Clinical Risk > Volume 14, Number 6 > Pp. 222-226

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Prenatal diagnosis

Wrongful birth claim for missed antenatal diagnosis of Fragile X syndrome

Anne Winyard and Dr Darren Conway

Email: awinyard{at}leighday.co.uk

	Abstract

Top Abstract Background What is Fragile X? DNA Genetic inheritance What causes Fragile X... Fragile X testing -... Fragile X testing guidelines Wrongful birth claims Quantum issues and what... References and notes

 
This is an account (by the two solicitors who acted for the Claimant Mrs A) of some of the key issues encountered in a recently settled ‘wrongful birth’ claim, arising out of failed antenatal genetic diagnosis of an inherited condition called Fragile X.

	Background

Top Abstract Background What is Fragile X? DNA Genetic inheritance What causes Fragile X... Fragile X testing -... Fragile X testing guidelines Wrongful birth claims Quantum issues and what... References and notes

 
Mrs A had two sons at the time she became pregnant with her third child. Her oldest son was healthy, but in the early stages of her pregnancy with her third child, her second son was diagnosed as having Fragile X syndrome.

Fragile X (FraX or FRAXA) is a potentially seriously disabling inheritable condition causing intellectual, behavioural and physical problems.

Mrs A and her husband were clear they did not wish to have a second child with Fragile X syndrome and therefore requested prenatal diagnosis. They had decided that if the fetus was affected by Fragile X, Mrs A would terminate the pregnancy.

Testing for Fragile X was performed in 1998 in the early stages of the pregnancy (on fetal material from a chorionic villus sample [CVS]) and was reported as ‘all clear’. Mrs A was advised that her baby did not have Fragile X syndrome, so went ahead with the pregnancy and gave birth to her third son in 1999. Mrs A, though not herself affected, was diagnosed as a carrier of the Fragile X gene.

The baby boy was delayed in reaching his milestones. Mrs A asked for re-testing but this was refused. She and her husband were told the ‘all clear’ antenatal testing was conclusive. When her third son was 4 years old, Mrs A was so concerned about him she insisted that he was genetically reviewed. The family had by then moved and were in the catchment area of a different genetic testing laboratory. The child's DNA was re-tested and in 2003 he was diagnosed as having Fragile X syndrome, like his older brother. He has substantial intellectual, behavioural and some physical disabilities because of his Fragile X syndrome.

Mrs A brought a claim in respect of the birth of her third son and the substantial costs of meeting, for his lifetime, his special needs (resulting from Fragile X syndrome). Liability was admitted shortly after the issue of proceedings and damages of £1.8 m were agreed earlier this year, about a month before trial.

Interesting issues arose both on liability (specifically the method employed to test the antenatal sample) and on quantum. Before describing these issues, we provide some brief background about Fragile X and its method of inheritance.

	What is Fragile X?

Top Abstract Background What is Fragile X? DNA Genetic inheritance What causes Fragile X... Fragile X testing -... Fragile X testing guidelines Wrongful birth claims Quantum issues and what... References and notes

 
Fragile X (FraX or FRAXA) affects about 1 in 4000 to 9000 men and 1 in 7000 to 15000 women of all races and ethnic groups.

It is the most common known cause of inherited intellectual disability. Because the condition is inherited, the diagnosis of an individual with Fragile X has serious implications for other family members (who may be carriers) and their future children. Both men and women can be carriers of the condition and the condition itself affects both men and women.

In Fragile X, one of the genes (called FMR1¹) on the X chromosome is faulty, affecting synthesis of a protein necessary for brain development.²

The reason boys are usually more severely affected by Fragile X than girls is that they have only one X chromosome (paired with a Y chromosome). Girls may have only mild disabilities because they have a second normal X chromosome, which can mask the adverse effects of the faulty one.

Apart from intellectual disability, an individual with Fragile X may be hyperactive, autistic and suffer from attention deficit disorder, emotional and behavioural problems, social anxiety, gaze avoidance, mood swings and language disorder. Self-injury in the form of biting and repetitive behaviour such as hand-flapping and an insistence upon routine with a dislike of change are common. Physical features are variable but can include a large head with a long face and large jaw, large or poorly folded ears, flat feet and hyperextensible joints. Between one-quarter and one-third of people with Fragile X are affected by epilepsy.

To understand how Fragile X is inherited, it is necessary to understand a little about DNA and methods of genetic inheritance.

