COURT FILE NO.: CV-14-514950
DATE: 20211124
ONTARIO
SUPERIOR COURT OF JUSTICE
BETWEEN:
RHODALEE LECKIE, MARLENE PALMER, KIMISHA FORDEN and TAMGWENA LECKIE
Plaintiffs
– and –
DR. ABRAHAM CHAITON, ABRAHAM CHAITON MEDICINE PROFESSIONAL CORPORATION, JEAN PAUL LI CHEONG HAN, PHARMCARE SERVICES LTD. and HUMBER RIVER HOSPITAL
Defendants
Justin Linden, for the plaintiff Rhodalee Leckie
Junior Sirivar, Jessica Laham, for the defendant, Dr. Abraham Chaiton
HEARD: April 12 to 20, 2021
REASONS FOR DECISION
J.E. Ferguson j.
[1] This is a medical malpractice action which proceeded to trial on April 12 to 20, 2021. Only Dr. Chaiton remained as a defendant. The action is dismissed and these are the Reasons.
[2] After hearing the evidence, the trial was adjourned in order to obtain the trial transcripts and provide time for counsel to provide written submissions. Those have now been received and include the plaintiff’s submissions dated May 10, 2021; Dr Chaiton’s submissions dated May 31, 2021; and the plaintiff’s reply submissions dated June 7, 2021. I am not including the cites in these Reasons which reference evidence as they are correct.
[3] Dr. Chaiton is a community based rheumatologist practicing in North York, Ontario. At all relevant times, he held privileges at Humber River Regional Hospital (“HRRH”). Dr. Chaiton had practiced rheumatology for almost 35 years at the time he treated Ms. Leckie.
Preliminary issues raised by Dr. Chaiton
[4] Dr. Chaiton’s submission is that this court must exercise extreme caution in its assessment of the written closing submissions put forward by the plaintiffs. He submits that the plaintiffs’ written closing submissions are replete with factual assertions that are unsupported by the evidence adduced at trial; evidence is frequently summarized without any reference whatsoever to the record; and critical points are misstated, miscited, summarized inaccurately or, on occasion, stated in a manner that is manifestly incorrect or misleading. Counsel for Dr. Chaiton has provided a table of what he submits are some of the more egregious inaccuracies in the plaintiffs’ written submissions attached as Schedule “A” to these reasons. Plaintiff’s counsel disagrees. From my review of this table, compared to the evidence I heard at trial, I agree that there are many problems with the plaintiff’s submissions. However, I will keep an open mind as I decide this matter.
[5] In addition, Dr. Chaiton submits that the plaintiffs’ written closing submissions include allegations of breaches of the standard of care that were not advanced by their expert. They instead rely on literature which was not introduced as evidence at trial. This includes, but is not limited to, literature in the plaintiff’s “brief of exhibits” that was not ultimately introduced at trial. Counsel for Dr. Chaiton apparently raised concerns when counsel for the plaintiffs uploaded the “brief of exhibits” to caselines in advance of trial on the basis that it was not proper for the plaintiffs to have done so unilaterally without them having been properly introduced as exhibits at trial. I confirm that I did not access this brief and will not rely on anything which was not properly made an exhibit.
[6] Counsel for Dr. Chaiton submits that none of the materials which have been improperly put before this court without having been entered into evidence can be considered. They have provided a separate table which outlines materials relied on by the plaintiffs in their written closing submissions that were not put in evidence at trial. This is attached as Schedule “B” to these Reasons.
[7] Plaintiff’s counsel has provided an explanation and his belief that these have been properly adduced as evidence. I have to comment that there was a somewhat haphazard use of the medical literature by plaintiff’s counsel.
[8] Counsel for Dr. Chaiton also submits that the new theory of misdiagnosis of gout (as not occurring) has not been pleaded properly and that I should not allow it. On that issue, I will give the plaintiff’s pleading a wide reading and allow it.
The Witnesses
[9] Ms. Leckie testified as did her daughter, Marlene Palmer (“Ms. Palmer”). Dr. Laurence Rubin (“Dr. Rubin”) a rheumatologist also testified for the plaintiff. Ms. Leckie had no expert on causation.
[10] Dr. Chaiton testified. His expert Dr. Philip Baer (“Dr. Baer”), a rheumatologist testified as did his causation expert, Dr. Michael Rieder (“Dr. Rieder”), a clinical pharmacologist.
The Law
A. The Standard of Care
[11] In an action alleging medical negligence on the part of a physician, the plaintiffs bear the burden of proof. To meet the standard of care, a physician must exercise the degree of skill and care expected of a normal, prudent physician with comparable training and experience in the same circumstances.[^1] The Supreme Court of Canada articulated the physician’s standard of care in ter Neuzen v. Korn as follows:
It is well settled that physicians have a duty to conduct their practice in accordance with the conduct of a prudent and diligent doctor in the same circumstances. In the case of a specialist, such as a gynaecologist and obstetrician, the doctor's behaviour must be assessed in light of the conduct of other ordinary specialists, who possess a reasonable level of knowledge, competence and skill expected of professionals in Canada, in that field. A specialist, such as the respondent, who holds himself out as possessing a special degree of skill and knowledge, must exercise the degree of skill of an average specialist in his field.[^2]
[12] A specialist owes a higher degree of skill.[^3]
[13] A doctor must take a proper history from the plaintiff.[^4]
[14] A doctor must employ all usual diagnostic aids.[^5]
[15] The standard of care is reasonable care, not a gold standard.[^6] A physician’s honest and intelligent exercise of judgement will satisfy the standard of care.[^7] A doctor is not responsible, at law, for every bad outcome a patient may have.[^8]
[16] The physician’s care must be assessed in light of the medical knowledge and circumstances that they ought to have been aware of at the time of the alleged negligence – without the benefit of hindsight. The Supreme Court of Canada explained this as follows:
[T]he conduct of physicians must be judged in the light of the knowledge that ought to have been reasonably possessed at the time of the alleged act of negligence. As Denning L.J. eloquently stated in Roe v. Ministry of Health; Woolley v. Ministry of Health, [1954] 2 All E.R. 131 (C.A.), at p. 137, “we must not look at the 1947 accident with 1954 spectacles”. That is, courts must not, with the benefit of hindsight, judge too harshly doctors who act in accordance with prevailing standards of professional knowledge.[^9]
[17] The focus should be on whether the physician behaved similarly to a reasonably prudent and diligent fellow physician in the same circumstances:
To ask, as the principal question in the general inquiry, whether a specific positive act or an instance of omission constitutes a fault is to collapse the inquiry and may confuse the issue. What must be asked is whether that act or omission would be acceptable behaviour for a reasonably prudent and diligent professional in the same circumstances. The erroneous approach runs the risk of focusing on the result rather than the means. Professionals have an obligation of means, not an obligation of result.[^10]
[18] The approach should not be outcome-based or retrospective. Physicians are not liable for errors in judgment when the physician’s judgment was exercised honestly and intelligently in contemplation of the relevant facts known at the time the decision was made.[^11] An error of judgment, including one which may prove wrong or have unexpected consequences, does not amount to negligence if the medical professional appropriately applied clinical judgment.[^12]
[19] A physician is not required to know everything about a medication being prescribed to a patient. The physician is only required to have the knowledge of the average competent practitioner in the same specialty.[^13]
[20] A physician is also not expected to have immediate knowledge of every new publication, nor change his practice, in respect of every new development. The court has stated the following:
The dissemination of new literature takes some time, and a medical doctor is not expected to react immediately, or change standard practices, in response to every new article that is published. Often new studies and recommendations are received with some scientific scepticism, while replication of the results is awaited. Immediate response to every publication is unrealistic.[^14]
[21] A finding of a breach of the standard of care must be grounded in evidence from appropriate experts:
In assessing the performance of skilled professionals… courts must be cautious to base their conclusions upon the expert evidence before them, and not to speculate as to the adequacy of professional standards in the absence of expert evidence attacking those standards.[^15]
[22] The Supreme Court of Canada has repeatedly cautioned courts that great care must be taken in assessing (and second-guessing) the actions and decisions of medical doctors in the course of discharging their professional obligations. Courts cannot prefer the prevailing opinion of the majority of physicians over a smaller but equally competent and responsible body of opinion. The plaintiff must prove that the course of action was not a choice that would have been made by a reasonable, competent physician in the circumstances. The Supreme Court of Canada stated this principle as follows:
What the surgeon by his ordinary engagement undertakes with the patient is that he possesses the skill, knowledge and judgment of the generality or average of the special group or a class of technicians to which he belongs and will faithfully exercise them. In a given situation some may differ from others in that exercise, depending on the significance they attribute to the different factors in light of their own experience. The dynamics of the human body of each individual are themselves individual and there are lines of doubt and uncertainty from which a clear course of action may be precluded. There is here only the question of judgment; what of that? The test can be no more than this: was the decision the result of the exercise of the surgical intelligence professed? Or was what was done such that, disregarding that it may be the exceptional case or individual, in all the circumstances, at least the preponderant opinion of the group would have been against it? If a substantial opinion confirms it, there is no breach or failure.[^16]
[23] There are often alternative courses of action and reasonable professionals may disagree on which course of action to adopt. As noted by the court “[d]ifferences of opinion are a common experience in the medical and other professions”[^17]:
Where the subject matter is one requiring expert knowledge of a specialized area, and qualified respected specialists cannot themselves reasonably agree on the appropriate conduct, common sense dictates that the court should not decide that one body of opinion is more persuasive than another. Where reasonably informed people disagree, one of them cannot be labeled negligent.[^18]
[24] A finding of a breach of the standard of care must be grounded in evidence from appropriate experts:
In assessing the performance of skilled professionals…courts must be cautious to base their conclusions upon the expert evidence before them, and not to speculate as to the adequacy of professional standards in the absence of expert evidence attacking those standards.[^19]
[25] Where there are conflicting expert opinions, the court must weigh the conflicting testimony and ultimately assess the weight to be given to the evidence.[^20] The assessment of the appropriate standard of care expected of a physician should be done through the eyes of a physician of the same background and training, in the same circumstances. Those “same circumstances” include the community in which the physician works, and the resources available to the physician in that community. The standard of care applicable to a physician is determined by reference to the degree of learning and skill possessed by the physicians “in similar communities in similar cases”.[^21]
[26] Common sense dictates that physicians who have the benefit of working in an academic setting are, in general, better-equipped, better serviced and have greater exposure to new medical literature. In Stepita v. Dibble, this court accepted that where the defendant was a community physician, the opinion of an expert community physician should be preferred to that of a specialist practicing in a tertiary care:
On the narrow issues in this case where Dr. Weeks’ opinion is at odds with that of Dr. Myers, Dr. Weeks’ evidence ought to be preferred for six reasons…First, Dr. Myers is not a peer of Dr. Dibble. He is a cardiologist at a tertiary care centre, whereas Dr. Dibble (like Dr. Weeks) practices at a community hospital.[^22]
[27] The standard of care in this action is the standard of care expected of a normal, prudent, rheumatologist of comparable training and experience similarly situated to Dr. Chaiton in 2012.
[28] While a finding that a physician breached the standard of practice must be grounded in expert evidence, evidence of an expert’s own practice is not evidence of the standard of care. As stated by this court:
To the extent that an expert testifies as to what he himself would do in a situation, rather than what the standard of care requires, his testimony does not establish the standard of care nor demonstrate that the defendant doctor breached a standard of care. As the court wrote in Campbell v. Hess (June 8, 1994), Toronto 51145/90 (Ont. Gen. Div.):
I note particularly that although Dr. Wiggle stated that he himself would not have discontinued the Coumadin he did not state in his evidence that Dr. Hess fell below the standard of care for a cardiologist in March 1989 in the circumstances that presented themselves. Thus Dr. Wiggle did not give opinion evidence concerning the standard of care; it can be argued that the inference can surely be drawn from his evidence that that is his view. It may well be his view but such an important piece of evidence that is an expert opinion on the standard of care, in my view, ought not to be left to a conclusion drawn by inference in the case of a negligence claim against a professional specialist.[^23]
[29] A negative inference can be drawn when a physician’s record-keeping is lacking:[^24]
[The physician’s] lack of proper medical records makes his evidence quite incredible. ... Because of the lack of charting of any information given to [the patient] and her consent, I am also of the view that she did not consent to the treatment of Haldol during that year. [^25]
[30] When records are incomplete, the court will generally favour the testimony of the plaintiff who has good reason to recall important information over the doctor where the interaction was just one more in a busy practice. The court stated the following:
It is unfortunate that Dr. Munthali did not make careful notes. This was a routine house call to him and he did not hear of the death until notified by the College of Physicians and Surgeons some months later. On examination for discovery he said he did not hear of the death until served with the writ but he was clearly mistaken. Mrs. Dale's memory of the events leading up to her husband's death would, of course, be sharpened by the impact of his death. In retrospect this was not just a routine house call to her and I think she would tend to remember every detail of what occurred. [^26]
B. Informed Consent
[31] The test for informed consent in a medical negligence action requires the plaintiff to establish both that: (i) there was inadequate disclosure of the nature of the treatment and its risks; and (ii) the lack of disclosure caused the damage complained of.[^27] Even if the plaintiff can establish that there was inadequate disclosure, she will not succeed unless she can also establish that she would not have consented to the treatment if adequate disclosure had been made. Considering whether the plaintiff would have consented to the treatment had disclosure been made requires both a subjective and objective analysis.
