Royal Courts of Justice
Strand, London, WC2A 2LL
Before :
MR JUSTICE HICKINBOTTOM
Between :
PETER LUKE HOGG (a Protected Party through his Mother and Litigation Friend CHERRYL DIANE HOGG) | Claimant |
- and - | |
THE SECRETARY OF STATE FOR HEALTH | Defendant |
Philip Havers QC and Jeremy Hyam (instructed by Leigh Day) for the Claimant
Margaret Bowron QC (instructed by DAC Beachcroft LLP) for the Defendant
Hearing dates: 19, 20, 21, 22, 23 and 28 January 2015
Judgment
Mr Justice Hickinbottom :
Introduction
The Claimant Peter Hogg was born at the London Hospital, Whitechapel, on 18 February 1986.
He has been diagnosed with septo-optic dysplasia (“SOD”) with structural brain abnormalities, visual defects, anterior and posterior pituitary deficiencies with resultant diabetes insipidus, adipsia (an inability to perceive thirst), sleep apnoea and severe learning disabilities. In these proceedings, he claims that his condition was caused by the negligent performance of an amniocentesis on his mother when pregnant with him, at the London Hospital on 14 August 1985, such that the amniocentesis needle punctured his head and damaged his brain. The procedure was performed by Dr Gillian Robinson and a sonographer, for whom the Defendant is vicariously responsible.
The trial, at which the Claimant was represented by Philip Havers QC and Jeremy Hyam and the Defendant by Margaret Bowron QC, was restricted to issues of liability. In addition to the Claimant’s mother and father (who was also present at the procedure) and Dr Robinson, I heard oral evidence from two other medics who worked at the London Hospital at the relevant time, Dr Nigel Armstrong and Dr Roger Harris. I also had the benefit of written and oral expert evidence from a number of experts. The following were instructed on behalf of the Claimant:
Mr Myles Taylor (Consultant Obstetrician and Gynaecologist at the Centre for Women’s Health, Royal Devon & Exeter Hospital)
Dr Waney Squier (Consultant Neuropathologist at the John Radcliffe Hospital, Oxford)
Dr Amanda Ogilvy-Stuart (Consultant Neonatologist and Endocrinologist at the Rosie Hospital, Cambridge)
Dr Willie Reardon (Consultant Clinical Geneticist at Our Lady’s Hospital for Sick Children, Dublin)
Dr Brian Kendall (Consultant Paediatric Neuroradiologist at HCA Wellington Hospital, London)
Professor Alistair Fielder (Professor Emeritus of Ophthalmology at City University, London, and formerly Consultant Ophthalmologist at Hillingdon Hospitals, London) and
Dr Lewis Rosenbloom (Consultant Paediatric Neurologist with Alder Hey Children’s Hospital, Liverpool).
The following were instructed on behalf of the Defendant:
Mr Gerald Mason (Consultant in Feto Maternal Medicine)
Dr Tom Jacques (Consultant Paediatric Neuropathologist at the UCL Institute of Child Health and Great Ormond Street Hospital for Children)
Dr John Reckless (Consultant Physician and Endocrinologist with the Royal United Hospital, Bath)
Professor Michael Patton (Professor Emeritus of Medical Genetics and Consultant Clinical Geneticist at St George’s Hospital Medical School and Portland Hospital, London)
Dr Kling Chong (Consultant Paediatric Neuroradiologist at Great Ormond Street Hospital for Children)
Mr John Elston (Consultant Ophthalmic Surgeon at the John Radcliffe Hospital, Oxford) and
Dr Gayatri Vadlamani (Consultant Paediatric Neurologist at Leeds Royal Infirmary).
At the outset, I thank Counsel and all of the experts for their assistance which has been considerable and much appreciated.
Medical Background
Tests upon the fluid that surrounds a developing fetus in the amniotic sac within the womb have been devised which can pre-natally detect chromosomal and other fetal abnormalities, such as Down’s Syndrome. These require the extraction of samples of the fluid for testing, usually by a procedure known as amniocentesis, by which a needle in inserted through the mother’s abdominal and uterine walls into the amniotic sac, followed by the attachment of a line and syringe so that fluid can be aspirated. The procedure carries with it a small but significant risk of miscarriage (about 1:200), and so it is generally reserved for situations where there is an unusually high risk of fetal abnormality, e.g. because of the mother’s age.
A number of steps are taken to ensure that the sample is aspirated from free fluid, so that a sample is obtained sufficiently large to produce a reliable test result. First, the procedure is not usually performed until 16 weeks after conception, because the amount of amniotic fluid greatly increases – almost doubling – from weeks 13-16. Second, ultrasonography is used to identify an area within the womb where there is a free pool of fluid. These steps also reduce the risk of the needle puncturing the fetus; although such risk is very small, with (as I understand it) only seven possible cases of damage to the fetal head being reported by 2000 (Footnote: 1).
The procedure has developed over time. In its early days, the ultrasonographer would perform a scan in the radiology department of the hospital, and physically mark the mother’s body where the insertion should be made, before returning the patient to the doctor who then performed the insertion of the needle “blind”, going through the various anatomical layers by “feel”. To reduce the risks of (e.g.) the fetus moving between the time of an earlier scan and the needle insertion, some hospitals moved to a procedure where the sonographer still marked the mother’s body, but the doctor performed the amniocentesis immediately, in the Radiology Department, albeit blind. However, from the mid- to late 1980s, the procedure was adapted such that an ultrasound scan and insertion of the needle were performed at the same time, which meant that the doctor had the advantage of seeing the scan on screen in real-time, during the procedure. Some hospitals had a stage where the sonographer did the live scanning whilst a doctor inserted the needle; but the procedure evolved in the 1990s to one in which the doctor performed the procedure without assistance, two-handed, doing the live scan with one hand and inserting the amniocentesis needle with the other. As I understand it, that is how such procedures are performed today.
