of probabilities, having regard to all the evidence, her action
against the defendant fails.
The “but for” causation test must be applied in a robust common
sense fashion. There is no need for scientific evidence of the
precise contribution the defendant’s negligence made to the injury.
See Wilsher v. Essex Area Health Authority, [1988] A.C. 1074 (H.L.),
at p. 1090, per Lord Bridge; Snell v. Farrell, [1990] 2 S.C.R. 311.
B. OVERVIEW
(a) Terminology and Anatomy
[87] Ms. Boyd’s dissection began in the RVA at the C1-C2 level of her
upper spine and extended inside her skull and inside the dura that surrounds
the brain. I will simply refer to this as area as “intracranial”.
[88] When a dissection occurs, involving a tear in the inner lining of the
artery, the inner layer is exposed to blood flow which triggers a clotting process.
Clots can form at the point of the tear and grow. A clot that breaks away is an
“emboli”. The emboli can be carried by the blood flow and lodge in an artery.
Natural processes in the body dissolve blood clots over time.
[89] The relevant anatomy is as follows:
(a) the RVA extends intracranially and there is an artery that branches
off called the posterior inferior cerebellar artery (“PICA”);
(b) as blood flows toward the brain, beyond PICA, there is another artery
that branches off called the anterior spinal artery (“ASA”); and
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(c) beyond the ASA, the RVA joins the left vertebral artery (“LVA”) at a
junction (the “Junction”) and together they form the basilar artery.
[90] Ms. Boyd’s major stroke was caused by the blockage of the ASA just
prior to the Junction.
[91] This blockage caused tissue death (referred to as “infarction”), in
both the upper area of the spine and the lower part of the brain stem. This is an
area in which motor pathways from the left and right side of the brain cross. The
right and left side of the brain control the opposite side of the body. Tissue
death in this critical area results in quadriplegia.
[92] Other terms I will refer to are:
(a) edema – the swelling that is caused when tissue that has been
damaged leaks fluid resulting in swelling;
(b) hematoma – blood that has gathered where it should not ordinarily
be, such as between artery walls or blood seeping into tissue causing
a bruise;
(c) lumen – the space within the artery through which blood flows;
(d) methemoglobin – blood which has seeped into tissue and is not
moving but which will be resorbed into the body over time;
(e) resorption – when natural body processes remove and recycle blood
that has seeped into tissue;
(f) SAH – sub-arachnoid hemorrhage which is the breaking of a blood
vessel within the brain typically with devastating or fatal
consequences; and
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(g) thrombus – also referred to as a clot, is congealed blood within an
artery or vein.
[93] It was common ground that all of the expert witnesses were qualified
to give opinion evidence on causation.
(b) The Expert Witnesses
(i) Plaintiffs’ Experts
[94] Dr. Pelz has practiced as a neuroradiologist for 30 years and is
Professor Emeritus in the Departments of Medical Imaging and Clinical
Neurological Sciences at the University of Western Ontario. Since 1993, he has
served on the editorial board of the Canadian Association of Radiologists
Journal. He has conducted research studies and published and presented
extensively.
[95] Dr. Sharma has been a neurologist since 1991. He is the Chair of
the Canadian Stroke Consortium, which is involved in research and education,
and a director of the Canadian Stroke Network, which is a nationally funded
agency devoted to improving stroke care. He is currently an Associate
Professor of Medicine (Neurology) at McMaster University. Previously he was
the Director of the Regional Stroke Program in Ottawa and an Assistant
Professor of Medicine (Neurology) at the University of Ottawa. He typically
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sees at least 20 stroke patients each week and patients with dissections twice
per month. He has conducted research projects and published extensively on
the subject of stroke.
[96] Dr. Young has been a neurologist since 1977. He is a Professor in
the Department of Clinical Neurological Services at the University of Western
Ontario and the editor-in-chief of the Canadian Journal of Neurological
Sciences. He treats stroke patients in the course of his practice and estimates
he has seen 2000 or more cases of stroke or suspected stroke. While he has
conducted research and published extensively, the focus has not been related
to stroke.
(ii) Defence Experts
[97] Dr. Farb has practiced as a neuroradiologist for 20 years. He is a
staff neurologist in the Department of Medical Imaging in the University Health
Network, which is comprised of a number of major Toronto hospitals. He has
been an editor on a number of professional journals, conducted research, been
granted a patent related to a MR angiography technique and has published and
presented extensively.
[98] Dr. Teal has been a neurologist since 1990, after ten years of
experience in emergency medicine. He is a Clinical Professor in the Faculty of
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Medicine at the University of British Columbia. He has been the Director of the
stroke program at Vancouver General Hospital since 1992. Vancouver General
admits 1400 stroke patients each year and there are typically one or two
patients with VAD at any one time. He also consults on stroke patients by
telephone and video. He has conducted research, published and presented
extensively on a broad range of stroke-related topics.
[99] Dr. Silver has been a neurologist since 1983. He has been the
Director of the University Heart Network Stroke Program since 1993 and is a
Professor of Medicine, Neurology at the Faculty of Medicine, University of
Toronto. He has conducted research, published and presented extensively on
a broad range of stroke-related topics. He has extensive clinical experience
and sees one to four patients with VAD every month. He was involved in
drafting the Canadian Best Practice Recommendations for Stroke Care.
C. WOULD LHSC HAVE ACCEPTED IMMEDIATE TRANSFER OF MS.
BOYD?
[100] In the opinion of Dr. Young, who is on staff at LHSC, if Dr. Edington
had called after his initial assessment of Ms. Boyd, she almost certainly would
have been transferred then. Dr. Sharma agreed based upon his experience in
Hamilton and Ottawa.
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[101] Dr. Teal, whose experience has been in British Columbia, said the
major reason to transfer a patient having a stroke is if you are within the time
window to administer tPA. Ms. Boyd was not and, as she was stable when first
assessed, most doctors would not seek to transfer her at that time. Dr. Silver
regarded it as reasonable for Dr. Edington to monitor Ms. Boyd and consider
treating her BP.
[102] In considering the weight to give to the evidence of Dr. Teal and Dr.
Silver on this issue, I bear in mind the basis for their opinion. They both
regarded Dr. Edington as having formulated a reasonable differential diagnosis
which included alcohol impairment. They viewed the signs as confounding
which made a decision to monitor and await further developments more
reasonable. I have, however, concluded Dr. Edington was negligent in
formulating his differential diagnosis.
[103] In any event, Dr. Young was in the best position to address what
steps LHSC would have taken. Dr. Sharma, who has extensive experience in
Ontario, shared Dr. Young’s opinion that if consulted, Ms. Boyd would have
been transferred. They approached the issue from what I have found was the
proper perspective, namely that there were indications that Ms. Boyd was
suffering a stroke or had some other focal neurological problem.
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[104] While I have also considered the fact that Dr. Young’s relationship
with the Boyd family may have influenced his evidence on this issue, I conclude
that it did not. Dr. Young, to his credit, acknowledged that he did overstate
aspects of his evidence on the standard of care issue.
