King v Western Sydney Local Health Network
[2011] NSWSC 1025
•07 September 2011
Supreme Court
New South Wales
Medium Neutral Citation: King v Western Sydney Local Health Network [2011] NSWSC 1025 Hearing dates: 11/04/2011; 13/04/2011; 14/04/2011 Decision date: 07 September 2011 Jurisdiction: Common Law Before: Garling J Decision: 1. Judgment for the defendant.
2. Plaintiff to pay the defendant's costs.
Catchwords: CIVIL - Medical negligence - Duty of Care - Foetal plaintiff when breach of duty occurred - Hospital owed duty of care to plaintiff which became enlivened upon her birth
CIVIL - Medical negligence - Breach of Duty - Civil Liability Act s 5B - Risk of Harm - Risk of plaintiff being born with congenital varicella syndrome (CVS) - Foreseeable - Requisite state of knowledge - Treating doctor consulted specialist to determine if mother should be treated with immunoglobulin - Widely known risk of plaintiff being born with CVS between one and two per cent - Not Insignificant risk of harm - Reasonable person would have taken precautions - Expert evidence - Plaintiff's mother should have been advised about availability, benefits and been administered with immunoglobulin - No evidence of possible serious adverse effects - Defendant breached duty of care
CIVIL - Medical negligence - Breach of Duty - Whether defence under s 5O Civil Liability Act - Onus on defendant - Whether deferral of immunoglobulin injection pending serology results widely accepted by peer professional opinion as competent professional practice - Relevant exposure to chickenpox within 96 hour window for immunoglobulin treatment - Expert evidence that deferral of treatment only acceptable when serology results available within six hours - Defence not made out
CIVIL - Medical negligence - Causation - Civil Liability Act s 5D - Whether, if administered, immunoglobulin injection would have been effective to prevent plaintiff's mother being infected with varicella - Particular harm - Congenital varicella syndrome - Whether plaintiff's mother would have accepted immunoglobulin treatment - Scientific and expert evidence - Research on comparable cohort of patients - Study quality issue - Differential dosage issue - Strike rate issue - Evidence of possibility only - Research and clinical practice on non-comparable cohort of patients - Evidence of effectiveness in different cohorts only - Probability of effectiveness in population circumstantial evidence of possibility of effectiveness in plaintiff - No causation
EVIDENCE - Medical Negligence - Contemporaneous hospital and medical records more reliable and accurate source upon which to rely when making findings of fact - Honest and truthful witnesses - Frailty of human recollection over time when partisan interest in an outcome
EVIDENCE - Medical negligence - Unchallenged evidence plaintiff's mother would have accepted immunoglobulin treatment - Evidence not illogical or inherently improbable - Evidence acceptedLegislation Cited: Civil Liability Act 2002 Cases Cited: Adeels Palace Pty Ltd v Moubarak (2009) 239 CLR 420
Ali v Nationwide News Pty Ltd [2008] NSWCA 183
Benic v State of New South Wales [2010] NSWSC 1039
Bolam v Friern Hospital Management Committee [1957] 1 WLR 582
Bolitho v City and Hackney Health Authority [1998] AC 232
Dobler v Halverson (2007) 70 NSWLR 151
Edward Wong Finance Co Ltd v Johnson Stokes and Master (A Firm) [1984] 1 AC 296
Ellis v Wallsend District Hospital (1989) 17 NSWLR 553
Fox v Percy (2003) 214 CLR 118
Herron v McGregor (1986) 6 NSWLR 246
Hucks v Cole (1993) 4 Med LR 393
Onassis and Calogeropoulos v Vergottis [1968] 2 Lloyds Law Rep 403
Paric v John Holland Constructions Pty Ltd (1984) 2 NSWLR 505
Poricanin v Australian Consolidated Industries Ltd (1979) 2 NSWLR 419
Roads and Traffic Authority of New South Wales v Dederer (2007) 234 CLR 330
Roads and Traffic Authority of New South Wales v Refrigerated Roadways Pty Ltd [2009] NSWCA 263
Rogers v Whitaker (1992) 175 CLR 479
Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262
Sidaway v Board of Governors of the Bethlem Royal Hospital and the Maudsley Hospital [1985] AC 871
Sydney South West Area Health Service v MD [2009] NSWCA 343
The T J Hooper 60 F 2d 737 (2nd cir 1932)
Wilson v Nilepac Pty Ltd [2011] NSWCA 63
X and Y v Pal (1991) 23 NSWLR 26Texts Cited: David Ipp, Review of the Law of Negligence, (Sept 2002) Can Print Communications Pty Ltd
Fleming's The Law of Torts, 10th Ed (2011) Thomson Reuters (Professional) Australia LtdCategory: Principal judgment Parties: Tamara King bhnf Phillippine King (P)
Western Sydney Local Health Network (D)Representation: Counsel:
D Wheelahan QC / R N O'Neill (P)
M Windsor S / S A Woods (D)
Solicitors:
McDonnell Schroder (P)
Gild Insurance Litigation Pty Ltd (D)
File Number(s): 2005/269149 Publication restriction: Nil
Judgment
On 1 November 2002, Tamara King was born to Phillippine and Kevin King. She is their second daughter. Their first, Shania, was born in August 1998.
Tamara has a number of features which are suggestive of her having Congenital Varicella Syndrome (CVS). She claims that her CVS came from her mother, Phillippine, whom she alleges was infected with varicella (or chickenpox) whilst she was pregnant with her.
Tamara, through her tutor, sues the Western Sydney Local Health Network, which is the entity legally responsible for Blacktown Hospital. She claims that when Phillippine attended at the Hospital on 6 May 2002 and told a member of the medical staff, Dr Davidson, that her first born daughter, Shania, had been diagnosed with chickenpox that very morning, Phillippine ought to have been given an injection of Varicella-Zoster Immunoglobulin (VZIG).
Tamara claims that this injection would, on the probabilities, have prevented her mother, Phillippine, being infected with varicella, and as a consequence, she would not have suffered from CVS.
The issues in this case deal with chickenpox, how it can be transmitted, what can be done to prevent its transmission, and whether the various features from which Tamara now suffers, were the result of her mother contracting chickenpox.
The facts to which I will shortly turn are in relatively brief compass. However, first it will be convenient to describe the limited nature of the hearing before me, and to outline some terms which will enable a more ready understanding of this judgment.
Nature of Hearing
On 1 May 2009, Price J decided that the question of liability of the Local Health Network to Tamara for damages ought be heard and determined in advance of and separately from, the remaining issue of quantification of damages.
It is that separate hearing which I conducted and which I determine in this judgment. The parties accepted before me that the hearing involved these issues:
(a) Whether the Hospital owed Tamara a duty of care, and if so, its nature and content;
(b) Whether the Hospital was in breach of that duty of care;
(c) Whether the features of Tamara's condition observed, prior to and after her birth, amounted to CVS; and
(d) Whether Tamara's CVS, was caused by, or else materially contributed to by, the Hospital's breach of duty.
The Local Health Network admitted that the Hospital owed a duty of care to Tamara, but otherwise disputed all of the other issues.
It will be convenient in this judgment to refer to the defendant which is the Local Health Network as the Hospital, since the Hospital was the active agent of the Local Health Network in the events which occurred.
Decision
I have decided, for the reasons which follow, that the issues the subject of the separate hearing should be answered as follows:
(a) The Hospital owed Tamara a duty of care.
(b) The Hospital was in breach of its duty of care to Tamara because it did not administer VZIG to Phillippine King on 6 May 2002, when it ought to have done so.
(c) Tamara has proved that she suffers from CVS, which was caused by her mother being infected with chickenpox, having been exposed to Shania during the period when Shania was infectious.
However, on the evidence, I have not been satisfied on the balance of probabilities that had the VZIG been administered on 6 May 2002, it would have prevented the chickenpox infection in Phillippine King. The evidence only satisfies me that it was possible that VZIG would have prevented the infection, which in law, is insufficient to make the Hospital liable for Tamara's CVS.
Accordingly, there will be a judgment for the defendant.
Definitions
It is appropriate here to set out some definitions of terms which are to be used throughout this judgment, which were not in issue between the parties:
(a) Varicella, or chickenpox, is a highly contagious disease caused by the Varicella-Zoster Virus. The disease is characterised by fever, malaise and an itchy rash that develops into crops of maculopapules which become vesicular and crust over before healing;
(b) Varicella-Zoster Virus (VZV) is a virus of the herpes family that is transmitted by respiratory droplets or direct personal contact with vesicular fluid, or, sometimes, indirectly. VZV causes a systemic infection that usually results in lifetime immunity.
(c) Maculopapules are large superficial solid elevations on the skin;
(d) A vesicule is a blister or circumscribed elevation on the skin containing serous fluid and ranging in size up to 1cm;
(e) Congenital Varicella Syndrome (CVS), which may be caused by chickenpox infection in a pregnant woman, may be characterised by any one or more of the following:
(i) skin scarring in a dermatomal distribution;
(ii) eye defects (chorioretinitis, microphthalmia, cataracts);
(iii) hypoplasia of the limbs;
(iv) neurological abnormalities including microcephaly, cortical atrophy, mental retardation and dysfunction of the bowel and bladder sphincter.
(f) Varicella-Zoster Immunoglobulin (VZIG) is a sterile solution of the globulin fraction of human plasma, primarily immunoglobulin G (IgG) mixed in a stabiliser with a preservative. It is administered by injection intra-muscularly. In this judgment, I will also refer to Zoster Immunoglobulin (ZIG). Unless specifically noted, VZIG and ZIG can be used to refer to similar products. For the purpose of this judgment, the terms should be regarded as interchangeable.
(g) Significant exposure to VZV infection is defined to include living in the same household as a person with active chickenpox or herpes zoster (shingles), play contact of longer than one hour, classroom contact or other close prolonged exposure.
Factual Findings
The principal evidence about what occurred, and which forms the basis of these factual findings, was that given by the Mr and Mrs King, together with the contemporaneous hospital and medical records.
Mr and Mrs King were giving evidence about events which had taken place nine years earlier. Although their honesty and truthfulness was not in issue, the accuracy and reliability of their evidence was. I am satisfied that the contemporaneous records are a much more reliable and accurate source upon which to rely when making findings of fact. To the extent that there is a difference between the accounts of Mr and Mrs King and the contemporaneous records, I propose to base my findings on the latter.
This approach to the evidence recognises the frailty of human recollection over time. Memories fade and can, unknowingly, become distorted by external influence: see Herron v McGregor (1986) 6 NSWLR 246 at 254E-255B per McHugh JA.
Gleeson CJ, Gummow and Kirby JJ in Fox v Percy (2003) 214 CLR 118 noted the caution that the trial judge should take in relying solely or principally on demeanour as a method of rational decision making. At [31] they said:
"Considerations such as these have encouraged judges, both at trial and on appeal, to limit their reliance on the appearances of witnesses and to reason to their conclusions, as far as possible, on the basis of contemporary materials, objectively established facts and the apparent logic of events. This does not eliminate the established principles about witness credibility; but it tends to reduce the occasions where those principles are seen as critical."
