Rothonis v Lattimore

Supreme Court of NSW|2016-06-29|Before: Fagan J

Solicitors: Ms Virginia Hart, Virginia Hart Medical Lawyers (Plaintiff) Ms Louise Hazelton, Norton Rose Fulbright File Number(s): 2013/153895

Judgment

In early September 2006 the plaintiff was referred to the defendant, a cardiologist, for investigation of possible involvement of her heart in neurological symptoms which she had recently experienced. The plaintiff alleges the defendant negligently failed to carry out sufficient investigations and failed to diagnose or to prescribe treatment for a patent foramen ovale ("PFO"). That is, an opening through the interatrial septum, being the membrane dividing the left and right upper chambers of her heart. On 7 June 2007 the plaintiff suffered a stroke which has left her significantly disabled. The plaintiff claims damages for alleged negligence upon the ground that the defendant failed to identify the PFO in September 2006 and allowed it to go untreated and to cause the stroke.

Plaintiff's first consultation with defendant, 4 September 2006

The defendant first saw the plaintiff in consultation for approximately half an hour on 4 September 2006. I accept the defendant's evidence that she received from the plaintiff the following history and other information on this occasion: 1. The plaintiff had been referred to a neurologist for opinion on her recent symptoms but had not seen that specialist and was not sure of his name. (The plaintiff was in fact referred to Associate Professor Ell by letter from her husband dated 8 September 2006. Associate Professor Ell saw her on 13 September 2006, issued to Dr Rothonis a written report of that date and provided further information and opinion orally on about 15 September - all of which is referred to in more detail below). 2. The plaintiff was 44 years old, living with her husband and four children ranging in age from 15 years to 2½ years and also caring for her parents-in-law, who were elderly and unwell. 3. She had felt "dizzy" on and off since her last pregnancy. 4. For the preceding two weeks she had experienced the following:

feeling "dizzy … like I was losing my step";
"not able to focus" whilst driving;
no sense of a curtain of darkness coming down during the driving incident and no patches of darkness;
seeing "little lines";
no palpitations whilst driving but experience of them when anxious or stressed;
no feeling of chest tightness but one episode of sharp chest pain;
no "greying out" or loss of consciousness during the driving incident (recorded by the defendant as "No presyncope. No LOC").

The defendant did not recall specifically whether the plaintiff brought with her to the consultation a copy of the radiologist's CT scan of her head. It would have been the defendant's usual practice to record a note about such a report and to keep a copy, if she received it. On the balance of probabilities I find that she did not receive a copy, as there is no note in the defendant's consultation record about the report nor any copy on her file. This is not of great significance because the defendant had the essential information about the outcome of the CT scan from Dr Rothonis' letter of referral. Namely that it was reported by the radiologist as showing a lacunar infarct. It does not appear that the defendant received the MRI scan or the report on it. These went to Dr Rothonis: see [32].
During the consultation the defendant carried out a physical examination of the plaintiff and an electrocardiogram ("ECG") to trace the electrical activity of her heart. The results of both were normal. The defendant's usual practice in such a case was to order a transthoracic echocardiogram. That is, an ultrasound examination of the heart using a transducer external to the chest. At the time of the consultation the defendant was told by the plaintiff that she had already undergone this form of examination but neither the ultrasound images nor any report on them was provided to the defendant at the consultation.
The defendant arranged for the plaintiff, at future dates, to have her blood pressure monitored over a 24-hour period and to be fitted with a Holter monitor which would record her heart rhythm for three days.
The defendant's conclusions from this first consultation, which were preliminary and subject to the results of the echocardiogram and other tests ordered, were summarised by her in the following paragraphs of her witness statement, which I accept: "40 The time course of the plaintiff's symptoms and the vagueness of the symptoms did not suggest to me that the plaintiff was describing symptoms of stroke or TIA. 41 I formed the view that the plaintiff was safe to drive home from the appointment. I also formed the preliminary view that her symptoms were not likely to be sinister but were likely to be associated with stress and migraine, as she was a homemaker living with an extended family, two of whom were infirm, she had four children and she worked full-time."
In par 40 the abbreviation "TIA" means transient ischaemic attack. That is, a temporary occlusion of an artery interrupting blood flow to a part of the brain, which causes transient neurological symptoms but does not result in an infarct. Such an ischaemic event will not leave tissue damage which would stand as evidence of the temporary occlusion. The occurrence of a TIA can be diagnosed only from the patient's history of the symptoms which he or she has experienced. It is in the nature of such an event that the diagnosing clinician is usually entirely dependent upon the history given. Only the patient has experienced the neurological sensations and can describe them, except if some symptoms have been observed by another person during the attack (evidence of Professor Davis, T 560.21 - .38).

Transthoracic echocardiogram performed 30 August 2006

The transthoracic echocardiogram was done by Associate Professor Ian Wilcox (referred to here as "Dr Wilcox") on 30 August 2006. At the time he practised at the same premises as the defendant, within a grouping of specialists (including the defendant) who referred to themselves as "Central Sydney Cardiology". They occupied rooms at the Royal Prince Alfred Hospital Medical Centre in Newtown. The medical practices and professional responsibilities of these doctors were entirely separate although they shared common areas of their premises. They also shared some practice expenses including the salaries of administrative staff. The plaintiff had been referred to Dr Wilcox directly by Dr Rothonis. At the first consultation the plaintiff told the defendant she had already submitted to the transthoracic examination by Dr Wilcox.
Dr Wilcox's report dated 30 August records under the heading "Referral Diagnosis" the words "previous TIA". Any referral letter which Dr Rothonis may have written to Dr Wilcox is not amongst the records which the parties have been able to locate and tender. There is no evidentiary basis for a finding that any medical practitioner had, by 30 August 2006, made a diagnosis of the plaintiff's neurological incident whilst driving as a TIA. The terms in which the referral diagnosis is stated on the echocardiogram report may be no more than an abbreviated reference, by Dr Wilcox or one of his staff, to the circumstance that the echocardiogram was being undertaken because the plaintiff's neurological symptoms may have been caused by some ischaemic event.
The reported results of the transthoracic echocardiogram were as follows: "1. Normal valvular structure with physiological Doppler flows. 2. Normal aortic root/ascending aorta size. 3. Normal atrial size. 4. Normal ventricular size, wall thickness and contractility. 5. Mobile atrial septum without shunting. 6. No intracardiac mass or obvious cardiac source of embolus."
For present purposes finding number 5 is significant. A mobile septum is one which displaces laterally when the muscle of the heart contracts. The increased pressure in the right atrium forces blood downward into the right ventricle but if the atrial septum is mobile the pressure also causes it to bulge outward, into the left atrium. "Shunting" means blood passing through an opening (PFO) in the septum, from the right atrium into the left.
Although the defendant did not have this report or the associated ultrasound images at the time of her first consultation with the plaintiff, after the consultation she went to a computer in a room within the premises of Central Sydney Cardiology and looked at the images. They were recorded on a disc. Neither the images nor the professor's report on them would have been sent to her directly because she had not ordered the study. As the referral to Dr Wilcox had come from Dr Rothonis, a general practitioner, the report would have been sent directly to him. It was so addressed. This would have been treated in Dr Wilcox's practice as an "outside" referral for which he would not automatically provide the results to any cardiologist working within Central Sydney Cardiology.
By the date of the trial the defendant had no recollection of actually looking at the echocardiogram images in September 2006 or of when in that month she had done so. However she agreed it was very likely she would have seen them within days of her first consultation with the plaintiff. I find on the balance of probabilities that she viewed the images no later than 8 September. At the trial of the action the defendant had no recollection of what details she had seen on the images at that time. (The disc on which the images were recorded was mislaid sometime after July 2007 and it is not in evidence).
The defendant examined the images again in mid-2007 after having been informed by Dr Rothonis that his wife had suffered a stroke on 7 June that year. At the trial the defendant was able to recall from her review in 2007 that the images were "good" and "clear" and that they "very clearly demonstrated" a mobile atrial septum. A mobile septum is classified as an atrial septal aneurysm if the measure of displacement upon contraction of the heart muscle exceeds 10mm. The defendant's recollection of the ultrasound images in this case was that one could not tell whether this septum was mobile to that extent. She said that one does not attempt to measure the displacement on the images from a transthoracic echocardiogram, they are insufficiently clear.
However it appeared to her likely that the mobility of this septum would fulfil the criterion for aneurysm. That is, if a transoesophageal echocardiogram should be performed (with the transducer inserted down the oesophagus to close proximity with the heart) and if the resulting images permitted measurement (as would be expected from that type of study), then the measurement would likely exceed 10mm. I find that these features of the transthoracic ultrasound images were observed by the defendant when she examined them after her first consultation with the plaintiff and before 8 September 2006.
The defendant's reading of the echocardiogram images, when she reviewed them in 2007 and, I infer, when she first looked at them between 4 and 8 September 2006, was that either no shunting was occurring or any shunting was not of sufficient magnitude to be detected by the study. If shunting could be detected it would indicate a PFO.
Dr Rothonis' letter of referral to Dr Ell of 8 September 2006 (see [33]) stated that his wife's cardiac assessment by the defendant "was normal and [she] is due to have a 24 hour Holter at the end of this week". I infer that Dr Rothonis would not have written to Dr Ell in these terms unless he had received an oral report from the defendant to the effect that the plaintiff's heart appeared normal on the basis of investigations to that date.
I also infer that the defendant, knowing at the time of her consultation with the plaintiff on 4 September 2006 that a transthoracic echocardiogram had been done, would not have given Dr Rothonis an oral report in these terms without having looked at the images. Dr Rothonis' letter to Dr Ell identifies only the Holter monitor as a cardiac investigation still outstanding. I infer that the defendant must have made an oral report to Dr Rothonis after the blood pressure testing had concluded on 8 September 2006 and that by this time she had seen the echocardiogram images. I consider it a strong inference that Dr Rothonis' referral of the plaintiff to Dr Ell occurred promptly after he had received from the defendant her oral preliminary report that cardiological investigations had returned normal results.
Dr Rothonis gave evidence by way of a witness statement that on 8 September 2006 the defendant reported to him by telephone to the following effect: "I really don't think there is anything to worry about Theo. All the tests have come back normal. There is one further test I could do - a bubble test - but I really don't think that's necessary because everything is quite normal."
I do not accept that the conversation was in these terms. The defendant has disputed that she spoke to this effect, firstly, upon the basis that she would not have given a general reassurance in accordance with the first sentence and the last phrase of the above quotation at a time when the tests she considered necessary were incomplete. Secondly, she would not have referred to "a bubble test". Her understanding, then and now, of the use of "bubbles" is that in conjunction with a transoesophageal echocardiogram, aerated saline may be introduced into the patient's bloodstream to highlight shunting and to aid in the detection of a patent foramen ovale by ultrasound. It is (and was then) the defendant's view that aerated saline would not be used in conjunction with a transthoracic study because, if she considered there was sufficient indication for the performance of some further echocardiogram beyond the transthoracic which Dr Wilcox had already performed, she would have gone straight to a transoesophageal study. She would not have referred to a "bubble test" being used other than in conjunction with a transoesophageal echocardiogram. Further, she did not consider as at 8 September 2006 or at any later time that a transoesophageal study was indicated.
Dr Rothonis' recollection of this conversation is unreliable for the additional reason that it is highly unlikely the defendant would have referred to "one further test I could do" as being a "bubble test", making no reference to the use of a Holter monitor. As shown by the defendant's contemporaneous records, at the date of this conversation she intended the use of the Holter monitor as an additional test of the plaintiff's heart rhythm and had booked this to be carried out nine days later. Dr Rothonis' letter to Dr Ell of 8 September refers to the impending Holter monitor investigation but his version of the conversation does not attribute to the defendant any mention of it.
The defendant explained that in her view (in September 2006 and now) monitoring of the plaintiff's heart rhythm over an extended period using the Holter device was important to her investigation of whether the plaintiff''s heart was implicated in the suspected stroke. In her opinion, which has not been contradicted by any other evidence, the Holter monitor would be capable of detecting atrial fibrillation. This condition may compromise the flow of blood through the heart. It may cause pooling of blood and result in the formation of clots or thromboemboli. The defendant said that she would not have given Dr Rothonis assurances that there was not "anything to worry about" or that "everything is quite normal" before the Holter monitor study had been completed. Dr Rothonis' referral to her was to investigate the possibility of cardiogenic cause for a suspected ischaemic event. She did not purport to give Dr Rothonis a final assurance when an important test for possible cardiogenic embolism by fibrillation, the Holter, was yet to be done.
I would not accept Dr Rothonis' evidence about any aspect of his conversation with the defendant on 8 September 2006 unless supported by probability flowing from evidence of surrounding facts and events. In cross-examination at T 264 - 265 his recollection of the conversation was shown to be variable and unreliable.