	DNA

Top Abstract Background What is Fragile X? DNA Genetic inheritance What causes Fragile X... Fragile X testing -... Fragile X testing guidelines Wrongful birth claims Quantum issues and what... References and notes

 
Human genomic DNA is arranged on chromosomes. There are 23 pairs, giving a total of 46 chromosomes. Usually, we inherit one copy of each chromosome from each of our parents.

Each one of a pair of chromosomes is generally the same size as the other, with the exception of the sex chromosomes (the X and Y chromosomes – pair number 23³). They differ in length and in the number of genes they carry. Generally, females have two X chromosomes (‘46 XX’ in genetic shorthand) and males have one X and one Y chromosome (‘46 XY’ in genetic shorthand).

So a child's sex is determined by whether the child inherits the father's X chromosome (in which case the child is a girl) or the father's Y chromosome (in which case the child is a boy).

There are only four ‘letters’ in the alphabet of the DNA ‘book’. These ‘letters’ (representing DNA ‘bases’, or ‘nucleotides’) are known for short by their initial letters, as A, C, G and T. The ‘letters’ combine to make the ‘words’, i.e. genes. Each ‘word’ or gene has a functional role, necessary for life – for example, instructions telling the body how to manufacture a particular protein.

Each gene is ‘spelled out’ or ‘coded’ by a specific sequence of hundreds or maybe thousands or more of nucleotides. Different sequences of the four nucleotides code for different genes. Even a small change – a mutation – in the nucleotide DNA sequence can lead to abnormal function and give rise to genetic disease.

	Genetic inheritance

Top Abstract Background What is Fragile X? DNA Genetic inheritance What causes Fragile X... Fragile X testing -... Fragile X testing guidelines Wrongful birth claims Quantum issues and what... References and notes

 
You normally inherit two genes for each characteristic;⁴ one from each parent. There are a number of different ways in which genetic characteristics and conditions can be inherited. For example, some genes are ‘dominant’. This means that if you inherit the gene for that characteristic from either parent, then you will definitely have that characteristic. The gene for brown eyes is a dominant gene. Other genes are ‘recessive’ – in order to show the characteristic you have to inherit the gene for it from both your parents. The gene for blue eyes is a recessive gene. So if two brown-eyed parents have a blue-eyed child, this means the parents both have (recessive) blue-eye genes. Each parent has brown eyes, because in each case, the (recessive) blue-eye gene was ‘trumped’ by the (dominant) brown-eye gene.

The genes you carry are called your ‘genotype’. The characteristics you show as a result are called your ‘phenotype’. So, in the example above, the parents each have a brown-eye/blue-eye genotype, but a brown-eye phenotype, because the dominant brown-eye gene ‘trumps’ the recessive blue-eye gene. You cannot tell by looking at the brown-eyed parent (the phenotype) what that person's underlying genotype is. In fact each parent in this example is, so to speak, a ‘silent carrier’ of a blue-eye gene.

There are a number of other ways in which genetic conditions can be inherited. One is ‘translocation’, another is ‘duplication’ and yet another is an unstable type of mutation called ‘dynamic or expansion mutation’. It is expansion mutation that gives rise to Fragile X and, as earlier mentioned, the fact that girls have two X chromosomes (whereas boys have XY) is the reason girls are often less severely affected than boys by Fragile X. A girl's second normal X chromosome can compensate for the adverse effects of the abnormal one.

	What causes Fragile X – how is it inherited?

Top Abstract Background What is Fragile X? DNA Genetic inheritance What causes Fragile X... Fragile X testing -... Fragile X testing guidelines Wrongful birth claims Quantum issues and what... References and notes

 
Fragile X is caused by an increase in size of part of the FMR1 gene on the long arm of the X chromosome, resulting from so-called ‘dynamic or expansion mutation’.⁵ That part of the FMR1 gene consists – whether you have Fragile X or not – in a number of repeats of the nucleotide triplet CGG.

The difference between having and not having Fragile X is the length of the repeat; the repeat is longer where Fragile X syndrome is present. When the length of the repeat is above a critical threshold (the full mutation), symptoms of Fragile X are present and increase in likelihood and severity with greater repeat length.