The fluid is aspirated into a syringe. The aspiration is known as a “tap”, which would usually comprise about 15ml of fluid in a fetus of 16 weeks gestational age. A “dry tap” is where no fluid is aspirated, e.g. because the needle fails to puncture the amniotic sac. A “bloody tap” is where fluid is aspirated, but it is contaminated with blood, which may be maternal or fetal. Where fetal blood appears in the tap, it may be the result of the needle puncturing the fetal body itself, or the umbilical cord or the placenta, each of which have fetal rather than maternal blood.
The Case History
The Claimant’s mother is Cherryl Hogg, who was born on 15 March 1948. She married Peter Hogg, and they ran a public house in London. By 1985, they had two healthy children, born in 1970 and 1972.
In early 1985, Mrs Hogg was having problems with her contraceptive coil device, and was advised to have a replacement fitted. On 18 April 1985, her old coil was removed, which caused her some discomfort and some bleeding. As a result, she did not have a new device fitted immediately. However, before the replacement was fitted, she fell pregnant.
On 4 July 1985, she attended the Midwives Clinic at the London Hospital. Her weight (110kg, i.e. something over 17st) was recorded. Her notes were marked that her last menstrual period was on 18 April 1985 “certain”, and therefore her estimated date of delivery was calculated to be 25 January 1986. Because of her age – 37 years – an amniocentesis was discussed, and the procedure was agreed and arranged at a further appointment on 12 July. The procedure was booked for 14 August 1985 at the London Hospital.
The precise procedure that took place is very much in dispute; but there is some common recollection. Mrs Hogg was accompanied by Mr Hogg. During her oral evidence, Mrs Hogg said – and Dr Robinson later confirmed – that the procedure was conducted in the Radiology Department by Dr Robinson, who was a Registrar in Obstetrics and Gynaecology at the hospital at the time. The sonographer was a Ms Beverley Nicholls. All four were present throughout the procedure. Mr & Mrs Hogg and Dr Robinson gave evidence before me; Ms Nicholls did not.
Mrs Hogg gave confident and vivid evidence. She said she and her husband were shown to the Radiology Department, where she met two medics, a tall young woman with blonde hair, long and straight, with a white name badge with her name (Dr Robinson) and, underneath, “Houseman”; and a second woman, the sonographer, whose description she could not remember, but who was clearly Ms Nicholls.
She lay on a bed, with her husband at her left side; and she could see an ultrasound screen, quite high up, near the foot of the bed. Ms Nicholls was on the same side of the bed as Mr Hogg. Dr Robinson was on the other side. Dr Robinson put some jelly on Mrs Hogg’s stomach, and Ms Nicholls put a scanner probe over the stomach and the scan came up, live, on the screen. Mrs Hogg remembered the sonographer doing some initial observations and clicking the controls which, she thought were to do with measuring the fetus.
Mrs Hogg said Dr Robinson then explained that she would feel pressure when the needle was inserted; and then the doctor “froze” a small area of the stomach and inserted the needle. Throughout the procedure, the sonographer was scanning the stomach with the probe, and Mrs Hogg could see on the screen the needle moving from the top right. She could see the baby’s head upwards, with his back to the right of the screen. As the needle moved in, the baby’s head rotated backwards, and his head appeared to move towards the needle so that the tip of the needle could no longer be seen. Both Mrs Hogg and her husband said, “Mind the baby’s head!” – and Dr Robinson assured them that, although it looked as if the needle was touching the head, it had in fact gone behind it.
Dr Robinson then aspirated some fluid, but it was dark red with blood; and she said that she would have to take another sample. The Particulars of Claim (at paragraph 10) say that the needle was passed a second time, and that was the basis of the Claimant’s case at the start of the trial (see paragraphs 13 and 37 of Mr Havers’ skeleton argument); but, in her oral evidence, Mrs Hogg could not remember whether Dr Robinson used a second needle, or only a second syringe. In any event, she said a second sample was taken, with the ultrasound image still on the screen; although Mrs Hogg was by now largely looking at Dr Robinson. The second sample was also blood-stained, but not as much as the first. Dr Robinson said she hoped she had enough amniotic fluid to give an accurate test result. She said that the blood might have come from the placenta.
Mr Hogg gave evidence essentially to the same effect as that of Mrs Hogg, but perhaps with less confidence and clarity.
After all this time, Dr Robinson could not recall performing this particular procedure on Mrs Hogg. However, she said that, in 1985, she was a Registrar with no ultrasonography experience. She relied upon the sonographer to calculate the gestational age and confirm that it was at least 16 weeks, and identify and confirm that there was a sufficient pool of free fluid. Dr Robinson said – and I accept – that she would only continue if she received these confirmations. If she had been told that the gestational age was less than 16 weeks, she would not have performed the procedure, but would rather have postponed it. I am satisfied that Ms Nicholls told her that the Claimant’s gestational age was at least 16 weeks.
Dr Robinson made a contemporaneous note in the medical records: “14/8/85 AMNIOCENTESIS 1 tap (bloody) 4mls blood stained fluid…”. Ms Nicholls’ note indicates: “5ml bloody tap”. As I have indicated, although the Particulars of Claim refer to two needle passes, Mrs Hogg was unsure whether there were two passes, or whether there was one needle but two syringes to take two samples. The records do not refer to a second pass. They do however refer to two samples. They show that one sample of 3mls of the fluid, described as “heavily bloodstained” and “very bloodstained” was sent to the North East Thames Regional Cytogenetics Service and was subject to a normal array examination. The provisional karyotype report on the sample was reported as 46XY, i.e. a chromosomally normal male; and a post-natal karyotype undertaken on 24 April 1986 confirmed a normal array. 1ml of the fluid, described as “slightly bloodstained”, was sent to St Bartholemew’s Hospital, where a Kleihauer test on the sample showed unequivocally that it was fetal blood. Dr Robinson said that it was standard practice then to use separate syringes to take the two samples needed to send off for tests. She said that, had there been more than a single needle pass, she would have recorded that in the medical notes. On the evidence, I find that there was only one needle pass, but two fluid samples were taken using separate syringes.