MRI scan and consultation with Dr Ell

Two highly qualified and experienced neurologists gave evidence in the trial: Associate Professor Ell and Professor Stephen Davis. For brevity and with no disrespect to their full titles both will be referred to as "Dr" in the balance of these reasons. Dr Ell was not qualified as an independent expert by either party but was called as a witness of fact in the defendant's case. No objection was taken to his opinion evidence. He has impressive qualifications. He demonstrated confident and thorough knowledge of the discipline of neurology in the manner in which he gave oral evidence. There has been no suggestion that his expressed opinions were other than honestly held. I therefore have no hesitation in giving full weight to those opinions. Dr Davis was qualified by the defendant as an independent expert in neurology. He was equally impressive in his credentials and in his demonstrated knowledge of this field of medical science.
By letter of 31 August 2006 Dr Rothonis received a report from Dr Jonathan Seeff, a radiologist who had carried out an MRI scan of the plaintiff's brain upon Dr Rothonis' referral (see [6]). The report stated that "artefact from the patient's teeth" limited the study but that there was no evidence of "an acute area of ischaemia" or of "a focal cystic lacunar infarct". Dr Seeff identified a "cystic focus in keeping with a choroid fissure cyst" and said "[t]his can sometimes be considered a left lacunar infarct."
Dr Rothonis' letter of referral of his wife to Dr Ell was dated 8 September 2006 and was in these terms: "Thank you for reviewing my wife Anastasia Rothonis, aged 44, who was sent for scans of her head after complaining of visual changes on a couple of occasions where she had trouble actually seeing. She also had a feeling of pressure on her head and seeing squiggly lines on other occasions. Her CT scan seemed to show a [left] lacunar infarct which was not seen on the MRI, although these images were degraded by artefact. Do you think that she actually has had a small CVA [cerebral vascular accident]. She has had carotids and a cardiac assessment [by the defendant] last week which was normal and is due to have a 24 hour Holter at the end of this week."
Dr Ell saw the plaintiff on 13 September 2006. By reference to his notes Dr Ell gave evidence that the history and other information he received at this consultation was a follows: 1. The plaintiff had experienced visual disturbances, consisting of generalised blurring of vision for a few minutes. She had suffered no associated headache. 2. In the preceding month she had had episodes of seeing variable squiggly lines at various sites in her visual field for 10 minutes. She had had no headache associated with these symptoms affecting her vision. 3. The plaintiff had not previously suffered from migraine. 4. On examination Dr Ell found no bruits (heart murmurs). 5. Dr Ell had received, either before the consultation or during it, both the film and the report for each of the CT scan and the MRI scan.
At the end of his consultation notes for 13 September 2006 Dr Ell made a memo to himself: "Get films reviewed". Dr Ell's written report to Dr Rothonis dated 13 September 2006 was in the following terms: "[Anastasia Rothonis] … two, four and three weeks ago had episodes of generalised visual disturbance for a few minutes, not associated with headache. There has been some suggestion since that she may have had episodes of tachycardia and of course the visual episodes could be related to that on the basis of hypotension. In the last month she has had episodes of a variable nature of squiggly lines at various sites in the visual fields going on for about ten minutes with no associated headache. She is not a migraine sufferer and is quite well. She is not aware of any family history of migraine. She does not smoke or drink or take medications. A CT scan was done 23rd of August and this shows an abnormality adjacent to the lateral wall of the left lateral ventricle [of the brain] on one cut only. The abnormality was confirmed on an MRI of the 30th of August. Looking at the films I'm not sure what this is. It may be a lacune but it could be a very small hamartoma. In any case I think it is asymptomatic. She has been seen by a cardiologist and also had carotid ultrasound examinations which are normal. Examination was normal. Fortunately I doubt that there is anything significant wrong here. The visual phenomena described above are migrainous. I have taken the liberty of borrowing the CT and MRI scans and shall have them reviewed by the neuroradiologists at RPAH tomorrow and shall be in contact with you."
I find that this letter was sent in the above form on about 13 September 2006. No amended report was prepared after Dr Ell had consulted a neuroradiologist at the Royal Prince Alfred Hospital (in accordance with his intention stated in the letter) either the following day or on 15 September 2006. He took the CT and MRI films and reports to a neuroradiologist and obtained her opinion that the abnormality seen in both of these scans was not an infarct but a hamartoma, also known as a disembryoplastic neuro epithelial tumour or DNET. That is, a developmental abnormality which in Dr Ell's opinion would have been present from birth and entirely asymptomatic. It would cause no future symptoms or damage. He added to his clinical notes with respect to the plaintiff an entry in these terms: "15.9.06 Films reviewed - hamartoma. LMO [local medical officer] inf.".
Dr Ell regarded the finding of a hamartoma as "completely coincidental" to the plaintiff's experience of neurological symptoms whilst driving. He concluded there was "nothing to indicate that she had had a stroke or stroke like episode". He telephoned Dr Rothonis on 15 September 2006 and informed him: "the abnormality on the MRI scan and CT was a hamartoma and therefore harmless, and that she had not had a stroke. And I had previously told him that I didn't consider that she had had … a TIA, that the episode of visual disturbances that she experienced were migrainous."
Dr Ell gave an explanation, which I accept, that migraine: "is a highly specific neurological diagnosis. It is a condition that affects 15 per cent of the human population. It's probably genetically based. The actual abnormality in the brain that allows it to occur has not been worked out yet and it causes highly specific symptomatology, not just headache but also multiple other neurological manifestations. Now, a person who has migraine has shown by their history that they have a propensity to have repeated episodes and that is a person who has migraine. But it is possible for any individual at any time in their life to have an episode, a neurological episode, where the manifestations are identical to what is seen in migraine and, when that occurs […] the medical jargon for that is they are experiencing migraine equivalents but they do not have the condition of migraine. [Migraine, as a condition, is necessarily manifested by] repeated episodes and the episodes are usually highly specific and stereotyped".
Dr Ell identified differences between the symptoms of migraine and those of a transient ischaemic attack: "In a migraine attack the […] brain pathways at the base of the brain are activated and which pathways […] are activated determines the position of the headache in […] that particular attack so that, in the visual system, you get positive neurological symptoms. In other words, definite things are happening and moving […] whereas in a transient ischaemic attack you would have negative neurological symptoms where vision would be either partly or totally lost, usually with what's called a visual field distribution. In migraine, the visual symptoms evolve over time, whereas in the vascular or TIA cases they come on very rapidly. So […] on the basis of the analysis of the symptomatology, the visual symptomatology, […] one can determine accurately whether you are dealing with a positive phenomenon in other words migraine phenomenon, occurring as an isolated event in a non-migraine sufferer as opposed to dealing with a cerebrovascular event or transient ischaemic attack. […] [Patients suffering a migraine attack] get a progress restriction of visual field with subsequent blurring of central vision evolving over something like 15 to 20 minutes or […] they can get what are called photopsias. They get bright lights flashing or they can get brilliant kaleidoscopic visual disturbances and these […] occur in variable parts of the visual field and you can tell by their distribution in the visual field that they are not due to a primary cerebrovascular problem because of the distribution of blood flow that occurs, the underlying circulatory neuroanatomy that will determine what part of the visual field might be […] involved in a transient ischaemic attack."
Dr Ell's evidence extracted in the previous two paragraphs was confirmed by Dr Davis (T 557.34 - 559.44; 562.14 - 563.2; 563.35 - 564.7). The plaintiff did not call a neurologist. The history Dr Ell had obtained from the plaintiff was of generalised visual disturbance. He said that to get that from a circulatory problem one would have to have "global reduction of blood supply to both occipital lobes at the back of the brain where the visual centres are and that, firstly, would be extremely rare and, when you look at the cerebral circulation patterns, it would also cause multiple other neurological symptoms" (T 309.45 - .50). He had not received any history of such "multiple other neurological symptoms". Dr Davis would have diagnosed the symptoms presented to Dr Ell as migrainous (T 552.55, 558.15) and he considers that any neurologist would agree (T 562.8).

Plaintiff's second consultation with defendant, 18 September 2006

The blood pressure monitoring which had been ordered by the defendant on 4 September 2006 was carried out on 7 to 8 September and the results were normal. The Holter monitoring of the heart rhythm was conducted on 15 to 18 September and was also normal. Reports upon both of these investigations were in the defendant's hands by 18 September 2006 when she saw the plaintiff for a second time, for about 15 minutes. The defendant was told at this consultation by the plaintiff that she had undergone an MRI and that her neurologist had discussed the results of it with other specialists.
Dr Rothonis acted throughout as the plaintiff's general practitioner, coordinating referrals to specialists and communicating information between them. He did not provide the defendant with the MRI report or Dr Ell's letter of 13 September 2006. Nor did he pass on directly Dr Ell's supplementary oral opinion of 15 September confirming that the phenomenon seen in the CT scan was a hamartoma and that the plaintiff's visual disturbances had been migrainous.
Although full details of the MRI report and of Dr Ell's opinion were not formally conveyed to the defendant, the gist of the radiological and neurological assessments was provided, orally, by the plaintiff herself at the second consultation on 18 September 2006. A letter from the defendant to Dr Rothonis was dictated in the plaintiff's presence on that occasion and later typed and dated 19 September. It was sent to Dr Rothonis either on the 19th or the next day. In the words of that letter the plaintiff had told the defendant at the second consultation that "what had initially appeared to be a lacunar infarct did not on review appear to be a stroke". This is a contemporaneous record of something said by the plaintiff and I find it to be highly reliable evidence that at least this much was said.
When the defendant was informed, approximately nine months later, that the plaintiff had suffered a stroke she wrote to Dr Rothonis on 27 July 2007. This letter included the following: "When I last saw her in the rooms she buoyantly told me that the diagnosis of lacunar infarct had been revoked and other causes for her symptoms were being considered."
The defendant's evidence in the trial of the action, by way of a written evidentiary statement, was that the plaintiff had said to her at the beginning of the second consultation: "Sorry Jo-Dee [the defendant's Christian name], I think I've wasted your time. I've seen a neurologist and I have not had a stroke. I have just had a migraine."
The defendant was not directly challenged regarding her evidence that on 18 September 2006 the plaintiff reported having received a neurologist's diagnosis of migraine (T 452.25 - 453.12). In any event I accept the defendant's evidence about this, notwithstanding that her letters of 19 September 2006 and 27 July 2007 referred only to the plaintiff having said Dr Ell had excluded stroke. The neurologist had indeed excluded stroke. It is highly likely the plaintiff would have gone on to report Dr Ell's affirmative diagnosis. Namely that her symptoms were migrainous or, as the plaintiff may well have understood this, simply that she "had a migraine". The plaintiff's evidence was that Dr Ell had told her "it was migraine" (T 128.40 - .46). Dr Rothonis said his wife told him after the consultation what Dr Ell had said, in terms to the effect that she had experienced "something like migraine" (T 350.8).
I find no reason to doubt the defendant's recollection as quoted, at [45], from her statement. The plaintiff's loss of memory and brain function following the stroke in June 2007 prevented her from being able to recall at the trial any of her conversations with the defendant.