[105] I accept the evidence of Dr. Young and Dr. Sharma and find as a
fact that if Dr. Edington had consulted LHSC after his initial assessment, Ms.
Boyd would have been transferred at that time.
D. WAS THE STROKE THE RESULT OF A BLOOD CLOT OR ARTERY
DISSECTION?
(a) Introduction
[106] I will first summarize the expert evidence having regard to what were
identified as indicia as to the cause of Ms. Boyd’s stroke. I will then provide my
analysis and findings of fact.
(b) The Indicia – Clot or Dissection
(i) Blood Clot Is Most Often The Cause Of Stroke
[107] All of the experts agreed that in cases of artery dissection, the vast
majority of infarcts are caused by blood clots which embolize and not by the
dissection itself. Dr. Young cited a 2009 article regarding carotid and VAD,
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which found that 92 per cent of infarcts resulted from clot formation and
embolization.
(ii) Circumstances Conducive To Blood Clotting
[108] It was common ground among the experts that:
(a) when the wall of an artery is torn it exposes the inner layer to flowing
blood and this triggers the clotting process; and
(b) stagnation of blood results in clot formation.
[109] Dr. Sharma and Dr. Young were of the opinion that a combination of
the fact that the RVA was narrowed by the dissection itself, and that lowering
Ms. Boyd’s BP further reduced the blood flow, created conditions conducive to
clot formation and growth. Dr. Pelz also referred to December 28 imaging as
showing the RVA as narrow and irregular such that there would be slow flow.
[110] Dr. Teal testified that unless BP is reduced to shockingly low levels,
so that blood flow is reduced to a “trickle”, it does not put the patient at a higher
risk to develop blood clots. He also noted the venturi effect whereby fluid
passing through a narrowing in a vessel increases in velocity. Dr. Teal agreed
that you can have a dissection which narrows the artery and, in addition, a clot
which blocks the artery.
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[111] Dr. Silver testified that clot formation does not occur unless blood
flow slows to almost complete stagnation. He did not agree that a narrowed
artery and lowered BP would have this effect, unless there was almost no BP.
(iii) Does Any Of The Imaging Show A Blood Clot?
[112] While other witnesses commented on the imaging, it was common
ground that Dr. Pelz and Dr. Farb, as neurodiologists, had superior
qualifications to interpret the imaging. In addition, as experts retained for that
very purpose, they had focused on the imaging. I will, therefore, concentrate on
their evidence.
[113] First, the imaging prior to the stroke. Dr. Pelz was referred to
December 28 imaging and stated it indicated a concern there might be a blood
clot in the basilar artery. The basilar artery is, however, beyond the point of the
obstruction that caused Ms. Boyd’s stroke.
[114] Dr. Farb reviewed the same imaging and does not believe there was
a clot in the basilar artery. His reasons were as follows:
(a) the technique used to obtain the imaging is known to produce
“artifacts” which means something that appears on the image but is
not real;
(b) what appears as a spot on the basilar artery is not seen in images
taken only minutes later; and
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(c) if it was a clot, and it moved with the flow of blood toward the brain,
he would expect it to have caused infarcts.
[115] Turning then to the imaging immediately following Ms. Boyd’s stroke,
as discussed, the RVA and the LVA join at the Junction to form the basilar
artery. Blood flowing through the RVA and LVA toward the brain meets at the
Junction and continues through the basilar artery.
[116] Ordinarily blood would not, therefore, flow from the LVA into the
RVA. In the case of Ms. Boyd, however, the blockage in her RVA allowed some
blood flowing through the LVA to the Junction to then flow back into the part of
the RVA, just below the Junction, which lacked blood flow. This was referred to
as an area of retrograde filling.
[117] Dr. Pelz cited the MRI Consultation report of a LHSC
neuroradiologist, relating to images taken December 30, at 15:15, which
identified an area beyond PICA in which “no definite flow is seen – only TI hyper
intensity”. Dr. Pelz said this hyper intensity is characteristic of a clot. Dr. Pelz
stated that what appeared as a “sharp margin” at the end of the area of
retrograde filling in the RVA, indicates it is more likely a clot than a dissection
that caused the obstruction.
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[118] Dr. Pelz testified that imaging on January 5, showed flow in the RVA
through what he described as a grey tube of material. In his opinion, this was
probably a blood clot that had resolved to the point that blood could flow
through it.
[119] Dr. Pelz acknowledged in cross-examination that neuroradiologists
are expected to look for and identify clots as that may be important in
considering treatment. Dr. Pelz agreed that none of the LHSC neuroradiologists
made specific reference to a clot.
[120] Dr. Farb did not agree that there was a sharp margin at the end of
the retrograde flow which indicated a clot as opposed to a dissection. He
described the image as showing a tapering or flame shape caused by the
dissection.
[121] Dr. Farb referred to CT and MRI images on December 30. He did
not see an area of high signal intensity that would be indicative of a clot.
[122] While Dr. Pelz and Dr. Farb had superior qualifications, the evidence
indicated that neurologists are often required to themselves interpret imaging as
well as consult with neuroradiologists regarding the interpretation of imaging.
Dr. Sharma and Dr. Young essentially shared the opinion of Dr. Pelz. Dr. Teal
and Dr. Silver essentially shared the opinion of Dr. Farb.
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(iv) Is The Blockage At The Area Of Dissection Or Beyond It?
[123] To appreciate the expert evidence it is helpful to understand the
positions advanced.
[124] The position of the plaintiffs is that:
(a) there was no significant change in the nature and extent of the
dissection from December 28 to January 5;
(b) imaging indicates that the blockage was beyond the area of
dissection and so not caused by the dissection; and
(c) the ASA was blocked on December 30 causing the stroke and then, with no significant change in the dissection, open as of January 5.
This makes it is more likely that it was a clot, and not a dissection,
that caused the blockage.
[125] The position of the defendant is that:
(a) there were changes in the nature and extent of the dissection
between December 28 and January 5;
(b) imaging indicates that the blockage was at the end of the area of
dissection and caused by the dissection; and
(c) the dissection extended to block the ASA on December 30. By
January 5 the dissection had receded, by the normal process of
blood being resorbed into surrounding tissue, allowing the ASA to re-
open.
[126] Dr. Pelz selected images that in his opinion best demonstrated the
extent of the dissection on December 28 and on January 5. In his opinion, the
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images look the same. There is no extension of the dissection and no widening
of the artery. The only difference is that on January 5, there is blood flow
through the dissected segment of the artery. He does not, therefore, believe
that there was increased bleeding within the artery wall after December 28.
[127] In the opinion of Dr. Pelz, the blockage causing the stroke was
beyond the area of dissection. He noted that an MRI consultation report by Dr.
Lee, a LHSC radiologist, reviewing images obtained December 30, 2008 at
03:35, states: “There is probably focal occlusion of the intradural right vertebral
artery beyond the area showing some intramural hematoma” (emphasis added).
