Kerr v Minister for Health - [2009] WASCA 32

JURISDICTION : SUPREME COURT OF WESTERN AUSTRALIA

TITLE OF COURT : THE COURT OF APPEAL (WA)

CITATION: KERR -v- MINISTER FOR HEALTH [2009] WASCA 32

CORAM: WHEELER JA
BUSS JA
LE MIERE AJA

HEARD: 1 SEPTEMBER 2008

DELIVERED : 5 FEBRUARY 2009

FILE NO/S: CACV 79 of 2007

BETWEEN: MARIANNE KERR
Appellant
AND
MINISTER FOR HEALTH
Respondent

ON APPEAL FROM:
Jurisdiction              :  DISTRICT COURT OF WESTERN AUSTRALIA
Coram  :GROVES DCJ
Citation  :KERR v MINISTER FOR HEALTH [2007] WADC 61
File No  :CIV 2205 of 2004

Catchwords:

Appeal - Tort - Medical negligence - Pain relief - Post-operative prescription of pethidine - Failure to warn of risks of complication - Risk of seizure - Whether trial judge erred in finding that respondent was not negligent in failing to give any warning to the appellant of the risk of any complications associated with the proposed administration of pethidine - Whether trial judge erred in concluding that he was not able to be satisfied that the seizure was materially contributed to by the dosage of pethidine - Turns on own facts

Legislation:

Nil

Result:

Appeal dismissed

Category: B

Representation:

Counsel:

Appellant: Mr J R Johnson
Respondent: Mr D R Clyne

Solicitors:

Appellant: Julian Johnson Lawyers
Respondent: Minter Ellison

Case(s) referred to in judgment(s):

Bolam v Friern Hospital Management Committee [1957] 1 WLR 582
Chappel v Hart (1998) 195 CLR 232
Naxakis v Western General Hospital (1999) 197 CLR 269
Rogers v Whitaker (1992) 175 CLR 479
Rosenberg v Percival (2001) 205 CLR 434
Sidaway v Governors of Bethlehem Royal Hospital [1985] AC 87

WHEELER JA: I agree with Le Miere AJA.
BUSS JA: I agree with Le Miere AJA, for the reasons he gives, that the appeal should be dismissed.
The trial before the learned judge, Groves DCJ, concerned liability and damages. His Honour found against the appellant on liability, but did not make a provisional assessment of damages. He should have done so. If this appeal had been successful, it would have been necessary for the action to be remitted to the District Court for damages to be assessed. That outcome would have involved time and expense for the parties and a waste of judicial resources. Those consequences would have been unacceptable, and could easily have been avoided.
LE MIERE AJA: On 6 August 2003 the appellant was admitted to the Osborne Park Hospital for maxillary sinus surgery. At the end of the surgery bilateral nasal packs were inserted. Dr Beahan, an anaesthetist engaged by the respondent, had the management and supervision of the appellant's post‑operative pain relief. Dr Behan prescribed pethidine 100‑150 mg intramuscularly second hourly as needed and tramadol 100 mg orally four hourly as needed for pain. The appellant was returned to the ward at approximately 10.45 am on 6 August 2003. The appellant was given six doses, each of 100 mg pethidine, commencing at 12.25 pm on 6 August 2003 and concluding at 7.40 am on 7 August 2003.
At about 8.00 am on 7 August 2003 the appellant was sat up in bed so that her nasal packs could be removed as ordered by the surgeon who performed the maxillary sinus surgery. As a nurse started to remove the nasal packing the appellant began to fit and suffered a seizure. At about 8.10 am three nurses were present and commenced cardiopulmonary resuscitation (CPR) chest compressions. At about 8.12 am the appellant was noted to be breathing and at about 8.13 am to have a pulse of approximately 30 beats per minute. At about 8.14 am Mr Hennessy, an anaesthetist, arrived and confirmed the appellant was breathing and in sinus rhythm. At about 9.30 am the appellant was noted to be conscious with a heart rate of 135 beats per minute. At about 10.15 am the appellant was transferred to Sir Charles Gairdner Hospital (SCGH) for further assessment.
The appellant was discharged from SCGH on 8 August 2003. As a consequence of cardiac compressions during the CPR the appellant suffered injury to her sternum and her spine.

The judgment appealed from

The appellant alleged that she suffered the seizures and the consequent injury as a result of the breach of the duty of care owed to her by Dr Beahan for whose negligence the respondent was vicariously liable. The appellant alleged the following particulars of negligence:
(a)Prescribing doses of pethidine in excess of the recommended doses;
(b)Prescribing and administering pethidine in dosages which were known to cause, or ought to have been known to cause, the appellant to suffer:
i.neurotoxicity;
ii.seizures;
iii.rapid onset respiratory depression;
iv.peripheral circularatory collapse;
v.bradycardia;
(c)Failing to warn the appellant of the risks of complication pleaded in (b), which they knew, or ought to have known, were associated with the prescription and administration of pethidine in the dose proposed to be prescribed and administered (and in fact thereafter so prescribed and administered) and to thereby seek her informed consent to such medication.
In the statement of claim there are allegations of negligence in relation to the failure to use a backboard at the time the CPR was performed. However, those allegations were not pursued at trial and it is not necessary to refer to them further.
The trial judge found that the respondent was not negligent in failing to give any warning to the appellant as to the risks of any complication which may have been consequent on the prescribed dosage of pethidine [90]. The trial judge further found that the dosage of 600 mg of pethidine in 19 hours did not exceed the recommended safe dose [103] and the respondent was not negligent in prescribing doses of pethidine in excess of the recommended dosages or prescribing and administering pethidine in dosages which were known to cause, or ought to have been known to cause, the appellant to suffer toxicity, seizures and the other conditions pleaded. Finally, the trial judge found that he was not satisfied that the appellant's seizure was materially contributed to by the dosage of pethidine [109]. The trial judge dismissed the appellant's claim.
The appellant now appeals against the dismissal of her claim. The appellant seeks orders that judgment be entered for the appellant and the matter be remitted to the trial judge for assessment of damages. The trial judge did not make a provisional assessment of damages. He could have done so and it would have been desirable so as to avoid the consequence of the need for a new trial limited to damages if this appeal were to be successful.
The appellant does not pursue her case at trial that the respondent, by Dr Beahan, was negligent in prescribing and administering the doses of pethidine that were prescribed and administered to her. The appellant's case contains two grounds of appeal. The first ground is that the trial judge erred in finding that the respondent was not negligent in failing to give any warning to the appellant of the risk of any complications associated with the prescription and administration of pethidine in the dose prescribed and administered. The appellant says that the trial judge should have concluded that the respondent breached its duty and so was negligent in failing to give such warning and that had the appellant been warned, she would not have received pethidine or not in the dose administered.
The second ground is that the trial judge erred in finding that the appellant's seizure and consequent injuries were not caused by the dosage of pethidine. The appellant says that the trial judge should have found that the pethidine the appellant received and the consequent norpethidine in her body materially contributed to the seizure she experienced.