Defendant's reasonable exclusion of any cerebral ischaemic event

The defendant's impression from the plaintiff's description of her symptoms at the first consultation was that they were not indicative of an ischaemic event in the brain, either stroke or a transient attack. Dr Ell's explanation of the difference between (a) the presenting symptoms of a cerebral ischaemic event, either stroke or transient, and (b) the plaintiff's symptoms as given to him on 13 September 2006, shows that the defendant's impression was sound and in accordance with the exercise of reasonable professional skill. Dr Ell excluded ischaemia on a history essentially equivalent to that given to the defendant. Dr Davis would have made the same judgment (see [40]).
Important common features of the symptoms recounted to Dr Ell (summarised at [34]) and those described to the defendant on 4 September (see [9]) are the absence of partial or total blacking out of vision or darkening, the presence of active visual sensations ("little lines" or "squiggly lines") and the absence of vision loss in any part of the visual field which could be correlated with interrupted blood flow to a specific part of the brain. The defendant was told that only one event had occurred whilst the plaintiff was driving whereas Dr Ell was told of more than one event. That does not relevantly differentiate the histories received by the two doctors respectively. It was the nature of the neurological events and symptoms which was critical to their respective diagnoses.
The only reason for investigating the plaintiff's heart for a defect which might have caused an embolus to enter the cerebral arteries was, initially, the CT report of a cerebral infarct. The plaintiff gave evidence to that effect at T 469.23 - .41 as follows: "Q. [W]hy didn't you include in your impressions at the end [of the consultation notes of 4 September 2006] where you refer to the cardiac aspects anything about what had been suggested to you from the neurological symptoms described which was that they didn't appear to be stroke or TIA but rather stress and migraine? A. Certainly. Because we had a stroke there and stroke overwhelms all the other symptoms, if you've got, you can have no symptoms and have a CT scan with stroke on it and I will go down the path of looking for a cardioembolic source. So, we have the CT scan and so I was going down the path of looking for a cardioembolic source. The supporting symptoms were not required at that time and I did not mean to really go through differential of what was going on the supporting symptoms, it was a stroke on the CT scan and we needed to find out whether there was a cardioembolic cause of that stroke. Q. So it really wasn't material for you to be, is this what you're saying, it really wasn't material for you to be weighing up the likelihood or otherwise of the symptoms described by the patient as being those of an ischaemic event or otherwise because you were told straight out, CT scan, stroke, and you were looking for a cardioembolic cause of that. A. That's correct."
The tests and studies by the defendant up to 18 September 2006 were all non-invasive. A transoesophageal echocardiogram, which would be necessary to confirm the degree of mobility of the septum and, more importantly, to ascertain whether a patent foramen ovale was present, would be invasive. The defendant said she would not have proceeded with that in the absence of neurological confirmation that there had been an ischaemic event, either stroke or transient attack. Her investigation of the heart would be the same if either type of ischaemic event had occurred or remained under suspicion. If the defendant had not been told that the plaintiff intended to consult a neurologist she would have herself caused a neurologist to become involved. I have found that she acted with reasonable care in concluding that the symptoms the plaintiff reported to her did not positively support a diagnosis of an ischaemic event and that the only purported evidence for such an event was the CT report. In those circumstances she determined that she should refrain from proceeding to invasive investigation by transoesophageal echocardiogram unless and until she had a neurologist's confirmation of the CT report or a neurologist's diagnosis of an ischaemic cause of the symptoms upon some other basis.
The defendant gave this evidence at T 443.6 - 445: "[T 443.6] A. There […] is no point in going to the next step of investigations until you have the neurologist on board. … [T 443.42] A. So the next step is when you go to the transoesophageal echo cardiogram. … [T 444.31] Q. What do you mean by "onboard"? A. Well, Anastasia is actually the only young female who has ever been sent to me via a GP. […] they usually come from neurologists and then I'm asked about the cardioembolic source question and then we go down the path of transoesophageal cardiogram and deciding about whether we do any closures [of a PFO]. … Q. You do that if the referral from the neurologist is upon the basis that […] there have been symptoms of an ischaemic event. A. Yes. […] we really need to have the confirmation that what is on the scan is definitely a stroke or we have to have, you know, reason to believe that something is a TIA. And the history that I got did not lead me down that path. So I needed to hear from the neurologist what they thought was going on, on the scan side, before you would go - because although the transoesophageal echocardiogram has only … minor side effects, it's not nothing, it is invasive. I'm happy to go down the path of Holter monitors, blood pressures, echoes, there's nothing invasive, there's not even a needle put in for those ones. But if you're going to go up the ante, to the next stage where you're looking at the hospital, you're looking at putting lines in, you're looking at injecting things, you're looking at probes-- Q. All of which is associated with the transoesophageal echo? A. Yes. […] those things that have got the potential for significant side effects and discomfort, you want to know you're doing it for a reason. So you have to be firmly on board, knowing that if you find something, you will be wanting to take it to the next stage. You won't be just finding it to say, isn't that interesting and there's that there. So as we know with a mobile interatrial septum, there's a 50% chance that there will be a patent foramen ovale. So you need to know that you're wanting to actually act on that and actually do something about it, if you're going to put the person through, albeit minor risks, if you're going to use those resources. Q. The answer to this question may be implicit in what you've already said, but would you not consider yourself able to make the determination about whether the neurological symptoms were sufficient indication of something to be able to make your own assessment of those symptoms and go, as you put it, to the next step. Did you consider that you needed a neurologist assessment of those symptoms? A. Yes. So my assessment, I did not find anything that I could recognise as a TIA. I've done a year of geriatrics, I've seen a lot of TIAs during that time and I'm used to a TIA being something with a definite start point and time, something happens, something is lost, you know a blood vessel is blocked and then usually a gradual return of function. […] the story was not like that, there was not a, this is the moment. So at 8 o'clock this happened and it last[ed] for an hour and a half and the ambulance came and then as I got to hospital, things gradually improved and I can see that as a TIA, I can recognise it clinically. These symptoms were not like that. Q. But to go back to my question though, did you consider that you could make a definitive assessment of those symptoms, along the lines that you've just said, to reach a point where you decided that there was sufficient certainty that you did or did not have an indication of what had been experienced, being such that it warranted going the next step of the transoesophageal? A. Yes, so I did not have sufficient, from my - the symptoms that I got, to suggest you should be going to the next step. Q. Is that what you mean by saying that you - before going to the next step, you wanted a neurologist to look at it from a neurological point of view? A. A neurological respect, yes."
I have already noted that Dr Ell excluded stroke upon further review of the CT scan, as advised to Dr Rothonis in the letter dated 13 September 2006 and in the oral report on about 15 September 2006. The plaintiff correctly passed on this information to the defendant at the beginning of the second consultation. That left no basis at all upon which the defendant, acting reasonably and skilfully as a cardiologist, ought to have acted thereafter on the premise that the plaintiff may have suffered a cerebral ischaemic attack of some kind. I accept the evidence of Dr Bhindi (Ex 1, p 2032, pars 13 and 14; T 519.1) and Dr Wong (Ex 1, p 2058, par 13; T 518.43) that this was a neurological question and that it is reasonable and sound practice for a cardiologist to act upon a neurologist's diagnosis of symptoms and disorder within the neurological field.
Drs Bhindi and Wong are both eminent cardiologists called by the defendant to give expert opinion evidence. Drs Allan and Richards are similarly qualified and experienced in cardiology; both of them practice as interventional cardiologists. Dr Allan became a treating specialist for the plaintiff after her stroke in June 2007 and performed closure of the PFO which was identified at that time. Although Dr Allan was called in the capacity of a treating doctor rather than as an independent expert, I do not differentiate the weight to be attached to his opinion evidence on that account. I will refer to each of these four witnesses as "Dr" for brevity, whilst acknowledging that each of them enjoys the title of Professor.
Dr Allan, in a report of 20 October 2015 (Ex A, p 52, Q 14(c)), said the defendant was "not entitled to [rely upon Dr Ell's diagnosis] because the presumption was that a TIA had occurred". I do not give significant weight to this answer. First, because it was in response to a question which conflated the issue of "excluding a cardiac cause" with the issue of whether there had been a neurological event of a particular kind, for which a "cardiac cause" should be sought. Secondly, it would be quite irrational that the defendant should be bound by a "presumption" which had preceded the neurologist's examination of both the patient and the scans. The initial "presumption" was superseded by Dr Ell's definitive diagnosis.
Further, in his report of 1 June 2016 (Ex A, p 52, Q 3) Dr Allan said: "If the neurologist had stated that the symptoms were secondary to migraine then one would need to accept that as a cardiologist because this would not be a field of knowledge for a cardiologist" [emphasis added]. When this answer is taken together with Dr Allan's evidence at T 536.16 - .25 it becomes apparent that the only difference between Drs Bhindi and Wong on the one hand and Dr Allan on the other is that the latter would have regarded a finding by Dr Ell of "migraine" as a diagnosis whereas he considers Dr Ell's finding of "migrainous symptoms" not to be a diagnosis at all. Dr Ell's evidence summarised at [38] - [40] shows that this is, with respect, a misunderstanding. Dr Ell intended in September 2006 - and he still maintains - that by ascribing to the plaintiff's symptoms the description "migrainous" he was expressing the conclusion that their cause was other than an ischaemic event, stroke or transient. It was a diagnosis, negative for ischaemia.
Dr Richards gave the opinion, in a report dated 2 June 2016 (Ex A, p 109E .3), that "as an autonomous consultant cardiologist, Dr Lattimore was not bound to accept the opinion of a reputed neurologist (or anyone else) when a patient was referred by a medical practitioner to a cardiologist for cardiological assessment of the patient with symptoms consistent with TIA or stroke, or migraine". This opinion is of no weight on the present issue. The question for the Court is not whether the defendant was "bound to accept" Dr Ell's diagnosis but whether it was a reasonably careful discharge of her duty as a specialist to do so.
Further, Dr Richards' answer is, with respect, invalidated by its assumption that the plaintiff reported "symptoms consistent with TIA or stroke, or migraine". Contrary to that assumption, the issue of whether the defendant could reasonably rely upon the neurologist's opinion arises because in Dr Ell's clear view (and that of Dr Davis) the symptoms were not consistent with anything but migrainous cause. Dr Richards' opinions on the case, generally, are heavily affected by his express disagreement with the diagnosis by both Dr Ell and Dr Davis that the symptoms were migrainous: T 505.43 - 507.50. This is evidence in all of his reports and in his oral evidence. I give greater weight to the opinions of the neurologists on a question of neurology and ground my findings accordingly.
At T 506.46 Dr Richards said: "As a cardiologist, I could simply not accept a diagnosis of or a term migrainous, which is not a diagnosis, in a patient who presented with vague symptoms that may well be due to cerebral ischaemia."
In this Dr Richards is commending caution on the part of a cardiologist beyond what reasonable care in the circumstances would require. I find that adoption of a conservative view as to whether ischaemia has been excluded, by not accepting a neurological specialist's opinion to that effect, is not required in order to discharge the common law duty of a cardiologist. Such scepticism with respect to the opinion of another consultant who is more relevantly specialised in relation to the medical issue at hand is not required, by way of abundant caution or otherwise, for the exercise of reasonable care. Dr Richards' approach could lead to neurologically unnecessary intervention - by further testing, by surgical corrective procedure or by prescription of medicine, all of which would carry their own risks for the patient.
When the plaintiff informed the defendant on 18 September 2006 that the neurologist had ruled out stroke, I find that it was a reasonable exercise of the defendant's professional skill to proceed on the basis that the plaintiff had not suffered a transient ischaemic attack either. If, as I find, the plaintiff also reported Dr Ell's opinion that the plaintiff's symptoms had been migrainous then that was an affirmative opinion positively explaining the symptoms on a basis which excluded ischaemia of any type. I accept Dr Ell's explanation that the respective diagnoses are mutually exclusive (T 327.43 - 328.43). Even if the plaintiff did not pass on the affirmative diagnosis that the symptoms were migrainous, it was a reasonable exercise of professional judgment and skill for the defendant to have concluded that the sole putative basis for suspicion of any type of ischaemia, the purported infarct referred to in the CT report, had been removed.
In submissions plaintiff's counsel criticised the defendant for having relied upon the patient's oral report of what the neurologist had said. Dr Richards was critical of this at T 515.23 - .29. There was no breach of reasonable professional standards of care in this respect, given that all consultants' opinions were being obtained by the plaintiff's husband as general practitioner. The defendant's letter of 19 September 2006 informed Dr Rothonis that the patient had passed on Dr Ell's conclusion that there had been no stroke. This satisfactorily gave Dr Rothonis the opportunity to make a correction to the defendant if either his wife or the defendant had misunderstood Dr Ell's view. Dr Bhindi (at T 515.37 - .46) and Dr Wong (at T 516.14 - .24) supported this justification for the defendant's acceptance of information through the patient in this case, on the basis of usual clinical practice and experience. I accept their evidence in that regard. In any event, if there was any fault on the defendant's part in this respect it did not cause loss or damage. The defendant gained via the plaintiff's oral report a correct understanding of Dr Ell's conclusion. Having it in print would have made no difference.
The plaintiff has also argued that the defendant acted with less than reasonable care in relying upon Dr Ell's exclusion of ischaemia because Dr Ell had proceeded upon the assumption that the patient's heart was normal. The plaintiff says this assessment came from the defendant by way of conversation with Dr Rothonis on about 8 September 2006 and was passed on in Dr Rothonis' letter of referral to Dr Ell (see [24] - [30] and [33]). The plaintiff argues that the assessment of the heart as normal at that stage was erroneous and was carelessly given before adequate investigations had been completed, including by transoesophageal echocardiogram. Dr Ell's diagnosis is said to have been invalidated because it was given on a false premise of cardiac normality.
I reject this argument. It inverts the science. Whether or not there had been an ischaemic event was a diagnostic question squarely within the neurological specialty. The answer depended in part upon the interpretation by a neurologist and a neuroradiologist of the CT and MRI scans and in part upon ascertaining and interpreting the patient's symptoms. The answer would not be affected by information concerning the condition of the heart. Such information would not tell the neurologist, or any other specialist, whether there had been a stroke or a transient ischaemic attack. The required order of investigations was the reverse. If the neurological symptoms or the scans indicated that there had been an ischaemic event then there would be a basis for investigating whether it might be inferred that a condition of the heart was the, or a, cause. In 2006 - and still at the date of the trial - known methods of medical investigation were such that no amount of examining and reporting upon the condition of the heart would tell any specialist whether there had in fact occurred a cerebral ischaemic event.
To this point I have found that the defendant exercised reasonable professional skill and care in the following respects: 1. concluding that the plaintiff's symptoms did not bespeak a cerebral ischaemic event - [48], [51]; 2. accepting and acting upon communication of the opinions of Dr Ell via the patient, orally - [62]; 3. accepting and acting upon Dr Ell's neurological opinion that the CT scan did not reveal an infarct and that the plaintiff's symptoms were migrainous - [53] and 4. accepting the neurologist's affirmative diagnosis of migrainous cause as excluding a transient ischaemic attack - [61].