[32] The Supreme Court of Canada elaborated on the first branch of the informed consent test as follows:
In summary, the decided cases appear to indicate that in obtaining the consent of a patient for the performance upon him of a surgical operation, a surgeon, generally, should answer any specific questions posed by the patient as to the risks involved and should, without being questioned, disclose to him the nature of the proposed operation, its gravity, any material risks and any special or unusual risks attendant upon the performance of the operation. However, having said that, it should be added that the scope of the duty of disclosure and whether or not it has been breached are matters which must be decided in relation to the circumstances of each particular case.[^28]
[33] The law anticipates that the patient will communicate her concern about the treatment to the physician. It is only when such concern is communicated, that the physician can be expected to react to the specific concern of the patient.[^29]
[34] In determining whether a given risk is, in fact, material and should be disclosed, the Supreme Court of Canada noted that:
Expert medical evidence was, of course, relevant to findings as to the risks that resided in or are a result of a recommended surgery or other treatment. It will also have a bearing on their materiality.[^30]
[35] It is the physician’s responsibility to exercise professional judgment with regards to the information provided to a patient. The clinical judgment of a physician based on his knowledge and experience is an acceptable basis on which to determine the information necessary to be communicated to the patient to meet the standard of care.[^31] There can be no failure to inform of an alternative treatment unless the expert evidence establishes that such alternative treatment was medically indicated. A physician’s obligation to disclose treatment alternatives is limited to those alternatives the physician believes will offer the patient an advantage:
One further aspect of the physician's duty of disclosure is to advise the patient of "any available alternatives to the treatment being proposed, as well as the material risks associated with those alternatives"; however this extends only to alternatives which the physician believes "offer some advantage and are reasonably likely to achieve a beneficial result".(Picard, E.I. and Robertson, G.B. Legal Liability of Doctors and Hospitals in Canada, 3rd edition (Agincourt: Carswell, 1996), p. 130).[^32]
[36] Whether a physician has an obligation to disclose alternative treatment options will also depend on the patient’s factual circumstances:
It is impossible to delineate the reach of a doctor's disclosure obligation without regard to the facts and circumstances of specific cases. The extent to which a doctor must disclose and discuss alternative treatments will depend on a myriad of factual circumstances.[^33]
[37] The second branch of the informed consent test was described by the Supreme Court of Canada as follows:
…whether a reasonable person in the circumstances of the plaintiff would have consented to the proposed treatment if all the risks had been disclosed.[^34]
[38] The test recognizes that:
…fears which are idiosyncratic… cannot be considered… It ensures that a plaintiff would not be able to successfully prove causation simply by demonstrating an irrational fear which, had the physician disclosed all the risks, would have convinced the plaintiff to forego medical treatment.[^35]
[39] The patient’s own testimony as to what treatment she would have chosen is inherently unreliable because it cannot be expected that a patient bringing the action would admit that she would have agreed to the treatment, even knowing all of the accompanying risks. The appeal court cautioned the trial courts that:
The plaintiff will invariably state with all the confidence of hindsight and with all the enthusiasm of one contemplating an award of damages that consent would never have been given if the disclosure required by an idiosyncratic belief had been made. This would create an unfairness that cannot be accepted.[^36]
[40] Consequently, the court must consider the issue objectively, but based on “the patient’s particular circumstance”.[^37]
[41] A doctor has an obligation to educate and inform a patient. The Ontario Court of Appeal set out the approach to take:
…The ultimate decision whether to proceed with a particular treatment rests with the patient and not the doctor. The doctor must equip the patient with the information necessary to make an informed choice. Where there is more than one medically reasonable treatment and the risk/benefit analysis engaged by the alternatives involves different considerations, a reasonable person would want to know about the alternatives and would want the assistance of the doctor's risk/benefit analysis of the various possible treatments before deciding whether to proceed with a specific treatment. Put differently, a reasonable person could not make an informed decision to proceed with treatment "A" if that patient was unaware of the risks and benefits associated with treatment "B", a medically appropriate alternative treatment.[^38]
[42] Individuals have a fundamental right to make their own health care decisions which is protected in negligence law through the doctrine of informed consent. The Supreme Court, put it this way: “The doctrine of informed consent dictates that every individual has a right to know what risks are involved in undergoing or foregoing medical treatment and a concomitant right to make meaningful decisions based on a full understanding of those risks”. Our courts have appropriately placed the obligation on physicians to provide their patients with all the material information they need to consider proposed treatment. As a matter of law, doctors must, without being questioned, disclose "the nature of the proposed operation, its gravity, any material risks and any special or unusual risks attendant upon the performance of the operation".[^39] This includes the right to refuse unwanted medical treatment.[^40]
[43] Our courts have appropriately placed the obligation on physicians to provide their patients with all the material information they need to consider proposed treatment. As a matter of law, doctors must, without being questioned, disclose "the nature of the proposed operation, its gravity, any material risks and any special or unusual risks attendant upon the performance of the operation".[^41]
[44] In Ontario, the duty to obtain an informed consent has been codified in the Health Care Consent Act, which imposes a legal duty on a physician to obtain informed consent prior to undertaking any treatment of a patient[^42]. The Act specifies that a consent to treatment is only “informed” if the patient is told about:
• the nature of the treatment.
• the expected benefits of the treatment.
• the material risks of the treatment.
• the material side effects of the treatment.
• alternative courses of action.
• the likely consequences of not having the treatment.[^43]
[45] In analysing the quality and quantity of the information given to a patient under negligence principles, the test to be employed is not the professional medical standard, but the reasonable patient standard.[^44]A material risk is one that a reasonable person in the patient’s position would want to know before deciding whether to proceed with the proposed treatment. A failure to make full disclosure of material risks constitutes negligence[^45]. Information is much more likely to be classified as “material” where the procedure is elective.[^46]
[46] The court comments that diagnostic tests should be part of the informed consent discussion:
It should be noted that the defendant submits that the last item is not properly part of the informed consent discussion but rather part of a failure to diagnose. I disagree; I find that this properly forms part of the informed consent question. The process of informed consent involves determining whether sufficient information was given to the patient. In my view, the failure to provide a patient with information regarding two available diagnostic tests which would provide her with more information on pre-surgical options, forms part of this discussion. [^47]
[47] After establishing a failure to disclose material information, the plaintiff must still demonstrate, on a balance of probabilities, that the procedure would not have gone ahead, using the so-called modified objective test.[^48] The subjective component of this test takes into account factors unique to the patient. The objective component is based on what a reasonable person in the patient’s position would have done.[^49] Courts are to consider the issue objectively based on the “particular concerns” of the patient and any “special considerations affecting the particular patient”.[^50]
Causation
Factual Causation
[48] Even if a physician is found to have breached the standard of care, the plaintiffs’ claim will fail unless they can establish that the particular breach of the standard, on a balance of probabilities, caused the injury. If a breach of the standard did not cause the injury, on a balance of probabilities, the physician is not liable.[^51]
[49] The Supreme Court of Canada confirmed that the “but-for” test is the legal test for causation:
As a general rule, a Plaintiff cannot succeed unless she shows as a matter of fact that she would not have suffered the loss “but for” the negligent act or acts of the defendant. A trial judge is to take a robust and pragmatic approach to determining if a Plaintiff has established that the defendant’s negligence caused her loss. Scientific proof of causation is not required.[^52]
[50] The “but for” test “recognizes that compensation for negligent conduct should only be made ‘where a substantial connection between the injury and the defendant’s conduct’ is present”.[^53] In this way, it ensures that the defendant will not be held liable for injuries that “may very well be due to factors unconnected to the defendant and not the fault of anyone”.^54
[51] The Court of Appeal for Ontario has confirmed that the “but-for” test ordinarily applies in cases where the delay in diagnosis or treatment is in issue:
“[c]ausation in medical malpractice cases where the negligence lies in the failure to diagnose or treat a pre-existing condition requires that the plaintiff show, on the balance of probabilities, that but for the failure to properly diagnose or treat the condition, the plaintiff would have had a better medical outcome”.[^55]
[52] A “loss of chance” is not compensable in medical malpractice cases.[^56] Plaintiffs cannot suggest that they would have had a “better medical outcome” in the sense of having a better chance at a better outcome. The plaintiff must prove that the outcome would have been avoided. The Supreme Court of Canada stated the following:
It is worth repeating the traditional principle set out in Laferrière v. Lawson, 1991 87 (SCC), [1991] 1 S.C.R. 541, at pp. 608-9, where I found that causation must be established on a balance of probabilities and that the loss of a mere chance cannot be a compensable harm.[^57]
[53] The mere possibility of a casual connection between the alleged negligence and the damaged caused is insufficient.
[54] A defendant can defeat an inference of causation simply by advancing some evidence that the plaintiff’s injury would have occurred notwithstanding the defendant’s breach of the standard of care. The Supreme Court of Canada stated the following:
Where "but for" causation is established by inference only, it is open to the defendant to argue or call evidence that the accident would have happened without the defendant's negligence, i.e. that the negligence was not a necessary cause of the injury, which was, in any event, inevitable. As Sopinka J. put it in Snell, at p. 330:
The legal or ultimate burden remains with the plaintiff, but in the absence of evidence to the contrary adduced by the defendant, an inference of causation may be drawn although positive or scientific proof of causation has not been adduced. If some evidence to the contrary is adduced by the defendant, the trial judge is entitled to take account of Lord Mansfield's famous precept [that "all evidence is to be weighed according to the proof which it was in the power of one side to have produced, and in the power of the other to have contradicted" (Blatch v. Archer (1774), 1 Cowp. 63, 98 E.R. 969, at p. 970)]. This is, I believe, what Lord Bridge had in mind in Wilsher when he referred to a "robust and pragmatic approach to the facts" (p. 569).[^58]
[55] The plaintiffs’ causation theory is that Ms. Leckie did not need Allopurinol because she did not have gout and had she not been prescribed Allopurinol, she would not have developed Stevens-Johnson Syndrome.
[56] Dr. Chaiton’s causation theory is that Ms. Leckie had gout and would have gone on to develop Allopurinol‑induced Stevens-Johnson Syndrome regardless of the starting dose prescribed.
Legal Causation (Remoteness)
[57] A plaintiff may fail to establish liability in negligence, even where the plaintiff established that the physician breached the standard of care and that the breach factually caused the plaintiff’s injury. The plaintiff must also prove that her injury was caused in law, that is, was not too remote from the defendant’s breach. As the Supreme Court stated:
[E]ven where a duty of care, a breach, damage and factual causation are established, there remains the pertinent threshold question of legal causation, or remoteness.[^59]
[58] An injury that is factually caused by negligent conduct is too remote to be compensable if the injury was not a reasonably foreseeable consequence of that conduct. The Supreme Court of Canada has stated that “[s]ince The Wagon Mound (No. 1), the principle has been that ‘it is the foresight of the reasonable man which alone can determine responsibility’”.[^60]
[59] The underlying rationale for this test of remoteness is that “the law of tort imposes an obligation to compensate for any harm done on the basis of reasonable foresight, not as insurance”.[^61]
This Case
[60] The plaintiffs advance a number of separate causes of action:
[1] Dr. Chaiton breached the standard of care by not exercising the care of a specialist;
[2] Dr. Chaiton breached the standard of care by failing to establish a diagnosis before treating;
[3] Dr. Chaiton failed to offer or perform the gold standard diagnosis test in order to diagnose;
[4] Dr. Chaiton failed to obtain informed consent before prescribing Allopurinol;
[5] Dr. Chaiton failed to offer more conservative options before treating Ms. Leckie with Allopurinol. Informed consent demands that a doctor educate the patient about various options for treatment and then allow the patient to make the decision.
[61] Dr. Chaiton’s submissions include the following:
(i) this is a medical negligence action arising out of Dr. Chaiton’s treatment of Ms. Leckie’s gout in the fall of 2012. The plaintiffs’ case has transmogrified from its original form and now centres on an allegation that Ms. Leckie has never had gout and therefore did not require Allopurinol, a drug employed to lower elevated uric acid levels. This new theory requires the court to ignore express admissions in the statement of claim.
(ii) tellingly, although the plaintiffs pled thirty-four separate and specific allegations about Dr. Chaiton’s conduct, they did not allege that he misdiagnosed Ms. Leckie with gout. In fact, the plaintiffs specifically pleaded that Dr. Chaiton failed to identify or take appropriate steps to treat Ms. Leckie’s gout. The plaintiffs’ central allegation was that Dr. Chaiton should have prescribed Ms. Leckie a lower starting dose of Allopurinol on the theory that, had he done so, she would not have gone on to develop an adverse reaction to the drug.
(iii) this theory was eviscerated in December of 2017 with the service of Dr. Rieder’s report. Dr. Rieder’s unchallenged opinion was that subsequent genetic testing confirmed that Ms. Leckie would have gone on to develop Allopurinol-induced Stevens-Johnson Syndrome regardless of the starting dose prescribed. The plaintiffs were unable to proffer any expert evidence in response to Dr. Rieder’s opinion. Instead, they now attempt to reverse course and advance the theory that Ms. Leckie’s gout has never been confirmed through a joint aspiration – the so‑called “gold standard” in the diagnosis of gout.
The Experts
[62] Dr. Baer, like Dr. Chaiton, is a community rheumatologist. He has been practicing in the field of rheumatology for over 30 years, and has held a number of prominent positions in his field including the chair of the Section on Rheumatology of the Ontario Medical Association, executive member of the Ontario Rheumatology Association, and Editor-in-Chief of the Journal of the Canadian Rheumatology Association. Dr. Baer has a specialized interest in the management of gout. He was awarded the Community Rheumatologist of the Year Award in 2011 by the University of Toronto, academic division of Rheumatology.
[63] Dr. Baer testified that Dr. Chaiton met the standard in the care that he provided to Ms. Leckie in the fall of 2012, including his diagnosis of gout, his decision to initiate Allopurinol on November 5, 2012, and his management of Ms. Leckie’s symptoms when she presented to his office on November 29, 2012.
[64] In contrast, Dr. Rubin is a rheumatologist principally practising at St. Michael’s Hospital, a tertiary care centre in Toronto. He is an academic rheumatologist, not a community rheumatologist. I agree that Dr Dr. Rubin’s approach to the standard of care issue was academic, theoretical and often contradictory. Dr. Rubin’s evidence was based on what can only be described as ideal care one would hope to receive in a tertiary care centre. His analytical approach was divorced from what was actually happening in the community setting in 2012. As such, he tended to set the bar considerably higher than standard required.
[65] On the topics on which their opinions diverge, I agree that Dr. Baer’s opinion is preferred to that over Dr. Rubin’s. Dr. Baer, unlike Dr. Rubin, is a community rheumatologist, and is therefore similarly situated to Dr. Chaiton.
[66] The fact that Dr. Rubin’s perspective comes from that of an academic practice rather than a community practice became immediately apparent in his testimony. He was critical of Dr. Chaiton for failing to perform a joint aspiration despite the fact that “over 90%” of gout cases in Ontario are diagnosed without a joint aspiration. By his own admission, he is also “one of the few rheumatologists that has a microscope in their office” to examine synovial fluid.
[67] Moreover, in coming to his opinion regarding standard of care, Dr. Rubin took into account information that was not available to Dr. Chaiton at the time, including Ms. Leckie’s complete family physician records, hospital records, pharmacy records, and many records that post‑dated Dr. Chaiton’s care. He did so despite acknowledging that it would not be fair to criticize Dr. Chaiton’s care on the basis of information that was not reasonably available to him at that time:
Q. Dr. Rubin, I take it you would agree with me that it would not be fair to criticize or be critical of Dr. Chaiton’s care on the basis of information that he didn’t reasonably have available to him at the time?
A. If he didn’t have the information, no, it would be not appropriate. No, I agree.
Q. And the information that she had been previously prescribed HydrochloroThiazide in February of 2011 is information that you got from the records produced by his family physician; correct?
A. I actually got it from the prescription list.
Q. So, you - right. So, you got it from the prescription - the list of prescriptions she took that was generated and produced in this litigation; correct?
A. Yes.
Q. And so, I take it you’re prepared to agree with me that in October of 2012, Dr. Chaiton would not have had that prescription list; correct?
A. The prescription list? No, he wouldn’t have had it, I don’t think so, unless the family doctor provided it.
[68] Despite acknowledging that Dr. Chaiton would not have had Ms. Leckie’s prescription list, Dr. Rubin took this information into account in forming his views on whether Dr. Chaiton met the standard of care. He testified that it was important information that HydrochloroThiazide was, on his (unconfirmed) understanding, resumed on September 24, 2012. Dr. Rubin gleaned this information from his review of Ms. Leckie’s prescription list, which was generated after the litigation was commenced. When asked whether his opinion might change if this information was not reasonably available to Dr. Chaiton, Dr. Rubin stated “I don’t know how to answer that”.
[69] Dr. Rubin also failed to consider Dr. Chaiton’s evidence on his usual practice, despite having this evidence available to him, and despite it being well-established that evidence of usual practice should be given considerable weight.
[70] I agree that throughout the course of his testimony, Dr. Rubin acted more as an advocate rather than an impartial expert whose duty is to the court. I agree that during cross-examination, he was argumentative, repeatedly asked questions instead of answering them and, at one point, was forced to acknowledge that he was stepping outside of his role as an expert.
[71] Dr. Rubin applied a standard to Dr. Chaiton that he did not apply to other physicians. While he was highly critical of Dr. Chaiton for treating based upon a clinical diagnosis, he noted that treatment based on a clinical diagnosis without confirmatory imaging was “perfectly acceptable” by another physician involved in Ms. Leckie’s care:
Q. All right. Let’s talk about that. At page 722 of the joint document brief is his follow up note of October 30th, 2012 and he reports at the bottom Ms. Leckie has had peroneal tenosynovitis which responded to casting. What does it mean when he says that as far as you understand as a physician?