The medical evidence

Norpethidine is a metabolite of pethidine. The elimination half‑life of norpethidine is much longer than that of pethidine. Consequently, repeated administration of pethidine leads to accumulation of norpethidine in the body. Numerous cases of seizures have been reported in patients receiving pethidine over a period of days or in some cases hours. Less severe symptoms have also been associated with pethidine use.
In support of her case the appellant called evidence from Dr Raftos. Dr Raftos has practised as a specialist in emergency medicine since 1983. In his reports and in his oral evidence Dr Raftos made reference to the following articles in medical journals:
(a)Plummer J L, 'Is There Still a Place for Pethidine in the Management of Post‑Operative Pain?' (1995) 6 Current Anaesthesia and Critical Care 98;
(b)Plummer J L, Gourlay G K and Cherry D, 'Norpethidine Toxicity' (2001) 8 Pain Reviews 159; and
(c)Latta K S, Ginsberg B and Barkin R L, 'Meperidine: A Critical Review' (2002) 9 American Journal of Therapeutics 53.
Dr Raftos gave evidence that there are two possible causes of the seizure that the appellant suffered. One is that she fainted during the procedure to remove the packs from her nose and the resultant reduction in blood supply to her brain caused seizure activity. The second is that norpethidine induced the seizure. Dr Raftos, in his report dated 27 May 2004, opined that the pethidine given to the appellant materially contributed to the seizure. Dr Raftos explained:
Vasovagal syncope (fainting) occurs when a stimulus causes the vagus nerve to fire excessively. This excessive vagal activity causes a sudden reduction in heart rate. The resultant reduction in blood flow to the brain causes transient unconsciousness. Very infrequently, if the patient faints in the sitting position, the reduction in brain blood flow may be more profound because of the additional contribution of gravity and may therefore cause hypoxic seizure activity. Pain, or the anticipation of pain, are common precipitants of vasovagal syncope.
…
Concern about the adverse effects of pethidine has caused a large number of hospitals in Australia to restrict its use to those patients who are intolerant to morphine and, even in those patients, many hospitals recommend the use of other, apparently safer opiates such as fentanyl rather than pethidine. Twenty four hour dosage should be restricted to an upper limit of 600 mg. The adverse effects of pethidine have been well documented and widely discussed in the literature to the extent that any doctor who prescribes opiate analgesia should be aware of the risks involved in the use of pethidine compared to the apparently safer morphine and fentanyl.
…
The most likely course of events is that [the appellant] suffered a vasovagal syncope because of pain, or the anticipation of pain, caused by the attempted removal of the nasal pack. Her heart rate dropped because of vagal overactivity and may have been imperceptible for a time. The reduction in blood flow to her brain was worsened by her sitting posture. She had a seizure because of a combination of norpethidine toxicity and reduced blood flow to the brain and recovered spontaneously without any specific treatment. Evidence of normal breathing may well have been absent for a short time during the faint and subsequent seizure.
…
[The appellant] was given 600 mg of pethidine over some 19 hours. This dose exceeds the generally recommended upper limit for pethidine use of 600 mg over 24 hours and placed her at a significantly increased risk of suffering a seizure because of norpethidine toxicity. While the pethidine dosage may not have been the sole cause of her seizure, it is unlikely that she would have had a seizure in the circumstances if she had been treated with a safe dose of pethidine or with an opiate analgesic other than pethidine.
…
The excessive dose of pethidine was probably not the sole cause of [the appellant's] seizure but it contributed substantially to the development of the seizure. She probably developed reduced cerebral blood flow due to vagal overactivity but this, on the balance of probabilities, would not have caused seizure activity had she not had an elevated norpethidine level because of an excessive pethidine dosage regimen. Had she been prescribed an analgesic other than pethidine or had the dosage of pethidine been within the recommended safe level, she would not, on the balance of probabilities, have had a seizure (3) ‑ (5), (8).
At the time of the operation the appellant was taking the medication Zoloft for depression. Dr Raftos said that it was known that there is an interaction between the group of antidepressants known as SSRI, of which Zoloft was one, and pethidine. The interaction can cause an adverse drug reaction or serotonin syndrome, but it is also suggested that a combination of Zoloft and pethidine may lower the seizure threshold.
Plummer, Gourlay and Cherry in their article 'Norpethidine Toxicity' said:
High blood concentrations of norpethidine are associated with excitatory toxicity. Numerous cases of seizures have been reported in patients receiving pethidine over a period of days or in some cases only hours … When multiple doses of opioids are likely to be required, pethidine should be avoided. If it is used, patients should be informed of the risks and monitored closely for signs of toxicity.
…
The use of pethidine as a first‑line analgesic is clearly unjustified. Indeed, with the availability of a range of opioid and non‑opioid analgesics, the need to resort to pethidine should rarely arise. When pethidine is to be used in more than a single dose, the risk of norpethidine toxicity is great enough that patients should be warned about it (159), (169).
The respondent led evidence from Dr Beahan, Professor Paech and Mr Hennessy. Dr Beahan has practiced as a specialist anaesthetist since 1964. Professor Paech is the Professor of Obstetric Anaesthesia at the University of Western Australia, the senior specialist anaesthetist at King Edward Hospital and a visiting specialist anaesthetist at Royal Perth Hospital. Mr Hennessy has practised anaesthesia for some 15 years and has practised as a specialist anaesthetist since 2000.
Professor Paech gave evidence that it was extremely unlikely that there is a link between the amount of pethidine given to the appellant, and by implication the amount of norpethidine in her body, and the appellant's seizure. Professor Paech said that by far the most likely explanation for the appellant's seizure was that it followed a vasovagal collapse. Professor Paech said that the dose of 600 mg received by the appellant was not unusually high judged on typical post‑operative requirements and the dose fell within the extremely conservative dosing recommendations of the product information and regulatory recommendations. Professor Paech said in his report of 6 September 2006:
Although it may be appropriate to do so in some circumstances, it is still not usual practice in 2006 to warn patients of a risk of seizure after more than one dose (4).
In cross‑examination Professor Paech said:
It's possible that norpethidine may have contributed [to the appellant's seizure] but I think it's very unlikely to have and that wasn't substantial.
Professor Paech acknowledged that the use of Zoloft by the appellant may have conferred a possible reduction in her seizure threshold.
In cross‑examination Professor Paech also said that there is a very small risk of norpethidine toxicity but the dose prescribed by Dr Beahan is clinically acceptable. Professor Paech went on to say that opinion has changed since 2003 because rare cases of norpethidine toxicity have been highlighted and people in authority suggested that pethidine was not the ideal drug to use and most people have accepted that. Professor Paech said that the use of pethidine in the appellant's case involved an exceptionally small recognisable risk of seizures which would be considered to be clinically acceptable. Professor Paech then explained what he meant by clinically acceptable:
It means that on the basis of an individual case that quantifying, looking at all the potential risks of the drugs and the interventions and everything else that has been done, that something is viewed as acceptable or unacceptable. Obviously there is some degree of grey in there but that's the whole of medical practice is based on that fact … [T]here are many risks with everything you do and we have to make judgments on what is clinically appropriate and what isn't appropriate.
Professor Paech then gave the following evidence:
So is it a matter of saying that the risk is sufficiently small, that it can be taken by the doctor?‑‑‑Yes.
What role does the patient play in that decision? In your view?‑‑‑If the patient has a right to know if it is a significant risk or a risk to which they may attribute significance. So again, you have to make a decision about what, you know, informed consent, and in some situations if I was to prescribe pethidine in the post‑operative phase because I felt it was the best drug to use, and it may still happen, then I would explain to the patient that there was a very small risk of norpethidine toxicity and I would be watching closely to see how much they were using etc…. So in that setting I would explain the risk but it wouldn't be, certainly in the past, it was not normal practice, ever, to quantitatively explain a risk like that.
Mr Hennessy said that in his opinion it was unlikely that norpethidine had caused the appellant to have a seizure. He agreed that the antidepressant Zoloft had the potential to lower the seizure threshold. Similarly, body or electrolyte changes post‑operation may have lowered the seizure threshold. He accepted that potentially those two factors may have increased the risk of seizure from pethidine. In Mr Hennessy's opinion it was extremely unlikely that norpethidine toxicity contributed to the appellant having a seizure.