Thirty-five years earlier, Lord Pearce, in his speech in the House of Lords in Onassis and Calogeropoulos v Vergottis [1968] 2 Lloyds Law Rep 403, said at 431:
"It is a truism, often used in accident cases, that with every day that passes the memory becomes fainter and the imagination becomes more active. For that reason a witness, however honest, rarely persuades a Judge that his present recollection is preferable to that which was taken down in writing immediately after the accident occurred. Therefore, contemporary documents are always of the utmost importance."
Facts
On the evening of Sunday 5 May 2002, Kevin King first noticed a pink rash on the left arm of his daughter Shania. He described what he saw as a rash that " looked like prickly heat " (T58.14). On that day, it was only the left arm of his daughter which displayed the rash. There were no blisters.
Phillippine King also saw the same rash on the evening of Sunday, 5 May 2002. At that time, Shania slept in the same bedroom as Mr and Mrs King.
Early on Monday morning, 6 May 2002, Mr King took his daughter to see a general practitioner, Dr Kodsi. Dr Kodsi diagnosed chickenpox. He advised that Shania should stay home for a period of 14 days and that Mrs King should sleep in a separate bedroom to Shania. Mr King told his wife about this advice.
The reason why the advice was given to sleep in a separate bedroom was that Mrs King was pregnant. Her last menstrual period was recorded both by Dr Kodsi in his notes (Ex M, p2), and in her pre-natal records at Blacktown Hospital (Ex G) as being 2 February 2002. Her estimated date of confinement was 9 November 2002. Accordingly, at the time Mrs King's pregnancy was well established.
Dr Kodsi recorded his consultation with Shania on 6 May 2002 in this way:
"6.5.02: Fever, spots of vesicles Panadol/Calamine Lot[ion], ?chicken pox, advice to preg[nant] mother."
At about 10.15am on Monday 6 May 2002, Mrs King presented to the Triage Nurse at Blacktown Hospital. Although her memory is different, I am satisfied that Mrs King presented primarily because she was having vaginal bleeding which had started that morning. She was also complaining of back pain and abdominal pain. She was distressed and teary. She told the Triage Nurse that she was 12 weeks pregnant and that she had an ultrasound two weeks earlier which had confirmed a viable pregnancy. She did not tell the Triage Nurse of her close contact with her daughter who was infected with chickenpox.
Mrs King was admitted to the emergency department and placed in a bed. Her observations (or "vital signs") were taken at 10.39am.
At about 11.45am, Mrs King was attended by Dr Jane Davidson. The Hospital did not call Dr Davidson as a witness to give evidence. Accordingly there is no material available about her particular expertise, her level of training or her experience. The notes that she made of the consultation are in evidence.
The first part of Dr Davidson's consultation notes record in detail Mrs King's history as it relates to her pregnancy. In particular, the notes record that her last menstrual period was 2 February 2002, and that a pelvic ultrasound carried out on 13 April 2002 showed her pregnancy as 10/40, that is, it was 10 weeks since conception.
Given that the visit to the Hospital was on 6 May 2002, which was 23 days after the ultrasound, Mrs King would have been a little under 131/2 weeks' pregnant. In other words, she was in the 14 th week of her pregnancy.
After completing the history relating to her pregnancy, the consultation notes record: " Also adds - daughter developed chicken pox yesterday - she does not believe she has had chicken pox ". This note suggests, and I accept, that contrary to the evidence of Mrs King, her main concern which led her to attend the Hospital was not her daughter's chickenpox, but rather her pregnancy related symptoms.
Dr Davidson examined Mrs King externally. She attempted a vaginal examination which was unsuccessful due to discomfort. She formed the impression that there may have been a threatened miscarriage.
In so far as the issue of chickenpox was concerned, and the appropriate treatment for Mrs King, Dr Davidson wrote this note:
"D/W O+G re need for zoster immunoglobulin - is in second trimester not given - suggested blood taken for Zoster IgM IgA - he will check at ANC on 9/5."
I take from this note, in the context, and having regard to the well-known abbreviations used in notes such as this, that Dr Davidson discussed with an obstetrician and gynaecologist (probably the Registrar) the need for Mrs King to be given Zoster Immunoglobulin (ZIG). I infer that other relevant history was provided. The obstetrician and gynaecologist advised Dr Davidson that since Mrs King was in her second trimester, there was no need for the administration of the Zoster Immunoglobulin on that day. She was advised that a blood test ought to be taken to check for the presence of antibodies to chickenpox which was intended to establish whether Mrs King was immune to VZV. She also advised that the results would be checked at the ante-natal clinic on 9 May 2002 and such treatment as was then appropriate would be provided.
I am not in any doubt that the substance of this advice was conveyed to Mrs King. In short, that advice was that in so far as the chickenpox was concerned, she was not treated at that time, but rather reassured, blood was taken and she was told that the obstetrician and gynaecologist would review her on 9 May 2002 at the ante-natal clinic.
Although Mrs King claims that she was told on 6 May 2002 at the Hospital that she was "immune", I reject that evidence. It is not consistent with the contemporaneous note and it is not consistent with the fact that she had blood taken for testing to establish the extent of her immunity which was to be advised to her at the ante-natal clinic.
Mrs King left Blacktown Hospital at about 12.45pm on 6 May 2002. Mrs King gave evidence that she returned directly home from the Hospital and remained there. But that account is unlikely to be correct because on that day, Mrs King attended for an ultrasound examination at the Blacktown rooms of North West Radiology. Their report noted:
"The appearances suggest a normal early gestation at approximately 13.5 weeks."
On 8 May 2002, Mrs King attended the Castle Towers Medical and Dental Centre and saw a general practitioner. The evidence does not enable me to identify the particular general practitioner. She was diagnosed with a viral infection and found to be unfit for work from 6 May 2002 until 10 May 2002. There is no other factual material about this consultation. Mrs King has no recollection of it. It is somewhat curious that if she had a viral infection and was unfit for work on 6 May 2002, that Mrs King did not report the existence of the viral infection whilst she was at Blacktown Hospital on that day. One possible reason which would explain the existence of this visit and the obtaining of the medical certificate of unfitness for work would be the need for Mrs King to stay at home to care for Shania.
However, on the evidence, such a finding would be speculative. Ultimately there is little if anything of relevance, which can be drawn from this consultation.
On 9 May 2002, Mrs King attended at the ante-natal clinic at Blacktown Hospital. The note of that visit records nothing about the issue of chickenpox exposure or her recently diagnosed viral infection. Mrs King gives no evidence about this consultation. She said that she has no recollection of it (T43.23).
The notes of the ante-natal clinic (Ex G) are also generally uninformative. In addition to recording Mrs King's weight, blood pressure and urinalysis, all of which are routine observations, the notes record this:
"will bring results next time. US [ultrasound] booked 20/6/02."
I am unable to infer that there was any consideration of, or discussion about, the issue of Mrs King's exposure to Shania's chickenpox on that occasion. I think that is unlikely that any such discussion occurred.
On 17 May 2002, Mrs King again presented to the Castle Towers Medical and Dental Centre where she was seen by Dr Ron Shapeira. He noted the following:
"Since yesterday, has developed chickenpox with very sore throat. Since 3am - pain epigastric - now moved to RIF [right iliac fossa], tender. Some guarding. ? Appendicitis."
Although Mrs King does not recall this consultation, I am satisfied that this note accurately records what happened.
On 18 May 2002, Mrs King attended upon her General Practitioner, Dr Kodsi. His note (Ex M) records:
"15/40 preg(nant), chicken pox, will have u/s [ultrasound] in 2/52".
On 19 May 2002, Mrs King again attended at Blacktown Hospital Emergency Department. The Triage Nurse recorded the presenting problem as: " vesicular eruptions on chest for couple of days ".
Mrs King was attended by Dr Naval. She gave the doctor a history which included that she was presenting with the vesicular rashes all over her body which had "... started last Friday " (that is, 17 May 2002).
Dr Naval carried out an examination which established that Mrs King had a vesicular rash on her face, chest and abdomen. The rashes were thought to be in different stages. She had a very sore throat, which when examined demonstrated a few vesicules in her oropharynx. The doctor thought that the throat was inflamed and congested with lesions. Mrs King was admitted to Hospital and remained there until 22 May 2002.
The three consultations of 17, 18 and 19 May 2002, which I have just described all consistently point to Mrs King being diagnosed with symptoms of chickenpox on 17 May, when a number of vesicules were seen on her chest. The symptoms which were associated with the chickenpox included a sore throat which ultimately was seen to be related to vesicules. The symptoms of epigastric pain and tenderness in the right iliac fossa seen on 17 May 2002 are unlikely to be indications of chickenpox. However, their co-existence does not cast doubt on the conclusion which I have reached which is that Mrs King did become infected on 17 May 2002 with chickenpox.
The history obtained and the findings of these consultations do not suggest that chickenpox developed any earlier than 17 May 2002. The entry of Dr Shapeira on that day is unclear as to what actually developed " ... since yesterday ... ". That entry is consistent with the interpretation that the symptoms had developed since, that is in the sense of, after, yesterday, being on the day of the consultation from the early morning. The entry is also consistent with the interpretation that since yesterday, that is, during the course of the day before the note was written, that is, yesterday, she had developed chickenpox.
In my view, having regard to the history given to Dr Naval on 19 May 2002, the first of those two interpretations is likely to be the correct one, and the one which I accept.
There were further obstetric consultations in the ante-natal clinic at the Hospital which do not require elucidation.
On 19 September 2002, the Hospital notes (Ex G) record that Mrs King contacted the ante-natal clinic at the hospital asking for a referral for an ultrasound because of concerns for the baby. She was asked to attend for an assessment, which she declined to do.
On 21 September 2002, Mrs King again contacted the ante-natal clinic because she was "... upset after having an ultrasound today " (Ex G).
Apparently, at least according to the Hospital notes (Ex G), the ultrasound of the plaintiff was reported as showing " scattered calcifications of the liver and ? an enlarged kidney . "
She was asked to bring the ultrasound report to the clinic where she would be seen by both an obstetrician and a paediatrician. It is not clear from the Hospital notes whether she did so. There is an entry on 1 October 2002 which records, as part of the progress notes, that an ultrasound scan "... shows echogenic spots in the liver - ? varicella ." It is not clear by whom the note was made. I would be prepared to infer from the content of the entire note, that the maker of the note was a doctor but their speciality and experience, if any, is not recorded.
On 31 October 2002, Mrs King was admitted to the Hospital in preparation for Tamara's birth. Tamara was born on 1 November 2002 at about 9pm. She was managed in the Special Care Nursery. The neonatal discharge summary of the Hospital dated 6 November 2002, recorded the following facts and statistics about Tamara:
"Baby KING was born at 21:16:00 hours with a birth weight of 2560 grams (8 th centile), length of 47cm (11 th centile), and a head circumference of 31.8cm ( 3 rd centile)."
It was suspected that Tamara had a congenital varicella infection. Various investigations were carried out. The TORCH screen was undertaken to rule out other infections. A CT scan of Tamara's head showed a small (2mm) area of calcification of the basal ganglia on the right side. An echocardiograph was carried out which detected a heart problem, namely a ventricular septal defect.