Defendant's duty of care

For each of the findings listed in the preceding paragraph I take the defendant to have owed a duty of care to the plaintiff arising out of the professional relationship between them, as articulated by the High Court in Rogers v Whitaker (1992) 175 CLR 479 at 483; [1992] HCA 58: "…The law imposes on a medical practitioner a duty to exercise reasonable care and skill in the provision of professional advice and treatment. That duty is a 'single comprehensive duty covering all the ways in which a doctor is called upon to exercise his skill and judgment' [Sidaway v. Governors of Bethlem Royal Hospital [1985] UKHL 1; (1985) AC 871, per Lord Diplock at p 893]; it extends to the examination, diagnosis and treatment of the patient and the provision of information in an appropriate case [Gover v. South Australia (1985) 39 SASR 543, at p 551]. It is of course necessary to give content to the duty in the given case. The standard of reasonable care and skill required is that of the ordinary skilled person exercising and professing to have that special skill [Bolam v. Friern Hospital Management Committee (1957) 1 WLR 582, at p 586; see also Whitehouse v. Jordan [1980] UKHL 12; (1981) 1 WLR 246, per Lord Edmund-Davies at p 258 and Maynard v. West Midlands R.H.A (1984) 1 WLR 634, per Lord Scarman at p 638] … ."
The defendant does not dispute that she owed the plaintiff a duty of care at common law. The first requirement in the analysis of breach is to identify the risk of harm to the plaintiff to which any exercise of reasonable care should have been directed: Roads and Traffic Authority of New South Wales v Dederer (2007) 234 CLR 330; [2007] HCA 42 at [59] (Gummow J). See also Wyong Shire Council v Shirt (1980) 146 CLR 40; [1980] HCA 12 at [13] - [14] where Mason J (as his Honour then was) recognised implicitly that identification of the relevant risk is a pre-requisite to evaluating the factors (now enacted in s 5B Civil Liability Act 2002 (NSW)) which bear upon what precautions a defendant may be required to take to discharge his or her duty of care.
On the plaintiff's case the risk, for the avoidance of which the defendant should have undertaken further investigation, advice and treatment in order to discharge her duty of care was that her patient, with a probable aneurysm and a possible undiagnosed PFO, might suffer a stroke. An immediate difficulty for the case in negligence constructed upon this risk is that as at September 2006 it was not known in medical science whether a PFO, either alone or in conjunction with an interatrial septal aneurysm is causative of stroke. As at the date of the trial this appears still to be unknown.
Many strokes are cryptogenic. That is, of unknown origin. Once the ischaemic event has occurred it is commonly not possible to ascertain from whence the blood clot or other embolus came, to cause occlusion of a cerebral artery. A presumed mechanism of the involvement of PFO in some cryptogenic strokes, as described by the defendant and in literature tendered by the plaintiff, is as follows. A thrombus, or blood clot, could form in de-oxygenated blood entering the right atrium and could pass through a PFO to the left atrium. It could thereby enter the arterial circulation and pass via the carotid artery to the brain, causing ischaemia and cerebral infarct.
A blood clot is more likely to form in the venous system which returns de-oxygenated blood to the right atrium, than in the arterial system, because blood in the venous system is more slow-moving. When de-oxygenated blood is pumped from the right atrium down into the right ventricle and back to the lungs - its normal course - clots will generally be filtered out in the lungs. Oxygenated blood returning from the lungs to the left atrium (thence passing to the left ventricle and on to the arteries) will therefore usually be free of clots. A PFO may permit de-oxygenated blood carrying thromboemboli to pass from the right atrium directly to the left, and from there to enter the arterial system, bypassing the usual course of filtration in the lungs.
As at September 2006 published results of clinical studies had not established that PFO is in fact a cause of stroke, either alone or when coincident with septal aneurysm. A 1993 study compared 100 young (under 55) patients who had suffered cryptogenic stroke with a control group of 50 patients who had not suffered a stroke but with respect to whom transoesophageal echocardiograms were performed for other reasons. PFO and aneurysm were both found to be present in a higher proportion of the cryptogenic stroke patients than of the control group. The disparity between the two groups was greatest for the combination of PFO and aneurysm. The results of the study were published in Stroke, the Journal of the American Heart Association. This and other studies of the same subject were reviewed in a May 2004 article in the Archive of International Medicine. Notwithstanding the association of PFO and aneurysm with cryptogenic stroke the review article recorded the following: "The high prevalence of PFO in the general population notwithstanding, the clinical significance of PFO in patients with stroke remains unclear."
The article went on to acknowledge that current data (of the kind referred to in the 1993 study mentioned above) "suggest a cause-effect association between PFO and an as yet undetermined percentage of cryptogenic strokes". The article referred to the postulated mechanism of PFO involvement in stroke (the presumed role of paradoxical embolism described at [69] - [70]) and considered a range of findings some of which appear to be for and some against causal involvement of PFO. A 2014 article by Anthony Furlan MD pointed out, for example, that difficult to detect atrial fibrillation and other undiagnosed causes may be at work and the statistical association between cryptogenic stroke, PFO and aneurysm may be coincidental.
The defendant acknowledged awareness of these studies and of the comparative percentages they revealed for incidence of PFO and/or aneurysm in patients who had suffered cryptogenic stroke (T 432, 436 - 437). In her view the lack of established causal connection and the high incidence of PFO and aneurysm in the general population are considerations which dictate that the presence of either or both of these features in the heart is not an indication for treatment: T 432.37 - 433.4. The incidence of aneurysm which all witnesses accepted is at least 1 in 30 to 1 in 40. In the defendant's words (T 433.13) "there are a lot of people you'd have to treat in order to try to fix one or two strokes". On the basis that 1% to 2% of the population have both the aneurysm and the PFO, the defendant maintained that it could not be justified to treat 1 in 100 or 1 in 50 of the total population upon these indicia alone, given the lack of evidence of causal relationship in current research.
It was common ground between the defendant and all of the medical experts in the case that an important matter for the defendant to ascertain, as an aspect of identifying and treating any condition of the plaintiff which might otherwise contribute to realisation of the identified risk, was whether the plaintiff had already experienced one or more strokes or transient ischaemic attacks. It was also common ground that if it should be found she had suffered an ischaemic event, this would be relevant to the defendant deciding (a) what investigations of the plaintiff's heart should be made in order to form a view on whether the ischaemia had a cardioembolic source and (b) advising whether any and if so what treatment should be undertaken. It follows that discharge of the duty with respect to the risk identified at [68] required, as a first step, reasonable care in finding out whether the patient had suffered a cerebral ischaemic event.
The findings summarised at [65] constitute my conclusion that the defendant took reasonable care in reaching satisfaction that the plaintiff had not suffered an ischaemic event. It may be said that these findings and the conclusion of reasonable care are made from overabundant caution because the evidence permits me to find as a fact - and I do find - that the plaintiff had not suffered any instance of ischaemia up to the defendant's last consultation with her in September 2006. The symptoms she had experienced are documented in the contemporaneous consultation notes of the defendant and of Dr Ell. I am satisfied on the basis of the opinions of Dr Davis, Dr Ell and the defendant herself that these symptoms did not disclose an ischaemic attack of any kind but were migrainous. It may be said that as the defendant was correct in fact to proceed on the basis that there had been no ischaemic event, my finding that she exercised reasonable care in reaching this conclusion is superfluous.
The plaintiff's case is that reasonable care on the part of the defendant in September 2006 to address the risk identified at [68] required her to carry out a transoesophageal echocardiogram of the plaintiff's heart to ascertain whether or not there was a patent foramen ovale in the atrial septum. This putative requirement of the duty is contested. Resolution of the issue is capable of determining the plaintiff's claim.
I find that had a transoesophageal echo study been done a PFO would have been found. That conclusion is inescapable because a PFO was discovered when such a study was undertaken in June 2007 after the plaintiff had suffered a stroke. The defendant did not conduct a transoesophageal echocardiogram in late 2006 or recommend any drug therapy or interventionist procedure. In her letter to Dr Rothonis of 19 September 2006, after recording that the plaintiff had informed her the apparent lacunar infarct on the CT scan "did not on review appear to be a stroke" (see [43]), the defendant summarised the results of her investigations of the plaintiff's heart. The results were essentially normal. The letter concluded as follows: "Anastasia therefore has a structurally normal heart and an appropriate conducting system, with episodes of sinus tachycardia which are in response to her busy lifestyle. Her blood pressure is also in the normal range. She does not therefore require any medications or further intervention. I have not made a follow up appointment, but as always I am happy to see her again, if there are ongoing problems."
The plaintiff contends that if the PFO had been discovered as a result of the defendant carrying out a transoesophageal echocardiogram in September 2006, her duty of care would have required that she would then have advised the plaintiff to take anticoagulant (Warfarin) and/or antiplatelet (Aspirin and Clopidogrel) medication and/or to undergo a procedure for closure of the PFO. These further alleged requirements for the discharge of the duty of care are also contested. The defendant says that even with the PFO revealed in late 2006 it would not have been appropriate to advise such remedies and she would not have done so.
On causation the plaintiff contends that had such advice for treatment been given she would have accepted and acted upon it and that the therapy adopted would be have been effective to prevent the stroke which occurred in June 2007. It is inherent in this case that the plaintiff contends the cause of the plaintiff's catastrophic stroke in June 2007 was a blood clot which had passed through the PFO which was at that time found to exist in her atrial septum. The expert witnesses are in agreement that embolism is likely to have passed through the PFO to cause the stroke in 2007, in the absence of any other identified pathology. Accepting those opinions, I find as a fact for the purposes of the case that the PFO was a cause of the stroke. The defendant disputes that she would have advised the plaintiff to accept anticoagulant, antiplatelet or closure therapy if a PFO had, hypothetically, been discovered in late 2006. The plaintiff therefore disputes that discovery of the PFO would have led to intervention or prevented the stroke.