A. My understanding is that in his opinion the application of the cast resulted in a reduction of the inflammatory component that he diagnosed as peroneal tenosynovitis. I would also say to be fair without doing confirmatory imaging on his part he made a clinical diagnosis which is perfectly acceptable. He made a clinical decision, introduced a tool or a treatment that helped. At the end of the day that’s really all that matters. I’m not going to be able to say with certainty that, that his diagnosis was correct or not.
[72] Dr. Rubin also substantially changed his evidence on re-examination to try to repair the damage done to the plaintiffs’ case. On the topic of informed consent, Dr. Rubin testified in chief that when prescribing drugs, he “does not talk about lethality,” and in cross-examination, he agreed that if Dr. Chaiton disclosed to Ms. Leckie the risk of a rash and what to do if a rash appeared, he would have met the standard of care.
[73] Yet, on re-examination, Dr. Rubin did an about face. He asserted, for the first time, that the standard of care required a physician to disclose that the drug could result in a life‑threatening complication, despite his own earlier evidence that he does not do so in his own practice.
[74] I agree that Dr. Rubin took on the role of an advocate, rather than a neutral expert whose duty is to the court and that he held Dr. Chaiton to a standard considerably higher than that which he acknowledged applies to himself and other physicians.
[75] It is also important to distinguish Dr. Rubin’s evidence about his own practices at St. Michael’s Hospital from his evidence about what the standard of care required of Dr. Chaiton. There were many instances throughout his testimony where Dr. Rubin described what he would have done in a given situation, however, it is well established that an expert’s practice should not be taken as evidence of the standard of care.[^62]
[76] I agree that Dr. Rubin’s actual evidence at trial must also be distinguished from assertions made by the plaintiffs in their written closing submissions that have no evidentiary foundation. In their closing submissions, the plaintiffs allege that Dr. Chaiton was negligent in nineteen different ways, most wholly unsupported by expert evidence. In support of some of their one-line propositions, they do not cite not the evidence of Dr. Rubin, but to literature that was never put in evidence at trial.
[77] I agree that it is somewhat difficult to discern precisely what Dr. Rubin’s opinion was regarding the standard of care. He frequently answered questions by responding with what he would have done, or otherwise did not provide responsive answers. A review of the transcript of his evidence reveals that he in fact only opined that Dr. Chaiton fell below the standard of care in the following respects:
(a) by failing to perform a joint fluid analysis to confirm the diagnosis of gout;
(b) in his decision to initiate Allopurinol on November 5, 2012 prior to doing a joint fluid analysis, prior to assessing and addressing Ms. Leckie’s kidney function, and prior to receiving the results of Ms. Leckie’s bloodwork from that day;
(c) in his documentation with respect to informed consent for the prescription of Allopurinol;
(d) in his decision to initiate Allopurinol at a starting dose of 300 mg; and
(e) in his decision not to refer Ms. Leckie to hospital immediately on November 29, 2012.
[78] The remainder of the criticisms levelled against Dr. Chaiton in the plaintiffs’ closing written submissions are not supported by expert evidence.
[79] Equally important to what Dr. Rubin’s opinion is, is what it is not. Dr. Rubin’s opinion is not that Ms. Leckie did not have gout. Indeed, he never took the position that the diagnosis of gout was incorrect, only that further investigation – namely, a joint fluid aspiration – should have been done prior to reaching a diagnosis and initiating treatment.
[80] Dr. Rubin’s opinion is also not that Ms. Leckie should have never been prescribed Allopurinol – only that it was not necessary to initiate Allopurinol on November 5, 2012, prior to a joint fluid analysis having been done. Indeed, his evidence was that it might have been appropriate to start Allopurinol as soon as December, one month later:
…Now the question is does she need long term urate lowering therapy? That’s the next question and she may have or may still need to but at the time that’s the central issue. No reason to initiate Allopurinol in November of 2012, maybe in December, maybe in January – who knows when – but at that time with the information that was at hand there was no reason to do so…
[81] Dr. Rubin acknowledged that Dr. Chaiton is a very experienced rheumatologist; skilled, diligent, and well-respected. He also acknowledged that Dr. Chaiton, had the opportunity to physically assess Ms. Leckie’s ankle and was in a better position to assess her affected ankle than he is now. He also acknowledged that reasonable physicians can see the same patient and reach different conclusions on the recommended treatment plan, because there can be differences in clinical judgment and there is not always one answer.
[82] The dispute between the experts regarding the diagnosis of gout is narrow. Drs. Baer and Rubin agree that based on Ms. Leckie’s presentation when she first saw Dr. Chaiton on October 4, 2012, crystal arthritis was the most likely diagnosis for Ms. Leckie based on her presentation, and the other diagnoses on the differential, osteomyelitis and sickle cell crisis, were very unlikely. As Dr. Rubin stated:
First of all, Ms. Leckie had sickle cell trait, she does not have sickle cell disease and so sickle cell crisis would have been very unusual. In fact she had never had to my knowledge any episodes that would be consistent with [sickle cell] because she [only] has a trait. She only has – I think it’s, it’s her hemoglobin in essence is 22 percent. It’s a low level. So she, she carries the trait but she doesn’t have the disease which is good. Osteomyelitis would be a – or even infected, infection – would still be a possibility because she was febrile and even though the initial culture was negative sometimes one can have these infectious conditions [indiscernible] hidden and it may take several days or because it’s in the bone itself it may not be, be accessible to culturing but the imaging that was done didn’t suggest any gross osteomyelitis and there was no penetrating wounds, there was no recent events in her clinical course that would suggest that she would get a blood borne infection and ankles are rarely ever infected unless there’s previous trauma, damage or instrumentation. In other words someone sticks metal in them [sic] part of the procedure and that’s the usual cause of joint infection is surgical intervention or trauma or penetrating wounds and osteomyelitis – she was not diabetic. It would have been very low on the differential. So I think the main differential was [sic] the question of infection. It’s highly unlikely but they did put a needle in that joint, they did take fluid out and for that alone you have some assuredness and they did put her on Prednisone and she did have a partial response and over time the x-rays never showed any evidence to suggest a progression of bone infection. That’s never been the case. It’s always been, you know, soft tissue swelling or this or that.
[83] In Dr. Rubin’s view, crystal arthritis was “at the top of the list”:
Well I think crystal arthritis was still very much at the top of the list. The type of crystal one of two, maybe more. Infection seemed unlikely given the previous aspirate. Osteomyelitis very less likely. Sickle cell trait doesn’t cause bone or joint injury. Trauma did not seem to be the case.
[84] With respect to diagnosis, the only real issue in dispute between the experts is whether Dr. Chaiton should have performed a joint aspiration and fluid analysis, which would have provided a definitive diagnosis for gout, if crystals had been found in the fluid analysis. As Dr. Baer explained, even a joint fluid analysis is not perfect, in that there can be false negatives or false positives.
[85] Critically, no other diagnosis has been advanced that would plausibly explain Ms. Leckie’s presentation. In their closing submissions, the plaintiffs appear to suggest that an old ankle tear could have been the cause of Ms. Leckie’s symptoms, however, their expert, Dr. Rubin, gave no evidence to support this theory, and indeed, it was specifically rejected by both Drs. Chaiton and Baer.
Dr. Chaiton’s submissons on standard of care and causation
[86] I accept and rely upon Dr. Chaiton’s submissions in reaching this decision. They are factually correct and are based on the evidence. The plaintiff’s submissions are unreliable.
[87] By the time Ms. Leckie saw Dr. Chaiton in October of 2012, she had been suffering from significant and progressive gout symptoms for over two years and, by her own evidence, had been told by four separate physicians that she had gout.
[88] Ms. Leckie’s own evidence, and the contemporaneous medical records introduced as business records at trial, overwhelming established that she had a longstanding history of gout prior to Dr. Chaiton’s involvement in her care. In the roughly two‑year period leading up to her first visit with Dr. Chaiton, Ms. Leckie was told by multiple physicians that she had gout. She was also prescribed, and took, a number medications to treat her gout and its related symptoms throughout that time.
[89] The plaintiffs’ attempt to minimize this evidence by ignoring the medical records in this time period. In fact, they make no reference at all in their written closing submissions to records prior to September of 2012, aside from Ms. Leckie’s decoded OHIP summary.
[90] At the time Ms. Leckie first saw Dr. Chaiton, she had:
(a) an inflamed ankle joint with intense ankle pain that had not settled, despite the use of potent ant-inflammatories and analgesics;
(b) previous joint inflammatory reactions in a pattern consistent with gout, including the classic presentation, podagra, and other lower extremity swelling;
(c) a prior history of gout, having been told before by multiple physicians that she had gout;
(d) a pattern of repeat hospital visits, which is not unusual for a crystal induced arthritis;
(e) significant hyperuricemia (elevated uric acid level);
(f) a negative culture and recent completion of a course of antibiotics, ruling out the possibility of septic arthritis or infection;
(g) fluid in the joint on ultrasound, consistent with an arthritis, and not osteomyelitis or sickle cell disease; and
(h) pain and swelling in one ankle upon examination.
[91] Ms. Leckie also fit the expected profile of a woman diagnosed with gout, being 53 years of age and post-menopausal.
[92] Dr. Chaiton’s evidence is that the combination of all of this information led him to believe that gout was the most likely diagnosis. This was further confirmed when bloodwork done on October 4, 2012 returned a uric acid level of 792 umol/L – one of the highest values Dr. Chaiton has ever seen– and when Ms. Leckie later responded to treatment with Prednisone, as would be expected for a patient with gout.
[93] I agree that although the plaintiffs in their closing submissions make much of the fact that Dr. Chaiton did not find any crystals in ultrasounds done on Ms. Leckie’s ankle, Dr. Chaiton testified that it is not common to see crystals on ultrasound, nor did he expect to see them:
Q. Not once did you observe crystals, fair?
A. It is not a common finding, sir.
Q. And you don’t see crystals; correct?
A. I didn’t expect to see them, sir.
[94] Dr. Rubin, by his own admission, does not have the ultrasound skills that Dr. Chaiton has. He did not provide any evidence as to the significance of a lack of crystals on ultrasound, despite the plaintiffs’ urging in their closing submissions that this was a significant finding. Indeed, his only evidence with respect to the ultrasound was that even if Dr. Chaiton had found crystals on ultrasound, a joint aspiration was still necessary.
[95] Significantly, Dr. Rubin conceded that gout can be diagnosed clinically:
Q. [T]he third way that you can diagnose gout is ... the presence of six of the twelve clinical, laboratory, and X-ray phenomena listed in Table 5 [of the “Wallace” article]. Correct?
A. Yes.
Q. And, in fact, as you testified in your examination in-chief, that’s what the overwhelming majority of physicians, greater than 90 per cent of the physician[s] who diagnose gout, diagnose it clinically in Ontario; correct?
A. Yes.
[96] Dr. Rubin also conceded that as of October 4, 2012, Ms. Leckie met the criteria for a clinical diagnosis of gout based on the “Wallace” criteria that he himself had cited in a presentation he prepared on the treatment of gout. Dr. Rubin acknowledged that Ms. Leckie met the following six “Wallace” criteria in October of 2012:
(a) a history of more than one (gout) attack;
(b) monoarticular arthritis;
(c) a history of first MTP pain/swelling;
(d) hyperuricemia;
(e) asymmetric swelling; and
(f) negative organisms on culture.
[97] Dr. Baer also agreed that Ms. Leckie met the criteria for a clinical diagnosis of gout, having had at least eight factors present when a minimum of six are required to make a diagnosis. Not only was Dr. Chaiton’s diagnosis reasonable, it was correct. Dr. Baer noted:
Q. And, in your opinion, doctor, did Ms. Leckie have gout when she presented to Dr. Chaiton in October 2012?
A. Yes, she did. That was a reasonable diagnosis. And, to me, that was the correct diagnosis as well. I don’t see any evidence for any other diagnosis being tenable at that point. That was the diagnosis.
[98] Dr. Rubin did not advance an alternative diagnosis that would have explained Ms. Leckie’s symptoms. His evidence was that a joint aspiration with crystals could have shown with certainty that this was in fact gout.
[99] It is undisputed that a joint fluid analysis is the “gold standard” to definitively diagnose gout (assuming crystals are found). However, the gold standard is not the standard of care.[^63] Dr. Rubin’s own evidence was that fewer than 10% of patients diagnosed with gout ever have a joint fluid analysis done:
[I]t’s well known that ten, less than ten percent of patients diagnosed with gout are, ever have a joint aspirated and that’s a problem because it means that 90 percent of them haven’t had a confirmatory test early on and that’s the problem with gout is that very often it is not diagnosed early, it’s years and years into the condition and people are having complications or damage from it…
[100] Dr. Rubin also conceded that the decision to do a joint fluid aspiration was a decision that must be left to Dr. Chaiton, as a known skilled clinician:
A. Which is, is a bit limited in it’s scope. He then described her ankle, swollen, and he also states there’s absolutely no involvement, the MTPs (ph) are [sic] tophi, are very important point because tophi as we said would indicate much more serious than uric acid overload. He then has excellent skills in ultrasound and, and undertakes an examination. [indiscernible] really you know excellent. This is a skill set that you know a lot of our younger folks are learning. It’s actually part of the protocol in European programs and finds a, a fusion in the subtalar joint which is under the ankle and a small residual area of fluid connection in the tibiotalar joint. Now at that point it would have been great to have stuck a needle in there and, and – but maybe he felt that there just wasn’t enough. I don’t know because I, I – you know I have to, I have to leave that decision to a skilled clinicians, a known skilled clinician and again he repeats the sentence in that paragraph that he wrote in the paragraph before about there not being any ongoing inflammation of the feet or any tophi. He had already said that in the paragraph before and then...
[101] It is significant that Dr. Rubin acknowledged that the decision to aspirate is one that is to be left to the judgement of the “known skilled clinician”. Dr. Chaiton, a highly experienced and skilled clinician, exercised his judgment and determined that a joint aspiration was not warranted in the circumstances:
Q. And, Doctor, Dr. Rubin has been critical of you for starting her on Allopurinol without definitively diagnosing crystal arthritis through an aspiration of her joint. Why didn’t you aspirate her joint at any of the occasions you saw her prior to putting her on Allopurinol?
A. I did not feel that I needed to subject her to that invasive procedure. I was very confident and secure with the diagnosis of gout. It was supported by her ultrasound study, by her biochemistry, by her history. So, I made a reasonable, I felt, clinical diagnosis of gout, and felt that identifying the uric acid crystals in her joint fluid would add very little to both the diagnosis or my proposed course of treatment. So, that’s how I made that decision.
[102] Dr. Baer testified that the standard of care did not require that a joint fluid analysis be done. In addition, in his own practice, he has never had success aspirating an ankle joint in the office for a patient with gouty arthritis.
[103] Neither of the rheumatologists who saw Ms. Leckie in 2014 and 2015, Drs. Amba and Kreidstein, performed a joint aspiration although they each recommended urate lowering therapy for the treatment of Ms. Leckie’s gout. I agree that this should be taken as further evidence that a joint aspiration is not standard practice, even amongst rheumatologists.
[104] Dr. Rubin testified that the rationale for doing a joint fluid analysis is because failure to do so leads to an under diagnosis of gout. It therefore makes little sense that Dr. Rubin was critical of Dr. Chaiton, a rheumatologist with decades of experience, for making the diagnosis clinically.
[105] Dr. Chaiton also had the benefit of being able to directly see and assess Ms. Leckie. He considered other possible diagnoses and exercised his clinical judgment to determine that gout was the most probable diagnosis for Ms. Leckie. His decision to diagnose and treat Ms. Leckie for gout was reasonable and met the standard of care.