[128] In cross-examination, Dr. Pelz was referred to Exhibit 28, p. 15 and
agreed that there was some indication of the intramural hematoma in the
December 28 image, but not in the January 5 image. He agreed that some of
the intramural hematoma may have resorbed by January 5.
[129] Dr. Pelz agreed that as of December 28 the dissection was within
approximately 8mm of the Junction and so close to the point of blockage.
[130] Dr. Pelz agreed that there is a normal mechanism by which if the
artery collapses due to a dissection, it can re-open as a result of the blood flow
that is attempting to get through.
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[131] Dr. Farb testified that when there is a dissection you get some
enlargement of the artery structure. His opinion was that the artery structure
became larger, and there had been a reduction in the intramural hematoma,
between December 28 and 30.
[132] Dr. Farb testified that there was a moderate decrease in the
intramural hematoma in the RVA over the 30-hour period from 03:15 on
December 30 to December 31, at 09:29 by which time flow had been re-
established. He attributed this to a natural process where the hematoma is
resorbed. He said the dissection was changing and this can occur in a matter of
hours.
[133] As further indication that the dissection had receded, Dr. Farb noted
that while a January 5 image no longer showed the hematoma, the artery walls
were visible. He testified the walls would only be visible if they were thicker
than normal due to edema.
[134] Eighty to eighty-five per cent of the population have an ASA
branching off both the RVA and LVA. In Dr. Farb’s opinion Ms. Boyd was in the
15 to 20 per cent of the population that have only one ASA, and that her ASA
branched off her RVA. If Ms. Boyd had a second ASA branching off her LVA it
would have provided collateral blood flow to the area that became infarcted.
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[135] Dr. Farb explained that a dissection can progress due to blood being
pushed into the tear in the inner arterial wall causing the artery walls to tear
apart. In turn, this tearing apart causes additional bleeding into the area
between the artery walls causing further separation. The separation can cause
the dissection to extend along the artery in the direction of the blood flow or
cause the artery to narrow and pinch off blood flow through the artery.
[136] Dr. Farb testified that sometimes the tear in the artery will heal and
the hematoma decrease very slowly. Sometimes the tear reopens so there is
further progression. It is not possible to accurately measure the amount of
hematoma in an artery wall. You have to rely on your eyes.
[137] Dr. Farb referred to two images from approximately 03:00 on
December 30. His interpretation is that there is methemoglobin in the artery
wall, indicating an area of dissection, although there is still some retrograde
filling into that area. From this he concludes that the dissection has extended
slightly past the point of blockage.
[138] When asked further questions he said it was difficult to actually pin
point how high the dissection went and that the dissection “seemed” to go to the
level of the blockage and “possibly a little higher”. He also referred to the
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dissection as having entered “in the ballpark” of a bone structure he referred to
as a landmark in reviewing the images.
(v) Could A Dissection Extend Beyond PICA Yet Not Block PICA?
[139] It is common ground in terms of anatomy that the RVA supplies
blood to PICA and, further along, the RVA supplies blood to the ASA. In Ms.
Boyd’s case, PICA maintained some flow both before and after her stroke. The
stroke itself was caused by a blockage of blood flow to the ASA.
[140] Dr. Pelz stated that if the dissection had extended to block blood
flow to the ASA he would not expect PICA to remain open. Dr. Sharma agreed
and stated that in his opinion, it was highly improbable that the dissection would
have extended to cause a blockage past PICA, while allowing continued blood
flow to PICA.
[141] Dr. Silver testified that dissections involve a dynamic process and
can spiral around an artery. Dr. Teal testified that a dissection can also block
off small penetrating arteries thereby causing infarction.
[142] Dr. Farb also testified that a dissection could compromise the blood
flow in PICA, but not block it, and then progress to block the ASA.
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(vi) No Additional Areas of Infarction Identified
[143] Dr. Pelz agreed that if a clot is seen in an artery and later not seen, it
has usually fragmented or moved on. There was no evidence of the clot moving
elsewhere.
[144] As mentioned, Dr. Pelz testified that a January 5 image showed flow
in the RVA through a grey tube of material which he interpreted as a blood clot,
which had resolved to the point that blood could flow through it.
[145] Dr. Farb noted that as of December 31, blood flow had returned to
the RVA. If a clot caused the blockage as of December 30, but blood flow later
resumed, the clot must have moved. There is, however, no evidence of the clot
causing infarcts further on.
[146] Dr. Teal stated that all of the infarcts suffered by Ms. Boyd could
have been caused by the dissection expanding by 1-3 mm in circumference or
length. He described the area in question as some of the most important neuro-
anatomy in the body.
(vii) Step Like Progression Of Signs And Symptoms
[147] Dr. Silver testified that dissections usually extend by steps, as
opposed to a steady progression. In the case of Ms. Boyd, the VAD was in
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progress by December 20, when the headaches she had been having
intensified. Arteries are sensitive to pain and the tearing of the arterial walls in a
dissection causes pain. The symptoms exhibited by Ms. Boyd on December 27,
when she went to Hanover Hospital, were consistent with the VAD having
extended intracranially, reducing blood flow to arteries and affecting her brain
stem. Ms. Boyd’s condition was then stable until about midnight on December
29, when her condition deteriorated abruptly resulting in quadriplegia. Dr. Silver
testified that a step progression is a classic example of a VAD advancing.
(c) Analysis and Conclusion
[148] Dr. Pelz and Dr. Farb are both eminently qualified radiologists.
They, however, disagree on a number of key points.
[149] The imaging shows what Dr. Pelz was concerned might be a clot on
December 28. Dr. Farb interprets this to be an artifact. No staff radiologist at
LHSC noted a clot. The staff radiologists interpreting this image at the time
would obviously have been able to give it far less attention than Dr. Pelz and Dr.
Farb who no doubt spent many hours considering their opinions.
[150] Dr. Pelz interprets a December 30 image as having a sharp margin
at the area of blockage, which most likely indicates a clot. Dr. Farb sees a
tapering, which likely indicates a dissection.
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[151] Dr. Pelz sees no material change in the dissection from December
28 to January 5. Dr. Farb sees evidence of the dissection having decreased in
size from December 30 to 31 due to the natural process of blood being
resorbed.
[152] The defence asked that I discount the weight to be given to Dr.
Pelz’s evidence on the basis that he was involved in the treatment of Ms. Boyd
and at the time, did not identify a blood clot or a concern of a blood clot in the
imaging he reviewed. Dr. Pelz first reviewed imaging on January 5 and his
report stated he reviewed the December 31 imaging for comparison purposes.
He reviewed imaging on January 22 and his report stated that he reviewed
January 5 and December 31 images for comparison purposes. He also
reviewed imaging on February 5, and his report stated he referred to “multiple
previous MRIs” for comparison purposes. It is, therefore, probable that in the
course of viewing these images, he did not review the December 28 imaging.
By January 5, Ms. Boyd had already suffered her stroke and blood flow in her
RVA had been restored. By that time, the focus would be on her condition and
prognosis, not a forensic analysis of what caused the obstruction days earlier.