The duty to warn ‑ legal principles

English courts have determined the standard of care to be observed by a medical practitioner by application of the so‑called Bolam principle that a doctor is not negligent if he acts in accordance with a practice accepted at the time as proper by a responsible body of medical opinion even though other doctors adopt a different practice: Bolam v Friern Hospital Management Committee [1957] 1 WLR 582; Sidaway v Governors of Bethlehem Royal Hospital [1985] AC 871.
In Australia the question is not whether the defendant's conduct accords with the practices of his profession, or some part of it, but whether it conforms to the standard of reasonable care demanded by the law. In Rogers v Whitaker (1992) 175 CLR 479 (Rogers) the High Court said:
The law should recognise that a doctor has a duty to warn a patient of a material risk inherent in the proposed treatment; a risk is material if, in the circumstances of the particular case, a reasonable person in the patient's position, if warned of the risk, would be likely to attach significance to it or if the medical practitioner is or should reasonably be aware that the particular patient, if warned of the risk, would be likely to attach significance to it. This duty is subject to the therapeutic privilege (490).
Under the Rogers test a risk is material if: (1) in the circumstances of the case, a reasonable person in the patient's position would be likely to attach significance to it (the objective limb); or (2) the medical practitioner was, or should have been, aware that the particular patient would be likely to attach significance to it (the subjective limb). In this case the appellant relies upon the objective limb. Important factors in considering whether the risk was material include the extent or severity of the potential injury, the likelihood of the injury actually occurring and the availability of alternative treatments: Rosenberg v Percival (2001) 205 CLR 434, Gummow J [77], [79].
In Rosenberg v Percival Gleeson CJ said that in Rogers the court had made it clear that the relevance of professional practice and opinion was not denied, what was denied was its conclusiveness. The chief justice said that in many cases professional practice and opinion will be the primary, and in some cases it may be the only, basis upon which a court may reasonably act [7].