Defendant's reasons for not undertaking a transoesophageal study

The issues identified in [76], [78] and [79] concern the scope or content of the defendant's admitted duty of care. The scope is to be determined on the premises 1. that from 18 September 2006 the defendant reasonably and correctly understood there was no history of stroke or transient ischaemic attack; 2. the only feature of any note with respect to the plaintiff's heart was the mobile atrial septum observed in the transthoracic study and 3. there was a 50% probability that the plaintiff would also have a PFO in her interatrial septum.
Before enumerating the statutory and case law criteria for deciding whether the measures propounded by the plaintiff should be regarded as necessary to discharge the defendant's duty of care, I will summarise the defendant's given reasons for not having ordered a transoesophageal study and the reasons why she would not have prescribed anticoagulant, antiplatelet or closure therapy even if the presence of a PFO had been established in late 2006.
The defendant gave evidence that in her professional judgment, for a young patient (less than 55) who has not suffered an event of cerebral ischaemia, the fact alone of the atrial septum being mobile, probably to the point of aneurysm, is an insufficient clinical indication to perform a transoesophageal echocardiogram for the purpose of finding or excluding a patent foramen ovale (see [51] - [52]). The defendant accepted that interatrial septal aneurysm is found in between 0.23% and 4% of patients who are investigated by transthoracic echocardiogram (T 422). Dr Allan gave a figure of 1.86% (Ex A, p 58, Q 11) and Dr Wong gave up to 5% (T 518.11). Random studies of the general population for the incidence of septal aneurysm have not been undertaken. It is therefore assumed in cardiology practice, as an approximation, that the incidence will be the same across the whole population. The defendant did not consider this phenomenon to be a "rare" finding on these percentages (T 422).
I accept the defendant's evidence that about 25% of the population have a PFO and that, of patients with a septal aneurysm, about half also have a PFO. The incidence of PFO was confirmed by Dr Davis (T 559.12), Dr Bhindi (Ex 1, p 2301), Dr Wong (Ex 1, p 2054; T 492.22) and Dr Richards (Ex A, p 99.6). Combining the incidence of aneurysm with the 50% association with PFO leads to the conclusion that up to about 2% of the population have both features (T 433).
In the defendant's opinion the presence of an interatrial septal aneurysm even in conjunction with a PFO would only be significant as a stroke factor if the patient had previously suffered stroke or a transient ischaemic attack (T 424.48 - 425.9; 425.24 - .28). Upon her view that there was no evidence of a stroke or transient ischaemic attack once the neurologist had dismissed the CT scan the defendant considered there was no clinical indication for an intrusive study (using a transducer inserted via the oesophagus) to ascertain whether a PFO was present. No treatment would be indicated in the absence of a history of cerebral ischaemia even if a PFO should be found. Therefore it would have been pointless to search for this feature of the plaintiff's heart.

Factors to be considered in determining the scope of the duty

The considerations in sub ss (1) and (2) of s 5B Civil Liability Act bear upon the requirements for discharge of a duty of care and hence they bear upon whether a breach has occurred. This is so notwithstanding that the heading "Division 2 - Duty of Care" appears immediately before s 5B: Adeels Palace Pty Ltd v Moubarak (2009) 239 CLR 420; [2009] HCA 48 at [13]; Grills v Leighton Contractors Pty Limited [2015] NSWCA 72 at [93] - [95].
With respect to s 5B(1)(a) and (b), the defendant does not dispute that the possibility of the plaintiff (or any patient) suffering a stroke was reasonably foreseeable to a cardiologist and was in fact foreseeable to her. The risk of this occurring in a patient with no history of a cerebral ischaemia and with a septal aneurysm and a PFO (if one should be found) was not known to medical science to be significantly greater than the risk of a cerebral vascular event for the general population because of the lack of evidence of causal connection (see [71] - [73]). For the purposes of s 5B(2)(a) the probability that stroke would occur if reasonable care were not taken to diagnose a PFO in the plaintiff's heart is simply not established, again for want of scientific evidence that a PFO is causal of cerebrovascular embolism. On the other hand, with reference to s 5B(2)(b), the seriousness of the harm that might be suffered by the plaintiff if she should sustain a stroke was very great.
The consideration in 5B(2)(c) is inapplicable because the defendant was engaged for reward to undertake whatever precautions were reasonably necessary to avert the risk of harm to the patient. No burden would fall upon the defendant at all. She would do whatever was reasonably required, in consideration for her professional fee. The consideration in s 5B(2)(d) (social utility of the activity that creates the risk of harm) does not arise.
The decisive consideration with respect to whether any breach of duty occurred is that prescribed in in 5B(1)(c): whether a reasonable person in the defendant's position would have taken the precautions for which the plaintiff contends against the risk of stroke. The plaintiff has propounded a case that the exercise of reasonable care to avert this risk required that the plaintiff should have 1. performed a transoesophageal echocardiogram to ascertain whether a PFO was present (see [76]) and 2. upon confirming that pathology of the plaintiff's heart, prescribed anti-coagulant medication (such as Warfarin) and/or prescribed anti-platelet medication (such as Aspirin and Clopidogrel) and/or performed closure of the PFO.
Closure of the PFO could have been effected by delivering a small device into the heart by catheter inserted through a vein into the heart and then through the PFO. The device is released inside the heart to block the hole in the septum and prevent the flow of blood across it. This is what Dr Allan did after the stroke, in mid 2007.
The defendant's case is that a reasonable person in her position as a cardiologist would not have taken these precautions because a reasonably skilful cardiologist would make the following assessments and take the following actions: 1. In the absence of any history of cerebrovascular ischaemia, stroke or transient, there was no occasion or cause to make any further investigation of the patient's heart directed to whether it might be a source of thromboembolism which might in future cause ischaemia. 2. In the absence of any history of cerebrovascular ischaemia, stroke or transient, the finding of a mobile atrial septum (probably qualifying as an aneurysm) combined with the 50% chance that there would also be a PFO, were not clinical indications of a heightened risk of thromboembolic stroke in a patient of the plaintiff's age. 3. Further investigation to determine the presence of a PFO was therefore not warranted because 1. the investigation would necessarily be by transoesophageal echocardiogram, which is invasive and carries some risk to the patient; 2. even if a PFO should be found no treatment would be warranted 1. for the reasons given in (2); 2. because closure of the PFO would be invasive, carry risks to the patient and not assure prevention of stroke in any event and 3. because anti-coagulant and anti-platelet medication would both carry risks of harmful side effects and would potentially affect adversely the patient's quality of life.

Consideration of the positive case on breach before the s 5O defence

Section 5O Civil liability Act provides as follows: "5O Standard of care for professionals (1) A person practising a profession (a professional) does not incur a liability in negligence arising from the provision of a professional service if it is established that the professional acted in a manner that (at the time the service was provided) was widely accepted in Australia by peer professional opinion as competent professional practice. (2) However, peer professional opinion cannot be relied on for the purposes of this section if the court considers that the opinion is irrational. (3) The fact that there are differing peer professional opinions widely accepted in Australia concerning a matter does not prevent any one or more (or all) of those opinions being relied on for the purposes of this section. (4) Peer professional opinion does not have to be universally accepted to be considered widely accepted."
Section 5O does not apply in connection with the giving of warnings about risks associated with medical procedures: s 5P. The present is not a case about warning of risk and s 5O is engaged. It is defensive in nature: Dobler v Kenneth Halverson; Dobler v Kurt Halverson (by his tutor) (2007) 70 NSWLR 151; [2007] NSWCA 335. It follows that the Court should, in the first instance, put to one side the consideration of wide acceptance by peer professional opinion in Australia as it arises under s 5O and determine whether the defendant's conduct fell short of reasonable care upon other relevant considerations. If the answer is that there was a breach of duty on this analysis then the applicability of s 5O would fall for consideration and the defendant might nevertheless not "incur a liability [to the plaintiff] in negligence" if her acts and omissions in September 2006 should be found to satisfy the test of wide acceptance.
This not being a case on warning of risk, it is consistent with Rogers v Whitaker that the Court may give considerable weight to evidence of the practice of cardiologists in circumstances such as those which confronted the defendant in September 2006, for the purpose of deciding whether she exercised reasonable care. The common practices of the specialisation are relevant at the first stage, of deciding what steps and precautions the duty of care called for and whether those matters were sufficiently undertaken, before coming to the application of s 5O by way of defence - if the latter arises.