While I consider the content of Dr. Pelz’s reports and the nature and extent of
his prior involvement, I do not believe there is any reason to discount his
opinion on this basis.
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[153] The defence also submitted that I should attach significance to the
fact that Dr. Pelz viewed the images using the LHSC software while Dr. Farb
reloaded the images on a different program that allowed computer
reconstruction of the images and facilitated taking measurements. I do not view
this as significant. Dr. Pelz took into account the opinion and reports of Dr. Farb
prior to testifying. I have no doubt that if he believed going back and using
different software would have enhanced the reliability of his evidence he would
have done so.
[154] Dr. Pelz and Dr. Farb both impressed me as conscientious
professionals endeavouring to provide fair and accurate opinions. Nothing in
their evidence suggested to me they were favouring one side over the other. I,
therefore, conclude that their areas of disagreement reflect the fact that the
interpretation of images, and the complexity of the processes at work, creates
considerable uncertainty despite their eminent qualifications.
[155] It is common ground that imaging on December 28 demonstrates
that the dissection had extended to within approximately 8 mm of the point of
blockage. In other words, the dissection was close to the point of blockage
approximately 36 hours prior to the stroke.
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[156] Having said that, the dissection process had been going on for some
time. Ms. Boyd’s headaches began in early December. The defence experts
agreed that her headaches were caused by the extension or expansion of the
VAD. In other words, the dissection had been ongoing for some time and
progressing in a step like fashion. The question is whether it took another step
around midnight on December 29 or whether a clot caused the stroke.
[157] If this was a dissection it somehow progressed past PICA, without
blocking it, to block the ASA. Dr. Farb and Dr. Silver explained, and I accept,
that it is possible that a dissection can spiral around an artery and so bypass
PICA and progress to block the ASA. I also accept the evidence of Dr. Pelz and
Dr. Sharma that it is improbable that a dissection would extend and cause a
blockage beyond PICA yet leave PICA open. The fact that PICA remained
open weighs heavily in favour of this being a clot.
[158] I also accept that the fact that no additional areas of infarction were
identified weighs in favour of the dissection theory. It is common ground,
however, that there is a natural process in the body whereby clots dissolve.
That is a plausible explanation for the fact that no additional areas were
infarcted.
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[159] I also accept Dr. Silver’s evidence that a dissection typically
progresses in a step like manner. The step like progression of a dissection,
however, is not inconsistent with a clot and emboli causing Ms. Boyd’s major
stroke. As noted in the vast majority of dissections, strokes are caused by a
clot and not the dissection.
[160] It was also common ground that clotting is a natural process initiated
if a dissection exposes the inner layer of the artery to flowing blood. It was also
common ground that at some point, a low rate of blood flow promotes clotting.
The experts parted company as to whether the rate of flow in Ms. Boyd was
compromised to the point it promoted clot formation. As I will later explain in
detail, I prefer the evidence of the plaintiffs’ experts on this point and find that
the lowering of Ms. Boyd’s BP and the state of her RVA promoted clot
formation.
[161] In summary:
(a) the lowering of Ms. Boyd’s BP and her irregular, narrowed RVA
created conditions that promoted the formation of blood clots;
(b) the imaging evidence is fairly evenly balanced;
(c) it is improbable that a dissection would not block PICA yet extend
beyond it to block the ASA and this weighs heavily in favour of a
blood clot having caused the stroke;
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(d) the fact there were no additional infarcts weighs only slightly in favour
of the dissection theory as it can also be explained by resorption of
the clot; and
(e) the step like progression of symptoms is equivocal and so not helpful.
[162] Considering the indicia just discussed, and based on the totality of
the evidence, I find that Ms. Boyd’s stroke was caused by a clot and not an
extension of the dissection.
[163] In addition, while I have not relied upon it in making my finding, I
note that the overwhelming statistical probability that Ms. Boyd’s stroke was
caused by a blood clot could provide additional support for this conclusion.
E. DID LOWERING BP AND DELAY IN ADMINISTERING HEPARIN
CAUSE THE STROKE?
(a) Introduction
[164] I have already concluded that as a result of Dr. Edington’s
negligence, Ms. Boyd’s BP was lowered drastically and the administration of
heparin was delayed by eight hours. For the reasons that follow, I conclude that
but for the negligence of Dr. Edington, Ms. Boyd would not have suffered the
stroke which debilitated her.
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(b) Lowering of BP by Dr. Edington
[165] Dr. Edington administered three doses of drugs which had the effect
of reducing Ms. Boyd’s mean BP by 37 per cent in the three hours from 23:15 to
02:15.
(c) LHSC BP Orders
[166] The defence position was that if Ms. Boyd had been transferred
earlier, the LHSC doctors would similarly have administered drugs to reduce
Ms. Boyd’s BP.
[167] On December 28, at 13:30, when the order was made to administer
heparin, an order was also written to administer hydralazine to control BP, only
if the systolic BP exceeded 180 or the diastolic BP exceeded 110.
(d) Plaintiffs’ Expert Evidence
(i) Lowering BP
[168] Dr. Young testified that in his opinion, lowering Ms. Boyd’s BP was
inappropriate and probably caused the left-sided weakness or paralysis that
occurred prior to her transfer to LHSC. Lowering the BP is harmful because it
reduces the blood flow through the narrowed blood artery which allows clots to
form and embolize. Dr. Young said that in the hours leading up to the transfer
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to LHSC, clotting progressed and the longer it went on, the less chance there
was of helping Ms. Boyd.
[169] In his opinion, if there had been an immediate neurological
consultation and a transfer, Ms. Boyd’s BP would not have been lowered and
clotting would have been avoided or lessened. Ms. Boyd would not have
suffered a devastating stroke and any deficits would have been limited to what
she presented with initially. These deficits often improve over time.
[170] In cross-examination, Dr. Young agreed that stroke was not his
primary area of expertise and that he did not research or publish in that field.
[171] Dr. Sharma cited the 2007 American Heart Association / American
Stroke Association, “Guidelines for the Early Management of Adults with
Ischemic Stroke” which stated that:
(a) drugs should not be administered to reduce BP unless diastolic BP
exceeds 120 or systolic BP exceeds 220;
(b) some strokes may be secondary to “hemodynamic factors” (meaning problems related to the flow of blood and pressure) and as a result
lowering BP may lead to neurological worsening; and
(c) BP should be lowered cautiously and a reasonable goal would be to
lower BP by 15-25 per cent within the first day.
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[172] Dr. Sharma testified if a stroke is suspected, you should only lower
BP if absolutely necessary, and then slowly and to a limited extent. BP should
only be reduced in an ICU-type setting under continuous monitoring.
Neurologists are taught that generally there should be no lowering of BP prior to
transfer.
[173] Dr. Sharma noted that Dr. Edington reduced Ms. Boyd’s BP by 37
per cent in three hours, which is far beyond the guideline of 15-25 per cent in 24
hours in the worst cases of hypertension. Dr. Sharma testified that in his
opinion, the immediate and direct effect of lowering Ms. Boyd’s BP was to
cause paralysis by reducing the blood flow. This also promoted the growth of
clots.