After discharge, Tamara came under the care of Dr Marea Murray, a specialist paediatrician at the Hospital. She was referred to Dr Cheryl Jones at the Children's Hospital at Westmead. Dr Jones, a paediatric infection specialist, reported on 6 December 2002 about Tamara's condition. She noted the ante-natal ultrasound findings of calcification in the liver and adrenal glands. She also noted a retardation of intra-uterine growth at 33 weeks. She noted that Dr Murray had:
"... excluded other congenital infections and looked for occult manifestations of congenital VZV. CMV urine and IgM were negative ...".
Dr Jones also noted that an eye examination had detected left chorioretinitis in a perimacular distribution. Dr Jones described her as small child. She concluded that Tamara was likely to have CVS.
Duty of Care
The plaintiff pleaded that the Hospital (and hence the Local Health Network) owed to her a duty which became "enlivened" upon her birth. The content of the duty was pleaded as including an obligation to advise the plaintiff's mother of the availability of VZIG and its potential beneficial effects in preventing or ameliorating chickenpox. It also alleged that the Hospital ought to have offered to administer the VZIG to the plaintiff's mother.
This is a relatively conventional pleading, even though the plaintiff, as at 6 May 2002, was still en ventre sa mer: X and Y v Pal (1991) 23 NSWLR 26 at 30A-D per Mahoney JA, 41F per Clarke JA (Meagher JA agreeing).
The defendant admitted the existence of such a duty of care. There is no need for further discussion on this question.
Breach of Duty
The issue of breach of duty must be considered by reference to s 5B of the Civil Liability Act 2002: Adeels Palace Pty Ltd v Moubarak (2009) 239 CLR 420 at [13].
Although the Local Health Network is a public authority, neither of the parties submitted that the principles referred to in s 42 of the Civil Liability Act were relevant on the facts and circumstances of this case. Accordingly, that provision can be put to one side.
As well, although s 5C of the Civil Liability Act is also potentially relevant in claims such as this, neither of the parties submitted that it had any role to play. Accordingly, it too can be put to one side.
It is appropriate to commence this analysis with the particular provisions of s 5B of the Civil Liability Act . They are:
" 5B. General principles
(1) A person is not negligent in failing to take precautions against a risk of harm unless:
(a) the risk was foreseeable (that is, it is a risk of which the person knew or ought to have known), and
(b) the risk was not insignificant, and
(c) in the circumstances, a reasonable person in the person's position would have taken those precautions.
(2) In determining whether a reasonable person would have taken precautions against a risk of harm, the court is to consider the following (amongst other relevant things):
(a) the probability that the harm would occur if care were not taken,
(b) the likely seriousness of the harm,
(c) the burden of taking precautions to avoid the risk of harm,
(d) the social utility of the activity that creates the risk of harm."
Risk of harm - s 5B(1)
In considering whether there has been a breach of duty in this case, the first step is that the plaintiff must identify a risk of harm against which she alleges the defendant would be negligent for failing to take precautions. Section 5 of the Civil Liability Act defines " harm" as meaning "harm of any kind, including... personal injury or death ...".
It is essential in considering this first step to carefully identify the particular risk of harm to which the later steps of the analysis of the provisions of s 5B will be applied: Roads and Traffic Authority of New South Wales v Dederer (2007) 234 CLR 330 at [59]-[61] per Gummow J.
In this case, the risk of harm was identified by senior counsel for the plaintiff as being, in the context of all of the facts and circumstances of the case, the risk of the plaintiff being born with Congenital Varicella Syndrome.
My analysis will proceed upon the basis that this is the relevant risk of harm, against which precautions should reasonably be taken.
The next step is to identify and address each of the three elements in s 5B(1) of the Civil Liability Act . The statute requires that a trial judge must be satisfied that each of the three elements in s 5B(1) are established before a finding of breach of duty can be made: Roads and Traffic Authority of New South Wales v Refrigerated Roadways Pty Ltd [2009] NSWCA 263 at [442]-[444] per Sackville AJA.
The three separate elements in s 5B(1) represent the concepts of foreseeability, probability and reasonableness of precautions: see David Ipp , Review of the Law of Negligence, (Sept 2002) Can Print Communications Pty Ltd, par 7.11.
Foreseeable - s 5B(1)(a)
The first element required by the section is that a plaintiff must establish that the risk of harm was foreseeable to the defendant. As can be seen from the statute, in order to establish foreseeability, a plaintiff must establish either actual knowledge in the defendant of the risk of harm, or else constructive knowledge (that is, the defendant ought to have known) of the risk of harm.
In the context of the present defendant, and the Hospital for which it is liable, it is a matter of establishing knowledge either in the corporate body itself, or else its responsible employees. Here there is no difficulty in establishing the identity of the relevantly responsible employee, because the care of the plaintiff's mother, Mrs King, when she attended at Blacktown Hospital on 6 May 2002 was entrusted by the Hospital to a medical practitioner who worked in the Emergency Department, Dr Jane Davidson, and those of the medical staff, with whom she consulted.
I am satisfied that Dr Davidson, and hence the Hospital, knew of the risk of harm. The knowledge of the relevant risk was, I infer, the reason why Dr Davidson consulted with an obstetrician and gynaecologist on 6 May 2002 whilst attending Mrs King, and why a discussion took place about whether Mrs King was in her first or second trimester, and therefore whether she was an appropriate patient to whom VZIG should be administered.
If I be wrong in drawing this inference, the evidence of the experts and the scientific articles which were tendered, all satisfy me that the risk of the plaintiff being born with CVS was between one and two per cent. It was widely known that there was such a risk of CVS in children born of pregnant mothers who were exposed to the VZV. The Hospital, and its medical staff, including Dr Davidson, ought to have known of that risk.
Accordingly, I am satisfied that the requisite state of knowledge has been proved, and as a result, the relevant risk of harm was foreseeable: s 5B(1)(a).
Not Insignificant - s 5B(1)(b)
The plaintiff must next demonstrate that the risk of harm was not insignificant.
I have previously reviewed a variety of sources and gathered together what seems to me to be an appropriate approach in interpreting the phrase "not insignificant". It is not necessary in the context of this case to repeat those principles. They are to be found in Benic v State of New South Wales [2010] NSWSC 1039 at [101]. The defendant in this case did not submit that the risk of harm, identified by the plaintiff, was not " not insignificant ". This was unsurprising having regard to the known rate of occurrence of CVS in children born of mothers exposed to VZV and the potential for serious consequences in those children.
I am satisfied that in this case, the risk of harm was a not insignificant one: s 5B(1)(b).
Reasonable precautions - s 5B(1)(c)
The third element which needs to be determined is whether the risk of harm is one against which a reasonable person would take precautions. The provisions of s 5B(2) need to be considered in drawing this conclusion.
As I have earlier indicated, the risk of a baby being born with CVS is between one and two per cent, where the mother has been exposed to infection with VZV in the first or second trimester. But the effects of CVS can be very serious.
According to Guideline 13 of the Royal College of Obstetricians and Gynaecologists, Chickenpox in Pregnancy , (July 2001) (Ex L), CVS can be characterised by one or more of the following consequences in a baby:
(a) skin scarring;
(b) eye defects such as microphthalamia, chorioretinitis and cataracts;
(c) hypoplasia of the limbs;
(d) neurological abnormalities including microcephaly, cortical atrophy, mental retardation and dysfunction of bowel and bladder sphincters.
These features are commonly permanent and can be very disabling. The effects of CVS are such that the possibility of their occurrence cannot be simply ignored.
The administration of VZIG is directed at preventing, or ameliorating maternal chickenpox, with the result that the infection of the foetus will be prevented. It is also directed at ameliorating the effects of varicella in the mother. Thus, there are two possible beneficiaries from the administration of VZIG, the mother and the child.
As Dr Philip Brunell puts it in his chapter, "Passive antibody prophylaxis", which is published A Arvin and A Gershon (eds), Varicella-Zoster virus, Virology and Clinical Management (2000) Cambridge University Press at 437 (Ex L):
"Varicella can be a life threatening illness during pregnancy ... . The seriousness of the illness in pregnancy and the potential for possible beneficial effect on [foetal] outcome would indicate that VZIG prophylaxis should be given to exposed susceptible pregnant women."
I agree. This opinion mandates the conclusion that the risk of harm is one against which a reasonable person would take precautions.
The joint report (Ex C) of the six experts who gave evidence concurrently, recorded the agreement of five of them (Dr R J Jones offered no comment) that:
(a) Mrs King, on 6 May 2002, ought to have been advised of the risk for her and Tamara developing chickenpox or CVS, as a result of Mrs King's exposure to Shania's infection;
(b) Mrs King, on 6 May 2002, ought to have been advised of the possibility of treatment by VZIG;
(c) In Australia, in 2002, it would not have accorded with proper and reasonable professional practice, to have failed to administer VZIG to a pregnant woman where exposure had occurred within the 96 hour period prior to administration.
From these opinions, I readily draw the conclusion that a reasonable person in the position of the Hospital, acting through its medical staff, would have taken the precaution which the plaintiff alleged should have been taken, namely, that Mrs King ought to have been advised about the availability and potential benefits of VZIG, and the appropriateness, in her case, of her being administered that preparation.
There are two further publications which confirm the view to which I have come, to which reference ought be made.
The Australian Immunisation Handbook , 7 th ed (March 2000) Pirie Printers, Canberra (Ex L), records the following at 236-237:
"... general guide to appropriate practice ...
Recommendations
ZIG should be given to individuals in the following categories if they are significantly exposed to varicella or zoster:
...
pregnant women who are susceptible to varicella infection (they should be tested for varicella-zoster antibodies);
...
"Significant exposure" is defined as household contact ... or other close prolonged exposure ...
...
ZIG must be given as early as possible in the incubation period - within 96 hours of exposure if possible."
A 2002 publication by P Palasanthrias, M Starr and C Jones (eds), Management of Perinatal Infections (2002), Australasian Society for Infectious Diseases) provides a treatment algorithm, which recommends the administration of ZIG to a pregnant woman within 96 hours of exposure to a person with active chickenpox in the same household, where the woman has no history or else an uncertain past history of chickenpox, and either, they are seronegative for varicella having had a blood test, or else serology is not available.
Both of these publications recorded clear advice for Australian medical practitioners, which was contemporaneous with the events in this case, which I am satisfied was reasonable to follow and would have been unreasonable to ignore.
None of the experts in their reports or evidence, and none of the publications which were tendered, identified any possible serious adverse effects from the administration of VZIG. As I have noted earlier, a failure to administer VZIG would have significant potential adverse consequences.
Having regard to the circumstances which surrounded the presentation of Mrs King to the emergency department at Blacktown Hospital on 6 May 2002, I am satisfied of the following matters, all of which were known to, or could have been deduced by, the Hospital's medical staff:
(a) Mrs King was 13.5 weeks pregnant;
(b) Mrs King had no history, or else an uncertain past history, of chickenpox;
(c) her daughter Shania, with whom she had close contact as a member of the same household, had developed chickenpox on the evening of 5 May 2002;
(d) Mrs King had been exposed to infection on a continuous basis since the evening of 3 May 2002, being 48 hours prior to the development of Shania's rash.
I am satisfied that, subject to the particular defence raised under s 5O of the Civil Liability Act to which I will shortly come, that the staff of the Hospital failed to act reasonably because they did not advise Mrs King about the availability of VZIG and its purpose and benefits, and they did not offer to administer it to her whilst she was a patient in the emergency department. There was a breach of duty by the Hospital.