Ground 1

The appellant says that the trial judge erred in fact and law in deciding that the respondent was not negligent in failing to give any warning to the appellant of the risk of any complications associated with the proposed administration of pethidine. The appellant says that the trial judge should have concluded that the respondent breached its duty and was negligent in failing to give such warning.
Counsel for the appellant submitted that the trial judge in effect applied the Bolam test and failed to enquire whether a material risk of injury was inherent in the proposed administration of pethidine and whether Dr Beahan had breached his duty to warn the appellant of that material risk.
The trial judge addressed the appellant's claim that the respondent had failed to warn her of the risks of complication in the use of pethidine in [87] ‑ [89] of his reasons for decision and then concluded at [90] that 'in the circumstances but having regard to the whole of the evidence' he was not able to conclude that the respondent was negligent in failing to give any warning to the appellant as to the risks of any complication which may have been consequent on the prescribed dosage.
In [87] ‑ [89] the trial judge referred to four matters. First, the trial judge referred to the statement in Plummer's 2001 article that when pethidine is to be used in more than a single dose the risk of norpethidine toxicity is great enough that patients should be warned about it. Second, the trial judge referred to Professor Paech's view that he did not consider the circumstances of this case to present a significant risk so as to warrant any such warning. Third, the trial judge referred to the long experience of Dr Beahan in prescribing pethidine and the fact that in his experience he had 'had really no problems with [pethidine] in the past' [84] with the dose prescription he made in this case whilst he was aware that larger doses over a prolonged period could lead to norpethidine toxicity. The trial judge said that Dr Beahan did not have any concern that would have warranted any warning to the appellant. Fourth, the trial judge said that it was Professor Paech's 'opinion that although it may be appropriate to do so in some circumstances, it is still not usual practice in 2006 to warn patients of a risk of seizure after more than one dose' [90].
The trial judge failed to address whether there was a material risk inherent in prescribing or administering to the appellant pethidine in the prescribed dosage. Whether the risk was material required the judge to consider whether, in the circumstances of this case, a reasonable person in the appellant's position, if warned of the risk, would be likely to attach significance to it. The first matter referred to by the trial judge does not support the trial judge's finding. The second matter, that is Professor Paech's opinion that he did not consider the circumstances of this case to present a significant risk so as to warrant a warning, might be understood to be an assessment of the magnitude of the risk. However, the language used by the trial judge refers to the opinion of Professor Paech whether a warning should be given rather than to the likelihood of injury occurring. More importantly, the third and fourth factors referred to by the judge concern medical practice at the time rather than an assessment of the extent or severity of the potential injury and the likelihood of the injury occurring. The third factor was the practice and experience of Dr Beahan in prescribing pethidine. The fourth factor was Professor Paech's opinion about the usual practice in 2006. I am satisfied, after considering all those matters, that the trial judge primarily had regard to responsible medical practice at the time and did not consider the extent or severity of the potential injury, the likelihood of the injury actually occurring and the availability of alternative treatments. The trial judge did not undertake the necessary intellectual exercise to enable him to decide whether a reasonable person in the appellant's position would be likely to attach significance to the risk of injury associated with the proposed administration of pethidine.
It is therefore necessary for this court to consider whether or not the respondent breached its duty to warn the appellant of a material risk inherent in administering pethidine in the prescribed dosage.
The question is whether the risk was material. The evidence of Professor Paech, Mr Hennessy, Dr Raftos and the medical articles referred to showed that at the time of the operation it was known, or ought reasonably to have been known, by an anaesthetist such as Dr Beahan that administering multiple doses of pethidine to the extent of 600 mg within 19 hours entailed a small risk of causing seizures or other adverse complications.
I find that there was a material risk inherent in the administering of pethidine to the appellant. The risk was of a seizure or other adverse complications. The risk was material because a reasonable person in the appellant's position, if warned of the risk, would be likely to attach significance to it. I find that is so for the following reasons.
First, the potential injury was severe. There was a risk of seizure. Dr Raftos said that a seizure had the potential for injury to body parts and the potential for sudden death during seizure. Dr Raftos was not cross‑examined on that evidence and it was not contradicted.
Second, the likelihood of the injury actually occurring was small but not farfetched or fanciful. Professor Paech said that the risk is exceptionally low but said that there is a known risk of seizures and that was one of the reasons people have been encouraged to not use pethidine in the post‑operative setting. Professor Paech also said that it was possible that the appellant's seizure threshold was reduced as a result of taking Zoloft and because the operation itself leads to changes in fluids and electrolytes which can lower a patient's threshold for seizure.
Third, there were alternatives to pethidine which are safer and there was no substantial reason for administering pethidine in preference to the alternatives, morphine and fentanyl. Professor Paech said that morphine and fentanyl were safer than pethidine and he could see no particular advantage in using pethidine rather than morphine or fentanyl. Where an analgesic carries a risk of serious injury, even when it is only a very low risk, and there are alternatives which are safer and there is no advantage is using the more risky analgesic, a reasonable person in the patient's position would be likely to attach significance to the risk of injury.
For those reasons there was a material risk inherent in the administering of pethidine and Dr Beahan had a duty to warn the appellant of that material risk. By Dr Beahan failing to do so the respondent breached its duty of care to the appellant.