[174] In cross-examination, Dr. Sharma was referred to two Cochrane
Collaboration reviews in 2001 and 2009 entitled “Interventions for Deliberately
Altering BP in Acute Stroke (Review)”. These are reviews that search and
compile the results of all relevant research and literature. The 2001 review of
studies that lowered BP concluded there was not enough evidence to decide if
drugs that lowered BP should be used. The 2009 review considered 11 trials
that lowered BP, and one that raised it, and again concluded there was not
enough evidence to decide if drugs that lower or raise BP should be used.
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(ii) Delay in Administering Heparin
[175] Dr. Sharma testified that clots build up over hours and after
formation are unlikely to be successfully treated. Heparin would stop the
process of clotting. In his opinion, the blockage occurred despite Ms. Boyd
being on heparin for 36 hours, because the clot was well-established when the
heparin was first administered.
[176] Dr. Sharma was directed to recent guidelines published by the
American Heart Association / American Stroke Association and the American
College of Chest Physicians as well as best practice recommendations
published by the Canadian Stroke Network. These are the most
comprehensive and authoritative guidelines available. None of the guidelines
recommend the use of heparin to treat acute ischemic stroke.
[177] Dr. Sharma testified that these guidelines and recommendations are
prepared by a committee which synthesizes all of the data. The quality of much
of the data is poor because high quality randomized control trials would be
extremely difficult to do and to date have not been done.
[178] Dr. Sharma also pointed out that in any aggregation of data a patient
like Ms. Boyd, a young female with a VAD, would be underrepresented and far
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different from a typical stroke patient. There is little data regarding
anticoagulants for a patient with her profile.
[179] In cross-examination Dr. Sharma was again referred to the American
and Canadian guidelines and recommendations. He agreed that these
guidelines addressed the treatment of patients with artery dissections including
VAD and did not recommend heparin (except in cases of atrial fibrillation which
Ms. Boyd did not have).
[180] Dr. Sharma stated that Dr. Teal and most neurologists would have
treated Ms. Boyd with heparin; and in his opinion, there was a high probability
treatment would be successful unless the clot was already well-established.
[181] Dr. Sharma testified that the majority of neurologists would have
treated Ms. Boyd with heparin and not simply aspirin. Dr. Sharma agreed that
there is no treatment that can be said with certainty to be effective.
[182] Dr. Sharma was referred to the 2008 “American College of Chest
Physicians Evidence Based Guidelines”. The guidelines recommended against
the use of heparin. The recommendation was immediately followed by:
Remarks: Some experts recommend early anti-coagulation for various
specific stroke subgroups including [. . .] documented intraluminal
thrombus, or arterial dissections. Clinical trials have not, however,
adequately evaluated adjusted dose IV anticoagulation in these selected
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stroke patients. To our knowledge, no adequately powered trials have
evaluated the role of very early anticoagulation (<12 h after stroke onset) in
any stroke population. The risk of hemorrhage may outweigh any benefits.
[183] It was suggested to Dr. Sharma that the remarks recognized that
some experts had a different opinion than the panel that wrote the guidelines.
Dr. Sharma disagreed, stating that the remarks indicated only that there was
inadequate data.
[184] Following re-examination, I asked Dr. Sharma to clarify his comment
to the effect that the guideline process does not usually result in a report on the
consensus recommendations of experts. Dr. Sharma said that there has been
a concern over the years that guidelines be reproducible, like an experiment. In
other words, based on data and not simply the opinion of the experts in the
room. As such, committees writing guidelines generally avoid trying to form a
consensus statement if evidence is absent, of poor quality or conflicting.
(iii) Typical Outcomes for VAD Patients – Efficacy of Treatment
[185] Dr. Young cited a number of studies which found that the vast
majority of patients, in the order of 70-90 per cent with VAD, had generally
favourable outcomes. By that I mean minor defects that did not affect the
patients’ ability to work, live independently and lead a normal life.
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[186] Dr. Sharma testified that the three major determinants of stroke
outcome are the patient’s age, the severity of the initial stroke and the time to
treatment. Age and the relatively mild deficits when she attended Hanover
Hospital were in Ms. Boyd’s favour. Time to treatment at LHSC was, however,
delayed.
(e) Defence Expert Evidence
(i) Lowering BP
[187] Dr. Teal testified that the reduction in BP was not overly aggressive
and that the extent of the drop in BP cannot be controlled precisely. In any
event, it was not lowered to a level that would be of concern.
[188] In acute ischemic stroke, extremely high or extremely low BP is bad,
but the most appropriate intermediate BP is not known. A potential benefit of
reducing BP in the case of dissection is that it reduces the pressure of the blood
flowing into the dissected area. A potential disadvantage of reducing BP is that
a precipitous drop may reduce perfusion to the brain. In Ms. Boyd’s case,
however, her BP was not reduced to a “shocky hypotensive” range such as a
systolic level of 70. Ms. Boyd’s BP was sufficient to allow perfusion.
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[189] In fact, the rate of blood flow in a narrowed vessel increases due to
the venturi effect. Risk of clotting due to slow flow would only occur if blood flow
was reduced to a trickle, and there is no evidence of that.
[190] A major risk of BP being too high is bleeding into the brain.
[191] In cross-examination, Dr. Teal agreed that you can have a dissection
that narrows the artery. A stagnation of blood can possibly cause clotting. A
fragment of a clot, called an emboli, can break off and cause damage.
[192] Dr. Silver testified that Ms. Boyd’s BP was only reduced to a normal
level. Systolic BP coming down to 112-115 would not impact cerebral perfusion.
The orders at LHSC were consistent with what Dr. Edington did and if she had
been transferred earlier, he would have expected her BP to be lowered at
LHSC.
[193] In 2008, and up to today, whether and when to treat BP remains
controversial. In the case of an intradural dissection, there are some reasons to
keep the BP low. High BP can push more blood into the tear, increasing the
dissection. Lowering the BP can also lessen the chance of an SAH caused by
bursting of the outer wall. If, however, arteries are narrow, then reduced BP will
reduce perfusion.
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[194] Ms. Boyd’s major neurological deterioration at Hanover occurred at
02:45. Her lowest BP was two hours later at 04:45. Dr. Silver does not believe
lowering the BP caused the deterioration at 02:45. In his opinion, the
deterioration occurred because the VAD was tracking up and blocking off small
branches that supply blood to the spinal cord and the brain stem.
[195] This is a dynamic process. Sometimes the dissection spirals around
the artery and causes a further narrowing. After a dissection moves intradurally,
there are a multitude of vessels and the symptoms worsen in a step fashion.
Fluctuation exists. It is somewhat difficult to explain, but if the perfusion is
precarious, often the motor deficits will fluctuate over hours and days. A
dissection is usually a step progression, not a steady progression.
[196] When a pipe is narrowed, the flow speeds up. You do not get clot
formation until you have almost complete stagnation and then, if a clot forms on
the tear, it can break away. Dr. Silver was asked, assuming you have a narrow
artery and you lower the BP, whether that allows a clot to form. He said it did
not. You would need almost no BP to retard the flow to the point that it was
almost blocked in order to cause blood stagnation.