Below this threshold there is a range of repeat lengths (called the premutation range) where that part of the gene becomes unstable during reproduction. Normally that part of the FMR1 gene contains less than 50 CGG nucleotide triplets. A person with Fragile X generally has more than 200 CGG nucleotide triplets. If the number of CGG nucleotide triplets on the FMR1 gene is between about 59 and 200,⁶ the person is a premutation carrier – though not generally adversely affected her or himself – with an unstable area on the FMR1 gene. If the fetus inherits from its mother her X chromosome with the unstable area, that unstable area can expand, generating extra repeats of the CGG nucleotide triplets and causing Fragile X in the child. A father with an abnormal number of repeats on his X chromosome will pass that X chromosome to all his daughters, but the unstable area will not normally expand during reproduction. There is a 50% chance that each child of a carrier parent will inherit the X chromosome with the unstable area.

	Fragile X testing – what went wrong in this case?

Top Abstract Background What is Fragile X? DNA Genetic inheritance What causes Fragile X... Fragile X testing -... Fragile X testing guidelines Wrongful birth claims Quantum issues and what... References and notes

 
Only one form of DNA testing, ‘polymerase chain reaction’ (PCR), was used to test the fetal DNA from Mrs A's antenatal CVS. If an additional and complementary form of DNA test, called ‘Southern Blot’, had also been used to test the antenatal sample, the Fragile X would not have been missed.

PCR is more rapid and easy to perform than Southern Blot. It is an indirect screening test, which detects normal and premutation numbers⁷ of the CGG trinucleotide repeat. But standard PCR cannot show the presence of the full mutation – that is, the high and pathologically expanded number of CGG repeats⁸ which causes Fragile X.

So PCR tests for Fragile X by default; the assumption is that if the presence of the shorter ‘normal’ or ‘premutation’⁹ sequences is shown, this must – in a male fetus, i.e. a fetus with only one X chromosome¹⁰ – exclude the presence of a full Fragile X mutation. That was the assumption made in Mrs A's case.

PCR preferentially amplifies smaller CGG trinucleotide repeat lengths. So if a sample contains even a tiny amount of DNA with smaller repeat lengths, these will be amplified and detected. A false assumption may then be made that the sample does not contain any of the long full mutation Fragile X repeat lengths.

This preferential amplification and detection of smaller repeat lengths present in a sample can cause such ‘false assumption’ problems if, for example, a fetal sample is contaminated with maternal DNA containing a shorter repeat length, or if the affected male fetus is ‘mosaic’ for CGG trinucleotide repeat length.

A genetic ‘mosaic’ is an individual in which different cells have different genotypes – some cell lines contain DNA with one variant (or ‘allele’) and other cell lines contain DNA with a different variant. So in the case of Fragile X, if you are mosaic for the X chromosome CGG trinucleotide repeat length, some of your cells will have DNA with one X chromosome CGG trinucleotide repeat length (for example, the normal length) whereas other cells will have DNA with the premutation length or the full mutation Fragile X repeat length. It is estimated that around 1% of full mutation Fragile X males also have a normal range repeat length, which can be amplified and detected by PCR.¹¹

The risk either of maternal contamination or of mosaicism in the fetus means that when testing a male fetus you cannot assume that, in all cases, demonstrating the presence of a shorter (‘safe’) repeat length by PCR excludes the presence of the pathologically expanded Fragile X repeat length in the fetus.

Southern Blot on the other hand is a diagnostic test for the full Fragile X mutation. It is a test for the presence (as opposed to the presumed absence) of the mutation that causes Fragile X. It requires more genetic material than is required for PCR testing. In Mrs A's case there was sufficient fetal genetic material from the CVS sample to allow Southern Blot testing to be carried out.

But in Mrs A's case only PCR testing was used to test the fetal DNA from the antenatal CVS. If the CVS had also been subjected to the ‘Southern Blot’ test, the fetal Fragile X mutation would not have been missed.

The liability issue therefore boiled down to whether it was acceptable for the Defendants to rely upon a (properly conducted) screening test, or whether they should have double-checked by using a diagnostic test. But it was in fact not at all simple either to define or to determine that issue.

Firstly, the ‘factual’ investigation – what tests had been conducted and what had gone wrong – was itself extremely complicated, detailed and technical. It helped that one of the authors had obtained a PhD in molecular genetics before qualifying as a solicitor. Shortly before we were instructed, the Defendant Trust had written a letter to the laboratory that diagnosed Mrs A's third son with Fragile X syndrome, detailing at length the number, range and extent of a series of investigative experiments by which they had tried, and failed, to identify their diagnostic error. The Trust was and, we speculate, still is unable to identify the exact nature and timing of their error. We in the end thought there had probably been maternal contamination, not of the CVS (although this could not be ruled out) but of the PCR samples which were visualized and interpreted one way, although there was a second (correct) interpretation that, if considered, ought to have mandated a Southern Blot test.