Reasonable care did not require transoesophageal echocardiogram 88

I find that reasonable care on the part of the defendant with respect to averting the risk of stroke did not require that a transoesophageal echocardiogram be carried out to establish whether or not a PFO was present. The primary basis of this conclusion is precisely that stated by the defendant at T 444 - 445 (see [52] and [90]). That is, even if a PFO had been found and if the mobility of the plaintiff's septum had been confirmed at the level of aneurysm, in the absence of a history of at least one cerebrovascular event, reasonable care would not have called for any intervention or treatment. The evidence for this independent of the defendant's is identified at [109] - [124]. My findings that no intervention or treatment would reasonably have been called for are set out in those paragraphs.
I accept the defendant's reasoning that a transoesophageal echocardiogram resulting in confirmation of interatrial aneurysm and identification of a PFO would be pointless given that a reasonably careful cardiologist would not in those circumstances advise any therapeutic action when armed with the additional information. The history of no cerebral ischaemic event would remain unchanged and would determine that no treatment be undertaken.
A second basis for rejecting the plaintiff's case on breach in this respect is that I accept the evidence of Dr Bhindi (Ex 1, p 2031, par 5; p 2032, pars 16 and 18; T 511 and 517) and Dr Wong (Ex 1, p 2054). Namely, that the carrying out of a transoesophageal echocardiogram was not called for upon the results of the defendant's adequate tests and investigations up to 18 September 2006, with cerebrovascular incident having been excluded by Dr Ell. At T 511.3 - .35 Dr Bhindi expressed the following views, which I accept, about carrying out a trans oesophageal echocardiogram on the basis of nothing more than the identification of a mobile interatrial septum: "It's subjecting someone to invasive procedure when there's no clinical context. Your clinical context in this particular instance has been determined by Dr Lattimore and by Professor Ell as not being a TIA or stroke. I'm not a neurologist. The symptoms are not clear-cut by any stretch of the imagination. I take Professor Richards' point. When the general practitioner of the patient, the plaintiff's husband, had referred the patient onto Dr Lattimore, in his referral note he says 'an incidental stroke was identified on CT', and provided that even in his assessment the word 'incidental' suggests that perhaps he himself may not have suspected a stroke. So there were three clinicians at the time that had assessed the patient and none of them had come up with a prima facie diagnosis of a neurological TIA or a stroke. On that basis you wouldn't perform a transoesophageal echo whether you had a mobile interatrial septum, whether you had a PFO. That would not make any difference. The primary issue here is whether there was a diagnosis of TIA or a stroke and in this case I think [if] I knew an expert neurologist with the help of his clinical skills and neuroradiology has determined that the patient has not had a transient neurological event. I as a cardiologist […] I wouldn't be game I think to override a neurologist unless I really felt that the symptoms were classical, and we might be here under different circumstances if a transoesophageal echo had been performed and the patient suffered a complication of the transoesophageal echo, and then we might be debating well the patient has had a TOE without having a stroke. HIS HONOUR: The transoesophageal study is not without risk? WITNESS BHINDI: It's an invasive test. It has small risks. The risks - the complication rates are small but it does involve sedation, it does involve a patient swallowing a tube and that can, that tube can make a hole in the oesophagus, it can cause an unpleasantness for the patient. So subjecting a patient to any invasive test requires there to be a good indication."
I accept the further evidence of Dr Bhindi at T 517.35 - .39 as follows: "I think the presence of interatrial septal aneurysm was entirely relevant [scil irrelevant], completely irrelevant. A diagnosis of stroke or TIA is not based on the presence of interatrial septal aneurysm and that has to be made unequivocally clear. It's made on the basis of a clinical assessment and other neuroradiological findings. The presence of an interatrial septal - I just want to repeat that again. The presence of an interatrial aneurysm does not mandate any further investigation in isolation."
The contrary opinions given in the reports of Drs Allan and Richards to the effect that a transoesophageal study should have been undertaken were clearly based upon the premise that a cerebrovascular event had occurred before the defendant saw the patient. As is commonly the case where medical negligence is alleged, the appearance of divergent clinical approaches has been created by the adoption of different assumptions by the expert practitioners - in this case, on the part of Drs Allan and Richards, an erroneous assumption in my judgment.
The critical impact of Dr Allan's assumption that the plaintiff needed to be investigated because she had suffered cerebral ischaemia can be seen at the following references in Ex A: 1. Report of 23 September 2011, p 45. 2. Report of 20 October 2015, p 47.
Dr Allan went so far as to assume that the defendant had actually assessed the plaintiff as having suffered a transient ischaemic attack, which I find not to have been the case (report of 20 October 2015, Ex A, pp 48, 50, 52).
Dr Richards' assumption that cerebral ischaemia had occurred and the extent to which it underpinned his conclusion that the defendant should have done a transoesophageal study may be seen in his reports at the following references in Ex A: 1. Report of 6 May 2013, p 93.9. 2. Report of 28 May 2014, p 98 - 102. 3. Report of 2 June 2016, p 109D - 109F.
Dr Richards adhered to his assumption in oral evidence (T 505 - 510), disagreeing expressly with the opinions against stroke or transient ischaemic event given by the neurologists (see [58]). I have found that he is in error in his rejection of the diagnosis of Dr Ell and in his criticism of the defendant for having acted upon that diagnosis. I do not accept his contention that a transoesophageal study was called for, that view being founded upon the erroneous basis that a history of cerebral ischaemia should have been assumed.
Given the inutility of conducting a transoesophageal echocardiogram (because no treatment recommendations would follow from the findings it could reveal), it is not strictly necessary to take into account, in the calculus of breach, the risks and/or the costs associated with this investigative procedure. Should it be necessary to consider those factors, the risks and costs were not insignificant and they would be further factors weighing against a finding that the procedure was required, in the circumstances which operated here, as a matter of reasonable care.
The assumption adopted by Drs Allan and Richards causes me to put their opinions aside. I have no hesitation in accepting the views of Drs Bhindi and Wong on the issue (see [96] and [97]). It has been mentioned that they are both highly experienced clinicians. They impressed me through the reasoning in their reports and through their measured and carefully considered responses in oral evidence. The view which they share, against undertaking a transoesophageal study in the circumstances with which the defendant was dealing in September 2006, is compellingly rational upon the basis of there being no indication for treatment even if the further procedure had identified a PFO.
In cross-examination by the defendant's counsel at T 528.23 - 532, Drs Allan and Richards had great difficulty bringing themselves to answer the question whether a transoesophageal echocardiogram was indicated if, contrary to their assumption, cerebral ischaemia had been excluded in a manner upon which the defendant could reasonably rely. Dr Allan protested that the question asked him to "dislocate her symptoms" (T 528.46). He maintained that he would have conducted the transoesophageal study merely on account of the patient's description of symptoms, irrespective of their diagnosis by a neurologist (T 529.5). I do not accept that reasonable care on the part of the defendant required her to pursue an invasive investigation on the basis of symptoms for which a cardiologist might not have been able to make a firm diagnosis but in respect of which a neurologist had excluded ischaemia.
Dr Allan accepted that there would be no indication to carry out a transoesophageal echocardiogram if the plaintiff was diagnosed with "clear-cut migraine". The following are examples of his answers to this effect: [T 510.17] "Normally, I don't think transoesophageal echo would play a role in the detection of abnormalities in a patient that had clear cut migraine. That's a clear cut neurological diagnosis. I think on this occasion I agree with Professor Richards that Professor Ell did not provide a diagnosis, he provided a recount of the symptoms and that's why he's called it migrainous symptoms." [T 510.25] "So we haven't got a diagnosis from him, actually, we've got a cluster of things that he thinks are called migrainous, but he didn't want to say she had migraine and he didn't want - well, I don't think he did say that she did not have TIA, I think he was quite firm about that. So back to your question, I would not normally investigate someone that had just migraine […]" [T 530.29] "WEINSTEIN: For the purposes of this question Profession Allan, can you assume that an ischaemic event, whether a transient ischaemic attack or a stroke, has been ruled out but there has been a diagnosis of migrainous symptoms, was there an indication in those circumstances for the TOE? WITNESS ALLAN: You mean the diagnosis wasn't migrainous symptoms, the statement was made that she had migrainous symptoms. I think it's not a diagnosis. HIS HONOUR: Taking it that way then Professor Allan-- WITNESS ALLAN: Well no I'd still want the transoesophageal echo in the presence of a mobile atrial septum because I hadn't a diagnosis as to what the neurological event was. It was a symptom that was described by the neurologist, not a diagnosis. HIS HONOUR: Would it make a difference if the diagnosis was migraine? WITNESS ALLAN: Yes I wouldn't have proceeded with the transoesophageal echo."
Dr Allan used the expression "clear-cut migraine" in contradistinction to Dr Ell's finding that the symptoms were "migrainous". But it is clear from Dr Ell's evidence (see [38] - [40]) that the distinction is not material to the question whether further investigation of the heart by transoesophageal echocardiogram was required. This is the misunderstanding referred to at [56]. Although migrainous symptoms may be experienced only on one or more isolated occasions, without the repetition which is necessary for a diagnosis of the full condition of migraine, the neurological categorisation of the symptoms as migrainous necessarily excludes ischaemic cause. For the purpose of determining whether further investigation ought be undertaken to find or exclude cardiogenic embolism, the categorisation has exactly the same consequence as a diagnosis of "clear-cut migraine". It rules out ischaemia and renders the search for a source of embolism in the heart irrational and unnecessary. That is the effect of the evidence of Drs Ell and Davis which I accept.
Dr Richards asserted that even a diagnosis of migraine would indicate that the further echo study should be done and, if a PFO should be found, treatment should follow (T 532.4). I reject that position as going beyond the requirements of reasonable care on the part of the defendant. None of the other witnesses supported Dr Richards in this and no scientific literature was identified by any witness to underpin his view (Dr Allan (Ex A, p 55, Q1 and p 58, Q 10); Dr Bhindi (T 532.44 - 533.14); Dr Wong (T 533.20)). The evidence of the other three cardiologists satisfies me that there is (and was in 2006) no scientific evidence to establish that the presence of a PFO is implicated in causation of migrainous symptoms. Here there would have been no justification for the defendant to continue her investigations of the heart on account of such symptoms. If she had done so and found the PFO the migrainous symptoms would not have warranted medication or closure. Dr Allan's evidence extracted at [106] directly contradicts Dr Richards.