Ground 2

Ground 2 is that the trial judge erred in fact and law in concluding that he was not able to be satisfied that the seizure was materially contributed to by the dosage of pethidine. The appellant says the trial judge should have found that the pethidine the appellant received (and the consequent norpethidine in her body) materially contributed to the seizure she experienced.
Causation in this kind of case requires satisfaction of two criteria. The first criterion is a breach of the duty to warn of a material risk, that risk having eventuated and caused, in the physical sense, injury to the appellant. The second criterion is that, had the warning been given, the injury would have been averted, in the sense that the appellant would not have had the treatment in question: Rosenberg v Percival [86].
The second criterion is a subjective one. The question is whether the appellant would not have had the pethidine given to her had a warning been given: Rosenberg v Percival [87]. In evidence‑in‑chief the appellant was asked what she would have done if she had been advised before she received any pethidine that there was a very small risk of side effects, including seizure. The appellant said that she would have asked if there was a safer alternative and if there had not been a safer alternative she would have asked if they could have just given it to her when she requested it, that is when she felt she needed it. A plaintiff's evidence on this issue will be self serving, even from the most careful witness. The veracity of the plaintiff's evidence must be assessed against the objective evidence, such as the availability and effectiveness of alternative treatments. In this case, the evidence is that morphine was much safer and no less advantageous than pethidine. That consideration supports the appellant's evidence that, in effect, she would have asked for a different medication if she had been warned of the risk of side effects from pethidine.
The trial judge made no express finding on this issue but appears to have accepted the appellant's evidence because his Honour said that the key issue for the court's determination concerns the cause of the seizure experienced by the appellant and more particularly did the 600 mg of pethidine received by the appellant in the 19 hours prior to the seizure materially contribute to the seizure? Ground 2 challenges the trial judge's finding on that issue.
Whilst the legal burden of proving causation remains throughout the proceedings on the plaintiff, the evidentiary onus may shift, in the sense that, where the plaintiff has proved a breach of duty by the defendant and can establish that the breach increased the risk of injury and that risk eventuated, the defendant will be held liable in the absence of proof of an alternative cause. In Chappel v Hart (1998) 195 CLR 232 McHugh J said:
The onus of proving that the failure to warn was causally connected with the plaintiff's harm lies on the plaintiff. However, once the plaintiff proves that the defendant breached a duty to warn of a risk and that the risk eventuated and caused harm to the plaintiff, the plaintiff has made out a prima facie case of causal connection. An evidentiary onus then rests on the defendant to point to other evidence suggesting that no causal connection exists. … Once the defendant points to such evidence, the onus lies on the plaintiff to prove that, in all the circumstances, a causal connection existed between the failure to warn and the injuries suffered by the plaintiff [34].
This line of reasoning was followed by Gaudron, Kirby and Callinan JJ in separate judgments in Naxakis v Western General Hospital (1999) 197 CLR 269.
The appellant led evidence that the pethidine given to her, and the resulting norpethidine in her body, was a possible cause of the seizure. In the 2001 article by Plummer and others the authors said that numerous cases of seizure have been reported in patients receiving pethidine over a period of days or in some cases only hours. Dr Raftos gave evidence that in his opinion the pethidine given to the appellant caused, or contributed to, the seizure. In his report of 27 May 2004 Dr Raftos said that if the appellant had been given an analgesic other than pethidine, or had the dosage of pethidine been within the recommended safe dosage, she would not, on the balance of probabilities, have had a seizure. In his report of 12 May 2006, having considered the report of Professor Paech dated 21 February 2005, Dr Raftos said that he maintained his opinion that it is more likely than not that the pethidine given to the appellant contributed to the occurrence of the seizure. Dr Raftos said that the norpethidine, created from the pethidine given to the appellant, either caused her seizure or lowered her seizure threshold to a level at which the vagal stimulation caused by removing her nasal pack precipitated seizure activity.
In his oral evidence, Dr Raftos said it was possible that the vasovagal syncope alone caused the seizure but said that the dose of pethidine suggested to him that pethidine neurotoxicity was involved in the causation of the seizure. He said that 'the influence of the pethidine may well make the difference between whether the patient does have a seizure or not'.
The respondent discharged any evidential onus on it by calling evidence from Professor Paech and Mr Hennessy to the effect that the seizure was caused by a faint and not by the pethidine or norpethidine. The effect of the evidence of Professor Paech was that it was extremely unlikely that the pethidine contributed to the appellant's seizure. Mr Hennessy opined that the appellant had a vasovagal bradycardic arrest which was followed by a seizure. Mr Hennessy said it was likely the appellant had a significant fear response to having her packs removed which caused the faint. In his written statement of evidence, Mr Hennessy said he did not believe that pethidine caused the faint. He said that pethidine does not cause fainting, rather it tends to cause tachycardia. In his oral evidence, Mr Hennessy said that in his opinion it is unlikely that norpethidine caused the appellant to have a seizure. In cross‑examination, Mr Hennessy said that he thought it was extremely unlikely that pethidine contributed to the appellant having a seizure.
Since the respondent has discharged any evidential onus on it, the question is whether the appellant discharged the legal onus of proving causation. The trial judge found that the appellant did not discharge the legal burden of proving that the pethidine dosage materially contributed to the seizure.