The Claimant was born on 18 February 1986, and initially all appeared well. However, shortly after the birth, his mother noticed a small lump on the Claimant’s head, described in the medical records as a “blue hairy nevus on Rt parietal area”, to which I shall return (see paragraphs 59(iii) and 72(ii) below). Worryingly, within a month, his parents considered there was something seriously wrong. The Claimant was admitted to the London Hospital for jitteriness, vomiting and concerns that his eyes were not fixing. Investigation showed an absence of septum pellucidum, some distortion of the third ventricle and dilation of the anterior part of the third ventricle. A radiological diagnosis of SOD was suggested. That diagnosis has since been confirmed.
Mr & Mrs Hogg have subsequently had a fourth, healthy child.
The Relevant Anatomy
It will assist briefly to describe the parts of the brain implicated in this case.
Within the brain is a system of interconnected cavities or ventricles, which produce the cerebrospinal fluid in which the brain and spinal cord float. Three ventricles lie within the brain: two lateral ventricles (left and right), and the third ventricle tucked underneath in a narrow cavity between the thalamus and hypothalamus. Each lateral ventricle consists of a body and a number of “horns”, including, at the front, the anterior horn. They are connected to the third ventricle by channels known as the interventricular foramina or the foramina of Monro.
The lateral ventricles lie within the two cerebral hemispheres (left and right), which form the major part of the brain. The surface of the hemispheres is folded into a series of gyri (ridges) and sulci (furrows) which have the effect of greatly increasing its surface area.
Each hemisphere consists of an outer cortex of grey matter and an inner mass of white matter. The germinal matrix is a part of the central brain forming a layer in the lateral ventricle, where cells form and from which they then migrate to their final position in the brain. As I understand it, there are a variety of mechanisms by which this migration can occur. Relevant to this case is radial migration of grey matter neurons from the germinal matrix outwards through the white matter towards the cortex of the frontal lobes where they form the outer cortex.
Blood is supplied to the frontal lobe and medial surface of each hemisphere by the anterior cerebral arteries.
The dura lines the skull. Between the hemispheres is the cerebral falx, a fold in the dura which descends vertically in the longitudinal fissure which separates the hemispheres, within which many of the main structures that control the majority of the body’s activities lie.
The corpus callosum or callosal commissure is found in the depths of this fissure. It is a thick, flat band formed from nerve fibres or axons which are projected from each hemisphere during the development of the brain, and which facilitate interhemispheric communication. Where there is agenesis of the corpus callosum (i.e. it does not form), these fibres remain in the hemispheres, and are known as the bundles of Probst. The genu is the most anterior part of the corpus callosum, which curves downwards so that the end is under the main body and posterior facing. The rostrum is the end part of the genu.
Immediately above the corpus collosum is the cingulate gyrus (which connects the limbic system with the cerebral cortex), which is itself below the cingulate sulcus, which curves round the front of the head following the line of the corpus callosum and genu.
The septum pellucidum is developed as a pair of thin, triangular membrane running vertically from and below the corpus callosum, separating the left and right anterior horns of the lateral ventricles. They merge into a single membrane in adulthood.
The lower edge of the septum pellucidum is attached to the upper face of the fornix, a bundle of fibres that forms part of the limbic system. These are C-shaped, starting from the hippocampus as two pillars or crura (left and right), joining mid-brain, before separating again to form the anterior pillars or columns. The fornix relays signals from the hippocampus to the thalamus, via the mammillary bodies, a pair of small round bodies that lie on the undersurface of the brain at the ends of each anterior fornix arch. In axial cross section, the corpus callosum runs across the top of the lateral ventricles, which, on each side, spread out laterally to form a cornu or horn. The septum joins the corpus callosum at the mid-line, forming a T-junction; or, more accurately, a Y-shaped junction.
The thalamus comprises two egg-shaped masses of grey matter or nerve cells lying each side of the mid-line, deep within the brain. The hypothalamus lies below it, separated by a shallow groove (the hypothalamic sulcus). The hypothalamus is the main link between the central nervous system and the endocrine system, controlling the function of the pituitary gland: the anterior and posterior lobes of the pituitary gland are just under the hypothalamus, and regulated by it. They have different functions. The anterior pituitary lobe secretes substances which influence the thyroid and adrenal glands, and produces growth factors. The posterior lobe produces hormones that (e.g.) increase blood pressure and decrease urine production.
The hypothalamus is just behind the optic chiasm, which is the point where the optic nerves cross over as they travel from the eyes to the back of the brain where the visual area of the brain lies. Beyond the chiasm, this bundle of nerves is known as the optic tract.
The Claimant’s Brain Abnomalities
Based on an MRI scan on 5 November 2009 (which the expert neuroradiologists agreed is the best in quality, and shows the abnormalities disclosed on other neuroimaging), the Claimant has the following abnormalities of the brain.
The septum pellucidum is completely absent.
The posterior part of the corpus callosum is well-formed; but the anterior part of the genu is asymmetrically defective, being more marked to the left of the mid-line. The rostrum is absent.
The frontal horns of the lateral ventricle are abnormally configured; the anterior half of the third ventricle and foramen of Munro are very wide; and there is an abnormality in the lateral wall of the third ventricle and in the anterior part of the left ventricle in the radiological form of a mild “scoop” out of the side of that ventricle.
Posterior to the abnormalities in the left thalamus, there is a cystic abnormality to the right thalamus.
The posterior parts of the fornix appear to be normal; but the anterior columns and mammillary bodies are small.
There is an abnormality, left of mid-line, between the left frontal horn and the overlying frontal cortex lobe. This appears as an ectopic pocket of grey cells, within the deep white matter, falling short of a complete cleft (i.e. schizencephaly), and appears to result from an abnormality in neuronal migration. Furthermore, there is thickening of the grey matter of the medial surfaces of the frontal lobes immediately anterior to the lateral ventricles.