Closure would not have been indicated if a PFO had been found 88

I am satisfied that in 2006 there were not available to a cardiologist in the defendant's position results of any study which would demonstrate that, in a patient with a septal aneurysm and a PFO but no history of cerebral ischaemia, closure of the PFO would reduce the risk of ischaemia from cardio embolic cause. This is unsurprising as, up to 2006 and indeed up to the date of the trial, it has not been the practice of cardiologists in Australia, to carry out closure in the absence of a history of at least one cerebral ischaemic event. This appears not to have been the practice in the United States either. None of the experts identified scientific evidence or literature supporting efficacy of closure in the absence of a past history of ischaemia. This was encapsulated in Dr Bhindi's report of 22 March 2016 (Ex 1, p 2032, par 17): "Based on a PFO being incidentally identified on trans-thoracic echocardiogram on 18 December (scil September) 2006 in the situation where there has been no evidence of stroke there were (sic) no indication to recommend closure of a patent foramen ovale as there was no accepted prospective evidence in the literature to support his (scil this) practice."
The lack of evidence of efficacy of closure in a patient such as the plaintiff as at September 2006 is one strong factor against the plaintiff's proposition that a recommendation for closure (if the PFO had been discovered) would have been required in discharge of the defendant's duty. A second factor is the existence of known risks of the procedure. To understand these one must consider in more detail what closure involves.
As explained by Dr Allan a catheter is fed into the right atrium through the femoral vein. It is pushed through the patent foramen ovale and the closure device is then deployed through the catheter. The device is "like two buttons held together with a bit of string". Each button is made of metal in filament form, woven into a disc. These are capable of being distorted sufficiently to be able to pass through the internal diameter of the catheter. Once released from the end of the catheter they open out to recover their disc shape. The first button is opened out on the left side of the septum. The catheter is then withdrawn to the right side of the septum and the other button is allowed to open out. The "string" between the two buttons holds them together and presses them upon the flaps of the septum thereby closing the aperture.
The risks, as identified by Dr Allan at T 494 - 496, are as follows: 1. Bleeding around the femoral vein through which the catheter is inserted into the heart. 2. Introduction of clots into the left atrium whilst the catheter is being inserted through the PFO and before the closure device has been deployed. Any blood clots introduced to the arterial system at this point could cause stroke, which is a "documented risk". 3. The tissue of the heart may be excited by the presence of the closure device and this may induce palpitations. These would usually last "about two or three minutes, or up to an hour at the most, but one in 1000 cases, the patient will be left with an arrhythmia, a permanent rhythm disturbance". 4. The closure device may dislocate and may be lost while the attempt is being made to place it. "That's very rare and it can usually be retrieved. It will generally go into the lungs and we have retrieval systems to pull it out of the lungs without requiring surgery". 5. Infection may result from the introduction of the foreign body into the interior of the heart. For six months after placement, until tissue has grown over the device, it may become a point of collection for pathogens. During this interval antibiotic protection is required in connection with dental and other medical procedures. 6. Aspirin and Clopidogrel are prescribed prior to placing the device and for three months afterwards, to reduce the risk of accumulation around it of platelets or clots.
A third consideration, bearing upon whether reasonable care would have required that closure should have been recommended had the plaintiff's PFO been detected in 2006, is that the judgment of cardiologists expressed through guidelines published by the American Heart Association and American Stroke Association ("AHA/ASA") is against closure in the absence of a history of cerebral ischaemia. For the risk factor of patent foramen ovale the AHA/ASA guidelines made the following recommendation in 2006. This remained unamended at the date of the trial: "For patients with an ischaemic stroke or TIA and a PFO, antiplatelet therapy is reasonable to prevent a recurrent event. Warfarin is reasonable for high-risk patients who have other indications for oral anticoagulation such as those with an underlying hypercoagulable state or evidence of venous thrombosis. Insufficient data exist to make a recommendation about PFO closure in patients with a first stroke and a PFO. PFO closure may be considered for patients with recurrent cryptogenic stroke despite medical therapy."
Significantly, closure is only recommended in case of a second cerebral vascular event occurring despite the administration of anticoagulant and/or antiplatelet medication following a first event. These guidelines are and were in 2006 accepted by Australian cardiologists. They are and were then considered authoritative and appropriate to be followed by Dr Bhindi (Ex 1, p 2032, pars 11 and 17), Dr Wong (Ex 1, p 2059, par 3) and Dr Allan (Ex A, p 45, par 4(c); p 49, Q 7) - with the qualification in Dr Allan's case that he has a practice of recommending closure of the PFO "after a single episode of proven stroke" where a mobile interatrial septum is evident in combination with a PFO and where free flow (or shunting) across the PFO can be seen on echocardiogram. All agreed upon the applicability of the guidelines as representing sound cardiological practice, at T 527.44 - 528.21.
Commencing in 2006 and concluding in 2013 a group of patients in the United States, each of whom had a PFO and had experienced at least one cerebral vascular event, were invited to participate in what became known as the RESPECT trial. Of the volunteers half were designated for treatment with either Aspirin and Clopidogrel or Warfarin, the other half for closure of the PFO. The number of patients in each group who suffered a further cerebral vascular event was very low so that the statistical significance of the results is questionable.
Subject to that qualification, the results are interpreted by Dr Allan as showing that closure is as effective as or more effective than long-term medication (T 498). This data was not available in 2006. In any event it says nothing about the efficacy of either form of treatment as against none in a patient, such as the plaintiff in September 2006, who has never had an ischaemic event. No doubt the absence of any study or data on patients of that class is attributable to the fact that, in accordance with the above-mentioned guidelines, such patients are not treated with either medication or closure in cardiological practice in the United States. The evidence of the RESPECT trial is irrelevant to the issues which I have to decide.
Upon the considerations summarised at [109] - [116] if a PFO had been found in the plaintiff's heart in September 2006 in conjunction with a septal aneurysm, in the circumstances of Dr Ell having rejected any indication of stroke on the scans and having diagnosed her neurological symptoms in terms which excluded ischaemic cause, reasonable care on the defendant's part would not have indicated that she should recommend closure of the PFO. On the contrary, reasonable care would have indicated that in light of its risks closure should not be undertaken. I accept the defendant's evidence that in the hypothetical circumstances described she would in fact not have advised closure and, for reasons similar to those advanced by other medical witnesses as summarised below, nor would she have advised medication therapy.

Warfarin would not have been indicated if a PFO had been found

All four expert cardiologists agreed that Warfarin should not be prescribed for a patient who had not experienced stroke or transient ischaemic attack and whose risk factors for such an event were limited to atrial aneurysm and PFO (T 485.8 - 489.5). They cited significant difficulties in managing an appropriate dosage of the drug to maintain clotting capacity of the blood within an acceptable range. Risk factors include haemorrhage in the event of a fall and even spontaneous haemorrhage into joints and body cavities. Long term commitment of the patient is required, with restrictions on activities and interference with lifestyle to avoid the risk of injury and internal bleeding.
Drs Allan and Richards said that in the absence of past stroke or transient ischaemic attack Warfarin might be prescribed for a patient with a septal aneurysm and a PFO if there was also a history of deep vein thrombosis in the legs or a predisposition to the formation of blood clots (thrombophilia) or a history of sleep apnoea. None of those additional risk factors for thromboembolism applied to the plaintiff in September 2006. I accept the unanimous expert opinion of the four cardiologists and conclude from it that reasonable care would not have required prescription or recommendation of Warfarin for the plaintiff, in the absence of an event of ischaemia, if she had been found in 2006 to have a PFO as well as an atrial septal aneurysm.

Aspirin would not have been indicated if a PFO had been found

Dr Allan explained the possible utility of Aspirin and Clopidogrel in combination for a patient with a PFO. (I will refer to these drugs compendiously as "Aspirin" hereafter). Aspirin inhibits aggregation of platelets, which otherwise may occur around the aperture in the septum which constitutes the PFO. It is considered that such aggregations at this location may break free into the arterial blood flow upon the patient coughing or straining. These platelet emboli may cause symptoms depending upon where in the arterial system they are carried.
All four specialists recognised side effects and risks associated with long-term prescription of Aspirin for prevention of platelet emboli formation in a patient with a PFO and a septal aneurysm (T 489.7 - 494.15). Risk of gastrointestinal bleeding is particularly significant. Dr Wong gave evidence of considerable experience with the use of this medication by patients suffering from atrial fibrillation, who are at risk of clot formation in the heart (see [29]). He has experienced a significant rate of fatality through gastrointestinal bleeding in such patients (T 493.6). This experience has been in cases of secondary prevention, which is the circumstance in which Aspirin is used. That is, cases where the patient has already had a myocardial infarction (from occlusion of a coronary artery) or a cerebral vascular event (stroke or transient ischaemic attack). In those cases Dr Wong explained that the risk of gastrointestinal bleeding or other complication from Aspirin may be accepted in order to reduce the risk of a subsequent possibly fatal cardiac or cerebral vascular event.
Dr Wong's experience with these cases of secondary prevention has shown that the risks associated with the medication are significant. Consequently he does not consider its use desirable, let alone necessary as a matter of reasonable care, in cases of primary prevention. That is, when no thromboembolic event has yet occurred (T 493.9 - .44). Both Drs Bhindi and Wong were emphatic that Aspirin should not be prescribed, in view of its inherent risks, in the case of a patient with a septal aneurysm and a PFO but no prior history of ischaemic event. For example, Dr Bindi said at T 491.29 - .38: "there is no evidence, there's no systematic respective evidence in the literature to support the routine use of aspirin outside in, in the case of a patent foramen ovale and an aneurism in the atrial septum in the absence of there being a clinical context. So if there's not been a stroke, there's not been a TIA, if there are no vascular risk factors that would otherwise make aspirin necessary, aspirin would not be indicated. I - the mechanism of action of aspirin has been well articulated [by the other cardiological experts] and I agree with that and there are some theoretical potential benefits but that's never been tested and has never been shown to be beneficial."
Dr Allan agreed at T 493.49 - 494.2: "I agree that if there was no symptoms and no signs to match your septal aneurysm and the PFO, then one would not embark on therapy until there was a reason. Purely because of the risks of the therapy."
Dr Richards did not opine on this directly (T 494.4 - .15). I accept the evidence of Drs Bhindi, Wong and Allan. Drs Bhindi and Wong, in particular, gave cogent reasons for refraining from Aspirin therapy in the absence of scientifically acceptable proof of benefit (Dr Bhindi) and in the face of demonstrable risk of doing harm (Dr Wong). On this evidence I do not consider that reasonable care would have required the defendant to prescribe or to recommend Aspirin if a PFO had been discovered in late 2006 - absent any history of ischaemic event and with the septal aneurysm as the only other notable feature of the heart.

The plaintiff's particulars of negligent breach

The plaintiff has particularised the alleged breach by the defendant of her duty of care as follows at par 46 of the Amended Statement of Claim: 1. failing to act upon the abnormality detected on the transthoracic echocardiogram; 2. [deleted]; 3. failing to order a transoesophageal echocardiogram; 4. advising and/or allowing the plaintiff and the plaintiff's general practitioner to understand that a cardiac cause for her symptoms had been excluded; 5. failing in fact to exclude a cardiac cause for the plaintiff's symptoms; 6. advising the plaintiff's general practitioner that the plaintiff's heart was structurally normal; 7. failing to establish, or alternatively, failing in any adequate attempt to establish, a valid alternative diagnosis to that of cardiac cause for the plaintiff's symptoms; 8. failing to advise the plaintiff and/or her general practitioner that the cause of her symptoms had not been identified.
In par (a), the "abnormality detected" is the mobile septum. The alleged failure "to act" refers to the defendant not having conducted a transoesophageal study and not having discovered the PFO or recommended treatment. For reasons given at [94] - [108] it was not a breach of the plaintiff's duty to refrain from conducting the further echocardiogram merely on the basis of the probable aneurysm seen in the transthoracic study. Further, in any event no damage was caused by the defendant not performing a transoesophageal study because if that had been done and had revealed the PFO the defendant would not have recommended treatment and she would have acted with reasonable professional care and skill in not doing so.
Paragraph (c) is disposed of by my findings in relation to par (a).
Paragraphs (d), (e), (g) and (h) are answered by what I have found in relation to Dr Ell's advice to Dr Rothonis at [35] - [39]. Without input from the defendant, Dr Ell's opinion that the symptoms were not of an ischaemic event meant that they had not been caused by cardiogenic embolism. These particulars are therefore not made out. Once the symptoms had authoritatively been categorised as migrainous by an eminent neurologist, cardiac cause was thereby excluded. There were no longer under consideration any symptoms of ischaemia in respect of which it could make sense to speak of - or seek to exclude - cardiac cause.
Paragraph (f) is not made out because the defendant's advice that the heart was structurally normal, as elaborated in her report of 19 September 2006 was sound and was reasonably based upon the results of the tests she had carried out. Although the PFO had not been found and was not mentioned, it was not inaccurate to report the heart as structurally normal on that account. A feature which is found in 25% to 30% of the population can fairly be described as a "normal variant" (in the phrase of Dr Bhindi). There was disagreement between the witnesses whether one could properly describe a heart with a mobile septum, possibly constituting an aneurysm, as "normal". On one view, at up to 5% incidence, this might be regarded as another "normal variant". But the failure to identify the mobile septum as a qualification to the "normal" report caused no loss or damage. Had the aneurysm been mentioned the defendant's reasonably careful advice with respect to it would have been that it did not warrant further investigation or treatment, absent evidence of an ischaemic event.