Reasons of trial judge

The trial judge considered the recommended safe dose of pethidine. It was the opinion of Dr Raftos that 24 hour dosage should be restricted to an upper limit of 600 mg which would be a safe and acceptable prescription. However, in Dr Raftos' opinion the dosage of 600 mg over 19 hours exceeded the generally recommended upper limit. Professor Paech's evidence was that the total dose of 600 mg was well within the Product Information recommended dose range, that is up to 150 mg 3 ‑ 4 hourly for no longer than 24 to 36 hours, that is a potential dose of 1200 mg in 24 hours. The trial judge noted that Latta and others in their 2002 article referred to 1200 mg per day as being a 'safe' level with a 600 mg per day limit in clinical practice suggested. The trial judge had particular regard to the Product Information referred to by Professor Paech. In his first written report, Professor Paech referred to the recommended dose as being an 'extremely conservative dosing recommendation'. The trial judge concluded that a dosage of 600 mg of pethidine in 19 hours did not exceed the recommended safe dose. The trial judge then went on to consider whether the pethidine materially contributed to the appellant's seizure.
The trial judge referred to Dr Raftos' opinion that 'the excessive dose of pethidine … contributed substantially to the development of a seizure' [104]. The trial judge said that Dr Raftos stood alone in concluding that the dosage of pethidine was excessive and that his conclusion was premised on that basis. The trial judge said that, in view of his finding that the dosage was not excessive, he was not able to accept Dr Raftos' conclusion [105].
The trial judge then said that the weight of evidence, being that of Professor Paech and Mr Hennessy, is contrary to Dr Raftos' conclusion [106]. The trial judge referred to the evidence of Professor Paech in cross‑examination that there is a very low likelihood that norpethidine contributed at all to the seizure. The trial judge also observed Professor Paech's opinion that a vasovagal syncope fitted with the clinical signs described. The trial judge referred to the opinion of Mr Hennessy in cross‑examination that he thought that it was extremely unlikely that pethidine contributed to the appellant's seizure [108].
In his conclusion the trial judge referred to his earlier observations that the clinical indicators, that is the appellant's symptoms, bradycardia and being sat up in the bed, are consistent with a vasovagal collapse which led to a hypoxic seizure [109]. The trial judge said that it was possible, albeit unlikely or improbable, that norpethidine toxicity may have contributed to the seizure. The trial judge concluded that, given the weight of evidence he had described, he was not able to be satisfied on the balance of probabilities that the seizure was materially contributed to by the dosage of pethidine.

Appellant challenges findings of trial judge

The appellant attacks the findings of the trial judge on a number of bases. First, the appellant submits that the trial judge should have found the onus was upon the respondent to establish that such pethidine did not cause, at least in part, the seizure. The appellant submitted that an evidentiary onus rested on the respondent to point to evidence suggesting that no causal connection exists between the pethidine dose and the seizure. The appellant submitted that, had this approach been applied, the trial judge should have found that the pethidine received by the appellant was a cause of her seizure because the respondent did not discharge the evidentiary onus it bore.
I have already found that the respondent did discharge any evidentiary onus upon it. The evidence of Professor Paech and Mr Hennessy discharged that onus. The legal onus was then upon the appellant to prove, on the balance of probabilities, that the pethidine materially contributed to the seizure.

Appellant warned of likely pain

The second basis on which the appellant attacks the findings of the trial judge is that the trial judge misunderstood, or wrongly attached weight to the evidence presented at trial relevant to the causation question. Counsel for the appellant submitted that the trial judge did so in six respects. First, counsel submitted that the appellant did not concede that she was warned of likely pain associated with removal of the relevant nasal packs. The trial judge said:
Having been forewarned that there would likely be pain associated with the removal of nasal packs she said that the thought of that procedure was not a cause for concern to her [13].
The appellant gave evidence that she knew she was to have nasal packs removed. When asked how she knew that the appellant said:
Dr Sakarapani had told me the procedure before I had gone in as to what would happen, so I was aware that the packs would be removed. I'm not too sure if a nurse also had said it in the time that I had been in there.
The appellant was then asked how she was feeling in relation to the fact that this was going to happen and she responded:
It didn't bother me. I had been, you know, forewarned. It was just a bit of cotton gauze that they would pull out and I've had far worse things happen in my life than a bit of cotton coming out my nose.
The trial judge had the advantage of seeing and hearing the appellant give her evidence. When the appellant said that she had been 'forewarned' the trial judge understood the appellant to mean that she had been told that there would likely be pain associated with the removal of the nasal packs. In the context in which the appellant was speaking the usual meaning of being forewarned is to be warned in advance of something painful or uncomfortable. The appellant's evidence that she had been forewarned but that it did not bother her and she had far worse things happen in life indicates that she had been warned in advance of something that was likely to be painful or uncomfortable. The trial judge made no error in understanding the appellant's evidence in the manner he did. Furthermore, the nurse on duty, Ms Durkalic, gave evidence that first thing that morning she explained to the appellant that she would have her nasal packs removed but prior to removing the nasal packs the appellant would be given pethidine for pain relief because it is uncomfortable to have the nasal packs out without any pain killers.

Symptoms not indicative of norpethidine toxicity

Second, the appellant submitted that the trial judge wrongly considered and attached weight to his finding that the appellant's symptoms reported shortly before her seizure were not consistent with the possible effect of norpethidine when the evidence was that they were and that the reported symptoms were very varied.
The appellant says that when she woke up on the morning of her seizure a nurse came in and gave her an injection and a short while after that the appellant started to feel a bit strange, a little bit like she was drunk, light headed. The appellant then said that when the nurse came back, and the appellant was talking to her, the appellant felt that the words she was trying to say sounded like they were coming from somebody else and when the nurse sat her up in bed she was about to tell the nurse that she was feeling a bit strange and she blacked out.
In their 2001 article Plummer and others said that a variety of symptoms have been ascribed to norpethidine in the literature but the full range has not been clearly defined. The authors said that the most characteristic appeared to be unpleasant subjective feelings, behavioural changes, myoclonus (jerking, involuntary movements of the arms and legs) and seizures. They said that the subjective feelings are described as 'shaky feelings'. The authors said that an inability to concentrate, loss of memory and feeling frightened have also been noted and that a patient has described feeling dysphoric. The authors noted that although subjective feelings and myoclonus appeared to have been indicative of a lesser degree of toxicity than seizures, they cannot be relied on as an early warning of more serious toxicity because seizures may occur without other symptoms first being observed.
Dr Raftos said that the symptoms the appellant reported were similar to the typical feeling before someone faints but sounded a little bit different. Dr Raftos said that there are all sorts of neurological changes associated with norpethidine toxicity and one of those is altered consciousness or delirium. Dr Raftos said that the symptoms which the appellant described could well be interpreted as altered mental state or altered consciousness.
Professor Paech considered that the symptoms described by the appellant did not change the probability that pethidine had contributed to the seizure. Professor Paech said that the symptoms described by the appellant were 'very non‑specific symptoms which could be due to a huge number of factors'. Professor Paech said that the classical symptoms of norpethidine toxicity are 'more jerkiness and jitteriness, muscle movements and seizures'.
Mr Hennessy said that in the cases of norpethidine toxicity he had seen the patient had exhibited twitching and agitation before seizure. Mr Hennessy considered that the appellant's report of a feeling of drunkenness and a sense that when she was speaking it did not feel or sound as if the words were coming from her mouth was consistent with normal opioid administration. Mr Hennessy said that the sense of derealisation is something that is commonly reported by people who are administered opioids. It was not something that he would describe as a toxic reaction to norpethidine.
The trial judge's finding that the symptoms described by the appellant were not of themselves an indicator of norpethidine toxicity and were consistent with typical feelings which precede a faint or with normal opioid administration was open to the trial judge.