Secondly, our expert evidence indicated a number of laboratories would at that time, when testing a fetus known to be male, have relied only upon PCR testing (a Bolam defence¹²). If so, and were we unable to establish Mrs A's PCR fetal testing had not been properly conducted, then for Mrs A's claim to succeed, we would have to establish that practice was not capable of withstanding logical analysis (the Bolitho argument¹³).

It is to the credit of the Defendants that they admitted liability shortly after the issue of proceedings and within three months of receipt of our complex and detailed letter of claim. We do not think that admission would have been forthcoming, but for our detailed investigative work, which allowed the basis of Mrs A's claim to be so clearly set out in our letter before action. But that unfortunately did not stop the Defendants issuing an unsuccessful costs capping application, which resulted in considerable time being devoted by both sides to that application, rather than in quantifying and settling the claim.

	Fragile X testing guidelines

Top Abstract Background What is Fragile X? DNA Genetic inheritance What causes Fragile X... Fragile X testing -... Fragile X testing guidelines Wrongful birth claims Quantum issues and what... References and notes

 
This legal case contributed to a significant tightening up of the UK testing guidelines to ensure antenatal Fragile X diagnosis does not fail because PCR alone is employed as a test for Fragile X.

The 1 May 1998 UK guidelines, in place at the time of Mrs A's testing, were replaced by new (and still current) UK guidelines following a Clinical Molecular Genetics Society (CMGS) workshop on 21 February 2005.¹⁴ The relevant passages read:

1998:‘One possible concern about using PCR for FRAX analysis was that affected males mosaic for normal and full mutations might be missed, as the PCR would only pick up the normal allele... The possibility of normal/permutation or normal/full mutation males should be given consideration, however, when testing in known FRAX families.’ [our emphasis]

2005:In relation to prenatal diagnosis, ‘... the risk of potential false-negative interpretations of PCR results due to maternal cell contamination of the CVS is particularly acute in Fragile X testing because of the widespread discrepancy in size between normal and expanded alleles, with consequent preferential amplification of the former. Therefore Southern blot analysis should be the method of choice to obtain a conclusive result in prenatal diagnosis.’
In relation to all molecular diagnosis, ‘It is recommended that all patients with a high prior risk or with a confirmed family history of Fragile X be tested by Southern blotting as well as by PCR’; and ‘Full mutations are large expansions... which can only reliably be detected by Southern blot analysis’; and ‘While a CMGS study did not find significant evidence of true mosaicism for a normal and full mutation allele, one should nevertheless beware of artificial PCR bands which may occur in the normal range being misinterpreted as normal alleles’. [our emphasis]

The revised UK guidelines are supported by the current US guidelines¹⁵ but, somewhat surprisingly, the current European guidelines are more equivocal. The 2006 European Molecular Genetics Quality Network (EMQN) guidelines¹¹ state: ‘One possible concern about using PCR for Fragile X diagnosis is that affected males mosaic for normal and full mutations might be missed (MoMN individuals), as the PCR would only amplify the normal allele... The possibility of size mosaics (normal/premutation or normal/full mutation) should therefore be taken into account especially when testing in known Fragile X families. A false-positive case has also been reported... while the CGG repeat was in the normal range. This underlines the need for complementing PCR analysis with Southern blotting.’ [our emphasis]

The current UK (CMGS) guidelines now make clear that Southern blot analysis is the method of choice to obtain a conclusive result in prenatal diagnosis. So we do not think any UK lab could now escape liability for a claim such as Mrs A's for failed antenatal diagnosis of Fragile X, having relied upon PCR alone without also doing Southern blot analysis, where that is technically possible.

While the differences between the UK (CGMS) and the European (EMQN) guidelines for Fragile X diagnosis may not help best practice, because they introduce a degree of confusion, we do not think a UK lab could rely upon the more equivocal message in the current European (EMQN) guidelines, successfully to defend such a claim.