The pituitary is hypoplastic (i.e. poorly developed). The Claimant has suffered complex pituitary failure, reflecting a primary hypothalamic (rather than discretely pituitary) abnormality. At 6 years of age, he showed precocious puberty (accelerated growth rate, pubic hair, testicular enlargement), which was controlled by hormone agonist analogues until age 10 when puberty was allowed to proceed. At 12, he developed diabetes inspidus. At 13, he developed central hypothyroidism. At 19, he was found to have growth hormone and cortisol deficiency.
The optic nerves on both sides and the optic chiasm are small.
Septo-Optic Dysplasia
In 1956, a report was published of a study by de Morsier involving 30 patients who had an absence of the septum pellucidum, nine of whom had an underdeveloped optic nerve (i.e. optic nerve hypoplasia) (Footnote: 2). He termed it SOD. In 1970, Hoyt et al reported a high prevalence of hypothalamic-pituitary dysfunction in SOD (Footnote: 3), a finding subsequently verified in a number of other studies (Footnote: 4).
A diagnosis of SOD is now dependent upon the patient exhibiting at least two of three morphological abnormalities: (i) absence of the septum pellucidum, (ii) optic nerve hypoplasia and (iii) pituitary hypoplasia with consequent hypopituitarism (i.e. abnormally diminished production of anterior pituitary hormones). About one-third of those diagnosed with SOD, which is estimated to occur in 1 in 10,000 live births, have all three elements. The diagnosis is based entirely on the presence of these anatomical abnormalities, and is not in itself suggestive of any particular aetiology. Where an individual has more pathology than the triad – as in the Claimant’s case – it is described as SOD plus; but that diagnosis is no more suggestive of cause.
SOD is “not well understood” (Footnote: 5) and its incidence sporadic. It is clear that the cases of SOD which have been studied are “clinically, radiologically and pathologically highly diverse” (Dr Squier’s Report, paragraph 20), exhibiting a “wide variation in the severity of the clinical features found, and in their association with other diagnoses, which follows no clear pattern” (Footnote: 6). The clinical expressions and radiological presentation of SOD are highly variable.
With regard to causes of SOD generally, paragraph 5 of the joint statement of the expert neurologists indicates that Dr Rosenbloom and Dr Vadlamani agree that “the exact pathogenesis of SOD is unclear and that multiple aetiological factors including genetic and environmental factors have been suggested”. None of the other experts casts any doubt on that proposition, which is supported by the medical literature to which I was referred. In respect of environmental factors, SOD has been associated with younger primigravidae, and with consumption by the mother of alcohol and drugs during pregnancy (Footnote: 7). Dr Squier said that she had seen cases of SOD following trauma to the mother, although there is no reported case of SOD being caused traumatically by an amniocentesis needle or, as I understand it, any other direct trauma to the fetus (as opposed to the mother). In respect of inherent factors, mutations of genes HESX1, SIX2, SOX3 and OTX4 have been reported; but, on the basis of published data, in no more than 5-10% of cases of clinically diagnosed SOD and related midline disorders (Footnote: 8). The genetics experts before me were agreed that the published data suggest a proportion of fewer than 5% (joint statement, paragraph 3). The genetic causes include both chromosomal abnormalities and mutations in homeobox genes, i.e. underlying developmental genes such as HESX2 that “control” other genes.
It has been suggested that the aetiology of SOD is likely to be multifactorial, involving a combination of genetic and environmental factors (Footnote: 9); and, elsewhere, that it may be the result of some form of genetic or extrinsic vascular disruption (Footnote: 10), (Footnote: 11). However, on current medical knowledge, for the vast majority of patients diagnosed with SOD, the aetiology remains unknown.
The Issues
By the end of the trial, the case gave rise to the following issues:
Issue 1: Were the hospital staff negligent in estimating the Claimant’s gestational age to be at least 16 weeks?
Issue 2: Was the amniocentesis performed with the benefit of real-time ultrasound scan? If not, was Dr Robinson negligent in not having a re-scan to check the position of the needle before the second aspiration?
Issue 3: Are the Claimant’s brain abnormalities the result of the amniocentesis needle penetrating his skull?
I will deal with those in turn.
Issue 1: Gestational Age
By the end of the trial, it was common ground that, as the date of the amniocentesis, the Claimant’s gestational age was 14 weeks 6 days. As I have indicated (paragraph 18 above), having taken the appropriate fetal measurements, Ms Nicholls told Dr Robinson that it was at least 16 weeks. Had she been told that it was less than 16 weeks, she would have postponed the procedure. Thus, the first question I have to consider is whether Ms Nicholls was negligent in assessing the age as she did.
The gestational age on the basis of last period appears to have been dubious; because the bleeding on 18 April 1985 (see paragraph 10 above) considered to be menstrual could equally have resulted from irritation from the contraceptive coil. However, the obstetric experts agreed that it was reasonable to fix an appointment for the amniocentesis of the basis of that date, subject to a check being carried out on by reference to fetal measurements taken from an ultrasound scan on the day (joint statement, paragraph 4).
Ms Nicholls unfortunately did not give evidence – she was not available to do so – but she did make and sign a contemporaneous note, which read as follows:
“BPD [biparietal diameter] = 34mm
Gestation [there is then written 15 and 16, one superimposed on the other] weeks -/+ [there is then written 1 and 3, again one superimposed on the other]
FL [femur length] 17mm
Posterior placenta. FHM [fetal heart motion] seen. Spine not well seen but NAD [no abnormality detected]
Amniocentesis Dr Robinson. 5ml bloody tap”
The biparietal diameter (“BPD”) is the transverse diameter of the head. From the available copy document itself, it is not possible to say whether the 15 was superimposed on the 16, or vice versa; similarly, the 1 and 3.
Dr Robinson said that Ms Nicholls simply confirmed to her that the gestational age was at least 16 weeks, and she did not know how that calculation was made; but, she said, there was a chart on the wall of the radiology room in which the procedure was performed. She could not recall the substance or even form of this chart; but she produced a table from a standard text book that she had, namely the second edition of Chudleigh & Pearce (Footnote: 12), which suggests that a 34mm BPD corresponds to a gestational age of 16 weeks 1 day. Although the book was not published until 1992, the data from which the table was complied came from a paper published in 1982 (Footnote: 13), i.e. before the procedure was performed on the Claimant’s mother in 1985.