Section 5O of the Civil Liability Act
The defendant pleads and raises an issue under s 5O of the Civil Liability Act as a basis for a finding that there was no breach of duty.
The legal position
Section 5O is in the following terms:
" 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 is the statutory embodiment of the Bolam principle, although in slightly different words.
The Bolam principle or the Bolam rule as it is also referred to, derived from the statement of McNair J in Bolam v Friern Hospital Management Committee [1957] 1 WLR 582, where his Honour said at 587:
"... [a doctor] is not guilty of negligence if he has acted in accordance with a practice accepted as proper by a responsible body of medical men skilled in that particular art ... merely because there is a body of opinion which would take a contrary view."
It has long been accepted in the United Kingdom that the consequence of the Bolam principle was that whilst it was the law which imposed the duty of care upon the medical practitioner, the standard of care was a matter for medical, and not legal, judgment: Sidaway v Board of Governors of the Bethlem Royal Hospital and the Maudsley Hospital [1985] AC 871 at 881 per Lord Scarman.
In Rogers v Whitaker (1992) 175 CLR 479 at 487 per Mason CJ, Brennan, Dawson, Toohey and McHugh JJ, it was noted that the Bolam principle was not always applied in Australia in cases involving diagnosis and prescription of treatment by a medical practitioner.
Gaudron J said at 493:
"Accordingly, even in the area of diagnosis and treatment there is, in my view, no legal basis for limiting liability in terms of the rule known as the 'Bolam test'. "
Professor Fleming regarded the High Court in this case as having rejected the Bolam principle as being a part of the Australian common law, holding that the ultimate question of negligence is one for the court and not the medical profession: see Fleming's The Law of Torts , 10 th Ed (2011) Thomson Reuters (Professional) Australia Ltd at pp 143-145.
Section 5O was introduced following the release of the Ipp Report. The Ipp Report at par 3.11 expressed the view that the " ...Bolam rule is not a reliable guide to acceptable medical practice ". It recommended against the statutory restoration of the rule in an unmodified form. However, the form of the "modified Bolam Rule" which it recommended was not wholly adopted by the legislation. The Ipp Report at 42 had the approach of identifying the relevant yardstick as " an opinion widely held by a significant number of respected practitioners ".
The legislation (s 5O(1)) uses the approach of "... a manner...widely accepted...as competent professional practice ..." rather than the words suggested by the Ipp Report. This is much closer to the Bolam phrase at 587 "... practice accepted as proper " than the recommendations of the Ipp Report. Both the current legislation and the application of the Bolam rule requires the acceptability of competent, or proper, practice to be that identified by peer opinion.
In those circumstances, it seems clear that the remarks of Lord Scarman in Sidaway are now applicable when considering a defence under s 5O of the Civil Liability Act . In other words, the standard of care is now a matter for medical judgment. This is consistent with the view expressed by Giles JA in Dobler v Halverson (2007) 70 NSWLR 151 where he said at [59] that: " ...subject to rationality that professional practice sets the standard of care ".
The reservation expressed by Giles JA in the words " ...subject to rationality... " is one of long standing in the common law. Although the source is debatable, it is clear that the judgment of Learned Hand J in 1932 in The T J Hooper 60 F 2d 737 (2 nd cir 1932) at 740 is an early example of the rejection by a Court of universal practices, in that case the practice of tugboats not carrying receiving radio sets, as being acceptable.
A more recent example of the "irrationality exception" is to be found in the judgment of the House of Lords in Bolitho v City and Hackney Health Authority [1998] AC 232, in the speech of Lord Browne-Wilkinson, where he said:
"But if ... it can be demonstrated that the professional opinion is not capable of withstanding logical analysis, the judge is entitled to hold that the body of opinion is not reasonable and responsible."
Other examples of the "irrationality exception" can be found in Hucks v Cole (1993) 4 Med LR 393, and Edward Wong Finance Co Ltd v Johnson Stokes and Master ( A Firm ) [1984] 1 AC 296.
In summary, the role of the Court, previously the sole determiner of the standard of care when considering the common law of Australia is now in New South Wales a very much more restricted one, as a result of the introduction of s 5O.
As Dobler sets out at [59]-[60], the process by which, in cases to which s 5O applies, proof of breach of duty will be achieved is:
(a) The plaintiff will call evidence to the effect that the defendant's conduct fell short of what is reasonably to be accepted having regard to any existing professional practice;
(b) The defendant will, if it wishes to challenge that evidence, call evidence as to whether the defendant's conduct breached the nominated professional practice or else whether the nominated practice was in fact accepted or reasonable;
(c) The defendant will, if it wishes to rely on a widely accepted practice different from that relied upon by the plaintiff, which it submits that peer professionals widely accept as competent, call evidence of that practice and seek to establish that the defendant's conduct, as a matter of fact, fell within that practice and hence that it was widely accepted by peer opinion as competent, thereby establishing a defence under s 5O.
The role of the court in determining issues raised by subparagraph (a) and (b) does not vary from the traditional common law position described in Rogers v Whitaker . But in considering subparagraph (c) the court has a more limited role, because it is the professional practice which sets the standard of care.
In this respect, the Court has to determine whether, as part of a defence, the defendant has established that the professional practice of which evidence is given meets the criteria of s 5O, namely:
(a) did the professional act in a manner which accorded with an identified practice;
(b) was the practice widely, but not necessarily universally, accepted by peer professional opinion;
(c) was the practice widely accepted as competent
Then, by way of a final issue, the court must be satisfied that the peer professional opinion is not irrational. Cases of this kind are likely to be rare. As a practical matter, the evidentiary onus of establishing that the particular peer professional opinion is irrational will fall on a plaintiff, where a defendant pleads and advances a defence under s 5O. That is because ordinarily it would be inferred that a widely accepted competent professional practice would be a rational one, unless it was proved otherwise.
Findings on the s 5O Defence
The defendant contends that the conduct of the Hospital in not administering VZIG to Mrs King on 6 May 2002, but asking her to submit to a blood test and then referring the results of that blood test for review at an appointment at the ante-natal clinic on 9 May 2002 was acting in a manner that "... was widely accepted in Australia by peer professional opinion as competent professional practice ."
The defendant submitted that there were two bases for concluding that Dr Davidson had acted in accordance with competent professional practice accepted widely in Australia by peer professional opinion. The first was that since, as a matter of fact, the exposure of Mrs King to the VZV had occurred more than 96 hours prior to her attending at Blacktown Hospital on 6 May 2002, widely accepted professional practice did not require the administration of VZIG.
The second basis upon which the defendant relied was that the treatment of Mrs King accorded with that recommended in Guideline 13 of the Royal College of Obstetricians and Gynaecologists at 3-4 (Ex L), which Guideline was agreed in the joint expert report (Ex C) to be competent professional practice, widely accepted in Australia by peer professional opinion.
Since s 5O is a defence, the onus of establishing that the defendant acted in accordance with it falls upon the defendant: Dobler at [59]-[61] per Giles JA (Ipp and Basten JJA agreeing); Sydney South West Area Health Service v MD [2009] NSWCA 343 at [21] per Hodgson JA, at [51] per Allsop P (Sackville AJA agreeing with Allsop P and Hodgson JA).
For the reasons which follow, I am not satisfied that the defendant has made out its defence based on s 5O of the Civil Liability Act .
The first argument advanced by the Hospital is that as a matter of fact Mrs King had been exposed to the VZV more than 96 hours prior to her attending at the hospital on 6 May 2002 and accordingly, professional practice did not require her to be administered VZIG.
In order to establish this defence, it was necessary for the hospital to prove when the exposure of Mrs King occurred and when she contracted the VZV.
The Hospital submitted that the evidence disclosed that Mrs King first suffered from symptoms of chickenpox on 16 May 2002 (Ex H). It submitted that the median time for the incubation of chickenpox was 14 to 15 days. The evidence in support of that submission was that given by Dr Hudson where he said (T89.45):
"I searched for that reference and in fact the mean and the median are not dissimilar, which would suggest it is normally distributed but the median is very useful when there is a skew in the distribution ... Most of the data is obtained from household contact exposure. The most well-studied examples are household contact exposure, so I think it is valid to say that in household contact exposure, the median is 14 or between 14 and 15."
Professor Curtis had earlier during the discussion of that topic said that whilst he agreed with the figure for the median, he wished to draw attention to the fact (T88.42):
"...I think the reference shows that the chickenpox incubation period certainly is normally distributed and therefore half of cases would have an incubation period greater than the median and half less than the median."
Professor Curtis went on to point out that the incubation period for chickenpox in an event of household contact, could be anything from 10-20 days. He accepted, as I have said, the median figure. He merely questioned the usefulness or its applicability in determining the specific position of Mrs King.
The defendant submits, based upon the mean period of incubation, that it must follow that Mrs King was infected with the VZV on either 1 or 2 May 2002. It submits that if infected on either of these days, the probability is that the infection occurred outside of 96 hours from the time of exposure to the virus.
It can be observed that this analysis relies upon facts which could not have been known to the staff at the Emergency Department of the Hospital when Mrs King presented on 6 May 2002. What was unknown to the staff was the date upon which, at some point in the future, if at all, Mrs King would show symptoms of having contracted chickenpox. Accordingly, the reasoning process which is relied upon by the defendant was not one which was open to the staff of the Hospital.
What was known to the staff at the hospital was that the first signs of chickenpox had been observed in Mrs King's elder daughter on the day prior to her attendance. In other words, her daughter had " ...developed chickenpox yesterday ". What was also known to the staff at the Hospital was that on the history which Mrs King gave them, she was not immune from becoming infected with VZV. That was because she told the staff " ...she does not believe she has had chickenpox ".
The evidence suggested that it was common knowledge for medical practitioners that a patient who had developed signs or symptoms of chickenpox was likely to be most infectious in the period 24 to 48 hours prior to the signs becoming apparent. This would mean that the period of exposure which was most likely to result in infection for Mrs King was in the period 24 to 48 hours before 5 May 2002, which was the date her daughter first showed signs of the infection.
On the basis that this was when exposure of the most relevant kind had occurred, this was well within the 96 hour cut-off period. It did not provide any reason to refrain, in accordance with accepted practice, from administering VZIG to Mrs King.
As well, the argument for the Hospital critically depends upon the proposition that Mrs King would have been infected at the time of the very first exposure to the infection in her daughter. However, as the evidence of Professor Curtis showed, by reason of there being a range in the number of days over which infection can occur before symptoms become visible in an individual, it is entirely possible that the very first time of exposure is not the time at which infection has occurred. In other words, in the case of Mrs King, the relevant exposure could well have occurred on the day before her presentation to the Emergency Department or the day before that. In other words, the relevant exposure could well have occurred between 24 and 48 hours prior to her presentation at the Emergency Department.
In those circumstances, this argument must fail. In order to succeed it was necessary for the hospital to prove that the relevant exposure was more than 96 hours before the morning of presentation on 6 May 2002. It has not done so and, on the facts before me, cannot do so.