[106] Dr. Chaiton’s decision to initiate Allopurinol therapy for Ms. Leckie on November 5, 2012 was a reasonable exercise of clinical judgment that met the standard of care. Again, the divergence between the experts is limited and is in relation to the timing of the introduction of Allopurinol.
[107] There was agreement amongst the experts that genetic testing was not required prior to the initiation of Allopurinol and that a failure to treat gout can have long-term consequences, including complications and joint damage.
[108] The experts also agreed that impaired renal function is not a contraindication for initiating Allopurinol therapy. To the contrary, it can be an indication for urate lowering therapy.
[109] Although Dr. Rubin’s view was that Dr. Chaiton fell below the standard by prescribing Allopurinol on November 5, 2012, his opinion was not that Allopurinol should have never been prescribed. His evidence was that he would have offered the drug “sometime in the future”, after doing a joint aspiration and repeating bloodwork:
…then he starts Allopurinol and I don’t, I don’t think that was the right thing to do at that point. I would have waited. I would have aspirated. I would have repeated the bloodwork. I would have had her followed up and then sometime in the future with all that information I would have brought her in and said listen this is what I found and this is what I think, these are the issues, this is what I’d like to do, these are the drugs and what do you think?
[110] Dr. Rubin suggested that in his opinion, there may have been an indication to initiate Allopurinol as soon as December 2012 or January 2013.
[111] As Dr. Baer testified, physicians frequently need to initiate treatment in the absence of 100% certainty as to diagnosis when a patient is symptomatic, as Ms. Leckie was at her appointment with Dr. Chaiton on November 5, 2012. She had attended before a number of physicians, including in the emergency department, with an extremely painful ankle over the course of approximately six weeks:
And so, we’re frequently faced with the fact that the patient obviously needs treatment, and while we may not be 100 per cent certain, we may be 99 per cent or 90 per cent or whatever it is, we have to get on the treatment because the patient is symptomatic and treatment is required, both for acute problems and for chronic problems.
[112] In Dr. Baer’s opinion, by October 15, 2012 – three weeks before Dr. Chaiton initiated Allopurinol – Ms. Leckie already had the “hallmarks” of a patient who requires pharmacologic urate lowering therapy:
Q. And in your opinion, was Ms. Leckie an appropriate candidate for Allopurinol therapy as of October 15, 2012?
A. Yes, she was.
Q. Why is that?
A. Well, as we’ve seen, she had not only exceedingly high uric acid levels, but she had the clinical features of recurrent gouty arthritis which was debilitating. And our philosophy as rheumatologists is we don’t want to be treating acute attack after acute attack because that lets the underlying disease process progress, potentially leading to chronic damage to the joint, chronic gouty arthritis and other issues with the kidneys and other parts of the body. So, this is the hallmark of a patient who needs pharmacologic urate lowering therapy to get their uric acid level below the target, if you can, of 360, which will stop them from having acute gouty arthritis and prevent any progression to chronic gouty arthritis and irreversible joint damage.
[113] Dr. Rubin was initially critical of Dr. Chaiton for failing to stop HydrochloroThiazide before initiating Allopurinol, and specifically cited the American College of Rheumatology October 2012 guideline recommendation to “consider elimination of non-essential prescription medications that induce hyperuricemia” as support for this opinion. However, Dr. Rubin omitted from his testimony in chief that these guidelines also caution against imprudent cessation of Thiazide treatment. As Dr. Baer noted:
…the TFP recognized the value of Thiazide treatment in many patients with hypertension, and cautioned against imprudent cessation of Thiazide treatment to lessen hyperuricemia at the cost of worsened control of blood pressure in difficult to control hypertension.
[114] Dr. Baer also noted that this guideline may not have even been available to Dr. Chaiton in October 2012:
And, even in the 2012 guidelines which had just come out, and which Dr. Chaiton and I may not have received by October 2012 for - because it was sent as a print journal and it took a month to get to Canada from the States. So, even though the article is dated October 2012, I didn’t receive it, I’m sure, till November 2012.
[115] Dr. Baer testified that he did not agree that Ms. Leckie’s HydrochloroThiazide needed to be stopped prior to Dr. Chaiton initiating Allopurinol, given the importance of controlling the patient’s blood pressure:
Q. Okay. Now, one of the points that Dr. Rubin made was that Ms. Leckie’s HydrochloroThiazide ought to have been stopped prior to the initiation of Allopurinol. Do you agree with that?
A. No, I do not. I can explain that a bit further if you would like.
Q. Yes. Why don’t you agree?
A. Okay. So, control of blood pressure is very important because if you don’t control blood pressure, you can end up with a heart attack or a stroke. If somebody is on a blood pressure medication, I wouldn’t want to abruptly stop it. And, I’m not in the business of treating hypertension as a rheumatologist. These are initiated by family doctors, cardiologists and others. So, I wouldn’t just stop it. You would have to replace it with something else, and that’s not generally what I would do. I would leave that to the treating physician.
I generally do make a recommendation in patients who have gout on a Thiazide to consider stopping it, if possible, and substituting something else for blood pressure control. It is not always possible, and I’ve seen in the - even in the 2012 ACR guidelines that have been referred to that it was not suggested that it had to be stopped. The impact of Thiazides on the uric acid level is not that great. It’s estimated, I’ve seen, between 6 and 21 per cent increase in uric acid, meaning if you stop it, you’re going to get, at most, a 6 to 21 per cent decrease. I’ve seen other studies suggesting it didn’t matter if you stopped it or not, the Allopurinol would overwhelm it in a way in terms of uric acid lowering. So, my practice would be to recommend that if something else could be used to try to use it, but you don’t have to stop a Thiazide when you are treating gout.
[116] Dr. Chaiton’s evidence was that he did turn his mind to the issue. Dr. Chaiton testified that his practice for any patient on a diuretic is to suggest the patient speak to her prescribing physician about selecting an alternative agent, and that he believes that he did that for Ms. Leckie. He testified that he makes this recommendation because HydrochloroThiazide can aggravate the underlying gout. His practice is not to discontinue medications prescribed by other physicians.
[117] Dr. Chaiton testified that he did not believe it was critical to stop the HydrochloroThiazide prior to the initiation of Allopurinol in this case because HydrochloroThiazide was not the only element related to the issue. It was Dr. Chaiton’s evidence that the impact of Thiazides on the uric acid level is not that great. Dr. Baer gave similar evidence on this point.
Ms. Leckie’s “gout” history
[118] By February of 2014, Ms. Leckie reported that she had been experiencing gout attacks lasting three to seven days, three times a year, for the past three years, further illustrating that she had a well-established history of gout attacks long before she first met Dr. Chaiton in October of 2012.
[119] Ms. Leckie attended at Dr. Anifowoshe’s office after hours in May of 2010 because of severe ankle pain and was advised that she had gout. Dr. Anifowoshe billed OHIP for an after‑hours appointment with a diagnostic code of ‘gout’ for this visit.
[120] Ms. Leckie’s symptoms were of such severity that on October 4, 2010 she attended the emergency department at HRRH with pain in her right thumb – pain which she had endured for two weeks despite the fact that she had not sustained any injury. The medical records from HRRH confirm that Dr. Lian diagnosed her with right thumb arthritis.
[121] Ms. Leckie returned to the HRRH emergency department on January 14, 2011, complaining of pain and swelling in her right big toe. As both Drs. Rubin and Baer confirmed, this is a classic presentation for gout. Ms. Leckie denied having injured her right toe. Dr. Ayow, the physician who treated Ms. Leckie in the emergency department, informed her that the pain and swelling were as a result of gout. Her pain was significant and she was prescribed Percocet and Indomethacin (itself associated with a risk of Stevens-Johnson Syndrome) for pain relief.
[122] On February 7, 2011, Ms. Leckie attended at Dr. Anifowoshe’s office because she was experiencing a gout flare up that was causing her significant pain. The OHIP billing for this visit confirms that Ms. Leckie was assessed that day for gout. Dr. Anifowoshe prescribed Indomethacin to treat Ms. Leckie’s gout, which Ms. Leckie took as directed.
[123] I agree that it is of some significance that two separate physicians independently prescribed Indomethacin, a drug with a known risk of Stevens-Johnson Syndrome. As with Allopurinol, the risk of Indomethacin-induced Stevens-Johnson Syndrome is extremely low. The fact that Ms. Leckie appears to have accepted the risk of Stevens-Johnson Syndrome associated with Indomethacin certainly is dispositive of the informed consent issue.
[124] Ms. Leckie attended with Dr. Anifowoshe on March 3, 2011 because of another flare up of her gout.
[125] Ms. Leckie returned to Dr. Anifowoshe on September 22, 2012 complaining of left foot pain. Dr. Anifowoshe recorded that there had been no injury and recommended that Ms. Leckie take Tylenol, another drug associated with a risk of Stevens‑Johnson Syndrome.
[126] On September 23, 2012, Ms. Leckie returned to the HRRH emergency department as a result of left ankle pain and swelling that she conveyed had been present since “Tuesday” – i.e., five days prior complaining that she had difficulty walking. She denied any history of injury and informed the physician who assessed her, that she had a history of gout. She was asked by nursing staff to rate her pain out of ten, with one being a little bit of pain and ten being the worst pain of her life. Ms. Leckie rated her pain as ten out of ten, as it was the worst pain she had experienced in her life. Ms. Leckie’s gout was clearly progressing during this time. As Dr. Rubin pointed out, this was before she had filled her latest prescription for HydrochloroThiazide, which was not filled until the next day.
[127] Ms. Leckie’s uric acid level was measured at 462 umol/L, well above both normal limits and the level at which monosodium urate crystals will form. A left ankle joint aspiration was undertaken and a synovial fluid culture proved negative. Ms. Leckie was given 600 mg Ibuprofen and was provided an appointment with the HRRH urgent care clinic. She was also started on a course of Ciprofloxacin and Prednisone.
[128] Ms. Leckie attended at the urgent care clinic at HRRH on October 1, 2012, as directed. She was seen on that occasion by an internist, Dr. Bina who recorded that Ms. Leckie had “pain in lt ankle C̅ edema. Cannot weight bear”. He also noted a past history of “hypertension, gout attack in the right foot and right toe as well as sickle cell trait”. Dr. Bina’s note states that Ms. Leckie was:
“[P]resenting with difficulty ambulating as well as a significant amount of pain in the ankle. She says she can no longer weight bear. She says she cannot manage this pain at home.”
[129] Dr. Bina also recorded “likely crystal arthropathy. On exam does not look like sickle cell attack or osteo but likely needs aspiration (Cxr microscopy for crystals), XR and pain control”. Dr. Bina discharged Ms. Leckie with a most responsible diagnosis of gout and Ms. Leckie was told that she had gout. Dr. Bina offered her a referral to the rheumatologic clinic but Ms. Leckie declined, indicating that she could not wait for another appointment. As a result, Dr. Bina offered for Ms. Leckie to attend at the emergency department.
[130] Dr. Bina’s referral note indicates that Ms. Leckie attended at the emergency department at HRRH later that same day, where she was seen by emergency physician, Dr. Lian who ordered an x-ray of the left ankle, and prescribed Percocet and Toradol for pain.
[131] Imaging done of the left ankle showed soft tissue swelling over each of the malleoli, with the ankle mortise intact and no fractures noted.
[132] Ms. Leckie was discharged with a diagnosis of “ankle swelling NYD. R/O gout/arthritis”. She was given instructions to follow up with the fracture clinic.
[133] The following day, October 2, 2012, Ms. Leckie attended the HRRH fracture clinic and was seen by an orthopaedic surgeon, Dr. Heller. She remained in extreme pain notwithstanding that she had taken the Percocet and Toradol. Dr. Heller noted that there was “moderate soft tissue swelling” of the left ankle, as well as a past history of gout, and an uric acid level of 467 umol/L. Ms. Leckie’s creatinine levels were also measured that day as 119 umol/L.
[134] Dr. Heller told Ms. Leckie that he thought her symptoms were caused by gout. Dr. Heller also noted that Ms. Leckie had been on anti-inflammatories, and that he anticipated resolution of her symptoms, which he felt to be secondary to gout.
[135] On October 4, 2012, Ms. Leckie again attended the emergency department at HRRH for left ankle pain and swelling. She again rated her pain 10/10. Her uric acid level was recorded as “450” on this occasion. On examination, her left ankle was noted to be warm and swollen.She was referred to see Dr. Chaiton that day. The physician who assessed her, Dr. Lian, had a differential diagnosis of sickle cell crisis versus gout versus osteomyelitis.
[136] Dr. Chaiton saw Ms. Leckie in his office on October 4, 2012. This was now her seventh medical attendance for severe left ankle pain in less than two weeks.
[137] It was Ms. Leckie’s evidence at trial that she brought all of her medications with her to the appointment so that Dr. Chaiton could understand what medications she was taking.
[138] Ms. Leckie’s evidence confirms that Dr. Chaiton took a detailed history, which includes the following that Ms. Leckie told Dr. Chaiton:
(i) her ankle pain;
(ii) a number of physicians had told her that she had gout;
(iii) that she was experiencing arthritis gout;
(iv) that she had had a number of prior gout attacks in the past, and that those attacks had caused her to go to the emergency room on a number of occasions due to the pain that she was experiencing; and
(v) some of the doctors had prescribed medication for her gout, including pain medications such as Toradol and Percocet.
[139] Dr. Chaiton examined Ms. Leckie’s ankle and noted it to be swollen and tender. He noted that there was no involvement of the metatarsophalangeal joints and no tophi evident. He performed an ultrasound, which revealed an effusion in the subtalar joint and a small residual area of fluid collection in the tibiotalar joint. This confirmed his clinical impression that Ms. Leckie was not experiencing osteomyelitis or a sickle cell disease, but rather that this was an arthritic process.
[140] Ms. Leckie’s evidence was consistent with Dr. Chaiton’s contemporaneous record, both of which confirm that Dr. Chaiton took a detailed history, undertook a thorough examination and ordered reasonable investigations in the circumstances. Having done so, Dr. Chaiton noted that Ms. Leckie had had prior attacks of monoarthritis in the left foot involving both the toe and ankle joint, and that she presented with a lingering synovitis of the left ankle that did not respond to joint injection.
[141] Dr. Chaiton felt that it was likely that Ms. Leckie was experiencing a flare up of gout. Given her presentation and history, he felt that sickle cell crisis and osteomyelitis were very unlikely (a conclusion shared by both Drs. Rubin and Baer).
[142] Dr. Chaiton also ordered bloodwork for Ms. Leckie, the results of which included a uric acid level of 795 umol/L.
[143] Based on a presumed diagnosis of gout, Dr. Chaiton prescribed Ms. Leckie Prednisone 50 mg/day and invited her to return for local injection if the problem failed to settle in the next five days.
[144] Although Ms. Leckie was instructed by Dr. Chaiton to return to his office if her problem failed to settle in five days, she did not return as instructed. Instead, Ms. Leckie attended the emergency department at HRRH on October 14, 2012, as her significant ankle pain continued to persist. Ms. Leckie again rated her pain as being ten out of ten, indicating that this was the worst pain she had experienced in her life. She was walking with crutches because she was unable to weight bear. She was seen again by Dr. Lian who ordered imaging of Ms. Leckie’s left ankle which confirmed that soft tissue swelling was present but that there was no bony injury.
[145] On that day Ms. Leckie’s uric acid was 642 umol/L, far outside of the normal range and, again, well beyond the range necessary for the formation of monosodium urate crystals. Ms. Leckie was given Percocet and an injection of Toradol for her pain, and discharged home with a diagnosis of “query gout” and an appointment with the fracture clinic the following day.