Section 5O: widely accepted cardiological practice re investigating for PFO

In view of my finding that no breach of duty occurred, upon the basis of my findings as to the requirement of reasonable care in the circumstances, the defence under s 50 does not require consideration. If it did, it would be clear from my earlier findings that I accept it was widely held to be competent practice amongst cardiologists in Australia in 2006 that, absent a firm neurological diagnosis of at least one cerebral vascular event, 1. a transoesophageal echocardiogram would not be carried out on the basis of a mobile septum (probable aneurysm) found on transthoracic study (see [96] - [97], [104], [106] - [108]) and 2. closure would not be performed and anticoagulant or antiplatelet medication would not be prescribed on the basis of septal aneurysm and PFO alone (see [114] - [115], [119], [123] - [124]).

Causation

If, contrary to my findings, the defendant was negligent in not carrying out a transoesophageal echocardiogram and identifying the PFO, nevertheless no damage was suffered by the plaintiff as a result. I accept the defendant's evidence that in the events described she would have advised no intervention or treatment. I find no basis in the evidence for concluding, on the balance of probabilities, that the plaintiff would have disregarded the defendant's advice and obtained either a prescription for anticoagulant or antiplatelet medication or engaged an interventionist to carry out closure.
Further, whilst all of the medically qualified witnesses agree that the stroke in June 2007 was probably attributable to the PFO, I am not persuaded on the balance of probabilities that it would have been averted by closure or medication, if either had been prescribed. In relation to closure, the evidence does not establish that this has in all cases been effective to prevent subsequent stroke where the procedure has been carried out in response to one or more prior ischaemic events. There is insufficient evidence from which I could find on the balance of probabilities that if the procedure had been performed on the plaintiff, in advance of her having had any proven ischaemic attack, this would have been preventive. The evidence may be sufficient to establish that closure would have improved her chances of not having a stroke in June 2007 but damages in an action such as the present cannot be awarded for the loss of a chance of a better outcome: Tabet v Gett (2010) 240 CLR 537; [2010] HCA 12.
The evidence referred to at [115] - [116] regarding the comparable efficacy of closure and of medical therapy for the prevention of recurrent stroke shows that there is similarly no basis for finding on the balance of probabilities that medical therapy applied from September 2006 would have averted the June 2007 stroke. Again, the evidence is insufficient for me to say any more than that anticoagulant or antiplatelet therapy may have improved the plaintiff's chances of not suffering the stroke in June 2007.

Damages

The plaintiff's claim fails because there has been no breach by the defendant of her common law duty of care and because it has not been shown that the acts and omissions complained of caused the plaintiff's stroke in June 2007. In case there should be an appeal from this decision and a different conclusion reached on liability I will assess the damages suffered by the plaintiff as a result of the stroke.
Immediately prior to the stroke the plaintiff, at 45 years of age, was an active mother of four children. By that date they ranged in age from 16 years down to 3 years. She also cared for her husband's parents who were in their 70s. They were in poor health. Understandably caring for these dependents and managing and organising the family home was a full-time occupation for the plaintiff.

Physical disabilities

When the stroke occurred the plaintiff lost consciousness which was not regained for several days. She remained hospitalised for 5 weeks. The plaintiff was then discharged in a wheelchair. At that time she had difficulty maintaining balance and could not be left unattended.
After discharge, within a period of months which is not established on the evidence, the plaintiff progressed to walking with a quad stick and after a further interval (also of uncertain duration) she was able to walk unaided. She continues to be able to walk unaided but with an irregular gait. She had to undertake outpatient rehabilitation at St George Hospital for several months after her discharge, continuing into 2008. She has had extensive private physiotherapy.
Approximately 9 months after the stroke the plaintiff's improvement in physical capability plateaued. At 12 months from the stroke, in June 2008, she suffered an epileptic seizure. She has been medicated for epilepsy ever since and has not suffered a further seizure.
The plaintiff has almost no movement of the left arm below the elbow and very poor control over movement of the left shoulder. Her left arm is practically useless. The mobility and strength of her left leg is poor. This deficit contributes to instability and to diminished capacity to recover from loss of balance. The plaintiff limps on the left side. She has reduced sensation to the left side of her body generally and consequently tends to bump into things. Also, her left side tends to slump or drop.
The plaintiff suffers bladder control difficulties as a result of the stroke. These include the frequent and urgent need to urinate. The plaintiff's eyesight is to a degree blurred and her hearing is reduced. She requires assistance with self-care, in particular with showering and bathing, drying herself, dressing and brushing her hair. The plaintiff is able to drive a motor vehicle. She undertakes gym and swimming pool exercises. However her physical limitations (and cognitive deficits referred to below) have precluded the plaintiff from fulfilling her former role of caring for all other family members and maintaining the family home. Much of this has had to be taken over by her husband and her children. The plaintiff feels keenly the loss of her role as a capable carer for her husband and children. She can now undertake only light duties and her dependence on others is an ongoing cause of loss of pride.
The description I have given of the plaintiff's physical impairments has been taken from her own evidence and that of her husband. It is fully supported by the expert evaluation of Dr Stephen Buckley, a consultant physician in rehabilitation medicine. I accept his evidence generally. His conclusions are contained for the most part in a report of 9 October 2014. Dr Buckley's report also confirms the cognitive disabilities of the plaintiff which I summarise in the following paragraphs, again from the evidence of the plaintiff and her husband.

Cognitive disabilities and effect on mental state

The plaintiff's thought processes have been significantly affected by the stroke. She becomes confused easily and has difficulty concentrating. She is thereby limited in her capacity for conversation. Her memory has been adversely affected and she has trouble understanding new information. These difficulties were evident to a degree when the plaintiff gave oral evidence. The plaintiff's husband testified that the cognitive effects of the stroke are evident in a lack of ability to manage money. Her forgetfulness prevents her from being able to complete a shopping list. She tends to act irrationally or at least imprudently in disposing of cash.
The tendency towards forgetfulness which has resulted from the stroke causes the plaintiff to lose her way when driving and to have great difficulty coordinating meetings with friends or family members at locations away from the home.
All these physical and mental impairments have had a depressive effect upon the plaintiff. She has become anxious about her condition and about the future. Dr Allnut has diagnosed the plaintiff as a suffering from a major depressive episode with associated panic attacks and a degree of sexual aversion. I have no difficulty accepting the doctor's opinion that these psychiatric disorders are consequent upon the "significant loss of self-esteem, and identity, a sense of futility and despair about her circumstances and her future" which the physical and cognitive consequences of the stroke have induced.
Notwithstanding all of this the plaintiff demonstrated strong character and preservation of her dignity in the manner in which she gave evidence. She spoke of her afflictions and of the diminution in quality of her life without any tendency to exaggerate or to try to manipulate sympathy. The plaintiff retains pride in her appearance, determination to improve her capabilities, courage and, despite everything, a sense of humour. I find her to be an entirely genuine claimant so far as the extent of her disabilities is concerned.

Quantum

Counsel on each side of the record agreed upon many of the numbers from which the plaintiff's damages are to be calculated, in a manner which has very sensibly narrowed the issues which I have to decide. They are to be commended for this approach which will have saved the parties significant legal costs in connection with this aspect of the case.
With respect to non-economic loss the plaintiff contends that she should be evaluated at 70% of the most extreme case ($416,000). The defendant argues for 60% ($356,500). I assess this component at 70%. The plaintiff's physical limitations amount to very severe loss of function of the whole of the left side of her body. The loss of cognitive function is still worse. For an intelligent capable woman to be so reduced in her faculties of understanding, memory, speech and ordered thought is an enormous loss. The physical and cognitive impairments, combined, in turn contribute to severe impact on her sense of happiness, security and well-being. These are pervasive and deeply affective forms of loss and damage.
The parties agree upon the following items:

past out-of-pocket expenses: $59,449;
past domestic assistance: $498,736;
aids and equipment: $3,680.

The plaintiff claims $50,000 as the cost of additional expenses and care in connection with taking vacations. Dr Buckley has expressed the opinion that the plaintiff would require a full-time travelling companion "for both physical assistance, particularly with luggage, and also for problem-solving with regard to the kind of problems which arise on vacation such as missed connections and lost bookings". I have formed the view that a full-time travelling companion would be excessive. Handling luggage and the other contingencies to which Dr Buckley refers could largely be taken care of by family members. I consider it likely that in most cases of travel a person with the plaintiff's disabilities would likely be accompanied by at least one family member. The defendant's concession of $25,000 on account of this contingency appears to me to be adequate.
The quantification of eight further categories of damage, all being items of anticipated future expenses of care, is dependent upon the plaintiff's life expectancy. Given her date of birth in December 1961, her life expectancy on the medium life tables is approximately 34 years. On the 5% tables for calculating the net present value of future periodic expenditure, that would yield a multiplier of 865.9.
The plaintiff accepts that her life expectancy should be discounted, having regard to the physiological effects of her stroke, by 5%. The defendant submits that the reduction of life expectancy should be 10%. The following circumstances are relied upon by the defendant as justifying a reduced life expectancy of that order: 1. The plaintiff has been diagnosed with epilepsy and is on medication for it. There is evidence before the Court that epilepsy is a recognised factor in shortened life expectancy. 2. There is a heightened risk of the plaintiff sustaining falls due to poor balance. 3. The plaintiff's left visual neglect exposes her to accident either as a pedestrian or as a driver. 4. The plaintiff's cognitive deficits affect her decision-making which places her at greater risk of accidents as a driver. 5. She will be a long-term user of aspirin, giving rise to the risks referred to at [121] - [124].
Dr Buckley was cross-examined about these possible factors in reduction of life expectancy at T 610 - 614. His answers do not provide any additional assistance on the issue. I am left to make my own assessment as best I can taking into account the five factors referred to in the preceding paragraph, each of which is, as a matter of fact, non-contentious. I consider that reduction by 10% to a life expectancy of 31 years, with a consequent multiplier on the 5% tables of 833.8, should be adopted. That gives rise to the following additional heads of damage, applying the multiplier as an integer in calculations which are otherwise a matter of agreement between the parties:

future care and assistance: $825,045;
future medical assistance: $94,851;
future occupational therapy: $11,224;
future case management, including a contingency amount of $5,000 for significant changes in arrangements every few years: $106,015;
future activities coordinator: $333,520;
gym membership: $41,690;
future physiotherapy: $16,868;
future massage treatment: $58,366.

The total of the five items referred to at [147] - [149] and the eight items listed in the preceding paragraph is $2,490,444. That is the quantum of damages which I would have awarded if I had found the defendant liable.

Orders 1. Judgment for the defendant. 2. Order that the plaintiff pay the defendant's costs of the proceedings.

DISCLAIMER - Every effort has been made to comply with suppression orders or statutory provisions prohibiting publication that may apply to this judgment or decision. The onus remains on any person using material in the judgment or decision to ensure that the intended use of that material does not breach any such order or provision. Further enquiries may be directed to the Registry of the Court or Tribunal in which it was generated. Decision last updated: 06 October 2016

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