	Wrongful birth claims

Top Abstract Background What is Fragile X? DNA Genetic inheritance What causes Fragile X... Fragile X testing -... Fragile X testing guidelines Wrongful birth claims Quantum issues and what... References and notes

 
A wrongful birth claim is one brought by a parent¹⁶ who was deprived of the opportunity to avoid conception¹⁷ or terminate a pregnancy because of negligent treatment, diagnosis or advice.

Where a healthy child is born as a consequence of such negligence, the House of Lords have decided unanimously that parents cannot claim for the costs incurred in bringing up that child;^18,19 though modest damages are recoverable for the pregnancy and birth and in recognition of the legal wrong which deprived the Claimant of the right to limit the size of her family.

Even if the mother is disabled, then so long as the child is healthy, no parental claim can be brought for the extra costs incurred in bringing up the healthy child, arising from the mother's disability; despite the fact that the disabled mother had sought the sterilization – in the event negligently performed – so as to avoid having a child because of fears about her ability to care for a child.¹⁹

Where a disabled child is born, the extra (disability-related) costs of caring for the child can be claimed.²⁰ The same applies where the child was born healthy, but subsequently developed a disabling condition as a result of an infection acquired during labour.²¹

In a ‘failed sterilization’ case, where a disabled child is born, you do not have to show that the sterilization or vasectomy was sought in order to avoid the risk of giving birth to a child with disability.²²

	Quantum issues and what happened in this case

Top Abstract Background What is Fragile X? DNA Genetic inheritance What causes Fragile X... Fragile X testing -... Fragile X testing guidelines Wrongful birth claims Quantum issues and what... References and notes

 
Where the child is disabled, as in Mrs A's case, general damages are awarded not only for the unwanted pregnancy and birth, but also for the difficulties in caring for a disabled child. But the main claim is for the extra costs that arise because of the child's disabilities. In other words, quantification of a parental claim in a wrongful birth case where the child is disabled involves a similar exercise to quantification of the child's claim in an acquired injury case, where the child is the Claimant.

Controversial areas include whether the costs of caring for the disabled child will extend beyond the age of 18 years and (where it is anticipated the mother will pre-decease the child) beyond the end of the mother's life.

Defendants almost invariably argue – as they did in Mrs A's case – that the answer to both should be ‘no’. But damages are regularly awarded for the costs of care beyond the age of majority.²³

It is certainly arguable that the claim for the costs of caring for a disabled child should continue for the life of the child. The mother who has cared for the child since birth will naturally wish, if she can afford to, to make provision for the child's care to continue after her own death – a 2006 JPIL article²⁴ makes this point, citing the remark of Lord Nimmo Smith in Anderson v Forth Valley Health Board²⁵: ‘I can see no reason ... to suppose that it was not in the parties’ contemplation that if the children were born suffering from disabilities the natural response of [the parents] would be to make reasonable provision for their care throughout the children's lives'.

It remains unclear whether a wrongful birth claim is one for personal injury or one for economic loss. On the one hand Defendants argue that the three-year limitation period for personal injury actions should apply to wrongful birth claims. The courts seem to agree with this argument.²⁶

But equally Defendants regularly apply the economic loss argument, as they did in Mrs A's case. The argument goes that although the claim includes one for personal injury to the Claimant, the loss and expense of caring for the child is a pure economic loss claim by the Claimant who is accordingly under a duty to mitigate her loss by reference to state provision. Thus, said the Defendants:

• S2(4) of the Law Reform (Personal Injuries) Act 1948 does not apply; so the requirement to ignore the availability of NHS care – when considering the reasonableness of any expenses claim – should not apply;
  
• the claim is outside the scope of the Social Security (Recovery of Benefits) Act 1997, so the Claimant must give credit for benefits received in respect of the child's disability, such as DLA.
  

In addition to these points of principle, the Defendant Trust in Mrs A's case raised a number of other customary arguments in relation to Mrs A's damages claims (for example, that the amounts claimed for particular items of loss and expense were in fact too high).

The case settled by negotiation, so there was no court adjudication upon all these issues. But the level of the agreed damages (between three and four times the amount in the Defendants' Counter Schedule) was a pretty clear indication that the Defendant Trust recognized they were unlikely to succeed on many of their ‘in principle’ quantum arguments.