However:
In addition to the table, the second edition of the work includes a chart derived from the same source showing BPD set against gestational age in the form of a graph, saying (Footnote: 14) that gestational age should be estimated from that chart and only by the table “if it is outside the normal range for postmenstrual age” (which, in the Claimant’s case, it was not). Using the median line from that chart, a 34mm BPD equates to a gestational age of less than 16 weeks.
The second edition of Chudleigh & Pearce was published in 1992. Even the first edition was published after the relevant events (Footnote: 15); but that edition did not have the table in it at all. Instead, it reproduced, as Figure 5.6, “the most widely used cephalometry chart [in the United Kingdom]”, in the same form as, but from a different source from that in, the later edition (Footnote: 16). Using the median line from that chart, again a BPD of 34mm equates to a gestational age of something clearly less than 16 weeks.
Furthermore, the second edition of the work – the one produced by Dr Robinson – says that “estimation of gestational age should not be made from a single parameter” (Footnote: 17). Mr Mason said that, whatever best practice might have been, it was common practice to rely only on BPD; but we know, from her contemporaneous note, that Ms Nicholls did in fact measure the femur length. Her only purpose for doing so would have been to estimate the gestational age from it. On the basis of a femur length of 17mm, the charts and tables in both first and second editions of Chudleigh & Pearce assess the gestational age, again, at clearly less than 16 weeks.
On the basis of the evidence before me, it is unclear from where Ms Nicholls might have concluded that the Claimant’s gestational age was at least 16 weeks. None of the experts was able to produce any chart or table from 1985 from which such a gestational age might have been calculated on the basis of a BPD of 34mm. The only table produced is from a 1992 work, and is in any event apparently not applicable to the Claimant’s case. The relevant chart in that work assesses the gestational age based on BPD as less than 16 weeks. The relevant chart in the earlier edition of that work gives the same assessment. In any event, the age based on femur length – by which Ms Nicholls appears to have cross-checked – was below 16 weeks. Furthermore, it seems clear that the initial age written down by Ms Nicholls was 16 weeks, later changed to 15 weeks: the 16 weeks must sensibly have been written down first, as that is the age given by her to Dr Robinson. It is not certain when or by whom the correction was made; but it is likely that it was made on the basis of the measurements Ms Nicholls had made and recorded, rather than (e.g.) being based upon later measurements which confirmed that the date of conception was later than Ms Nicholls’ calculation suggested (e.g. those made on 3 October 1985).
As I have recorded, it is unfortunate that Ms Nicholls was not available to give her explanation of why she informed Dr Robinson that the gestational age was at least 16 weeks. However, on the basis of all the evidence that was before me, I am satisfied that that she had no proper basis for doing so on the measurements that she had taken; and thus she was negligent in estimating the Claimant’s gestational age to be at least 16 weeks. Although Dr Robinson was not negligent in this regard, the Defendant is of course vicariously liable for the negligence of Ms Nicholls as well as any negligence on the part of the doctor.
Dr Robinson accepted that, had she been told that the gestational age was less than 16 weeks (as, I have found, she ought to have been), she would not have proceeded with the amniocentesis.
Issue 2: The Ultrasound Scan
With regard to the amniocentesis procedure, there is a stark factual dispute between the parties. The Claimant says that the procedure was done with the benefit of a real-time ultrasound scan by Ms Nicholls at the same time as Dr Robinson performed the amniocentesis procedure. If that were so, the experts are agreed that it would have been negligent for Dr Robinson to have pierced the Claimant’s skull during the procedure. The Defendant contends that the scanning was discrete: it was done first, and the scanner removed before Dr Robinson performed the procedure blind. If that were so, then there is a further issue between the parties as to whether Dr Robinson was negligent in not having a further scan between the first and second aspirations, to check where the needle was.
Mrs Hogg said that she had seen the needle and her son’s head on the screen during the procedure, as I have described; and, she said, it was not something that she would forget. Although the relevant events were nearly 30 years ago, Mr Havers suggested that, even prior to knowing the Claimant’s medical condition after his birth, having an amniocentesis was not something a mother is likely to forget.
He also submitted, with some force, that Mrs Hogg gave her evidence confidently and with some detail, such that I could and should accept it. For example, she recalled in her oral evidence that the procedure had taken place in the Radiology Department of the hospital, which Dr Robinson confirmed in her oral evidence was indeed the case: that had not been evidence before trial. Mrs Hogg also recalled – correctly – that the procedure was carried out in a room with Dr Robinson, Ms Nicholls, her husband and she all present, and it was room in which real-time ultrasound equipment was available. She also recalled that there were two samples taken, which Dr Robinson again confirmed.
Furthermore, the description of Mrs Hogg, of the fetal head moving and thus obscuring or coalescing with the needle tip, was consistent with (i) her account of the immediate conversation she and her husband had with Dr Robinson, and (ii) with the brain abnormalities actually suffered by the Claimant (see the section on Causation below).
In all the circumstances, Mr Havers submitted that Mrs Hogg’s evidence had the ring of truth about it; and the details she gave were convincing in evidencing that she correctly recalled seeing the real-time scan during the procedure.
Furthermore:
Although his evidence did not come over as robust as that of Mrs Hogg, Mr Hogg’s evidence supported his wife’s in the essential details. For example, his evidence as to the conversation they had with Dr Robinson when they saw the needle coalesce with the fetal head was identical to hers.
Miss Bowron suggested that, when recalling seeing a real-time scan, Mrs Hogg and her husband might have been mistakenly recalling the amniocentesis undertaken in respect of their fourth child. However, Mrs Hogg said – and I accept – that that later procedure was performed on a ward, not in the Radiology Department; and Mr Hogg was not present at all. They were essentially different.