The second argument by which the Hospital advanced its defence under s 5O was that the treatment accorded with Guideline 13 of the Royal College of Obstetricians and Gynaecologists. Relevantly, it reads at 3-4 (Ex L):
"6.3 In the pregnant woman who gives a history of contact with chickenpox
When contact occurs with chickenpox, a careful history must be taken to confirm the significance of the contact and susceptibility of the patient. If the pregnant woman is not immune to VZV and she has had a significant exposure, she should be given VZIG as soon as possible. VZIG is effective when given up to ten days after contact. ...
The history must be confirmed with particular respect to the certainty of the infection, the infectiousness (vesicular rash or development of rash within 48 hours of contact) and the degree of exposure (household, face-to-face for five minutes or indoors contact for more than 15 minutes). The UK Advisory Group on Chickenpox consider any close contact during the period of infectiousness to be significant. The susceptibility of the woman should then be determined by eliciting a past history of chickenpox. If there is a definite past history of chickenpox, it is reasonable to assume that she is immune to varicella infection. If the woman's immunity to chickenpox is unknown and if there is any doubt about previous infection, of if there is no previous history of chickenpox, serum should be tested for VZV IgG. ...
If the pregnant woman is not immune to VZV and she has had a significant exposure to chickenpox while the contact was infectious, she should be given VZIG as soon as possible. The administration of VZIG can be delayed until serology results are available. ..."
The defendant also relies upon the contents of Guideline 13 where it contains this statement in relation to serology testing:
"This can usually be performed within 24-48 hours and the virology laboratory may be able to use serum stored from booking ante-natal bloods."
The defendant submitted that, in 2002, a medical practitioner working at a public hospital in New South Wales, who was following the Guidelines, would have been entitled when treating Mrs King to undertake a treatment plan which included testing her for immunity and delaying the administration of VZIG until those serology results were available. It then submitted that if no immunity was present in the serology results, then VZIG could have been administered on 9 May 2002. The defendant submitted that this treatment plan was in effect what had occurred.
When examining this submission, it is important to record that in Ex C (the joint expert report) in answer to questions 32 and 34, all experts (except Dr Robert Jones who made no comment) were agreed that it would only have been acting in accordance with competent professional practice to defer administration of VZIG and to await results of serology testing to establish immunity, providing the results were available within six hours of the blood test having been taken.
Dr Davidson's notes from the emergency department referred to above at [32]-[33] describe a three day lag until the results would be either available to, or else acted on by, the obstetrician and gynaecologist at the ante-natal clinic. This is far in excess of the six hour time period, within which the experts agreed that a treatment plan of deferring ZVIG treatment until serology results were available, is acceptable.
As well, the Guideline posits a maximum period of 96 hours between exposure and VZIG administration. That is because it refers to contact between the patient and the infection within 48 hours and then it posits a maximum of 48 hours for the serum testing. Even if I were to ignore the joint expert view to which I have just referred, and I do not, the defendant's treatment, involving more than 96 hours between exposure and test results, did not comply with the guidelines.
Finally, I note that the defendant did not attempt to prove any of the necessary factual material about when the blood specimen of Mrs King was actively tested. It did not tender the printed report of the results of the test, which would demonstrate the date of collection and testing. An example of such a printed report is to be seen in Ex G, the hospital notes at p315. Nor did the defendant attempt to prove what the standard time period was at the Hospital in May 2002 for the processing of, and reporting upon, blood tests.
It is therefore not open for the defendant to rely on adherence to the above Guideline, and this submission also fails.
In conclusion, the submissions by the defendant that it is not liable in negligence via operation of s 5O of the Civil Liability Act cannot be supported.
Causation
It is now necessary to move to the issue of causation, because, even though I have been satisfied that the plaintiff has proved the existence of a duty of care and a breach of that duty, it is necessary that the plaintiff prove that the breach of duty caused, or materially contributed to, her suffering CVS.
Legal test - s 5D
It is appropriate therefore to firstly identify the legal test which the plaintiff is obliged to discharge in accordance with the Civil Liability Act . In claims of this kind, s 5D of that Act now prescribes the relevant test: see Adeels Palace at [41]-[44]. The common law test has no role to play.
Section 5D says:
" 5D General principles
(1) A determination that negligence caused particular harm comprises the following elements:
(a) that the negligence was a necessary condition of the occurrence of the harm ( factual causation ), and
(b) that it is appropriate for the scope of the negligent person's liability to extend to the harm so caused ( scope of liability ).
(2) In determining in an exceptional case, in accordance with established principles, whether negligence that cannot be established as a necessary condition of the occurrence of harm should be accepted as establishing factual causation, the court is to consider (amongst other relevant things) whether or not and why responsibility for the harm should be imposed on the negligent party.
(3) If it is relevant to the determination of factual causation to determine what the person who suffered harm would have done if the negligent person had not been negligent:
(a) the matter is to be determined subjectively in the light of all relevant circumstances, subject to paragraph (b), and
(b) any statement made by the person after suffering the harm about what he or she would have done is inadmissible except to the extent (if any) that the statement is against his or her interest.
(4) For the purpose of determining the scope of liability, the court is to consider (amongst other relevant things) whether or not and why responsibility for the harm should be imposed on the negligent party."
Senior Counsel for the plaintiff eschewed reliance on s 5D(2) and did not submit that the case was an exceptional one to which those provisions applied (T206). Accordingly, in this judgment there is no need to further consider those provisions.
Neither party submitted that it was not appropriate for the scope of the defendant's liability, if established, to extend to the plaintiff's CVS. Scope of liability (s 5D(1)(b)) was not an issue in the proceedings and can also be put to one side.
The "particular harm" which is necessary to be identified by the introductory words in s 5D(1) requires attention at the outset. It is necessary to note that when considering this phrase at this stage, it is quite separate from the phrase " risk of harm " used in s 5B of the Civil Liability Act , and to which I have earlier referred.
The " particular harm " which the plaintiff suffered must be identified with clarity, so that the question of whether that harm was caused by the offending negligence can be addressed.
Here, the plaintiff claimed that the harm that she suffered was a physical one, namely CVS. She claimed that she suffered CVS as a consequence of her mother having contracted VZV on 15 May 2002, whilst pregnant with the plaintiff.
As I have earlier held, the relevant breach of duty or negligence on the part of the Hospital was its failure, on 6 May 2002, to offer Mrs King an injection of VZIG together with the appropriate advice about its intended effect, its benefits and any adverse effects.
The question of causation in this case is encompassed by the term " factual causation " as used in s 5D(1)(a). Factual causation must be established by the application of the "but for" test: Adeels Palace at [55]; Wilson v Nilepac Pty Ltd [2011] NSWCA 63 at [132] per Tobias JA (Beazley JA agreeing).
Senior counsel for the plaintiff accepted (T182) that the central factual causation issue was properly described in this way:
Had, on 6 May 2002, the medical staff at Blacktown Hospital, appropriately advised about and administered 600 international units of VZIG to Mrs King, the plaintiff's mother, she would, on the balance of probabilities, not have contracted varicella on 16 May 2002.
Intermediate issue
Before proceeding further with the analysis of factual causation, it is necessary to deal with an intermediate issue, which requires a finding about a hypothetical fact. I have held that Mrs King ought to have been advised about, and offered the immediate administration of, VZIG on 6 May 2002. The intermediate and hypothetical issue, which must be determined, is whether, if so advised and if VZIG was offered to be administered, Mrs King would have accepted administration of the VZIG.
In her statement, Ex A, Mrs King said this with reference to ZIG at [53]:
"If I had been informed that such an injection could help myself, and in turn my unborn child I would have without any doubt had such an injection."
This statement was undoubtedly one which was influenced by hindsight. She was not cross-examined on it.
As Kirby P said in Ellis v Wallsend District Hospital (1989) 17 NSWLR 553 at 560E:
"However honest the patient may try to be, self-interest and the knowledge of the misfortunes that have followed the treatment will necessarily colour the patient's response to that question."
However, I see no reason why I would not accept the statement of Mrs King. The statement does not strike me as inherently improbable, as an illogical or unlikely response to the issue. After all, Mrs King was sufficiently concerned to mention the issue during her attendance at the Hospital. She allowed blood to be drawn for testing. The benefits of being administered VZIG were clearly able to be identified and communicated to her by the Hospital staff. Whilst it is not a totally benign injection, no significant adverse effects were identified in the evidence. I am satisfied that if, after securing adequate advice, Mrs King had been offered the administration of VZIG on 6 May 2002, she would have decided to receive that injection.
I regard the fact that senior counsel for the defendant did not cross-examine Mrs King on the statement which I have referred to earlier in this judgment at [ 153 ], as enabling the evidence to be regarded with a greater degree of assurance than might otherwise have been the case: Paric v John Holland Constructions Pty Ltd [1984] 2 NSWLR 505 at 507 per Samuels JA Huntley and Priestley JJA agreeing); Ellis at 586D-589C per Samuels JA (Kirby P and Meagher JA agreeing); Poricanin v Australian Consolidated Industries Ltd (1979) 2 NSWLR 419 at 426 per Hope and Glass JJA.
Further, the defendant did not submit that the evidence ought to be rejected, or else not accepted. Since, prima facie, unchallenged evidence ought, unless contradicted by other evidence, or else unless illogical or inherently improbable, be accepted: Ali v Nationwide News Pty Ltd [2008] NSWCA 183 at [112] per Tobias and McColl JJA, I am satisfied that the evidence of Mrs King on this issue ought be accepted.
The Central Causation Issue - Likely Effectiveness of VZIG for Mrs King
This finding means that in determining factual causation the central issue is, in short, whether, if administered, the VZIG would have been effective to prevent Mrs King being infected with VZV. I have set the issue out more compendiously at [151].
It is convenient to remind myself in this context of the principal factual setting that I have already found, namely that Shania was infected from 3 May 2005 onwards, and Mrs King was exposed to the varicella virus from that time until her visit to Blacktown Hospital on 6 May 2005.
In order to prove her case on causation, the plaintiff relied upon both scientific and expert evidence. The scientific evidence consisted of the reports of a variety of learned studies which are to be found in the medical and scientific literature. She also relied upon expert evidence from various medical practitioners with the appropriate expertise.
In accordance with principle, the proof of causation involves examining, and taking into account, all of the evidence. It is not a matter of simply looking at the scientific evidence, although that is clearly relevant: See Seltsam Pty Ltd v McGuiness (2009) 49 NSWLR 262.
As well, the plaintiff called in aid the application of common sense having regard to the desirable practice of administering VZIG to pregnant women and the many widely accepted recommendations to that effect.
Scientific and Expert Evidence
The Court took evidence concurrently from a panel of six experts. They had produced a joint report (Ex C), as a result of conferring together prior to the commencement of the hearing.
The panel consisted of:
(a) Two paediatric infectious disease experts: Professor Curtis from The Royal Children's Hospital, Melbourne in Victoria and Associate Professor Kesson from The Children's Hospital, Westmead in New South Wales;
(b) Dr Hudson who is an adult infectious diseases physician at the Royal North Shore Hospital;
(c) Professor Trudinger who is a qualified obstetrician and gynaecologist and is the head of the Maternal Foetal Medicine Service at Westmead Hospital;
(d) Professor Gillian Turner who is a highly experienced clinical geneticist, and
(e) Dr Robert Jones, who is a most experienced paediatric neurologist.