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(ii) Delay in Administering Heparin
[197] Dr. Teal testified that in 2008, he would have recommended treating
Ms. Boyd with heparin. He now would not recommend the use of heparin
unless there was evidence of a clot in the artery or an embolic stroke.
[198] Dr. Teal stated that if there was a need for Ms. Boyd to have an anti-
thrombotic drug, the fact is that she had aspirin in her system which, in
accordance with the guidelines, is the recommended therapy. The Hanover
Hospital records show that a blood sample from Ms. Boyd taken at 07:00 on
December 28, had a level of aspirin high enough to have the desired anti-
platelet effect.
[199] Dr. Silver testified that when he started practicing, it was standard to
administer heparin. Now, the consensus opinion as reflected in published
guidelines is that heparin should not be used, although there are exceptions. If,
as in the case of Ms. Boyd, the dissection is intracranial, heparin presents the
added risk of a SAH.
[200] Even if the benefit of heparin outweighs the risk in a particular case,
it does not follow that administering heparin will in fact improve the outcome.
Dr. Silver would not have used heparin to treat Ms. Boyd.
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[201] Dr. Silver testified that the weight of expert/medical/scientific opinion
is that heparin does not work. Starting a treatment that does not work earlier
cannot logically improve the outcome.
(iii) Typical Outcomes for VAD Patients – Efficacy of Treatment
[202] The defence experts agree that most patients with intracranial VAD
have favourable outcomes in the sense that any deficits do not affect the ability
of the patient to care for herself and be engaged in the ordinary activities of life.
The defence experts, however, point to the fact that a subset of patients die or
suffer severe disability despite timely and appropriate treatment.
[203] The defence experts also identified a great number of factors
associated with outcome, including the size of the dissection, the location of the
dissection and the anatomy of the patient. Dr. Silver reviewed the medical
literature and found only eight other cases in which VAD resulted in spinal cord
infarction. The defence submission was that the focus should be on the
characteristics of Ms. Boyd and not on statistics.
[204] The lack of effective treatment options is indicated by the following
data that both Dr. Young and Dr. Silver testified to:
(a) with tPA (“tissue plasminogen activator” - the clot busting drug) one
in eight or ten patients has a better outcome;
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(b) with heparin, 1 in 111 patients has a better outcome; and
(c) with aspirin, 1 in 100 patients has a better outcome.
(f) Analysis and Conclusion
[205] It was common ground that in the case of acute stroke it is beneficial
to keep BP within a specific range. In other words, physicians are to avoid
extremely high BP which can result in increased blood flow into a dissected
area and increased risk of an artery rupture and bleed. They are also
cautioned to avoid very low BP, which may reduce blood flow to tissue and
thereby cause infarcts.
[206] On presentation, Ms. Boyd’s BP was 170/112. The 2007 “American
Heart Association / American Stroke Guidelines” cited by Dr. Sharma,
recommend that in the setting of an acute stroke, BP should not be lowered
unless systolic BP exceeds 220 or diastolic BP exceeds 120. It was not
suggested that particular characteristics of Ms. Boyd made this guideline
inapplicable. (I recognize there are other guidelines which vary slightly). I also
note that at LHSC the initial BP orders were directed to maintaining Ms. Boyd’s
BP less than 180 systolic and 110 diastolic.
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[207] The most that can be said, from the defence perspective, is that on
presentation, Ms. Boyd’s BP was at a level where some doctors might consider
lowering it. Dr. Teal made the point that a doctor cannot predict or control how
quickly a particular dose will lower BP. For that reason it does not make sense
that steps to lower Ms. Boyd’s BP would have initiated just prior to putting her in
an ambulance for a two-hour trip. I am certainly satisfied, however, that if Dr.
Edington had met the standard of care and contacted LHSC after his initial
assessment, he would have been advised to not lower her BP.
[208] I do not accept the defence argument that lowering Ms. Boyd’s BP at
Hanover was immaterial because if she was transferred to LHSC earlier, the
doctors there would have lowered Ms. Boyd’s BP to the same extent Dr.
Edington did.
[209] At Hanover, Ms. Boyd’s systolic BP was never so high that the
LHSC orders would have called for it to be reduced. Ms. Boyd’s diastolic was
less than 10 per cent higher than the LHSC orders allowed.
[210] I am not satisfied that if Ms. Boyd had presented at LHSC with the
BP she presented at Hanover that her BP would have been lowered at all. Her
systolic BP was never in a range that called for intervention and her diastolic
BP was only slightly in the range. In the alternative, if LHSC had decided to
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lower Ms. Boyd’s BP, in accordance with Dr. Sharma’s evidence it would have
been at a controlled and much slower rate. As a consequence, any impact on
Ms. Boyd’s blood flow would have been much less than she experienced due to
her treatment at Hanover Hospital.
[211] In any event, even assuming LHSC would have administered drugs
to lower Ms. Boyd’s BP to the same degree as Dr. Edington, there is a very
significant difference between what would have happened if Dr. Edington met
the standard of care and what did happen:
(a) if Dr. Edington met the standard of care Ms. Boyd’s BP would only have
been lowered December 28 at 13:30 at LHSC at the same time heparin
was administered. As such, while the lowered BP would promote clot
formation the heparin would inhibit clot formation; and
(b) because Dr. Edington breached the standard of care, Ms. Boyd’s BP
was lowered by December 28 at 02:15 which promoted clot formation
while heparin, which would inhibit clot formation, was not administered
until approximately ten hours later.
[212] It is, therefore, much more probable that the clot which caused Ms.
Boyd’s stroke formed between 02:15 and 13:30 than at some later time.
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[213] As such, even if LHSC had lowered Ms. Boyd’s BP to the extent Dr.
Edington did, that would not change my reasoning and conclusion as to
causation.
[214] As Dr. Sharma explained, Ms. Boyd’s mean BP was reduced by
approximately 37 per cent in three hours, far outside the guideline
recommendation.
[215] Dr. Sharma testified that the lowering of Ms. Boyd’s BP had an
immediate and observable effect, being Ms. Boyd’s inability to move her left
arm. In Dr. Sharma’s opinion, the reduced blood flow promoted the growth of
clots. Dr. Young testified that with lower BP the artery narrows which allows
blood clots to be created and increase.
[216] Dr. Teal and Dr. Silver did not take issue with the fact that at some
point, low BP increases the risk of clotting and accelerates the growth of clots.
Dr. Teal said this would only occur if blood flow was reduced to a trickle. Dr.
Silver said you would need to reduce BP and retard blood flow to the point it
was almost blocked to cause blood stagnation. Dr. Teal and Dr. Silver point to
the fact that Ms. Boyd’s BP was only reduced to a normal range, supporting
their opinion that lowering her BP did not cause or contribute to clot formation.