[146] On October 15, 2012, Ms. Leckie saw Dr. Heller in the fracture clinic. He noted that Ms. Leckie’s left lateral ankle pain and swelling had recurred and noted tenderness at the peroneal tendons and moderate soft tissue swelling. Dr. Heller noted that he suspected peroneal tenosynovitis, which can be a symptom of gout, and offered various options. A below‑knee slab was applied, and Dr. Heller planned to see her again on October 30, 2012 to remove the slab and re‑examine.
[147] Following her attendance at the fracture clinic, later that same day, Ms. Leckie attended for an appointment with Dr. Chaiton for her ankle pain.
[148] Ms. Leckie advised Dr. Chaiton that she had been seen in the emergency department the previous day. She reported that the Prednisone Dr. Chaiton had previously prescribed had been helpful in relieving her pain, but that the pain had returned once she stopped the medication. Ms. Leckie reported intense pain in her left foot. Dr. Chaiton was unable to examine the foot as it was in a cast.
[149] In Dr. Chaiton’s view, the fact that Ms. Leckie’s pain had improved with Prednisone but recurred after stopping the medication was consistent with a presentation of gout.
[150] Dr. Chaiton told Ms. Leckie her uric acid level was exceedingly high, and recommended that she restart Prednisone and add Colchicine, with a view to starting her on Allopurinol at their next appointment.
[151] On November 5, 2012, Ms. Leckie returned to see Dr. Chaiton who noted that Ms. Leckie had seen a significant improvement with Prednisone, but that upon stopping the medication, there had been a slight recurrence in the left ankle area. Dr. Chaiton observed evidence of capsular thickening and a possible effusion in the ankle joint, talonavicular joint, and calcaneal cuboid joint under ultrasound. The ultrasound findings indicated to Dr. Chaiton that she had synovitis, a feature of gout, and that the inflammation in Ms. Leckie’s joint was low-grade, rather than acute.
[152] By this point, Dr. Chaiton was secure in the diagnosis of gout, which was supported by Ms. Leckie’s clinical presentation, ultrasound, biochemistry, and history. He recommended that Ms. Leckie restart Prednisone at a lower dose of 10 mgs a day to address the inflammation, Colchicine 0.6 mg daily (a lower dose than previous to reduce side effects) and begin Allopurinol at 300 mg daily.
[153] It was Dr. Chaiton’s evidence that his usual practice when prescribing Allopurinol was and is to tell patients that if they have a rash, or any other adverse reaction that they feel can be attributed to the drug, to contact him immediately:
Q. Doctor, you made the prescription for Allopurinol that day at 300 milligrams. What is your usual practice in terms of the risks of Allopurinol that you disclose to your patient?
A. Well, I’ve been prescribing Allopurinol for well over 50 years, I think, 40 years. It’s a very common drug that I prescribe. I’m very familiar with the common associated side effects, which are often rash, sometimes there’s gastric intolerance. My usual explanation is that if there is a rash, or any other adverse reactions that they feel that can be attributable to the drug, that they should immediately get in touch with me.
[154] Dr. Chaiton told Ms. Leckie that he would recheck her chemistry and see her again in three to four weeks. The results of the bloodwork taken that day (which Dr. Chaiton believes he received the following day) included an elevated creatinine level of 139 umol/L, an estimated glomerular filtration rate (GFR) of 41.14 mL/min (corrected for race) and a very high uric acid level of 672 umol/L, far beyond the point at which monosodium urate crystals form.
[155] Ms. Palmer, filled the prescriptions for Allopurinol, Colchicine and Prednisone on November 6, 2012. Ms. Leckie took the medication as directed and started the Allopurinol.
[156] Dr. Chaiton next saw Ms. Leckie on November 19, 2012, when he noted that her ankle synovitis was gradually resolving. He advised Ms. Leckie to remain on Allopurinol 300 mg daily but to reduce her Colchicine to 0.6 mg for a further two to three weeks and reduce Prednisone to 5 mg a day until her current prescription ran out.
[157] The results of the bloodwork taken that day included an elevated creatinine level of 127 umol/L, an estimated GFR (corrected for race) of 45.98 mL/min, and a uric acid level of 230 umol/L. This was the first time that Ms. Leckie’s uric acid levels were in the normal range since first being measured on September 23, 2012. Dr. Chaiton planned to see Ms. Leckie in three to six months, unless there were any interim gout flare ups.
[158] Ms. Leckie noticed a rash on November 29, 2012. She contacted Dr. Chaiton’s office that day, consistent with Dr. Chaiton’s instruction to patients to call immediately should the patient experience a rash. Ms. Leckie was given an appointment after hours that same day. Upon assessing her, Dr. Chaiton noted that she had developed an acute allergic reaction to Allopurinol, consisting of angioedema without wheezing and without hypertension. He noted no blisters, unusual skin lesions, or oral ulcers. Dr. Chaiton instructed Ms. Leckie to stop Allopurinol immediately and take Atarax and Prednisone 50 mg a day for five days. He instructed her to go to the hospital if she was not well.
[159] Ms. Leckie was admitted to HRRH with a generalized rash on December 1, 2012. She was ultimately diagnosed with Stevens-Johnson Syndrome which was thought to likely be secondary to Allopurinol. She was discharged home from HRRH on December 16, 2012, having recovered.
[160] In September of 2014, genetic testing performed on Ms. Leckie revealed that she was positive for the HLA B*58:01 haplotype. The undisputed evidence at trial was that this haplotype predisposed Ms. Leckie to Allopurinol-induced Stephens-Johnson Syndrome. Ms. Leckie was advised that she must avoid using Allopurinol and the implications for her first degree family members were also explained to her.
[161] During the appointment to discuss her genetic test results, Ms. Leckie advised that her gout was not controlled due to discontinuation of Colchicine and Allopurinol.
[162] Since her discharge from hospital in December 2012, Ms. Leckie has continued to be treated for gout:
(a) on April 26, 2013, Ms. Leckie saw Dr. Anifowoshe, for pain in the right foot, and was diagnosed with gout;
(b) on February 5, 2014, Ms. Leckie saw family physician Dr. McKinney, who referred her to rheumatologist Dr. Amba for management of her gout. In his referral request, Dr. McKinney noted that Ms. Leckie had developed Stevens‑Johnson Syndrome to Allopurinol and Colchicine and inquired whether there was another drug that could help prevention;
(c) on February 27, 2014, Ms. Leckie was seen by Dr. Amba for management of possible gout.At that time, Ms. Leckie reported a history of gout attacks lasting 3-7 days occurring three times per year for the past three years.Ms. Leckie reported that her last attack was in October 2013. Bloodwork ordered by Dr. Amba during that appointment showed a very high urate level of 621 umol/L;
(d) on March 14, 2014, Dr. Amba again assessed Ms. Leckie for gout in the setting of mild renal dysfunction and allergy to Allopurinol and Colchicine. He recommended that Ms. Leckie start on Uloric, an alternative urate lowering therapy indicated in the setting of Allopurinol hypersensitivity;
(e) on March 17, 2014, Ms. Leckie saw Dr. McKinney, who noted that Ms. Leckie was currently experiencing a gout attack, and that Dr. Amba had prescribed Uloric.Ms. Leckie did not want to see Dr. Amba again, so Dr. McKinney referred her to another rheumatologist, Dr. Kreidstein, for further management of her gout;
(f) on April 8, 2014, Ms. Leckie saw Dr. Kreidstein for management of her gout. On examination, Dr. Kreidstein noted that no subcutaneous tophi were present, but the left ankle was swollen, warm, and tender. Dr. Kreidstein told Ms. Leckie that she had gout that required urate lowering therapy, and explained to Ms. Leckie that she was eligible for Uloric since she was allergic to Allopurinol.Dr. Kreidstein made a request for Ms. Leckie to get Uloric under the Exceptional Access Program.Bloodwork ordered that day returned a urate level of 567 umol/L, again well outside of the normal range and beyond the level at which monosodium urate crystals form;
(g) on May 20, 2014, Ms. Leckie saw Dr. Kreidstein for management of gout. Dr. Kreidstein noted that Ms. Leckie was taking Uloric 80 mg every three days and advised that the Uloric would now be increased to every 2 days for the next two weeks and then daily thereafter.At that time, Ms. Leckie’s uric acid level was measured as 412 umol/L, still elevated but much closer to the normal range;
(h) on September 30, 2014, Ms. Leckie saw Dr. Kreidstein who noted that Ms. Leckie had stopped Uloric two weeks prior.Bloodwork taken that day returned a urate level that had climbed back to 498 umol/L, again well outside of the normal range. By December 2014, Ms. Leckie’s urate level had increased yet again to 540 umol/L;
(i) on July 6, 2015, Ms. Leckie was seen by Dr. McKinney for a flare-up of her gout.
[163] None of these physicians – including two rheumatologists, Drs. Kreidstein and Amba – performed a joint aspiration to check for crystals in the synovial fluid, although both rheumatologists prescribed Uloric for the treatment of gout.
[164] Ms. Leckie did not produce family physician or rheumatology records going beyond 2015. However, she confirmed under cross-examination that since seeing Dr. Kreidstein in 2015, doctors have told her that she continues to suffer from gout flare ups.
[165] I agree that the plaintiffs essentially ask this court to conclude that all of the doctors who told Ms. Leckie that she had gout were wrong. This court would also have to conclude that some of these physicians prescribed medications, including Indomethacin and Uloric, that Ms. Leckie did not need. The records speak for themselves. I agree that all of these doctors, like Dr. Chaiton, correctly diagnosed Ms. Leckie with gout based on her clinical presentation.
Ms. Leckie’s Submissions
[166] I am not going to summarize the plaintiffs’ submissions as there is absolutely no merit to the plaintiffs’ case. Four other doctors, apart from Dr. Chaiton, diagnosed Ms. Leckie with gout. She has gout. No evidence on causation (dealt with below) was led from Ms. Leckie, and Dr. Rieder was an eminently qualified clinical pharmacologist who provided causation evidence on behalf of Dr. Chaiton.
Other Comments
[167] Even if the plaintiffs can establish that Dr. Chaiton should not have prescribed Allopurinol on November 5, 2012 (which they did not), their own expert, Dr. Rubin, does not take the position that Allopurinol should never have been prescribed – in fact, his evidence is that it may have been indicated as soon as a month or two later:
…Now the question is does she need long term urate lowering therapy? That’s the next question and she may have or may still need to but at the time that’s the central issue. No reason to initiate Allopurinol in November of 2012, maybe in December, maybe in January – who knows when – but at that time with the information that was at hand there was no reason to do so.
[168] I agree that there is no evidentiary foundation for the assertion that Ms. Leckie could have avoided the Allopurinol, which was the ultimate cause of her allergic reaction in the form of Stevens-Johnson Syndrome.
[169] In their written closing submissions, the plaintiffs argue that Ms. Leckie could have controlled her gout through diet modification and cessation of HydrochloroThiazide alone, without ever requiring urate lowering therapy. I agree that this argument is unsupported by the evidence, which includes the following:
(a) in February of 2014, Ms. Leckie was referred to Dr. Amba for management of gout. Dr. Amba recorded that Ms. Leckie gave a history of attacks lasting 3 to 7 days occurring three times a year for the past three years, with her last attack in October 2013;
(b) in February of 2014, Ms. Leckie’s uric acid levels were measured as 621 umol/L, a very high level, far beyond where monosodium urate crystals will start to form;
(c) in March of 2014, Dr. Amba recommended Ms. Leckie start urate lowering therapy for treatment of gout;
(d) in April of 2014, Dr. Kreidstein determined that Ms. Leckie required urate lowering therapy in the setting of significant gout, and made an application for Ms. Leckie to obtain a prescription of Uloric under the Ontario Exceptional Access Program, due to her Allopurinol hypersensitivity;
(e) Ms. Leckie took Uloric as prescribed;and
(f) Ms. Leckie reported in October 2014 that her gout had not been controlled due to the discontinuation of Colchicine and Allopurinol.
[170] The plaintiffs’ submission that Ms. Leckie has not seen a rheumatologist since 2015 and “has not taken any urate lowering therapy including Allopurinol or Uloric for the last 6 years and has been fine” is somewhat irrelevant but also lacks an evidentiary foundation. The plaintiffs’ submission that “the uncontested evidence of Rhodalee Leckie and Dr. Rubin is that she has gone on for the last 6 years without any medication for gout at all and has been just fine” is a mischaracterization of the evidence.
[171] Dr. Rubin testified that Ms. Leckie has been fine for the past six years as far as he knows, not having seen medical records for that period. Importantly, Dr. Rubin also noted that it is “entirely possible” that Ms. Leckie is still on the pathway of gout.
[172] The plaintiffs did not produce, nor put in evidence, records from Ms. Leckie’s family physicians or a decoded OHIP summary for the past six years, to support their assertion.
[173] The prescription summary provided at trial, which they state “proves that Rhodalee has not taken any urate lowering medication” and “has been just fine” proves nothing except that no prescription for Allopurinol or Uloric was filled at that particular pharmacy. Ms. Leckie gave no evidence about whether she has been prescribed any urate lowering therapy in the past six years, nor did she give any evidence that she has not had gout flare ups in the past six years.
[174] While Ms. Leckie did testify that after she was discharged from hospital in December 2012, she “never really go to any doctor about gout”, “don’t take nothing” or “take a Tylenol at home”, when taken to the records, she admitted that she had seen Drs. McKinney, Amba, and Kreidstein for treatment of gout. She also testified that since seeing Dr. Kreidstein in 2015, other physicians have told her that she continues to suffer from gout flare ups.
[175] In any event, as Dr. Baer testified, this is not uncommon, nor does it obviate the diagnosis of gout:
I have patients come, I’ve put them on urate lowering therapy, they go back to their family doctor, they’re sent back 10, 15 years later, and they took the therapy for a while, and then they were off it for years and nothing happened, then things started to happen again, and that’s why they’re back. And, obviously, if nothing had happened, they wouldn’t be back and just carry on. So, you know, it doesn’t obviate the diagnosis of gout.
[176] I agree that in totality, the evidence leads to the conclusion that Ms. Leckie has gout which required urate lowering therapy and would have been prescribed Allopurinol, if not on November 5, 2012, then certainly at some point shortly thereafter.
Causation
[177] The other uncontroverted evidence was that because of Ms. Leckie’s genetic haplotype, it was inevitable that she would develop Stevens-Johnson Syndrome once she received Allopurinol ‑ regardless of when she started it, regardless of her starting dose, regardless of her renal function, regardless of whether she was taking a Thiazide diuretic, and regardless of whether she stopped taking the drug immediately upon noticing symptoms of a rash.
[178] Dr. Rieder is an eminently qualified clinical pharmacologist, the only expert to provide opinion evidence on causation. He is a Professor in the Departments of Paediatrics, Physiology, and Pharmacology and Medicine at Western University, and his practice and research focus on drug safety and adverse drug reactions. He has specialized interest and expertise in severe and life‑threatening drug reactions and has published widely in this area. He has particular expertise in investigating the pathogenesis of drug‑induced serious cutaneous reactions such as Stevens-Johnson Syndrome.
[179] I agree that Dr. Rieder’s opinion was straightforward: in light of Ms. Leckie’s HLA-B*58-01 haplotype, her risk of developing Stevens-Johnson Syndrome was dose-independent, and therefore, even if she had been prescribed a lower starting dose of Allopurinol, she would have nonetheless gone on to develop Stevens-Johnson Syndrome. Dr. Rieder also testified that the concurrent use of HydrochloroThiazides and Prednisone did not contribute to her reaction, and that her renal function also did not contribute to her reaction.