Dr Robert Jones took only a very minor role in the concurrent evidence. He expressed an opinion on the issue of whether the symptoms from which Tamara now suffers amounted to CVS. He otherwise did not feel able to offer any opinion because of his lack of expertise.
I note that the experts agreed that their opinions about the likely effectiveness of VZIG were limited to a maximum elapsed period of 96 hours from the time of exposure.
The factual causation question, which I have set out above in [151], was addressed to each of the experts directly at T141.39. It is convenient if I encapsulate their answers:
(a) Professor Curtis: "... on the balance of probabilities [the chickenpox] would have been prevented ..." (T143.7-8);
(b) Professor Turner: "... 50 per cent chance that [the administration of VZIG would] stop [the patient] getting varicella ..." (T143.37-38);
(c) Professor Trudinger: "... uncertain what benefit there was ..." (T145.18);
(d) Associate Professor Kesson: "... less than 50 per cent [and as time progresses, effectiveness] becomes less and less and less ... until it would have no effect ..." (T145.33);
(e) Dr Hudson: "... my answer to, is it more likely than not, is no" (T146.20);
(f) Dr Jones did not express any opinion on this issue.
It is to be observed that only Professor Curtis was prepared to advance the view that it was more likely than not that if the VZIG had been administered, Mrs King would not have developed varicella. The plaintiff submitted that I would accept the opinions of Professor Curtis in preference to the other expert opinions.
It is necessary therefore to examine carefully the opinion of Professor Curtis, to see if it ought be accepted.
Professor Curtis' evidence
The basis for Professor Curtis' view seems to include a combination of all of the following:
(a) the statistics contained in the table which was reproduced in answer to question 21 in the joint report (Ex C), which in turn was derived from Table 16.7 in Gisela Enders and Elizabeth Miller's chapter "Varicella and herpes zoster in pregnancy and the newborn" in Arvin et al (2000) at 335 (Ex L). It will be convenient to refer to this as the Enders Table;
(b) studies to which he referred in Table 3 of his report of 17 March 2008 (Ex D, appendix page 5);
(c) studies to which he referred in Table 4 of his report of 17 March 2008 (Ex D, appendix page 6); and
(d) his own clinical experience.
I will now examine each of these sources upon which Professor Curtis has relied.
The Enders Table
The Enders Table was relied upon to provide the principal source for Professor Curtis' opinion. He interpreted the Table to demonstrate by that:
"...VZIG prevented infection in 54% of women given VZIG1-2-3 days after exposure - therefore on the balance of probabilities the plaintiff's mother would not have been infected with chickenpox." (Ex C, footnote pp32-33).
Professor Curtis also made it clear in the course of his oral evidence that he regarded the figures in the Enders Table as being conservative, and that VZIG is more effective than those figures show.
An analysis of the Enders Table, the views expressed about it and the conclusions that can be drawn from it, is necessary.
The Enders Table was contained within a publication which all experts accepted was a peer-reviewed publication of appropriate standing by authors accepted as experts in the field. There were a number of features of the Enders Table about which the experts made comment including that:
(a) it was not compiled from the results of a randomised controlled clinical trial, but rather it was derived from one or more observational studies ("the study quality issue");
(b) the dosage used for the patients in the studies was 1750 international units of VZIG, whereas the standard dose used in Australia in 2002 was 600 international units which was the dose which ought to have been administered to Mrs King ("the differential dosage issue"); and
(c) the Table did not, in reproducing the numbers of patients who avoided being infected with varicella, take into account those who would have failed to become infected, even if they did not receive VZIG ("the virus strike rate issue").
I will examine each of these issues, in turn, to see what effect if any, they have on the Enders Table and conclusions to be drawn from it.
The Study Quality Issue
In the field of medicine there are different types of studies or trials which can be carried out. The results of these studies and trials are then used and relied upon for many reasons, including the formulation of public health policy or practice guidelines in accordance with evidence based practice. The studies and trials are also used as a basis for further research.
The July 2001 Guidelines on " Chickenpox in Pregnancy " of the Royal College of Obstetricians and Gynaecologists (Ex L at 8), describe the level of evidence obtained by the various studies in this way:
" Classification of evidence levels
Ia Evidence obtained from meta-analysis of randomised controlled trials.
Ib Evidence obtained from at least one randomised controlled trial.
IIa Evidence obtained from at least one well-designed controlled study without randomisation.
IIb Evidence obtained from at least one other type of well-designed quasi-experimental study.
III Evidence obtained from well-designed non-experimental descriptive studies, such as comparative studies, correlation studies and case studies.
IV Evidence obtained from expert committee reports or opinions and/or clinical experience of respected authorities."
The studies which have resulted in the Enders Table are, in essence, observational studies. They are not randomised control trials. They would fall into the category of Level III evidence.
To that extent, if other studies, of a higher evidentiary level were available, they would form a much sounder basis for drawing scientific conclusions.
However all of the experts agreed that notwithstanding this categorisation of the study, and the fact that 212 patients was a relatively small number for statistical satisfaction, the Enders Table was the best available material from which to understand the effects of VZIG in pregnant women.
I will keep in mind that the nature of the Enders Table is that it is derived from Level III evidence, but I do not draw any specific inference adverse to it or the conclusions expressed in it, from that fact.
The Differential Dosage Issue
This issue arises because of different practices around the world about the dose administered, as a matter of routine practice, of VZIG to non-immune pregnant women who have been exposed to VZV.
The routine dosage in Germany, in the patients included in the Enders Table, was 1750 international units. The recommended and routine dosage administered to patients in Australia was, in 2002, 600 international units. In the United Kingdom, the typical dose is 700 international units.
Thus the issue was raised in the course of the concurrent evidence about what, if any, allowance ought to be made to the statistical results in the Enders Table, and in the interpretation of it, to account for this significant difference in dosage practices, when applying the results to the practice in Australia in 2002.
Associate Professor Kesson in her evidence described the effect of VZIG in this way (T101.10):
"The effect of [VZIG] at 600 international units per adult dose, could be both to attenuate disease and to prevent infection. However, I think it is more likely to attenuate infection than prevent disease."
She used the expression "attenuate" to mean to reduce, or lessen, the adverse effects of the disease.
Dr Hudson gave evidence to a similar effect (T101.19):
"... [I]t is known that the higher dose is more likely to prevent infection and therefore attenuation of the disease is more likely to be seen with a lower dose than with a higher dose."
The other experts did not proffer any contradictory views to these expressions of general opinion which I accept.
There is a sound basis for these opinions, as Associate Professor Kesson explained, again without demur from the other expert witnesses, namely that the work which VZIG does as an antibody to counteract the VZV is "... just a numbers game " (T104.14).
Her fuller explanation, which I accept, is worthy of reproduction (T104.4-T104.21):
"But I would say from a pathophysiological point of view that what you are trying to do with antibody is prevent establishment of infection and what you do with cellular immunity is [to] clear, established infection. They are different arms of the immune response. So here we are trying to prevent establishment of infection. When one initially gets exposed to varicella, there will be a fixed amount of virus particles or virions, to which one is exposed. And if you have antibody, there is a fixed amount of antibody which you either had in your body, because you are immune, or that we administer to you as a form of passive immunity.
And this is basically a numbers game, and if there is not sufficient antibody to neutralise, which is an immunological concept to prevent establishment of infection, to neutralise the virus, then the virus will continue to replicate. So as time goes on from the point of exposure in your body and its entering cells and replicating, you're generating more and more virus particles. So it is just a numbers game. This is why antibody has no therapeutic effect when infection is established, because there are so many virus particles, compared to the antibodies."
The evidence of Associate Professor Kesson is supported by the conclusions reached, and the remarks of Dr Enders in her 2000 publication. At 335, Dr Enders discusses the fact that in the United Kingdom typically preparations used have 700 international units per dose, and in Germany between 1750 international units and 2000 international units.
Of the United Kingdom experience, Dr Enders says:
"Their effect is to attenuate disease rather than prevent infection (Miller et al., 1993)."
Of the German experience, Dr Enders refers to the Table and says:
"According to our experience in 212 seronegative pregnancies, about half of the mothers have clinical varicella virus if VZIG is given in the recommended dosage ... and a further 5% have subclinical infection."
As I see it, the end point of the differential dosage issue is that when considering the application of the Enders Table to Australian practice, where a much smaller dosage is used, it is likely that some of the people who are recorded in the Table as showing no infection, would, in the Australian context, have been likely to have been infected with varicella because the lower dose would not have prevented the infection, although it may have attenuated it.
It is not possible to now be precise about how many people that would have been. Accordingly, it is not possible to adjust with accuracy the actual numbers in the Enders Table to account for this issue. However, it is clear that with a lower dosage of VZIG a larger number of patients in any identified cohort are likely to be infected, than those in the cohort studied in the Ender Table.
The result is that in applying the results of the studies recorded in the Enders Table to the Australian practice, I am satisfied that if only 600 international units were administered, then a higher number of the patients would have been infected with VZV than was shown in the Table.
It follows that the Table overstates the effectiveness of VZIG in VZV prevention when considering its application to the Australian administration practice.
The Virus Strike Rate Issue
It was accepted by all of the experts that it was well established that for significant exposure to VZV infection, such as household contact, there was likely to be an 85 to 90 per cent strike rate of infection with the virus. In other words, where there has been household contact, statistics over time demonstrate that only 85 to 90 per cent (and not 100 per cent) of individuals who were not immune to VZV are likely to become infected. The corollary of this is that 10 to 15 per cent of those exposed and non-immune individuals will not be infected.
It was also accepted by the experts that administration of VZIG itself did not cause anyone to become infected with varicella. After all, only antibodies are being administered, not the virus itself.
It therefore follows that, in understanding the Enders Table and what conclusions can be drawn from it, it was necessary to accept that of the total group of 212 exposed non-immune individuals to whom VZIG was administered, 10 to 15 per cent would not have been infected in any event, even if VZIG had not been administered. It is appropriate to take the more conservative figure of 10 percent, in adjusting the Enders Table so as to understand the consequences of the virus strike rate issue. In other words, of the 212 group members, 21 of them would not have been infected with varicella regardless of the administration of VZIG. That is, the administration of VZIG had no causal relationship with their not being infected with the virus.
Professor Curtis agreed that it was appropriate to adjust the Enders Table to take account of the virus strike rate issue. However, he suggested that the only adjustment which needed to be made was to the "non infected" group of 84 (T161, T173). However, I think that he was mistaken in this view. The issue was raised for the first time during the course of the evidence by Dr Hudson. I had the distinct impression that Professor Curtis had not previously considered the matter and so had only a brief time to consider the real impact of the virus strike rate issue. Having heard submissions on the issue from counsel and had time to carefully consider the matter, I am satisfied that it is correct to adjust the Enders Table by reference to the virus strike rate issue consequences on the whole group of 212 people, and not just the "non-infected" group.