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[217] It is common ground that a dissection can expand the artery wall and
so narrow the artery or even block it. It makes sense to me, that with high BP,
a tipping point would be reached at which the artery opening would be
maintained and with a 37 per cent reduction in BP it would close. We know
from Ms. Boyd’s fluctuating symptoms that blood flow to the critical area
governing motor functions was tenuous. An inability to move limbs is indicative
of the fact that the brain and spinal cord cells are deprived of oxygen and sugar
without which the cells will eventually cease to function and die. It follows that in
certain areas Ms. Boyd’s blood flow was severely compromised, as Dr. Teal put
it to a “trickle”.
[218] To summarize, Ms. Boyd’s RVA was narrowed and irregular to the
extent that the blood flow to parts of her brain was tenuous resulting in her
fluctuating symptoms. The reduction in her BP was drastic. Dr. Sharma and
Dr. Young took account of these facts, as well as the temporal connection
between the drastic reduction in Ms. Boyd’s BP and her neurological
deterioration. They concluded that lowering her BP resulted in blood clots
forming. This all makes sense to me.
[219] As mentioned, Dr. Teal and Dr. Silver pointed to the fact that Ms.
Boyd’s BP was only reduced to a normal range as supporting their opinion that
BP did not cause or contribute to the formation of clots. This does not make
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sense to me. A number of witnesses analogized an artery to a hose. The
amount of water that will flow out of a hose is a function not only of the water
pressure but also the extent of any obstructions which may reduce the flow out
the other end.
[220] Dr. Teal and Dr. Silver also cited the venturi effect as supporting
their opinion. Far from reducing flow they suggested that areas of the artery
narrowed by dissection would experience accelerated flow. I fail to see how the
venturi effect has any application to an artery dissected over a considerable
length and narrowed to the point that brain perfusion was tenuous.
[221] In discussing their evidence on standard of care, I concluded that Dr.
Teal and Dr. Silver failed to focus on Ms. Boyd and resorted to the general
emergency department experience to support their opinion that alcohol was a
confounding factor. I concluded that this evidenced an element of partiality or
advocacy. I have similar concerns with the evidence just referred to. Ms.
Boyd’s BP was obviously not the only factor determining the rate of blood flow
in her RVA. My conclusion is that in arriving at their opinions that the lowering
of Ms. Boyd’s BP did not cause or contribute to clotting, Dr. Teal and Dr. Silver
again failed to focus adequately on the specific condition of Ms. Boyd. Their
evidence on these points similarly suggested partiality or advocacy on their
part.
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[222] I am satisfied and find as a fact that the lowering of Ms. Boyd’s BP at
Hanover Hospital reduced Ms. Boyd’s blood flow in her RVA to a “trickle” which
had the effect of promoting the formation and growth of clots. As already
explained, I have concluded that a blood clot caused Ms. Boyd’s stroke.
[223] It is common ground that:
(a) heparin is an anti-coagulant which has the effect of inhibiting the
formation of blood clots; and
(b) blood clots form and grow over time creating a higher risk of emboli and stroke.
[224] The opinion of both Dr. Sharma and Dr. Young was that if Dr.
Edington had initiated the transfer of Ms. Boyd to LHSC immediately after
assessing her, she would have received heparin earlier and this would probably
have inhibited clot formation resulting in a favourable outcome.
[225] Dr. Teal and Dr. Silver emphasized the fact that Canadian and U.S.
guidelines do not recommend the use of heparin under any circumstances. As
Dr. Silver put it, an earlier start to a treatment that does not work earlier does
not make any difference.
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[226] Dr. Sharma made the point that guidelines are necessarily based
upon large numbers of patients most of whom would have characteristics quite
different from Ms. Boyd.
[227] Despite the fact that the guidelines do not recommend the use of
heparin under any circumstances, the evidence is that it has been and
continues to be administered by leading stroke experts. Dr. Nicolle at LHSC
administered heparin to Ms. Boyd. Dr. Sharma would have administered
heparin and indicated that a majority of his colleagues would have done the
same. Dr. Young agrees. Dr. Teal also would have administered heparin at
the time. Dr. Teal would still administer heparin to treat a proven clot within an
artery, which is what I have concluded caused Ms. Boyd’s stroke. Dr. Silver
also acknowledged that there are exceptions to the general rule against heparin
use.
[228] This puts the guidelines in context and supports Dr. Sharma’s
evidence concerning them. The highly trained neurologists who have and
continue to administer heparin are not doing so because they prefer anecdotal
experience to evidence-based practice as reflected in the guidelines. They are
doing so recognizing that unique patient characteristics may render guidelines
and statistics unhelpful or irrelevant. They are doing so based upon their
clinical judgment, which is obviously informed by their years of practice, the
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thousands of cases they have handled and the tens of thousands of cases that
their colleagues have handled and they have learned about.
[229] It is also significant that guidelines are prospective in nature. They
address what should be done in average or common cases in light of all the
risks that the treatment presents. In giving their evidence, Dr. Teal and Dr.
Silver’s viewpoint was also prospective.
[230] In considering causation, however, I consider matters
retrospectively. A major concern with heparin is the risk of causing a bleed. In
the case of Ms. Boyd, where the dissection was intracranial, a particular risk
was a SAH which results in devastating injury or death. Patients with these
types of unfavourable outcomes are obviously included in research data and
these risks weigh heavily in determining general guidelines.
[231] The fact is, however, that in hindsight we know that Ms. Boyd was
administered heparin and did not suffer a bleed or SAH. Perhaps she was, as
Dr. Sharma said, atypical in that she was young and had an initial stroke with
an extremely small area of infarction. Perhaps Ms. Boyd was simply lucky to
have avoided these risks. The fact is she did.
[232] Given the stature of the expert witnesses, I am certainly satisfied
that the opinions were based upon all relevant scientific data available. I,
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therefore, infer and conclude that the state of science is such that it does not
inform a number of pertinent considerations such as:
(a) under what precise conditions do clots form;
(b) at what rate do clots grow;
(c) at what size and under what precise circumstances do clots
embolize;
(d) at what size do clots cause damage in particular blood vessels; and
(e) at what rate do clots dissolve due to natural body processes.
[233] We know with certainty, however, that blood clots form and grow
over time. We know with certainty heparin inhibits blood clots. We know with
certainty that since heparin inhibits clots, the earlier it is administered, the fewer
and/or smaller clots there will be. We know with certainty that Ms. Boyd
avoided the most significant risks associated with the use of heparin as she did
not have a bleed or SAH.
[234] I have considered the significance of Dr. Teal’s evidence that as of
07:00 on December 28, Ms. Boyd had aspirin in her body at a level that would
have an anti-platelet effect. There was limited evidence concerning the
distinction between aspirin, which inhibits blood platelets from adhering to each
other and artery walls, and heparin, which is an anticoagulant. As discussed,
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aspirin is recommended by the guidelines because it has benefits without the
increased risk of a bleed presented by heparin.