Mr Taylor explained that ultrasound would have picked up both the fetal head and the needle because they are echogenic structures, and so (he said) it would be unsurprising if Mr & Mrs Hogg had seen what they claim.
In all the circumstances, Mr Havers submitted that I could be confident that Mrs Hogg’s account was essentially correct.
I accept that Mrs Hogg’s evidence was forcefully given; and that she, and her husband, are now both firmly convinced that the amniocentesis was conducted with real-time ultrasound. However, after anxious consideration of all the evidence, I have concluded that their recollection, whilst sincerely held, is unfortunately incorrect. In coming to that conclusion, I have particularly taken into account the factors in relation to Mrs Hogg’s evidence set out above, but also the following.
Dr Robinson gave thoughtful and considered evidence. She accepted that she did not recall Mrs Hogg’s particular procedure; nor did she suggest that she recalled the exact details of the procedure for performing amniocentesis in 1985. However, she believed that the Hoggs were mistaken when they said that the procedure was performed with real-time ultrasonography. She said she was “very confident” of this, because she recalled being “taught the practice of performing amniocentesis with a continuous visualisation of the needle tip with an ultrasonographer being present at the Mayday Hospital” about 6 years later – she was there from April 1992 for about 18 months – some time before she moved on to doing the procedure alone, two-handed at the St George’s Hospital, for which she was also then trained.
Mr Havers submitted that Dr Robinson’s recollection was likely to be inaccurate, because she did not perform any amniocenteses between February 1986 (when she left the London Hospital) and, at the earliest, September 1991 or probably April 1992 when she went to St George’s Hospital. Prior to August 1985, she accepted that she had done few amniocenteses. Mr Havers submitted that she therefore had no established practice in performing the procedure prior to 1985, and no period of consolidation in the years following. Furthermore, the obstetric experts agreed that there was no standard form of training in 1985, and many medical procedures were performed on the principle, “See one, do one, teach one” (joint statement, paragraph 3). Mr Mason said that, although in a different hospital in Manchester, he witnessed a number of amniocenteses, was supervised in one and then allowed to perform them unsupervised. It was quite possible – and, Mr Havers submitted, probable – that, in 1985, whilst Dr Robinson did not have had any formal training in performing amniocenteses with real-time ultrasound by a sonographer, she had witnessed and/or been supervised on such a procedure and was thereafter allowed to perform them unsupervised.
However:
Although Mrs Hogg’s recollection was patently correct with regard to some details (e.g. as to where the procedure took place, and who were there), it was not correct in all particulars. Her description of Dr Robinson was, save for the hair colour, generally inaccurate: Dr Robinson is not tall, she did not have long hair at the time and she was not a “Houseman” but a Registrar. Dr Robinson said – and I accept – that it was not her practice to use freezing or anaesthetic gel, as Mrs Hogg recollected she used on her. Insofar as Mrs Hogg said that there were two needle passes – and that is set out in the pleading – Dr Robinson did not do so.
Furthermore, although I accept that both a fetal head and a needle are echogenic, scanning equipment in 1985 had its limitations; and the pictures from contemporaneous literature to which I was referred (Footnote: 18) suggest that they may not have been as clear as Mrs Hogg and her husband suggest and identifying what was occurring may not have been as straightforward as they suggest. The quality of the image would have been adversely affected as a result of both Mrs Hogg’s BMI (she was 17st at the time) and the fact that her abdomen was scarred from previous operations. Mr Mason (who was in obstetric practice at the relevant time) said that the quality of imaging in 1985 made it improbable that they could have seen what they assert they saw. That evidence was convincing.
It is noteworthy that the first intimation of a claim based on there being an ultrasound-guided procedure, with Mr & Mrs Hogg witnessing the needle near and then coalescing with the fetal head, was in the letter of claim dated 23 February 2012. It was not mentioned previously, e.g. in the earlier solicitor’s letter of 30 July 1996. There is some force in Miss Bowron’s contention that, had this important matter been recollected earlier by Mr & Mrs Hogg, it is surprising that it was not deployed sooner. Mr Havers submitted, correctly, that the main purpose of the July 1996 letter was to obtain the Claimant’s own medical records; but it is noteworthy that it mentions both the blood in the samples and the hairy naevus which Mr & Mrs Hogg then appear to have thought supported their case.
I accept that Mr Armstrong’s evidence was generally undermined by his recollection that, in 1985, the scanning and amniocenteses were done in different parts of the London Hospital, when they were clearly not; but he too said that the procedure was performed blind at that time.
Importantly, Mr Taylor (the Claimant’s obstetric expert) said in his report (at paragraph 47) that:
“The acceptable standard of performing amniocentesis in 1985 was to have had at least ultrasound prior to procedure, but not necessarily during it.”
In their joint statement (paragraph 1(a)), the obstetric experts agreed:
“In 1985 a typical amniocentesis involved the ultrasonographer identifying a pool of liquor and then marking the maternal abdomen over this spot. The ultrasound probe was then removed and the obstetrician would feel their way through the various layers into the uterine cavity…. In the mid to late 80s a few fetal medicine centres started to use real-time ultrasound during the procedure and in 1985 this would only have been available in a very limited number of fetal centres in the United Kingdom…”.
In 1985, whilst the London Hospital was a teaching hospital, Mr Mason (who was practicing in obstetrics at the time) said, Dr Robinson confirmed and I accept that it was not a recognised fetal centre. Mr Mason said that, when he joined a teaching hospital in Leeds in 1993, they were still doing amniocenteses blind.
Although Mr Havers questioned why it did not appear in her first statement – it was set out in a second statement dated 7 January 2015 – Dr Robinson’s evidence that she was not “taught the practice of performing amniocentesis with a continuous visualisation…” (in whatever form that teaching might have taken place) until she was at the Mayday Hospital was compelling. She took particular care in considering when she began performing amniocenteses with real-time ultrasound and, even taking account of the evidence as to how medical procedures were taught in 1985, her recollection of when being taught to do so was, in my view, compelling evidence and highly supportive of the proposition that, in 1985, she did not perform the procedure in that way.