	Footnotes

 
Anne Winyard, Partner, Leigh Day & Co, Dr Darren Conway PhD, formerly of Leigh Day & Co, now an Associate at Freeth Cartwright LLP

	References and notes

Top Abstract Background What is Fragile X? DNA Genetic inheritance What causes Fragile X... Fragile X testing -... Fragile X testing guidelines Wrongful birth claims Quantum issues and what... References and notes

 

1. Located in Xq27.3 and encoding an RNA-binding protein (FMRP)
2. See http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=309550
3. The first 22 pairs (called ‘autosomes’) are numbered from the largest (pair number 1) to the smallest (pair number 22)
4. With the exception of the (male) sex-determining gene SRY on the Y chromosome
5. This type of genetic mutation, in particular where there is an increase in severity of a disease or earlier onset of a disease over several generations, also causes some other inherited diseases. Other examples of diseases caused by this type of trinucleotide repeat mutation include Huntington disease (previously known as Huntington Chorea), Friedreich's Ataxia, Spinocerebellar Ataxia, Myotonic Dystrophy, Spinobulbar Muscular Atrophy and Dentatorubral-Pallidoluysian Atrophy (DRPLA)
6. Where the number of CGG nucleotide triplets is between 50–58 (‘intermediate’ or ‘grey zone’), transition to a full mutation in one generation has not been reported
7. Up to about 200 repeated CGG nucleotide triplets
8. Over 200 repeated CGG nucleotide triplets
9. A premutation genetic sequence will not cause Fragile X in the individual who carries it, but may do so in the child of a mother who is a premutation ‘carrier’
10. Different considerations apply to a female baby who has 2 X chromosomes, one of which is likely to be normal and therefore to have a ‘safe’ and lower number of CGG repeated nucleotide triplets
11. See http://www.emqn.org/emqn/BestPractice/mainColumnParagraphs/05/document/EMQN%20guidelines%20FRAX_2006.pdf
12. Bolam v Friern Hospital Management Committee [1957] 2All ER 118: ‘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... Putting it the other way round, a doctor is not negligent, if he is acting in accordance with such a practice, merely because there is a body of opinion which takes a contrary view’
13. Bolitho v City and Hackney Health Authority [1997] 4 All ER 771: ‘... the court in not bound to hold that a defendant doctor escapes liability for negligent treatment or diagnosis just because he leads evidence from a number of medical experts who are genuinely of the opinion that the defendant's treatment or diagnosis accorded with sound medical practice ... the court has to be satisfied that the exponents of the body of opinion relied upon can demonstrate that such opinion has a logical basis. In particular, in cases involving ... the weighing of risks against benefits, the judge before accepting a body of opinion as being responsible, reasonable or respectable, will need to be satisfied that, in forming their views, the experts have directed their minds to the question of comparative risks and benefits and have reached a defensible conclusion on the matter ... if, in a rare case, 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 or responsible’
14. See http://cmgsweb.shared.hosting.zen.co.uk/BPGs/pdfs%20current%20bpgs/Fragile%20X.pdf
15. See http://www.acmg.net/Pages.ACMG_Activities/stds-2002/fx.htm at FX 3.2: ‘Laboratories very often need to use more than one method because no single method can detect all types of mutations equally well or with equal precision. For instances, for carriers with pre/full mutation pattern it would be questionable whether PCR alone would detect the full mutation leading to a different risk assessment for Fragile X, FXTAS and POF. For this reason, the ACMG policy statement recommends that Southern blot analysis always be conducted, even if a premutation allele is identified by PCR.’
16. Nearly always the mother
17. For example because of failed sterilization or failed vasectomy
18. McFarlane v Tayside Health Board [2002] 2AC 59
19. Rees v Darlington Memorial Hospital [2004] 1AC 309
20. Majority decision of Court of Appeal in Parkinson v St James and University Hospital [2002] QB 266; though three of the seven Law Lords (Lords Bingham, Nicholls and Scott) who heard the appeal in the Rees v Darlington Memorial Hospital case expressed disapproval of the Court of Appeal decision in Parkinson
21. Groom v Selby [2002] PIQR P201
22. Parkinson v St James and University Hospital [2002] QB 266
23. See for example Rand v East Dorset HA [2000] Lloyds Rep Med 181; Nunnerly v Warrington HA [2000] PIQR Q69
24. By Robert Glancy QC: [2006] JPIL 271
25. [1998] SLT 588
26. Court of Appeal in Walkin v South Manchester HA [1995] 1 WLR 1543; Godfrey v Gloucestershire Royal Infirmary [2003] Lloyds Rep 398

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