Adjusted Table
It is appropriate to set out the Enders Table in a way which demonstrates the original figures, and those adjusted for the effect of the strike rate issue.
| ENDERS TABLE 16.7 (Ex M) | |||||||||||
| UNADJUSTED FOR STRIKE RATE | |||||||||||
| OUTCOME | |||||||||||
| TOTAL | INFECTION | NO INFECTION | |||||||||
| VZIG administration after exposure | (n) | (n) | (%) | (n) | (%) | ||||||
| TOTAL | 212 | 98 | 46 | 114 | 54 | ||||||
| ADJUSTED FOR VIRUS STRIKE RATE (10%) | |||||||||||
| OUTCOME | |||||||||||
| TOTAL | NO VIRUS STRIKE | INFECTION | NO INFECTION | ||||||||
| VZIG administration after exposure | (n) | (n) | (%) | (n) | (%) | (n) | (%) | ||||
| TOTAL | 212 | 21 | 10 | 98 | 46 | 93 | 44 | ||||
Conclusions to be drawn from the Enders Table
I do not accept the view of Professor Curtis, that the Enders Table demonstrates that more probably than not, the administration of 600 international units of VZIG to a non-immune pregnant woman who has been exposed to chickenpox, will prevent the woman becoming infected with varicella.
Without making any adjustments because of the differential dosage issue which are difficult, if not impossible, to quantify with precision, but merely to make the adjustments, to which all experts agreed in principle by reason of the virus strike rate issue, the Enders Table, as the best available scientific evidence, demonstrates that infection was prevented by the administration of VZIG in fewer than one half of the studied cohort. Put another way, notwithstanding the administration of VZIG, over one half of the studied cohort were infected with chickenpox.
Thus I conclude, based on this Table alone, that it has not been proved, more probably than not, across a population, that if VZIG had been administered it would have prevented infection. The Table does, however, clearly demonstrate that it was possible that infection may have been prevented.
It is important to note that even if I had concluded that the Enders Table had demonstrated that more patients in the cohort had not been infected if they had received VZIG than if they had not received it, whilst ever the numbers who did get infected, were at a level higher than an insignificant one, that would not have been sufficient to draw the conclusion which Professor Curtis did. It is important to note that even if I had concluded that the Enders Table supported the finding that it was probable that VZIG administration prevented chickenpox across a population, that would not have been sufficient of itself to draw the conclusion which Professor Curtis did that it was probable that ZVIG would have prevented Mrs King from contracting chickenpox.
The reason for this is that, in the context of this case, the question which is essential to be answered is what would have happened to Mrs King as an identified individual, and not just what would have happened across a population.
The difference between the effect across a whole population, and on an individual can be demonstrated by reference to the numbers in the unadjusted Enders Table which is reproduced at page 15 of the joint expert report (Ex C), in answer to question 21. Those figures demonstrate that of the cohort of 212, 114 or 54 per cent did not have any infection, whereas 98 or 46 per cent had a form of the infection. If one were to apply this infection prevention rate to a population of 100 people each of whom were infected with VZV and who did not receive VZIG, then the study demonstrates that 46 (or 46 per cent) of that group would have been infected even if they had received VZIG.
But in which of theses groups would Mrs King be found? That question is not answered simply by translating the scientific result to the legal test of causation.
That is because if one assumes that each member of the infected cohort were to bring proceedings which would be resolved on the approach taken by Professor Curtis, then all members of the cohort would succeed in law in proving causation. But it is clear that 46 per cent of them would have been infected notwithstanding the administration of VZIG. Clearly, that conclusion would not reflect the reality of the Enders Table and would distort the result.
This comes about because the law regards proof as sufficient on the balance of probabilities. However, the law does not necessarily accept that without more, one can properly apply the results of such a population study to any one individual within a population. General causation, which is the only conclusion open on the Enders Table, whether adjusted or not, is only evidence of possibility and not probability: Seltsam at [60], [78] per Spigelman CJ (Davies AJA agreeing).
This principle alone is sufficient to dispose of Professor Curtis' opinion. However, as I have explained, when correctly adjusted, the Enders Table does not do the work attributed to it by Professor Curtis.
But that conclusion does not entirely dispose of the plaintiff's claim. There are other factors to be considered before a final determination can be made on the question of factual causation.
I will now turn to the two other factors relied upon by Professor Curtis, to which I have made reference at [171] above, and to one final factor relied upon by the plaintiff, which are:
(a) the other studies referred to in Tables 3 and 4 of Professor Curtis' report of 17 March 2008 (Ex D). The full details of the articles, including their full names and authors and details of publication are provided at Appendix pages 5 and 6 of the report;
(b) Professor Curtis' own clinical experience;
(c) the inferences to be drawn from either the common practice of administration of VZIG to pregnant women exposed to varicella, the guidelines for administration of VZIG, and the generally held beliefs within the medical profession about the effectiveness of VZIG when administered within 96 hours of exposure. I will refer to this last issue as the common sense approval.
Other Studies
In Table 3 of his report of 17 March 2008, Professor Curtis summarises the results of four studies. Some discussion of each of these studies is necessary.
It needs to be observed, as Professor Curtis noted, that the studies are examining the effects of VZIG when administered in quite different contexts to that involved with the plaintiff's claim in this case. He also noted that they were studies which examined both prevention and attenuation (or amelioration) of the infection. The plaintiff's case here relates only to prevention of infection in her mother. She makes no claim with respect to the consequences of VZIG attenuating the disease.
Miller et al: Lancet (1989)
Miller, et al. Outcome in newborn babies given anti-varicella-zoster immunoglobin after perinatal maternal infection with varicella-zoster virus. Lancet 1989;12:371-3 was a study of 280 surviving infants whose mother had either chickenpox or herpes zoster during the peri-natal period (that is, during the last 28 days of pregnancy or the first 28 days post-delivery). The infants were given VZIG shortly after birth or the onset of postnatal maternal chickenpox.
The study found that 169 (or 60 per cent) of the infants were infected with chickenpox, 35 (or 13 per cent) of whom were without clinical features.
The following conclusions can be drawn from the study:
(a) VZIG did not prevent infection in the majority of cases in which it was administered;
(b) there was a particularly high infection rate (64 per cent) for babies exposed during the last week of pregnancy or first four weeks after birth with VZIG being administered within 72 hours of birth or contact.
The authors concluded at 373:
"We have shown that severe varicella can occur in 14% of infants ... despite the use of VZIG. This finding together with the occasional deaths reported in VZIG-treated infants, underlines the need for more effective measures to prevent or attenuate infection."
Hanngren et al: Scandinavian Journal of Infectious Diseases (1985)
This study, K Hanngren, et al. Effect of zoster immunoglobulin for varicella prophylaxis in the newborn. SJID 1985;17(4):343-7 seems to produce quite different results from those reported in the Brunell 1969 study to which I refer later.
The authors established that 50 per cent of 95 neonates given ZIG for prophylaxis, born to mothers with perinatal varicella, developed varicella.
The article itself was not tendered and accordingly, I cannot make any assessment of the conclusions in it. The entirety of the evidence about these results of the article is as I have just stated.
Hanngren et al: Scandinavian Journal of Infectious Diseases (1983)
This article was not tendered in evidence. No assessment can be made of it except by reference to what others have said about it.
Hanngren, et al. Zoster immunoglobulin in varicella prophylaxis. A Study amongst high-risk patients. SJID 1983;15(4):327-34, was in a study of 173 individuals who were not immune to VZV, the majority of whom were also immunocompromised, in whom the administration of VZIG had success in preventing varicella infection in a high proportion of cases. Professor Curtis noted that the infection was prevented in 80 per cent of cases. It is not clear if the cohort of patients were adults or children. If they were children, the results of this study would seem to reflect Professor Curtis' own clinical experience.
As well, it is necessary to keep in mind that as Dr Phillip Brunell says, the definition in medical science of an immunocompromised patient may not be precise. Some patients within that description may be more likely to become infected than others (Ex L, Brunell 2000) .
Whilst I note the study and its findings, I find it difficult to accord it much weight in understanding its possible application to the issues in this case in the absence of further detail. In short, without more, it does not provide much support for Professor Curtis' views.
Brunell et al: The New England Journal of Medicine (1969)
This study, Brunell, et al. Prevention of varicella by zoster immune globulin. N Engl J Med 1969;280(22):1191-4, involved twelve children, two each from six families. The children were aged between 21/2 years and 6 years. One child in each family was given human immunoserum globulin (IsG). The other ZIG. Results were compared.
The authors concluded that administration of ZIG to susceptible children (that is, those exposed to household contact within 72 hours) prevented clinical manifestation of infection. The study did not detect any antibody response in these children. The administered dosage of ZIG was not recorded in international units.
The authors said at 1193:
"... The absence of both clinical signs and detectible antibody responses suggests that passive immunisation with ZIG resulted in prevention rather than modification of infection."
The study provides useful data for the effect of ZIG in young children particularly when compared with IsG. However, the numbers enrolled in the study are very small, and accordingly, the significance of the results in an application to the broader population is open to question.
Conclusions to be drawn from the Table 3 Studies
The studies identified in Table 3 of Professor Curtis' report can be accepted as demonstrating that:
(a) in the case of peri-natal chickenpox (that is, 27 days before to 28 days after birth), where VZIG was administered to the newborn, between 50 per cent and 61 per cent developed infection but the infection was, on the probabilities, attenuated;
(b) in the case of older children (ie, aged between 21/2 years and 6 years), ZIG was successful in preventing varicella in all six cases in which it was administered;
(c) in the case of immunocompromised patients, VZIG was successful in preventing varicella in 80 per cent of the patients.
These studies do not, and Professor Curtis does not himself, suggest that the results are capable of direct application to the segment of the population in which Mrs King fell (that is, non-immune pregnant women). Nor do they suggest direct application to the Australian experience, because of the potential for differential dosages.
The evidence does not identify any particular reason for the disparity in results between the newborn cohort with perinatal exposure and infection, and the other two cohorts.
I am not able to find in any of the expert evidence and other material dealing with these studies any explanation for the difference in the study results, save to note that it seems clear that VZIG works differentially in different groups of patients to whom it is administered. These studies, by themselves, do not compel a conclusion, on the balance of probabilities that in the relevant cohort, that is, non-immune pregnant woman, VZIG will prevent varicella infection. They do provide some additional material about the effectiveness of VZIG in different cohorts.
Table 4 of Professor Curtis' Report of 17 March 2008
This Table identifies three studies which report the results obtained in preventing maternal varicella. It is appropriate to examine the studies.
Evans et al: The Lancet: 1980
This study, Evans, et al. Human anti-chickenpox immunoglobulin prevention of chickenpox. Lancet 1980;1:354-6, which followed patients to whom ZIG had been provided by a particular laboratory in the United Kingdom.
Of a total of 206 patients, who were followed up, 39 were adults. So far as this group were concerned, the study reported as follows (at 356):
"Thirty-nine adults were given Zig after contact with chickenpox or zoster. Nine were pregnant and the remainder immunosupressed or had malignant disease. Thirty-five of these thirty-nine adults had V-Z antibody in their pre-immunoglobulin blood-sample. Three of those without antibody were in their early twenties, and the other was aged 71. None developed chickenpox, but one woman who was pregnant became seropositive without overt illness."
The study concluded that the efficacy of ZIG to prevent chickenpox was not established. The authors caution that when assessing the value of immunoglobulin, the efficacy of the material can be overestimated without the immune status of the patient being ascertained.