[180] It was Dr. Rieder’s uncontested opinion that once Ms. Leckie started expressing symptoms (the rash), there was nothing that could have be done to prevent her from developing full‑blown Stevens-Johnson Syndrome. The plaintiffs adduced no evidence at trial that could establish that her outcome would likely have been different if she had been referred to the hospital two days earlier on November 29, rather than on December 1, 2012.
[181] The plaintiffs place some significance in their closing submissions on Dr. Rieder’s evidence that the risk factors for Allopurinol Hypersensitivity Syndrome (AHS) can include renal impairment, Thiazide diuretics, a high starting dose of Allopurinol, and the presence of the HLA B*58:01 haplotype. Dr. Rieder also acknowledged that the risk of Severe Cutaneous Acute Reactions (SCAR) is more than one in a million. None of this evidence was in dispute.
[182] I agree that the plaintiffs conflate the evidence as to the risk factors for AHS and SCAR generally, with the risk factors for Stevens-Johnson Syndrome specifically.
[183] As Dr. Rieder testified, AHS is a term used by rheumatologists to describe a number of adverse events associated with Allopurinol. Stevens-Johnson Syndrome is one very specific and rare subset of AHS:
Q. Doctor, you were asked a series of questions about Allopurinol Hypersensitivity Syndrome, and you drew a distinction between Allopurinol Hypersensitivity Syndrome and Stephens-Johnson Syndrome. Can you explain the difference?
A. Certainly. Rheumatologists tend to use the word Allopurinol Hypersensitivity Syndrome to cover - as I mentioned, I used the word “broad umbrella” because that’s it, which is not uncommon. Many clinicians use purely - term to cover broad - a broad range of disorders, especially with drugs when things go wrong. Stephens-Johnson Syndrome is a very specific thing. And it’s a specific - specific, very serious part of hypersensitive - drug hypersensitivity. And, so it’s a subset of the overall hypersensitivity syndrome.
So, I think part of the issue on Allopurinol hypersensitivity is it covers a ‑ not to use the better word of variety [indiscernible] of which Stephens‑Johnson Syndrome is a very important, but very rare part.
[184] Dr. Rieder also testified that SCAR covers a myriad of disorders.
[185] To the extent that Dr. Rubin and Dr. Rieder’s opinions on the risk factors for Ms. Leckie’s Stephens-Johnson Syndrome diverge, Dr. Rieder’s evidence is preferred to Dr. Rubin’s who, by his own admission, is not an expert in Stevens-Johnson Syndrome.
[186] Dr. Rieder’s opinion that Ms. Leckie would have gone on to develop Stevens-Johnson Syndrome regardless of her starting dose of Allopurinol, her renal impairment, her use of Thiazide diuretics, and her starting dose, was unchallenged. Ms. Leckie has failed to establish causation.
[187] The plaintiffs’ case is dismissed. They have failed to prove that Dr. Chaiton breached the standard of care. Ms. Leckie was appropriately treated by Dr. Chaiton for gout. Dr. Chaiton met the standard of care. Ms. Leckie as well was provided with informed consent. In any event, Ms. Leckie’s case fails on causation. She would have developed Stevens‑Johnston Syndrome no matter what dose of Allopurinol was prescribed.
[188] I can be provided with cost submissions, if necessary, delivered to my assistant at lorie.waltenbury@ontario.ca.
J.E. Ferguson J.
Released: November 24, 2021
COURT FILE NO.: CV-14-514950
DATE: 20211124
ONTARIO
SUPERIOR COURT OF JUSTICE
B E T W E E N:
RHODALEE LECKIE, MARLENE PALMER, KIMISHA FORDEN and TAMGWENA LECKIE
Plaintiffs
– and –
DR. ABRAHAM CHAITON, ABRAHAM CHAITON MEDICINE PROFESSIONAL CORPORATION, JEAN PAUL LI CHEONG HAN, PHARMCARE SERVICES LTD. and HUMBER RIVER HOSPITAL
Defendants
REASONS FOR DECISION
J.E. Ferguson J.
Released: November 24, 2021
SCHEDULE “A”
Examples of Misleading, Mischaracterized and False Factual Assertions in the Plaintiffs’ Written Closings
Paragraph Reference[^64]
Proposition (Underlining Added)
Actual Evidence at Trial
46 and 48
It is clear, that the only person who may have told her that she had gout is a non-doctor, who had no notes or records that any diagnosis was made.
None
This is plainly false.
Ms. Leckie testified that multiple physicians told her that she had gout prior to the time she saw Dr. Chaiton:
Q. In fact you had been told that you had arthritis gout prior to the time you saw Dr. Chaiton, correct?
A. Correct.
Q. And in fact, more than one doctor had told you prior to the time that you saw Dr. Chaiton that you in fact had arthritis gout, correct?
A. Correct.
(Leckie Cross, p. 82, lines 28-30, p. 83, lines 1-4)
48
There are no notes or records that any diagnosis of gout was made prior to Rhodalee seeing Dr. Chaiton.
None
This is plainly false.
See Exhibit 2, JBD, Tab 3, pages 572 and 576, which note that Ms. Leckie was discharged from Humber River Regional Hospital on January 14, 2011 with a diagnosis of gout.
In addition, the OHIP billing records for Ms. Leckie (JBD, Tab 11, p. 2596) reflect that billings with a diagnostic code of ‘gout’ were made on the following days prior to her first attendance with Dr. Chaiton:
• May 4, 2010
• January 14, 2011
• February 7, 2011
• March 3, 2011
• October 1, 2012
• October 4, 2012
3
Dr. Chaiton knew that people on Thiazide diuretics, people with renal impairment, and black persons, had a higher risk of sever (sic) reaction to Allopurinol.
None
This is a misleading statement. Dr. Chaiton testified that a heightened risk for Black people was not known in 2012:
Q. You do not record indicating to her that as a person who was black, she had a heightened risk of a hypertoxic reaction over white people; correct?
A. That was not known at that particular time in 2012.
(Cross-Examination of Dr. Chaiton, April 15, 2021, page 167, lines 14-19)
In addition, Dr. Chaiton’s discovery evidence read-in at trial was that the difference in risk is extremely small:
- Q. Sir, do you agree that people, non-Caucasians, so black people and people of African origin, had a higher susceptibility to hypertoxicity of Allopurinol?
A. The added risks accrued to black persons as opposed to white is extremely small. 369. Q. 4 to 1, 5 to 1?
A. There is a difference of 1 percent to 3 percent, in that range.
(Exhibit 1, Read-ins from Dr. Chaiton’s Examination for Discovery, p. 66, q. 368, 369)
67
Dr. Chaiton agreed at discovery, and it was read in at trial, that he knew black people and people of African origin, had a higher susceptibility to hypertoxicity of Allopurinol.
Plaintiff Transcript Brief, Tab 1, p. 66 – Dr. Chaiton Discovery Transcript at question 368-369, line 14-22
This statement is misleading.
Dr. Chaiton testified that a heightened risk for Black people was not known in 2012:
Q. You do not record indicating to her that as a person who was black, she had a heightened risk of a hypertoxic reaction over white people; correct?
A. That was not known at that particular time in 2012.
(Cross-Examination of Dr. Chaiton, April 15, 2021, page 167, lines 14-19)
In addition, Dr. Chaiton’s discovery evidence read-in at trial was that the difference in risk is extremely small:
- Q. Sir, do you agree that people, non-Caucasians, so black people and people of African origin, had a higher susceptibility to hypertoxicity of Allopurinol?
A. The added risks accrued to black persons as opposed to white is extremely small.
- Q. 4 to 1, 5 to 1?
A. There is a difference of 1 percent to 3 percent, in that range.
(Exhibit 1, Read-ins from Dr. Chaiton’s Examination for Discovery, p. 66, q. 368, 369)
99
Dr. Chaiton was also aware that the risk allele of Allopurinol Hypersensitivity Syndrome (AHS) is seen in approximately 7% of black people
Note 21
Dr. Chaiton did not testify that the “risk allele of AHS is seen in approximately 7% of black people.”
The reference cited is to an article Dr. Chaiton co-authored in 1980 (Exhibit 18). There is no reference whatsoever in the article to risk allele or race.
84
The defence argued that Rhodalee had a higher risk of severe reaction to Allopurinol because she had the HLA-B58:01 gene. It was known to Dr. Chaiton that Rhodalee could have had this gene as he admitted at discovery and at trial that Rhodalee had an elevated risk of severe reaction to Allopurinol as she was black, he also knew that she had an elevated risk as she had renal impairment and was on HydrochloroThiazide. Dr Chaiton did not take any action to mitigate the risk or warn Rhodalee of the risk.
None
There is no evidence cited for this proposition.
There was no evidence at trial that “it was known to Dr. Chaiton” that Ms. Leckie could have had the HLA-B* 58:01 allele. Dr. Chaiton was not asked and gave no evidence that it was known to him that Ms. Leckie could have had this genetic haplotype.
Both Dr. Rubin and Dr. Baer agreed that genetic testing was not required.
Dr. Rubin did not testify that Dr. Chaiton should have warned Ms. Leckie of an elevated risk because she was black.
Dr. Chaiton testified that it was not known in 2012 that black people had a heightened risk of a severe reaction. See Dr. Chaiton Cross on Page 167, line 14-19:
Q. You do not record indicating to her that as a person who was black, she had a heightened risk of a hypertoxic reaction over white people; correct?
A. That was not known at that particular time in 2012.
(Cross-Examination of Dr. Chaiton, April 15, 2021, page 167, lines 14-19)
260
A patient who was black, had renal failure and taking a Thiazide medication would not have agreed to take Allopurinol especially in the face of more conservative options being available. It is hard to imagine anyone consenting to taking Allopurinol for the rest of their life in these circumstances when there was such an extreme risk of a severe reaction to the medication.
None
There is no evidence cited in support of this proposition. In particular, no expert testified that Dr. Chaiton was required to inform Ms. Leckie that she was at greater risk because she was black (and indeed, the evidence was that the difference in risk is extremely small).
There was absolutely no evidence at trial that Ms. Leckie was at an “extreme risk” of a severe reaction to Allopurinol.
120
According to the product monograph, the Merck manual and Dr. Rieder the defence pharmacology expert, Rhodalee Leckie had three major risk factors for a severe reaction to Allopurinol; she is black, had renal failure and was on a Thiazide medication.
None
This statement is inaccurate.
Dr. Rieder did not provide any testimony with respect to the role played by Ms. Leckie’s race, nor did he testify that Ms. Leckie had renal failure.
Dr. Rieder testified as to risk factors for Allopurinol Hypersensitivity:
Q. Right. So, the risk factors, just so we’re clear, for Allopurinol Hypersensitivity Syndrome, are renal impairment, use of Thiazide diuretics, high starting dose of Allopurinol, and HLA B-Star 5801 genotype, correct?
A. With Allopurinol Hypersensitivity Syndrome overall, that is correct.
(Rieder Cross, p. 45, lines 12-17).
Dr. Rieder specifically testified that HydrochloroThiazide did not increase the risk of Stevens-Johnson Syndrome (Dr. Rieder chief, p. 29, lines 2-11):
Q. Now, we’ve heard evidence from Dr. Ruben about HydrochloroThiazide, and I’d like to take you now to one of the slides presented by Dr. Ruben in his examination in-Chief and specifically slide.... Doctor, Dr. Ruben testified that HydrochloroThiazide inhibits the [indiscernible] of oxypurinol and therefore increases the risk of Stephens-Johnson Syndrome, do you agree with that?
A. I agree that HydrochloroThiazide inhibits the excretion (ph) of oxypurinol. I do not agree that it increases risk of Stephens-Johnson Syndrome.
(Rieder Chief, p. 29, lines 2-11).
Additionally, to the extent the plaintiffs rely on this statement to argue that this information should have been disclosed to Ms. Leckie, the product monograph and Merck Manual both were published in 2017, long after Dr. Chaiton’s involvement in Ms. Leckie’s care and are therefore irrelevant. In addition, these documents were not put to either Dr. Rubin or Dr. Baer.
57
The Canadian Pharmacists Association product monograph lists the risk factors for hypersensitivity reactions to the medication which include renal impairment, Thiazide diuretics, and a high starting dose of Allopurinol.
Exhibit 32, Canadian Pharmacists Association, Product Monograph Allopurinol, 2017
The plaintiffs appear to be relying on this monograph for the proposition that Ms. Leckie should have been informed of these risk factors.
To the extent they are relying on this monograph to argue that the risks outlined in the document should have been disclosed, this document was not put to either Dr. Rubin or Dr. Baer, and no expert tied the risks that need to be disclosed to this 2017 document.
Moreover, the 2017 Canadian Pharmacists Association Product Monograph for Allopurinol is not relevant to the standard of care/informed consent issues as it was published five years after the care in issue.
3
Dr. Chaiton knew that people taking Thiazide diuretics should not take Allopurinol at the same time.
None
This statement misrepresents Dr. Chaiton’s evidence.
Dr. Chaiton testified:
Q: You have no note anywhere about this topic, do you? A: I do not, sir, but my standard of practice when I see a Thiazide diuretic in the face of gout, I always suggest that an alternative hypertensive be chosen, but it is not 100 percent required. It has nothing to do with sensitivity reactions.
(Cross-Examination of Dr. Chaiton, April 16, 2021, page 24, lines 10-16)
37
Dr. Chaiton testified his usual practice was to contact the family doctor and discuss changing medications that cause hyperuricemia. Dr. Chaiton testified that he did not do that with Rhodalee.
Dr. Chaiton cross, p. 23-24, lines 26-32, 1-11
This is not accurate.
Dr. Chaiton did not testify that his usual practice was to contact the family doctor and discuss changing medications that cause hyperuricemia. He testified that he tells the patient to contact the prescribing physician:
Q. You did not take those steps; correct?
A. Well, I believe I did. But, again, it’s not recorded in the record. My usual practice on anybody on a Thiazide diuretic is to inform the patient to suggest to her doctor who prescribed it to select another alternative agent.
Q. In this case, you did not do that, and you did not document doing that; correct?
A. I believe I did do that, but it’s not documented, sir.
(Chaiton Cross, April 15, 2021, p. 189, lines 15-23)
He testified again that his usual practice is to counsel patients to choose an alternative hypertensive:
Q. Well, I didn’t ask you that question, but I take it knowing that potential for hypersensitivity, you took no steps to take her off HydrochloroThiazide, or find an alternative drug, or discuss with her family doctor finding an alternative drug; correct?
A. No, that’s not correct. As I think I testified at discovery, my usual practice is to advise that Thiazide diuretic not be employed, but it had nothing to do with hypersensitivity reactions. It has to do with the fact that it aggravates the underlying primary condition which is gout.
Q. Sir, I take it you have not documented taking any steps to raise this issue with Mrs. Leckie; correct?
A. None that are documented, sir.
Q. And you certainly didn’t document any discussions with the family doctor about it; correct?
A. That’s correct.
Q. You have no note anywhere about this topic, do you?
A. I do not, sir, but my standard of practice when I see a Thiazide diuretic in the face of gout, I always suggest that an alternative hypertensive be chosen, but it is not 100 per cent required. It had nothing to do with sensitivity reactions.
Q. In this case, you have no recollection of doing that, fair?
A. Correct.
(Chaiton Cross, April 16, 2021, p. 23, lines 26-32; p. 24, lines 1-19)
This issue was raised a number of times in cross examination. On each occasion, Dr. Chaiton reiterated his earlier evidence that his standard practice is to suggest that an alternative hypertensive be chosen but that he has no specific recollection of having the discussion with Ms. Leckie (as distinct from not having had the conversation):
A. Well, as I said, I did, in my usual pattern of practice, counsel patients to get off Thiazide diuretics, unrelated to hypersensitivity reactions, but simply to the adverse effects on kidney function and their uric acid level.