Dosage was within a safe level

Third, the appellant says that the trial judge incorrectly attached weight to the proposition quoted in the 2002 article by Latta and others that:
It has often been stated in the literature that 1200 mg per day (a 100 mg every two hours parenterally) is a 'safe' level and a 600 mg per day limit in clinical practice is suggested (59).
In the article the authors go on to say that symptoms have been experienced by patients receiving significantly less than 1200 mg per day.
The trial judge referred to the reference in Latta and others to 1200 mg per day being a 'safe' level with a 600 mg per day limit in clinical practice being suggested [100] when considering whether 600 mg of pethidine in 19 hours exceeded the recommended safe dose. It is true that the trial judge did not go on to refer to the further statements in the article that symptoms have been reported in patients receiving significantly less than the reported dose of 1200 mg per day and that patients who are likely to have norpethidine neurotoxicity will experience symptoms at lower doses than those who may be tolerant to the effect of norpethidine. However, that shows no error by the trial judge. Dr Raftos, who produced and referred to the article by Latta and others, opined that 600 mg within 24 hours would be safe and acceptable. The trial judge observed that the dosage of 600 mg did not exceed a safe recommended dosage of 600 mg per 24 hours but that the appellant had received that dosage in less than 24 hours. The trial judge's finding that the dose of 600 mg of pethidine in 19 hours did not exceed the recommended safe dose was based primarily upon the evidence of Professor Paech that the Product Information was an extremely conservative dosing recommendation and it recommended up to 150 mg three to four hourly for no longer than 24 to 36 hours, that is a potential dose of 1200 mg in 24 hours.

Bradycardia

Fourth, the appellant submits that the trial judge erred in attaching weight to the occurrence of bradycardia as suggestive of no link between pethidine and the seizure and support for a link with a vasovagal spasm. The appellant says that her case was that the respondent conceded that she had fainted. Furthermore, the appellant says that it was norpethidine and not pethidine itself which caused the seizure and as such the fact that pethidine had a propensity to cause tachycardia was irrelevant.
At [72] the trial judge referred to the evidence of Mr Hennessy that one of the effects of pethidine is to speed the heart up (tachycardia) not to slow it down (bradycardia). The trial judge said that if a fast heart rate is a symptom of the use of pethidine then the event of bradycardia very much weighs against the cause of the seizure being pethidine related.
Mr Hennessy's evidence was:
One of [pethidine's] effects is to speed the heart up not to slow it down. When [the appellant] was initially noted to lose consciousness she was noticed to be bradycardic. This goes hand in hand with a neurological vagal phenomenon like a simple faint so I think that the fact that she was bradycardic when she initially had the event I think is more consistent with having had a faint.
In his reasons, the trial judge correctly referred to the evidence of Mr Hennessy that the event of bradycardia weighed against the cause of the seizure having been pethidine related - that is, related to the recent administration of pethidine but was consistent with a simple faint. Logically, the event of bradycardia does not exclude the possibility that norpethidine toxicity lowered the appellant's seizure threshold but it is consistent with the immediate cause of the seizure having been a faint. The trial judge's conclusion is not vitiated by his observation concerning the appellant being bradycardic when she lost consciousness.

Dr Raftos' opinion rejected - dose not excessive

Fifth, the appellant says that the trial judge erred in that his reason for not accepting Dr Raftos' opinion on the causation question was not reasonable. The appellant says that the trial judge's reasoning was based on the fact that Dr Raftos concluded that the dose of pethidine was excessive which was a reasonable conclusion.
The trial judge said at [105] that he was not able to accept Dr Raftos' opinion that the pethidine dose materially contributed to the appellant's seizure because Dr Raftos' opinion was premised on his conclusion that the dosage of pethidine was excessive and the trial judge had found that the dosage was not excessive. It was open to the trial judge to find that the dosage was not excessive and to not accept the conclusion of Dr Raftos that the pethidine dose materially contributed to the appellant's seizure because Dr Raftos' opinion was based on the dosage being excessive.
Dr Raftos' opinion was based upon the medical journals he referred to. In his report of 12 May 2006, Dr Raftos said that the recommended upper limit daily dose of pethidine in clinical practice in 2003 was 600 mg. Dr Raftos cited the article by Latta and others in support of that statement. In their article Latta and the other authors said:
It has often been stated in the literature that 1200 mg per day (100 mg every two hours parenterally) is a 'safe' level and a 600 mg per day limit in clinical practice is suggested. When looking at the ranges of use for the symptomatic groups, it is startling how much overlap there is. The shaky feelings group ranges from as little as 59 to 1080 mg/d the tremors/twitches group ranges from 46 to 1100 mg/day, and the most severe group, the myoclonus/grand mal, ranges from as low as 260 to only 540 mg/day. This is significantly less than the reported dose in the literature of 1200 mg/day. What becomes evident is that the patients who are likely to have meperidine/normeperidine neurotoxicity will experience higher iatrogenic events at lower doses than those who may be tolerant to the effect of normerperidine (59).
In cross‑examination, Professor Paech pointed out that Latta and the other authors were talking about patients who were on those doses every day for a prolonged period of time.
In his substance of evidence dated 15 July 2005 Professor Paech said:
My own research supports other studies, showing that when doses of pethidine up to 500 mg per 12 hours are used by patients after surgery (dose requirements up to 1000 mg in 24 hours are common) the levels of plasma pethidine and norpethidine remain well below the lowest level associated with seizures.
Professor Paech said in cross‑examination that the dose of 600 mg in 19 hours was well within the Product Information recommended dosage which itself was a conservative dosing recommendation. Professor Paech said that most of the cases of seizure activity are related to patients who have been on pethidine for several days, and usually more than 48 hours, although there are rare exceptions to that.
Mr Hennessy said that a dose of 600 mg over 19 hours was an inadequate dose to cause seizures. Both the amount, 600 mg, and the time, 19 hours, were inadequate for the required amount of norpethidine to build up in the appellant's system. Mr Hennessy said that it is likely to need about 36 hours for the appellant to metabolise the pethidine to the norpethidine and for that norpethidine to accumulate in such an amount as to cause a seizure.
Having regard to all of the evidence, the trial judge was correct to find that the dosage of pethidine received by the appellant was not excessive in the sense referred to by Dr Raftos.