[235] On the evidence before me it is clear, and I find, that heparin would
have been more effective in treating Ms. Boyd having regard to the following:
(a) Dr. Sharma would have administered heparin and he believes that
most stroke neurologists would have;
(b) Dr. Nicolle at LHSC administered heparin;
(c) Dr. Teal testified he will still administer heparin if there is evidence of
a clot in the artery; and
(d) Dr. Silver testified in select cases he will still administer heparin.
[236] For the reasons discussed, I prefer the evidence of Dr. Sharma and
Dr. Young to that of Dr. Teal and Dr. Silver as to the efficacy of heparin if it had
been administered earlier. I also accept the evidence of Dr. Sharma that the
guidelines are of very limited assistance in deciding this case given their
inherent limitations and the unique circumstances of Ms. Boyd. I find as a fact
that if Ms. Boyd had been administered heparin approximately eight hours
earlier it would have resulted in no, fewer and/or smaller clots.
[237] In my opinion this case is analogous to Clements, in which the
plaintiff, Ms. Clements, was a passenger on a motorcycle operated by her
husband. Mr. Clements was not aware a nail had lodged in one tire. The
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motorcycle was overloaded by 100 pounds and being driven 20 kph over the
speed limit at the time the nail dislodged and the tire deflated rapidly. Mr.
Clements lost control of the motorcycle resulting in a crash and severe injury to
Ms. Clements.
[238] In that case there were three factors to consider:
(a) the no-fault factor being the nail that fell out of the tire causing rapid
deflation;
(b) the at fault factor that the defendant was driving 20 kph too fast; and
(c) the at fault factor that the defendant overloaded the motorcycle by
100 pounds.
[239] The Supreme Court of Canada noted at para. 48 that the trial judge
accepted expert evidence that:
[A]fter the fact, it is not possible through accident reconstruction modelling
to determine at what combination of lower speed and lesser weight
recovery from the weave instability would have been practicable.
[240] Further, the court held that the trial judge erred in reasoning that
because expert scientific evidence could not determine the interplay of these
three factors, the plaintiff could not prove “but for” causation.
[241] Chief Justice McLachlin for the majority stated, at para. 49:
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As discussed above, the cases consistently hold that scientific precision is
not necessary to a conclusion that “but for” causation is established on a
balance of probabilities. It follows that the trial judge erred in insisting on
scientific precision in the evidence as a condition of finding “but for”
causation.
[242] Chief Justice McLachlin referred to the fact that:
(a) instability would increase with higher speed;
(b) instability would increase with overloading;
(c) the judge was left with no scientific evidence one way or the other as
to whether the accident would have occurred absent the excessive
speed and overloading; and
(d) ordinary common sense supported the relation between the
excessive speed and weight and the injury.
[243] The factors in our case are:
(a) the no fault factor being the VAD Ms. Boyd suffered can initiate the
clotting process;
(b) the at fault factor that Ms. Boyd’s BP was lowered drastically which I
have found created conditions that promoted clot formation and
growth; and
(c) the at fault factor that the administration of heparin, which inhibits the
formation and growth of blood clots, was delayed by eight hours.
[244] As in Clements, there is no scientific test or model which can
determine one way or the other whether the clot that caused Ms. Boyd’s stroke
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would have formed and grown to the size it did if Ms. Boyd’s BP had not been
lowered and if heparin was administered earlier.
[245] As in Clements, ordinary common sense supports the relation
between conditions promoting clot formation and growth, late administration of
heparin which inhibits clot formation and growth and Ms. Boyd’s stroke which
was caused by a clot.
[246] As I interpret Clements, it is my responsibility to determine whether
on the totality of the evidence, and taking “a robust common sense” approach
to causation. I am satisfied on a balance of probabilities that “but for” the
negligence of Dr. Edington, Ms. Boyd would not have suffered a debilitating
stroke.
[247] Ms. Boyd’s dissection probably began in early December 2008 and
was certainly in progress by December 20, when she started experiencing very
severe headaches. There was no evidence of clot formation prior to Hanover
Hospital. Dr. Edington lowered her BP precipitously, creating conditions
promoting clot formation and growth. Approximately 48 hours later, Ms. Boyd
suffered a stroke caused by a clot. For approximately 36 of those 48 hours,
she was being administered heparin which inhibits clot formation and growth.
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[248] For the reasons given, I prefer and accept the opinions of Dr.
Sharma and Dr. Young to the opinions of Dr. Teal and Dr. Silver as to the effect
of lowering Ms. Boyd’s BP. The evidence of Dr. Sharma and Dr. Young, and
the chronology just referred to, satisfies me on a balance of probabilities and I
find as a fact that the clot which caused Ms. Boyd’s stroke was the result of Dr.
Edington’s drastic lowering of Ms. Boyd’s BP. As a result, the plaintiffs have
established but for causation.
[249] I now turn to whether the plaintiffs have also established but for
causation by reason of the delayed administration of heparin.
[250] Blood clots grow over time and the larger the blood clot the more
likely it can block an artery and cause a stroke. Heparin inhibits the formation
and growth of blood clots. But for Dr. Edington’s breach of the standard of care
heparin would have been administered to Ms. Boyd approximately eight hours
earlier. It follows that the blood clot which caused Ms. Boyd’s stroke was larger
by reason of the delayed administration of heparin.
[251] Taking “a robust common sense” approach to causation, considering
the totality of the evidence, and given my reasons for preferring the evidence of
Dr. Sharma and Dr. Young to that of Dr. Teal and Dr. Silver, I am also satisfied
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on a balance of probabilities that “but for” the delay in the administration of
heparin Ms. Boyd would not have suffered a debilitating stroke.
[252] In reaching my conclusion I have not relied upon the evidence that
VAD patients generally have favourable outcomes. There are probably
hundreds of variables that affect stroke outcome. Most stroke patients have a
good outcome but some die. I cannot reliably reason that because most
patients have a favourable outcome, there is a greater likelihood that Ms.
Boyd’s outcome was caused by fault on the part of Dr. Edington.
F. DAMAGES
[253] The parties agreed that if liability was established damages should
be awarded in the amount of $15,000,000.
[254] It remains to consider costs and post-judgment interest. To allow
the parties time to try to resolve these issues:
(a) the plaintiffs shall submit their costs outline and written submissions within 60 days;
(b) the defendant shall respond within 30 days of receiving the plaintiffs’
submission; and
(c) the plaintiffs shall serve any reply within a further ten days.
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G. CONCLUSION
[255] This case was presented and defended very capably and
professionally by counsel. I thank them all for their assistance.
___________________________ Sproat J.
Released: February 20, 2014
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CITATION: Boyd et al. v. Edington et al., 2014 ONSC1130
COURT FILE NO.: 29/12
DATE: 2014-02-20
ONTARIO
SUPERIOR COURT OF JUSTICE
B E T W E E N :
DANIELLE EDITH BOYD, ELAINE LUCIE
FRETZ, RICHARD JAMES BOYD, and
KAIDEN RICHARD BOYD by his Litigation
Guardian, Elaine Lucie Fretz
Plaintiffs
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DR. RICHARD BRUCE EDINGTON
Defendant
REASONS FOR JUDGMENT
Sproat J.
Released: February 20, 2014
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