For those reasons, whilst I do not for a moment question Mr & Mrs Hogg’s sincerity, in my view their recollection is mistaken. I find that the procedure in August 1985 was performed blind, and without real-time ultrasound.
In those circumstances, Mr Havers submitted that Dr Robinson was negligent in failing to re-scan after the first and before the second aspiration. Aspirating 3mls of heavily blood-stained fluid strongly suggested that the end of the amniocentesis needle was in the wrong place, and the sonographer had recorded a posterior placenta. There was therefore at least a possibility that, at the time of the first aspiration, the needle was in the fetal body; and undertaking a second aspiration with it in that same place might damage or further damage that body. In the circumstances, he submitted, Dr Robinson was negligent in not requiring a re-scan before proceeding to the second aspiration. The procedure was, of course, taking place in the Radiology Department, with a sonographer present; and so there would have been no difficulties in re-scanning.
This was a late-running plea, for which Mr Havers sought permission to amend only during the trial itself. I am unpersuaded by it.
In 1985, bloody taps were common. I was referred to a 1983 paper which suggested the incidence was 8-40% (Footnote: 19). That is reflected in the evidence of Mr Mason, who, in paragraph 18 of his report, said that the incidence in the “old literature” suggested an incidence of “up to 25%” (Footnote: 20). It was Mr Mason’s evidence that in 1985, when a first sample of fluid was bloody, it was usual and acceptable practice simply to proceed to aspirate a second sample. I accept that evidence over the evidence of Mr Taylor that Dr Robinson should not, even in 1985, simply have ploughed ahead; noting that, unlike Mr Mason, Mr Taylor was not in obstetrics practice at that time. Dr Robinson said that this is what she did: she simply proceeded to take the second sample. There is no substantial evidence that to have proceeded in that way was not in accordance with a responsible body of medical opinion in 1985.
Issue 3: Causation
The Issue Identified
However, I have found that the Defendant was negligent in the assessment of the Claimant’s gestational age at the time of the amniocentesis. I thus turn to the question of causation; and, first, medical causation. In this case, that issue is particularly difficult.
Two possible broad aetiologies were canvassed before me, which each attempted to explain the abnormalities to parts of the brain which (i) are apparently disparate (including both sides of the mid-line) and (ii) develop at different times during gestation.
Mr Havers submitted that, on the evidence, it was probable that the abnormalities were caused by the amniocentesis needle traumatically damaging the brain, through one or more of three mechanisms, namely:
Direct trauma. The needle caused direct trauma damage to the septum pellucidum, corpus callosum including the genu and rostrum, the right thalamus (now exhibiting a cyst), and probably the germinal matrix.
Vascular disruption. A contusion to the left thalamus was caused by the needle pathway; and probably some form of vascular disruption was caused by damage to the anterior cerebral artery, which supplies blood to the relevant involved structures such that disruption to that blood flow is capable of causing hypoplasia in those structures.
Neuronal migration damage, as a result of the damage to the germinal matrix.
Miss Bowron submitted that I cannot be satisfied on the balance of probabilities that the abnormalities were caused by the needle; and, on the evidence, it is more probable that the abnormalities result from an intrinsic cause unconnected with the needle, and likely gene based.
It is clear from the evidence that no aetiological hypothesis can elegantly explain all of the abnormalities in this case without some challenges. There is no silver bullet: none of the experts said that there was a specific factor or combination of factors in this case that excluded either needlestick damage or an intrinsic cause. All said that, whilst there were difficulties for any hypothesis, the abnormalities were all consistent with either cause. Thus, each expert expressed a view on causation on what was, in his or her view, the most likely on the basis of the evidence and his or her expertise. Of the twelve causation experts, six consider it more likely that the abnormalities are the consequence of traumatic brain damage, whilst six consider an intrinsic cause the more likely.
Discussion
The decks can be cleared to some extent.
Whilst environmental factors have been associated with SOD, in this case there is no evidence of such factors being present in this case. Mrs Hogg, despite being a publican at the relevant time, is teetotal. There is no evidence that she drank, or took any relevant drugs, during pregnancy. Nor was she a young primagravida. There is no evidence of any relevant family genetic history. There is, in short, no evidence that the Claimant’s SOD resulted from any environmental insult or trauma other than from the amniocentesis needle.
Neither Mr Havers nor Miss Bowron suggested that the ophthalmic expert evidence was likely to assist me greatly; and I did not find that evidence helpful on the issue of causation. The experts agreed on much; in particular, they agreed that the Claimant suffers from optic nerve hypoplasia, i.e. from a failure of the optic nerves and chiasm to develop properly, one of the triad of diagnostic morphologies. That has resulted in each of the Claimant’s eyes having a very restricted visual field – less than 10 degrees – so that his peripheral vision is very poor. In addition, Professor Fielder considered that he also has right homonymous hemianopia, i.e. a loss of the right side of each field caused by an insult to the optic tract beyond the chiasm. This exhibited itself (he said) in the form of a vertical line in the right field on the Goldman perimetry chart obtained for the purposes of his report. Mr Elston did not agree with this additional diagnosis, because (a) the defect is not visible in the left field as it ought to be: he did not consider that the fact that the blue inner field in respect of the left field in that test represented such a defect, and (b) the defect was not replicated in a later test in 2014: he did not consider the “notch” on the right hand side of the field represented such a defect. In all the circumstances, I agree with Mr Elston: the ophthalmologic evidence does not assist in determining the cause of the Claimant’s SOD: although I note – and accept – Mr Elston’s evidence that the results of the Claimant’s sight tests are typical of an individual diagnosed with optic nerve hypoplasia as an element of SOD.
Some of the Claimant’s experts – notably Dr Kendall, but generally supported by Dr Rosenbloom – considered that the brain abnormalities are the result of direct trauma, by virtue of deep penetration of the brain by the amniocentesis needle. This was the Claimant’s primary case at the start of the trial, set out in paragraph 3 of Mr Havers’ skeleton argument. “Deep” here is, of course relative. The fetal BPD was only 34mm, and so the depth of penetration they considered occurred was in the region of, perhaps, 15-17mm.