This caution seems to me to have been overlooked by Professor Curtis who relies on the article to conclude that no individual developed chickenpox as a result of the administration of ZIG. The difficulty with this conclusion is that 35 out of the 39 adults were already immune to the varicella-zoster virus before the ZIG was administered. They were not at risk of infection. I do not accept that the value of ZIG can be assessed in these individuals.
One of the other four patients was a 71 year old whom I am prepared to conclude was not one of the nine pregnant women. Of the remaining three women who may have been pregnant, they were each in their early 20s, only one of whom was identified as pregnant and had evidence of varicella infection without clinical symptoms. No conclusion is available about the other two women.
I do not regard the study as providing any evidence about the value of ZIG in preventing maternal varicella, in non-immune women. I reject Professor Curtis' view that the study provides support for determining the effectiveness of preventing maternal varicella in non-immune women, and by extension in the circumstances of this case.
Enders et al (1984)
The comments of Professor Curtis in his Table 4, suggests that this study, Enders, et al. Varicella-zoster virus infection in pregnancy. Prog Med Virol 1984;29:166-196, had a small cohort of 12 non-immune women, seven of whom received ZIG and did not develop chickenpox, the other five of whom did not receive ZIG and of those five, four developed chickenpox.
Important factors such as dosage, time of exposure, timing of receipt of ZIG, and whether the study examined only clinical and not subclinical infection with varicella, are entirely unknown. As I understand it, this cohort of 12 women was included in the cohort of 212 women repeated in the Enders Table.
The report of the larger cohort would, in any event, be a far more reliable basis for judging the effectiveness of VZIG.
Enders et al: (1994)
Enders, et al. Consequences of varicella and herpes zoster in pregnancy: prospective study of 1739 cases. Lancet 1994;343:1548-51 was a large prospective study in Germany and the United Kingdom over a 13 year period involving a cohort of 1,739 women, 1,373 of whom had chickenpox and 366 of whom had herpes zoster during the first 36 weeks of pregnancy.
The study established that the risk of CVS following maternal infection was about one per cent during the first 20 weeks of gestation. The highest risk, which was about two per cent, was observed between 13 and 20 weeks gestation.
The authors concluded:
"Post-exposure prophylaxis with varicella zoster immune globulin attenuates disease and there was evidence from the present study that it may also reduce the risk of fetal infection."
The report of the study does not reveal whether the cohort of pregnant women were administered VZIG at any stage. Since the cohort consisted of pregnant women who contracted chickenpox or herpes zoster, had it included universal administration of VZIG within a short time after exposure, the size of the cohort ought to have provided compelling scientific results. But it did not.
As Professor Curtis reports, there were 97 cases within the cohort in which maternal varicella infection followed administration of post-exposure VZIG. But it is not possible to draw meaningful conclusions from this statement alone because the study does not reveal how many of the cohort received VZIG.
Conclusions to be drawn from the Table 4 Studies
From these studies, referred to in Table 4 of Professor Curtis' report, I am unable to draw any conclusion which assists in the resolution of the issue posed in this case.
I do not accept that they provide any support for, nor do they detract from, the opinions expressed by Professor Curtis. However, they do add to a limited extent, to the general knowledge base of VZIG effectiveness.
Clinical Practice
In the course of evidence, Professor Curtis said that his personal observations of the effectiveness of VZIG in the course of clinical practice were that it was highly effective to prevent varicella infection.
At T151.36, Professor Curtis said this:
"... in my everyday practice we give VZIG to children who are severely immunocompromised, children with cancer who have no immunity whatsoever. It is a highly effective product. It is considered a medical emergency to treat those patients and I have never seen VZIG fail in those circumstances. So I have a much higher opinion of VZIG, based on my personal observation and on the literature. I see [the Enders] table as providing conservative estimates."
In the course of her evidence, Associate Professor Kesson who had a clinical practice similar to that of Professor Curtis, agreed with the view which Professor Curtis had expressed, that in immunocompromised children, VZIG is "... efficacious and will ameliorate or prevent infection in a significant proportion of patients " (T155.38).
However, she expressed the view that (T155.40):
"I don't think that [this clinical practice] is analogous to this situation of giving VZIG to a pregnant woman to protect the foetus, because we have no data whatsoever that it is efficacious".
As I understand that evidence, what Associate Professor Kesson was saying was that the nature of the clinical practice in which she and Professor Curtis were each engaged, was not comparable with a clinical practice which would have included pregnant women such as Mrs King. Hence, their clinical practice provided no basis for confidence about the effectiveness of VZIG in the cohort of patients of which Mrs King would be a part.
Professor Curtis did not contradict the evidence to which I have referred above.
Later in the evidence, I asked the panel a question in order to identify the comparability, generally, of immunocompromised patients and pregnant women (T171.49-172.1). Associate Professor Kesson answered that, strictly speaking, pregnant women were immunocompromised by reason of their pregnant state but that in a practical sense, in terms of their vulnerability to varicella, they were not immunocompromised patients. There was no disagreement in principle from the other experts with this answer.
Whilst I accept that Professor Curtis and Associate Professor Kesson in the course of their clinical practice of treating severely immunocompromised children have found VZIG to be highly effective in preventing or ameliorating varicella infection, I am not satisfied that it is a sufficient basis for concluding that VZIG is more likely than not to be effective in preventing varicella infection in pregnant women, generally, or Mrs King in particular.
Summary of the Opinion and Evidence of Professor Curtis
I do not accept Professor Curtis' view that it is more likely than not that had VZIG been administered to Mrs King on 6 May 2002 she would not have contracted chickenpox.
Although the reasons for this appear from the lengthy discussion which precedes this part of the judgment, it is perhaps best to repeat them, in short form:
(a) the Enders Table, when adjusted properly to reflect the virus strike rate issue, in fact demonstrates that VZIG did not prevent infection in over half of the studied cohort;
(b) other adjustments ought properly to be made to the results of that Table which cannot now be precisely quantified, which would have the effect of making the prospect of VZIG preventing infection, if administered in Australia less likely than the results recorded in the Table;
(c) other studies, properly considered, do not support Professor Curtis' opinion;
(d) the observation in clinical practice of the effectiveness of VZIG in immunocompromised children does not assist in the elucidating the question about the effectiveness of VZIG administration to pregnant women within 96 hours of exposure to chicken pox.
Importantly, even if the Enders Table is accepted without adjustment, as Professor Curtis did, it does no more than provide a basis for an extrapolation across a population of the effectiveness of VZIG. It cannot be taken, without more, to directly apply to Mrs King. At best, it is circumstantial evidence of the possibility that in the case of Mrs King, if VZIG was administered, she may have avoided an infection.
I accept the opinions in which all experts agreed, including Professor Curtis, that it is possible that VZIG administered to Mrs King may have prevented her infection with chickenpox. I do not accept that it is more likely than not that it would have done so.
Commonsense Approach
Senior Counsel for the plaintiff, Mr Wheelahan QC, called in aid of proof of factual causation, in addition to the expert and scientific evidence two further matters, namely:
(a) the fact that the guidelines or recommendations for use of VZIG existed which, he submitted, suggested that VZIG was regarded as likely to be efficacious; and
(b) the fact of a broad prescription of VZIG would also supports its being likely to be efficacious.
I do not accept that either of these facts assists in the proof of factual causation in this case. They can be considered together because the broad based prescription of VZIG is guided by the recommendations and published guidelines.
The existence of guidelines or broad recommendations across a population, and the prescription of VZIG across a population, are both examples of steps taken for the protection of the population as a whole, and in particular that part of the population who are at risk of being infected with VZV.
However, the reasons for the publication and dissemination of a guideline and the practice which follows it, are likely to be informed by matters relevant to public health and not just the health of one or another individual. Much in the way in which vaccination programs are decided upon as being of an overall benefit to the public, so are measures such as those to which the plaintiff points.
VZIG may well be effective across a population. That was in substance the argument which Professor Curtis advanced. In order to be regarded in the public health sense as being effective across a population, it does not have to prevent infection in greater than one half of that population. In order to justify introduction by the publication of guidelines and subsequent prescribing practices, it may well be that the relevant authorities are satisfied if it is effective in a much lower percentage of cases. Matters of economics, and cost-benefit analysis are also relevant.
None of these issues were matters which the evidence directly addressed.
I would not be prepared to draw any inference with respect to any particular individual, and the effectiveness of VZIG, from the existence of the guidelines and the widespread practice of the administration of VZIG which follows it from the guidelines.
Summary on Causation
I have reached my conclusion on causation, namely, that whilst it is a possibility that VZIG, if administered to Mrs King, may have prevented her infection, it has not been proved that it was more likely than not to have been effective, by reference to the evidence.
This conclusion is consistent with the judgment of Spigelman CJ in Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262, and the approach to epidemiologic evidence which be there enunciated.
At [60] his Honour said in dealing with epidemiological studies this:
"Epidemiological evidence identifies associations between specific forms of exposure and the risk of disease in groups of individuals. Epidemiologists do make judgments about whether a statistical association represents a cause-effect relationship. However, those judgments focus on what is sometimes called in the epidemiological literature 'general causation': Whether or not the particular factor is capable of causing the disease. Epidemiologists are not concerned with 'specific causation': Did the particular factor cause the disease in an individual case?"
Having reviewed a series of scientific studies which were observational studies, the Chief Justice said at [78]:
"78. Epidemiology is ...concerned with the study of disease in human populations. It is not, of itself, directed to the circumstances of an individual case. For the purpose of determining whether exposure to a particular substance is the legal cause of a particular disease, epidemiology only provides evidence of possibility.
79. Evidence of possibility, including expert evidence of possibility expressed in opinion form and evidence of possibility from epidemiological research or other statistical indicators is admissible and must be weighed in the balance with other factors, when determining whether or not, on the balance of probabilities, an inference of causation in a specific case could or should be drawn. Where, however, the whole of the evidence does not rise above the level of possibility, either alone or cumulatively, such an inference is not open to be drawn.
80. The common law test of balance of probabilities is not satisfied by evidence which fails to do more than establish a possibility. ..."
In this case, the scientific evidence established a possibility of prevention of infection.
It is accordingly necessary to consider and determine whether there is any particular factor available on the whole of the evidence, which relates to Mrs King individually and which could form the basis of the conversion of a possibility which the evidence of Professor Curtis and the experts all support, to a probability that VZIG administered to her would have prevent her infection with VZV.
The plaintiff in her submissions did not refer to, or identify any fact, matter or circumstance in addition to those evidentiary facts and findings to which I have earlier made reference, which would support a conclusion that it was more probable than not that she would not have been infected with VZV if she has received VZIG.
The evidence about Mrs King's personal circumstances, her background, her state of health and her vulnerability or otherwise to infection was all very limited. There was nothing at all about any of that evidence which could support any conclusion of the necessary kind on the factual causation issue.
As consequence I conclude that the plaintiff has failed to demonstrate the necessary causal link between the breach proved of duty and her suffering from Congenital Varicella Syndrome.
Conclusion
Although, as I have said, the defendant owed to the plaintiff a duty to take care, and was in breach of that duty, I am not satisfied that the breach of that duty was causally related to the plaintiff's suffering Congenital Varicella Syndrome.
There must be a judgment for the defendant.
Orders
(1) Judgment for the defendant.
(2) Plaintiff to pay the defendant's costs.
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Decision last updated: 08 September 2011
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