Q. You actually don’t recall telling Mrs. Leckie that, do you?
A. Yes, we’ve been through that a few times, and I have no - I have no written document that I did that, but that is my usual pattern of practice, sir.
Q. All right. You agree with me you do not actually recall the discussion with Mrs. Leckie, do you?
A. No, I do not.
Q. Right. You do not recall the discussion with Mrs. Leckie, fair?
A. That is fair. That was 10 years ago.
(Chaiton Cross, April 16, 2021, p. 29, lines 1-15)
123
Dr. Chaiton testified his usual practice was to contact the family doctor and discuss changing medications that cause hyperuricemia. Dr. Chaiton testified that he could not recall doing that with Rhodalee and there is no evidence to suggest that he did.
Dr. Chaiton cross, page 23-24, lines 23-32, 1-11
Dr. Chaiton did not testify that his usual practice was to contact the family doctor and discuss changing medications. It is undisputed that Dr. Chaiton did not contact Ms. Leckie’s family doctor.
The cited evidence reads as follows:
Q. Well, I didn’t ask you that question, but I take it knowing that potential for hypersensitivity, you took no steps to take her off HydrochloroThiazide, or find an alternative drug, or discuss with her family doctor finding an alternative drug; correct?
A. No, that’s not correct. As I think I testified at discovery, my usual practice is to advise that Thiazide diuretic not be employed, but it had nothing to do with hypersensitivity reactions. It has to do with the fact that it aggravates the underlying primary condition which is gout.
Dr. Chaiton testified that he tells the patient to contact the prescribing physician:
Q. You did not take those steps; correct?
A. Well, I believe I did. But, again, it’s not recorded in the record. My usual practice on anybody on a Thiazide diuretic is to inform the patient to suggest to her doctor who prescribed it to select another alternative agent.
Q. In this case, you did not do that, and you did not document doing that; correct?
A. I believe I did do that, but it’s not documented, sir.
(Chaiton Cross, April 15, 2021, p. 189, lines 15-23)
86
She had Sickle Cell Trait and was taking the medication HydrochloroThiazide, which had been reintroduced in September 24, 2012 for her high blood pressure.
None
There is no evidence cited for the proposition that HydrochloroThiazide had been reintroduced on September 24, 2012.
The evidence was that a prescription for HydrochloroThiazide was filled on September 24, 2012. There was no evidence from Ms. Leckie that it was reintroduced at that time.
As Dr. Baer testified:
Q. And you’re aware of the fact that one of the intervening factors is what’s in the purple line, which is the addition of HydrochloroThiazide by the family doctor; correct?
A. I have had a lot of difficulty with that, looking at that and also looking at the pharmacy records, because Dr. Rubin stated that this was a newly added drug, but it had been prescribed in February 2011 as well. So, I wasn’t sure that it was something newly added. I see that there is a gap in the prescription record because in February 2011, she was given 100 tablets, and at one a day, that really shouldn’t have lasted until September 2012 when she got the next prescription dispensed at the pharmacy, and it raised some questions with me as to a couple of things.
One was that she was prescribed it, but perhaps there was some noncompliance, which is very common with anti-hypertensive medications, that they’re not taken every day and, therefore, the supply could have stretched, or that, in the interim, she went to another pharmacy whose records we don’t have and received other prescriptions for it. As I say, Dr. Rubin stated quite clearly that it was something newly added, and I was not at all comfortable with concluding that because it had been prescribed in the past.
(Baer Cross, p. 124, lines 15-32; p. 125, lines 1-4)
66
In fact, a closer look at the blood work by Dr. Chaiton would have revealed an elevated creatinine level contemporaneous with the introduction of HydrochloroThiazide, which had caused her a (sic) substantially elevated creatinine level to almost double.
None
There is no evidence that Dr. Chaiton had all of the blood work that the plaintiffs appear to refer to.
In addition, there is no evidence as to when HydrochloroThiazide was introduced, only that a prescription was filled on September 24, 2012.
Finally, both Dr. Chaiton and Dr. Rubin testified that there may have been other factors aside from HydrochloroThiazide that impacted Ms. Leckie’s creatinine.
Dr. Chaiton outlined other factors in the course of his cross examination:
Q. Do you agree with me the only intervening act between her level of 467 and her level of 795 was a new prescription of HydrochloroThiazide; correct?
A. No, there are a lot of contributing factors. It could be her hydration; it could be her diet. I mean, there are many factors that could alter the uric acid apart from HydrochloroThiazide.
Q. The only matter you are - you know of, the only intervening act you are aware of is the institution of HydrochloroThiazide; correct?
A. That’s the only pharmaceutical factor, yes.
(Chaiton Cross, April 14, 2021, p. 191, lines 10-19)
Dr. Rubin testified as follows:
Q. Other than the HydrochloroThiazide is there any other intervening act you’re aware of that would of caused the creatinine and the uric acid to almost double between the before and after within weeks?
A. I couldn’t find anything. That doesn’t mean there isn’t. The possibility is that taking a – the only other thing would be using anti-inflammatories. I believe she was given Ibuprofen in the emergency room. That could have also had an impact upon kidney function. So anti-inflammatories of that nature might have done so. I don’t know what else, other drugs that she may have taken, unknown, over the counter, whatever but – and I don’t know what her volume status was like and how well hydrated she was.
(Rubin Chief, April 14, 2021, p. 75, lines 8-20)
115
Dr. Chaiton failed to inquire with Rhodalee or her family doctor when she began taking HydrochloroThiazide. If Dr. Chaiton would have inquired, he would have seen that the HydrochloroThiazide was the intervening act that caused her uric acid and creatinine levels to significantly increase.
None
No evidence is cited for the proposition that HydrochloroThiazide likely caused Ms. Leckie’s uric acid and creatinine levels to significantly increase. The evidence was that this was a possible factor.
In addition, there was no evidence as to when HydrochloroThiazide was introduced, only that a prescription was filled on September 24, 2012.
As described above, both Dr. Chaiton and Dr. Rubin discussed other factors that could have contributed the change in Ms. Leckie’s uric acid and creatinine levels.
(Chaiton Cross, April 14, 2021, p. 191, lines 10-19; Rubin Chief, April 14, 2021, p. 75, lines 8-20)
29-31
Dr. Chaiton’s evidence at his Examination for Discovery and at trial was that he “suspected” that Rhodalee had gout.
Examination for Discovery transcript of Dr. Chaiton, p. 25, q. 131.
Dr. Chaiton cross examination page 3, lines 1-16
This statement is misleading and incomplete. The evidence cited was in relation to when Dr. Chaiton first saw Ms. Leckie on October 4, 2012. His evidence was that during that initial appointment, he suspected, but was not certain, that Ms. Leckie had gout.
At trial, Dr. Chaiton testified that when he saw Ms. Leckie on November 5, 2012, her significant improvement while on Prednisone confirmed his diagnosis:
Q. Would you agree with me that you had a presumptive diagnosis?
A. Yes, but presumptive and provisional are the same thing, sir.
Q. Presumptive means not certain, fair?
A. Yes.
Q. Presumptive means not definitive, fair?
A. It does mean that, sir. Yes, sir.
Q. So, you had a not certain, not definitive diagnosis; correct? Fair?
A. Yes. Yes, that’s fair.
Q. And in the setting of that, you note on November 5th, 2012 that she had a significant improvement, fair?
A. Which confirmed my diagnosis, yes.
Q. Well, it’s not what your note says, but let’s just talk about what I’m asking you. She had a significant improvement. I’ve just highlighted it in your note; correct?
A. Improvement to my recommended therapy that she followed.
Q. Now....
A. That would not have occurred if she had another condition.
(Chaiton Cross, April 16, 2021, p. 18, lines 7-28)
95, 110
Although Dr. Heller noted a presumed diagnosis of gout he later diagnosed Rhodalee with peroneal tenosynovitis (which is not gout).
On October 15, 2012, Rhodalee attended the fracture clinic at Humber River Regional Hospital and saw Dr. Heller. Dr. Heller commented on moderate soft tissue swelling of her ankle; no malleolar tenderness and diagnosed Rhodalee with peroneal tenosynovitis (this not gout).* (sic)
*underlining in original
Joint Document Brief, p. 709
It is misleading to state that peroneal tenosynovitis is not gout, given that the evidence was that this was likely a secondary event and could be a feature of gout.
Dr. Rubin testified that he suspected soft tissue injuries were a secondary event:
A: Soft tissue injuries as Dr. Heller suggested I think were a secondary event. (Rubin Chief, April 14, 2021, p. 104, line 32; p. 105, line 1)
Dr. Chaiton also testified that peroneal tendonitis can be a component of gout:
Q. Did you obtain the imaging that Dr. Heller obtained?
A. I recall obtaining a report that said that there was a peroneal tendonitis as the reason for his casting the ankle.
Q. Peroneal tendonitis is not necessarily gout; correct?
A. It can be a component of gout, yes, it can be.
Q. It could also be the product of an injury; correct?
A. Yes. (Chaiton Cross, April 15, 2021, p. 186, lines 22-32; p. 187, lines 1-3)
166
Instead he presumed a diagnosis and even after his diagnosis was proven incorrect by two ultrasounds, his confirmation bias led him to prescribe Allopurinol instead of dealing with the comorbidities and fully assessing Rhodalee’s health issues.
None
This statement misstates the significance of a lack of crystals. There is no evidence that the lack of crystals on ultrasound proved the diagnosis of gout incorrect.
Dr. Rubin did not testify as to the significance of a lack of crystals on ultrasound.
Dr. Chaiton testified that it is common not to observe crystals on ultrasound (cross-examination, April 16, page 8, line 32, p. 9, lines 1-11)
MR. LINDEN: Q. Now, sir, we can agree that you conducted multiple ultrasounds on Mrs. Leckie, is that fair?
A. Two, sir.
Q. Not once did you observe crystals, fair?
A. It is not a common finding, sir.
Q. That’s not my question. Not once did you observe crystals, fair?
A. That’s correct, sir.
Q. All right. You agree with me you can see crystals on ultrasound?
A. On occasion, sir. More typically in the big toe. She did not have a big toe inflammation when I saw her.
(Chaiton Cross, April 16, 2021, p. 8, line 32, p. 9, lines 1-11)
153
Dr. Chaiton testified that an ankle tear was found on the Ultrasound that he performed on Rhodalee. Dr. Chaiton testified that a tear could be painful. Dr. Chaiton testified that he did not record the tear in his notes and could not recall asking Rhodalee about it.
Dr. Chaiton Cross Examination Testimony, page 171-172, lines 13-32, 1-2
This is misleading and takes only a selective portion of Dr. Chaiton’s evidence. Dr. Chaiton testified that an old tear – what Ms. Leckie had – would not be painful:
The passage cited by the plaintiffs continues:
Q. Can you read the first line under – across from “ankle,” please?
A. “No tendon pathology, left ATFL not seen, old tear.”
Q. And tear, is that the word? Old tear?
A. Yeah.
Q. Tears can be painful; correct?
A. Not when they’re old.
Q. Well, if they don’t get better, you agree with me they might still be painful?
A. No.
(Chaiton Cross, April 15, 2021, p. 171, lines 31-32; p. 172, lines 1-10)
73
Both the plaintiff and defence experts all agreed that Dr. Lisa Stamp is the foremost expert of Allopurinol, and adopted at trial her published findings in her article on Allopurinol.
None
No expert testified at trial that Dr. Stamp is “the foremost expert of Allopurinol.”
Dr. Rubin was not questioned on nor did he provide evidence about Dr. Stamp or her articles whatsoever.
Dr. Baer testified that Dr. Stamp is an expert on gout and Allopurinol hypersensitivity syndrome:
MR. LINDEN: Q. So, my understanding is, in the report that you prepared, you comment on an article by Lisa Stamp; is that right?
A. Yes, she’s an expert on gout and, I believe, on Allopurinol hypersensitivity syndrome. She has written extensively on that, and I have seen some of her articles and commented on them, yes.
(Baer Cross, p. 99, lines 27-32, p. 100, line 1)
Dr. Rieder testified that Dr. Stamp has published extensively in the area of Allopurinol:
MR. LINDEN: Q. Dr. Rieder, do you know Dr. Lisa Stamp?
A. Dr. Lisa Stamp is a Professor of Rheumatology in Christchurch, New Zealand.
Q. All right. And you would agree with me that unlike you, she has actually studied Allopurinol and the adverse effects arising from that, correct?
A. Dr. Stamp is a rheumatologist who has a great interest in studying drugs for treatment of rheumatic disease, and she’s published extensively in the area of Allopurinol.
(Rieder Cross, p. 49, lines 24-30, p. 50, lines 1-3)
218
Although the defence theory from Dr. Chaiton was the risk of severe reaction was one in a million, Dr. Rieder conceded that this was wrong and that the risk was 690 times higher. Dr. Rieder testified on cross-examination that the numbers in Dr. Stamp’s study meant that the incidence of Allopurinol induced SCAR which include Stevens-Johnson Syndrome is much higher than one in a million.
Dr. Rieder cross examination, page 51-52, lines 12-32, 1-25.
This is incorrect and represents a fundamental misunderstanding of the evidence, and confusion between the risk of Severe Cutaneous Adverse Reaction (SCAR) as distinct from the risk of Stevens-Johnson Syndrome.
Dr. Chaiton testified that the risk of Stevens-Johnson Syndrome – not the risk of severe reaction - was in the range of one in a million:
Q. Doctor, did you tell Mrs. Leckie that the risk - that one of the risks of Allopurinol was Stevens-Johnson syndrome?
A. I did not.
Q. Why not?
A. As I said, in my experience, I had never run into that very rare and unusual reaction. I did not feel it was a likelihood. In my experience, it was a possibility in the range of one in a million. I didn’t feel it was necessary to disclose these kinds of rare events, but more typically deal with common events and to proceed on that basis.
(Chaiton Chief, April 15, 2021, p. 139, line 32, p. 140, lines 1-10):
Dr. Rieder testified that he agreed with this:
Q. Dr. Chaiton - Dr. Rieder, I’m sorry, Dr. Chaiton testified that the odds of getting Stephens- Johnson Syndrome from Allopurinol are in the order of one in a million, do you agree with that?
A. That would be in the range, yes.
(Rieder Chief, p. 25, lines 7-11)
Dr. Rieder agreed that the risk of SCAR is higher than one in a million:
Q. Right. And the incidence is far more than one in a million, fair?
A. The incidence is overall, from Dr. Stamp’s work, is higher than one in a million, yes, of SCAR.
(Rieder Cross, p. 52, lines 8-11)
133
Dr. Amba also notes that if there is a concern regarding gout her HydrochloroThiazide should be stopped and alternative medication to control her blood pressure should be used. This is precisely what Dr. Chaiton should have done instead of rushing to prescribe Allopurinol. This is precisely what the guidelines require.
None
The evidence was that the pertinent guidelines did not in fact require that HydrochloroThiazide be stopped.
As Dr. Baer testified, the relevant guidelines state: “consider elimination of non-essential prescription medications that induce hyperuricemia.*”
The guidelines go on to specifically state “ *…in discussion, and without a specific vote, the TFP recognized the value of Thiazide treatment in many patients with hypertension, and cautioned against imprudent cessation of Thiazide treatment to lessen hyperuricemia at the cost of worsened control of blood pressure in difficult to control hypertension.”