Weight given to medical literature

Finally, the appellant says that the trial judge attached inadequate weight to the medical literature before him. I do not accept that proposition. It was for the trial judge to attach such weight to each of the articles as he saw fit in light of the other evidence, including the opinions of the expert medical witnesses. The learned trial judge discussed at some length the two articles referred to by Dr Raftos and admitted them into evidence. His Honour had regard to them in assessing what is and is not an excessive dose of pethidine. The appellant has not demonstrated that the trial judge made any error in not having sufficient regard to any of the articles.

Finding of trial judge is correct

The trial judge found that the appellant had not discharged the legal onus of proof that the pethidine dose administered to her materially contributed to her seizure. The trial judge found that the appellant's symptoms, bradycardia and being sat up in bed were all consistent with a vasovagal collapse which led to a seizure. The appellant does not challenge that finding. Rather, the appellant's case is that the pethidine dose materially contributed to the seizure that was precipitated by the faint. The trial judge found that whilst it was possible that norpethidine toxicity may have contributed to the seizure the weight of evidence was against it.
The appellant did not display the classic symptoms of norpethidine toxicity prior to the seizure. The appellant described feeling a drunken type sensation and a sense that when she was speaking to the nursing staff the words were coming from someone else. Dr Raftos said that the symptoms that the appellant reported may have been the typical feeling before someone faints but sounded a little bit different. Dr Raftos said that those feelings were consistent with norpethidine toxicity. However, Professor Paech said that those symptoms were very non‑specific symptoms which could be due to a huge number of factors and the classical symptoms of norpethidine toxicity are more jerkiness and jitteriness which were not present. Mr Hennessy said that the feelings reported by the appellant were consistent with normal opioid administration rather than specifically norpethidine toxicity. When all of the evidence is considered, the symptoms or feelings reported by the appellant prior to her seizure are not indicative of norpethidine toxicity.
There was no objective evidence that the appellant suffered norpethidine toxicity, such as the appellant's norpethidine blood concentration. As I have said, the appellant did not exhibit the classic signs or symptoms of norpethidine toxicity. The only evidence that the appellant suffered norpethidine toxicity was an inference that might be drawn from the fact that she received 600 mg of pethidine over 19 hours and suffered a seizure. Dr Raftos opined that that dosage was excessive and that the excessive dose of pethidine contributed substantially to the development of the seizure. The trial judge, correctly, found that Dr Raftos' opinion was based on the premise that the dose of pethidine was excessive. Dr Raftos referred to the dose being excessive by reference to the discussion in the journals of a 'safe' level. The opinion of Professor Paech and Mr Hennessy, consistent with the articles of Latta and others and Plummer and others, is that it is very unlikely that a dose of 600 mg over 19 hours would cause, or contribute to, a seizure. Indeed, in their 2001 article Plummer and others wrote that:
An upper dose rate of 10 mg/kg per day has been suggested to provide a reasonable margin of safety. Using this upper dose limit, it was reported that no cases of norpethidine toxicity were seen in five years, except when the dose limit was ignored (168).
Professor Paech's opinion was that whilst it was possible that norpethidine toxicity contributed to the seizure it was extremely unlikely that it contributed at all. Professor Paech explained the basis of his opinion. There is a very plausible explanation for the seizure, that being a vasovagal collapse. A vasovagal collapse fitted 'very well with the clinical picture'. Professor Paech considered that the symptoms described by the appellant before her seizure were not the classical symptoms of norpethidine toxicity such as jerkiness. Professor Paech considered that it would be very rare for a patient receiving the dose of pethidine that the appellant received over the time period over which she received it to develop norpethidine toxicity and have a seizure.
Mr Hennessy's opinion was that it was unlikely that the norpethidine contributed to the seizure. His opinion was based upon the magnitude and timing of the dose. Furthermore, Mr Hennessy considered that the symptoms described by the appellant before the seizure were consistent with normal opioid administration and not a toxic reaction to norpethidine.
Dr Raftos' opinion that norpethidine toxicity contributed to the seizure is based on his opinion that the pethidine dose received by the appellant was excessive. That opinion was rejected by the trial judge. The trial judge made no error in doing so. The judge was right to conclude on the basis of the evidence of Professor Paech and Mr Hennessy that the appellant had failed to discharge the legal onus of proving that the pethidine dosage materially contributed to the seizure.
Ground 2 of the appeal is not made out.

Conclusion

I would dismiss the appeal.