(Exhibit 25, 2012 ACR Guidelines extract)
(Baer Chief, p. 70, lines 18-32, p. 71, lines 1-32, p. 72, lines 1-8)
119
Dr. Chaiton failed to follow the ACR guidelines as he failed to recommend diet and wellness changes and take Rhodalee off her Thiazide medication before prescribing Allopurinol. It is evident from Rhodalee’s history if Dr. Chaiton had done this it would have solved Rhodalee’s ankle issues as Rhodalee has subsequently been without any urate lowering therapy for 6 years and is currently asymptomatic.
None
There was no such evidence introduced at trial to support this retrospective assertion.
Ms. Leckie did not testify that she has been without urate lowering therapy for six years. She only testified that she is not currently taking Allopurinol (Leckie Chief, p. 69, lines 21-22).
The statement that if Dr. Chaiton had recommended diet and wellness changes and taken Ms. Leckie off Thiazide medications, it would have solved her ankle issues is entirely inconsistent with the evidence, including:
• Ms. Leckie testified that in October 2014 she told Dr. Shear that after discontinuation of Allopurinol and Colchicine that her gout was not controlled (Leckie Cross, p. 133, lines 4-12)
• In 2014, Ms. Leckie was prescribed and took Uloric, an alternative urate lowering therapy (Leckie Cross, p. 131, line 1-3)
• Ms. Leckie’s evidence is that since seeing Dr. Kreidstein in 2015, doctors have told her that she continues to suffer from gout flare up (Leckie Cross, p. 132, lines 10-15)
In addition, Ms. Leckie did not produce family doctor or rheumatology records past 2015, nor an updated decoded OHIP summary for the period past 2015.
Finally, even the plaintiffs’ own expert, Dr. Rubin, testified that lifestyle modifications will reduce a patient’s uric acid by at most, 15 percent, and may delay – not eliminate – the need for urate lowering therapy – for patients with a lower uric acid level and one attack:
A. Well this is very similar to what the European’s said, patient education, dietary modification – I spend time doing that. You know the fact of the matter is most people who present with gout, most middle ages males are overweight, hypertensive, eat all the wrong foods, alcohol consumption is God knows what, I mean there’s a lot of things that you can modify and you know it’s very, it’s very gratifying when the person comes back six months later and they feel better and they lose weight. Now all of those things will reduce uric acid by at most 15 percent. So if you start off with the uric acid level at 500 and you’ve had one attack it’s possible that you can push back the need for urate lowering therapy a number of years. If your uric acid level is 600 plus, 650 in a male with all those things the chances are that it’s good for you to do those things but it really depends on how frequently the attacks occur and that’s individually based but very much a reflection of the uric acid level in the blood…
(Rubin Chief, April 14, 2021, p. 68, lines 11-27)
137
Rhodalee has been off urate lowering therapy for 6 years, and as a result of diet modification, and not taking HydrochloroThiazide, has been just fine.
None
No evidence is cited to support this proposition, and no such evidence was adduced at trial.
In addition, Ms. Leckie did not produce family doctor or rheumatology records past 2015, nor an updated decoded OHIP summary for the period past 2015.
Finally, even the plaintiffs’ own expert testified that lifestyle measures will reduce a patient’s uric acid levels by at most 15 percent and may delay (not eliminate) the need for urate lowering therapy for a patient with one attack and uric acid level around 500. Ms. Leckie had uric acid levels well in excess of 500 umol/L and a history of gout attacks.
(Rubin Chief, April 14, 2021, p. 68, lines 11-27)
4
Most importantly, even if Dr. Chaiton presumed gout, he could have – and should have – started Rhodalee with conservative measures while he looked for the source of her elevated uric acid. The evidence suggests that this method would have been successful.
None
There is no evidence to support this proposition.
The statement that conservative measures would have solved Ms. Leckie’s ankle issues is entirely inconsistent with the evidence, including:
• Ms. Leckie testified that in October 2014 she told Dr. Shear that after discontinuation of Allopurinol and Colchicine that her gout was not controlled (Leckie Cross, p. 133, lines 4-12)
• In 2014, Ms. Leckie was prescribed and took Uloric, an alternative urate lowering therapy (Leckie Cross, p. 131, line 1-3)
• Ms. Leckie’s evidence is that since seeing Dr. Kreidstein in 2015, doctors have told her that she continues to suffer from gout flare up (Leckie Cross, p. 132, lines 10-15)
In addition, Ms. Leckie did not produce family doctor or rheumatology records past 2015, nor an updated decoded OHIP summary for the period past 2015.
Finally, even the plaintiffs’ own expert testified that lifestyle measures will reduce a patient’s uric acid levels by at most 15 percent and may delay (not eliminate) the need for urate lowering therapy for a patient with one attack and uric acid level around 500. Ms. Leckie had uric acid levels well in excess of 500 umol/L and a history of gout attacks.
(Rubin Chief, April 14, 2021, p. 68, lines 11-27)
131
The Allopurinol almost killed Rhodalee Leckie. She did not need this drug. This is proven by the fact that Rhodalee testified that for 6 years she has had no issues with her ankle and has not been on any urate lowering therapy at all. Rhodalee modified her diet and she has had no ankle issues.
Rhodalee Leckie Cross examination page 117, line 28-32;
Marleen (sic) Palmer, chief, page 25, line 18-25
This statement is retrospective and misleading. Ms. Leckie did not testify that she has had no issues with her ankle for six years. The cited passage of Ms. Leckie’s evidence reads:
Q. When, when, I want to talk to understand a little bit more about how your symptoms in relation to your arthritis gout, were dealt with my [sic] other doctors after you were discharged from the hospital? So, after you were discharged, were now talking in 2013, in April of the following year, you went to see Dr. Afinawasha (ph) again because you were having pain in your right foot, which Dr. Afinawasha (ph) told you was because of gout, correct?
A. Correct. After that you know, when I see what I go through, I never really go to any Doctor about it. I was just [indescribable]I don’t take nothing, or I take a Tylenol at home. And from then, and I change my diet, and thing like that so it don’t really act up.
This passage is immediately followed by Ms. Leckie’s admission that she saw several other physicians for her gout, including Dr. McKinney, Dr. Amba, and Dr. Kreidstein, and was prescribed Uloric, a urate lowering therapy for her gout. See Leckie Cross, pages 118-131.
Ms. Leckie’s evidence was that since seeing Dr. Kreidstein in 2015, doctors have told her that she continues to suffer from gout flare ups (Leckie Cross, p. 132, lines 10-15)
In addition, Ms. Leckie did not produce family doctor or rheumatology records past 2015, nor an updated decoded OHIP summary for the period past 2015.
The cited reference to Ms. Palmer’s evidence (which appears to erroneously refer to page 25 instead of page 15) simply confirms that Ms. Palmer has not collected a prescription for Allopurinol or Uloric for her mother in the past five or six years.
146
Dr. Chaiton testified in chief at trial that he had never seen a note from Humber River Regional Hospital that was in his chart.
Dr. Chaiton testimony in chief, page 141-142, lines 28-31, 1-5
The document referenced (Exhibit 2, Joint Brief of Documents, Tab 4, p. 2370) is not a Humber River Regional Hospital Record.
Dr. Chaiton testified that he believed these were his notes in relation to the November 29, 2012 visit:
Q. And I want to take you for a moment to 2370, to the very next page, and can you explain what this note is? And why is it in this form?
A. I don’t know. I think those are my notes referenced to the visit on the 29th.
Q. But is this form of note the new EMR you were just describing?
A. No. I don’t know what is – what that refers to. It might have been a brief – I don’t know. I can’t – this is the first time I’ve seen this, so I can’t comment, but it definitely deals with the events of the visit on the 29th.
(Chaiton Chief, p. 141, lines 27-32, p. 142, lines 1-5)
50
Dr. Baer testified and it is indicated in his presentation at slide 10 that primary care physicians more frequently misdiagnosed gout than they accurately diagnose it. In fact, 76% of their patients are taking a drug that they don’t need.
Dr. Baer cross, page 110, lines 10-16
This statement represents a misunderstanding of these statistics. The slide referenced cited a 1991 study where it was found that 1.7% of patients had gout, and 1.8% had been misdiagnosed as having gout. Of the 1.8% misdiagnosed with having gout, 76% were treated with Allopurinol.
SCHEDULE “B” Documents Relied on in the Plaintiffs’ Written Closings that Are Not in Evidence
Paragraph Reference[^65]
Document not in Evidence
Comments
15-16
CPSO Medical Records Documentation policy
This document was not discussed nor put to any witness at trial.
35, 115
Exhibit “B”, Chart prepared by Dr. Rubin
This chart was entered as a lettered exhibit, marked for identification purposes only.
38, 49
Rheumatology by Marc C. Hochberg
(Editor), Alan J. Silman, Josef S. Smolen, Michael E. Weinblatt, Michael H. Weisman
Published October 19th 2010
This document was not discussed nor put to any witness at trial.
39, 63
EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the standing committee for international clinical studies including therapeutics (ESCISIT), 2006 at page 1305
This document was not put to any witness at trial.
54
Exhibit “A”, Dr. Rubin presentation
This chart was entered as a lettered exhibit, marked for identification purposes only.
[^1]: Crits v. Sylvester, 1956 34 (ON CA), at paras. 13-14, aff’d 1956 29 (SCC), [1956] SCR 991; ter Neuzen v. Korn, [1995] 3 SCR 674, 1995 72 (SCC) at para. 33 [ter Neuzen].
[^2]: ter Neuzen, ibid at para. 33.
[^3]: Crits v. Sylvester 1956 34 (ON CA), [1956] O.R. 132-151 (Ont. C.A.) at QL pg. 7, aff’d 1956 29 (SCC), [1956] S.C.R. 991.
[^4]: Wade v. Nayernouri [1978] 2 L.M.Q. 67 (Ont. H.C.) at para. 22) [Wade].
[^5]: Wade, ibid at para. 16.
[^6]: Hillis v. Meineri, 2017 ONCA 2845 at para. 54 [Hillis].
[^7]: Turkington v. Lai, 2007 48993 (ON S.C.J.) at para. 69.
[^8]: Bafaro v. Dowd, [2008] O.J. No. 3474 (S.C.J.) at para. 24, aff’d 2010 ONCA 188 [Bafaro].
[^9]: ter Neuzen, supra at para. 34.
[^10]: St. Jean v. Mercier, 2002 SCC 15 at para. 53 [St-Jean].
[^11]: Wilson v. Swanson, 1956 1 (SCC), [1956] S.C.R. 804 at p. 812 [Wilson].
[^12]: Wilson, ibid paras. 21-23; Lapointe v. Hôpital Le Gardeur, 1992 119 (SCC), [1992] 1 SCR 351.
[^13]: Nattrass v. Weber, 2010 ABCA 64 at para. 26 [Nattrass].
[^14]: Nattrass, ibid para. 31.
[^15]: Hajgato v. London Health Association, [1982] O.J. No. 2564 (H.C.J). at para. 36, aff’d, 1983 1687 (ON CA), [1983] O.J. No. 2911 (C.A.) [Hajgato].
[^16]: Wilson, supra at p. 811-812.
[^17]: Ball v. Amendola, 2009 55309 (ON SC), [2009] O.J. No. 4114 (S.C.J.) at para. 137 [Ball].
[^18]: Ball, ibid at para. 138, citing Pittman Estate v. Bain, [1994] O.J. No. 463 (S.C.J.) at para. 258.
[^19]: Hajgato, at para. 36.
[^20]: Crawford (Litigation Guardian of) v. Penney, [2003] O.J. No. 89 (S.C.J.) at para. 245, aff’d [2004] O.J. No. 3369 (C.A.), leave to appeal refused, [2004] S.C.C.A No. 496.
[^21]: Wilson, supra at p. 817.
[^22]: Stepita v. Dibble, 2020 ONSC 3041 at para. 66 (xxxii)-67.
[^23]: Bafaro at para. 36, aff’d 2010 ONCA 188.
[^24]: Kolesar v. Jeffries et al. [1978] 1 S.C.R. 491, 1977 6 (SCC), at page 497.
[^25]: Wells (Litigation Guardian of) v. Paramsothy [2000] O.J. No. 2390 (S.C.). at para. 154; cited in Watson v. Soon, 2018 ONSC 3809 at para. 78.
[^26]: Dale v. Munthali, 1977 1135 (ON SC) at para. 5.
[^27]: Nichols v. Young, [2003] O.J. No. 4376 (CA) at para. 1.
[^28]: Hopp v. Lepp, 1980 14 (SCC), [1980] 2 S.C.R. 192 at p. 210 [Hopp].
[^29]: Hopp, ibid. at para. 12.
[^30]: Reibl v. Hughes, 1980 23 (SCC), [1980] 2 S.C.R. 880 at p. 894-95 [Reibl].
[^31]: Wei Estate v. Dales, [1998] O.J. No. 1411 (SC) paras. 87-88, aff’d, [2000] O.J. No. 2753 (CA).
[^32]: Cameron (Litigation Guardian of) v. Louden, [2000] O.J. No. 858 (S.C.J.) at para. 285.
[^33]: Van Dyke v. Grey Bruce Regional Health Centre, 2005 18841 (ON CA), [2005] O.J. No. 2219 (C.A.) at para. 67, leave to appeal to SCC refused, [2005] S.C.C.A. No. 335 [Van Dyke].
[^34]: Arndt v. Smith, 1997 360 (SCC), [1997] 2 S.C.R. 539 at para. 17 [Arndt].
[^35]: Arndt, ibid at para. 14.
[^36]: Arndt, ibid at para. 16.
[^37]: Reibl, supra at p. 899-900.
[^38]: Van Dyke, supra at para. 67.
[^39]: Hollis v. Dow Corning Corp, 1995 55 (SCC), [1995] 4 SCR 634, at para. 24.
[^40]: Starson v. Swayze, 2003 SCC 32, [2003] 1 SCR 722 at para. 75
[^41]: Hopp, at page 210.
[^42]: Health Care Consent Act, 1996, S.O. 1996, c.2 Sched A, at s. 10.
[^43]: Health Care Consent Act, ibid at s. 11.
[^44]: White v. Turner (1981), O.R.(2d) 773, 1981 2874 (ON SC) at para. 47 [White].
[^45]: Van Dyke, supra para. 63.
[^46]: White, supra at para. 69.
[^47]: Cory v. Bass, 2011 ABQB 360.
[^48]: Arndt, supra at para. 17.
[^49]: Bollman v. Soenen, 2014 ONCA 36, at paras. 20-21.
[^50]: Arndt at para. 6. See also Reibl at para. 25.
[^51]: Clements v. Clements, 2012 SCC 32, at para. 37 [Clements]; Cottrelle v. Gerrard, 2003 50091 (ON CA), [2003] O.J. No. 4194 (C.A.), at para. 36; leave to appeal refused, [2003] S.C.C.A. No. 549 [Cottrelle].
[^52]: Clements, ibid at para. 46.
[^53]: Resurfice Corp. v. Hanke, 2007 SCC 7 at para. 23, citing Snell v. Farrell, 1990 70 (SCC), [1990] 2 S.C.R. 311 (Q.L.) at p. 327.
[^55]: Van Dyke, supra at para. 44.
[^56]: Cottrelle, supra at para. 36.
[^57]: St-Jean, supra, 2002 SCC 15 at para. 106.
[^58]: Clements, supra note 39 at para. 11.
[^59]: Saadati v. Moorhead, 2017 SCC 28 at para. 20.
[^60]: Mustapha v. Culligan of Canada Ltd, 2008 SCC 27 at para. 12 [Mustapha].
[^61]: Mustapha, ibid at para. 16.
[^62]: Bafaro, supra at para. 36.
[^63]: Hillis, supra at para. 54.
[^64]: All references are to the Closing Submissions of the Plaintiffs dated May 10, 2021.
[^65]: All references are to the Closing Submissions of the Plaintiffs dated May 10, 2021.