Dr Kendall suggested a line of such trauma, running through the front of the head (but avoiding the eyes themselves: in oral evidence, he said the head would have been penetrated just above the left eye), then running transversally at a slight gradient downwards and axially almost down midline running an course from 1 o’clock to 7 o’clock on the usual axial cross-section, through the site of the septum pellucidum, genu and rostrum, and then through the left ventricle (affecting the germinal matrix) and finally to the position now occupied by the cyst in the right ventricle. He considered that the septum is entirely absent, because the genu and rostrum to which it relates had been primarily/traumatically damaged. He explained the damage to the left thalamus as occurring, not by direct trauma, but by bruising/bleeding which, he envisaged, would have affected a 5mm radius around the needle’s course. Dr Rosenbloom also generally favoured this mechanism of damage, although he also considered that some of the damage was caused by vascular disturbance etc, secondary to the primary trauma.
However, I have considerable difficulties in accepting that the abnormalities were caused as Dr Kendall suggested.
Dr Kendall accepted that his hypothesis could not explain all of the Claimant’s abnormalities, e.g. it could not explain the abnormality in the optic nerve which is not on the suggested line of trauma. Indeed, as Dr Kendall’s fellow expert neuroradiologist, Dr Chong, stressed, the Claimant’s abnormalities are anatomically separate, involving disparate parts of the brain, not readily open to explanation by a single axis of trauma. Dr Chong has two decades of recent experience in paediatric neuroradiology at Great Ormond Street Hospital; and he was a particularly impressive witness.
Although the relevant experts were agreed that such trauma might occur without leaving a skin lesion, Dr Chong said he would have expected to see such a lesion where the needle penetrated the skull on the axis of trauma. The genetics experts were agreed that the pigmented hairy naevus noticed by the Claimant’s parents (see paragraph 20 above) – and thought by them to mark an entry point, because it was specifically referred to in the July 1996 claim letter – has no likely significance (joint statement, paragraph 9). All of the five cases in Squier et al 2000 had an apparent skin lesion at the apparent point of needle entry; although Dr Squier said in her oral evidence that such a lesion might not be seen if (e.g.) it were in the scalp. Dr Kendall’s axis of trauma suggests that it entered through the Claimant’s face. On balance, the evidence was that such an entry would at least usually have left some mark.
There is no marked linear track within the Claimant’s brain. The expert pathologists were agreed that that does not in itself exclude a needlestick injury and, in their joint statement (at paragraph 4), they said that it was not possible to draw any inferences on causation from this absence because of a dearth of data. However, Dr Squier said in her report (paragraph 11) that the absence of a unilateral linear or tract-like pattern of damage argues against a needle injury; and, in her oral evidence, she was clear that she would have expected much more damage if there had been deep penetration of the brain by the needle, even if the penetration had been more or less midline and thus to an extent between the hemispheres. Such penetration would have caused, she said, “massive damage”. Squier et al 2000 was accepted by Dr Jacques as the principal study in the pathological literature. Case 1 in that paper concerned an amniocentesis, undertaken at 18 wks 6 days, known to have penetrated the fetal skull (because there was evidence of relevant tissue, including the germinal matrix, in the amniotic fluid). The fetus was aborted at 20 weeks. On pathological examination, the brain showed clear severe haemorrhaging in the deep periventricular tissue, with a tract leading to a large area of haemorrhaging and necrosis in the white matter of the brain. With regard to the degree of damage that might be expected from a deep penetration of the brain, Dr Jacques agreed (see his report at pages 6-7); as did Dr Chong, who also said that, although healing may occur over time, the needlestick theory does not readily explain the apparent normality of the Claimant’s brain between the two thalamic lesions.
Thus, whilst accepting that the brain could recover from trauma and it is possible that the track of a needle penetrating the brain might disappear over time, in the absence of a firm linear track of damage, neither expert pathologist considered it likely that there had been deep needlestick penetration of the brain in this case. It must be acknowledged that there are few recorded instances of pathological investigation in cases where the fetal brain has, or might have been, penetrated. However, with regard to this issue, I consider the paediatric neuropatholgists’ evidence generally – and Dr Squier’s evidence that it is unlikely that there was deep penetration of the brain by the amniocentesis needle in this case, in particular – especially compelling.
Although Dr Squier said that she would only expect microcephaly where (unlike this case) there was substantial tissue loss, and the evidence was that blood within the amniotic fluid may disperse over time, there is in fact no evidence of reduction in head growth, or any signs of bleeding or pooling blood on the later scans, which, if present, may have supported the contentions of those experts who favoured the direct trauma mechanism. As it is, the absence of microcephaly in this case does not assist on the issue of causation, one way or the other.
Nevertheless, Dr Squier did not consider the abnormalities to be genetic. Even if there was not deep penetration by the needle, that did not (she considered) exclude damage by the needle caused in some more subtle way.
In her view, the abnormalities were caused, not by deep penetration of the brain, but by the needle penetrating the head and damaging surface structures of the brain including the anterior cerebral artery. Such damage could cause bleeding and/or inflammation which could compromise the blood flow to the disadvantage of tissues at some distance from the initial traumatic injury. Bleeding at the surface of the brain might lead to the pooling of blood elsewhere in the brain, which might itself interfere with blood flow. Furthermore, while fetal blood vessels are not fully muscularised at that stage, she said that leptomeningeal arteries may have an identifiable layer of muscle by 16 weeks gestational age (Footnote: 21); and so such vessels could suffer from vasospasm, if there is interference with the blood flow.
However, I accept the evidence of Dr Jacques that such a theory is, at best, improbable and speculative. He said he was unaware of any literature that suggested the pooling of blood in the circumstances of this case was likely, because of the effects of amniotic fluid, the inevitable movements of the fetus and the limited effects of gravity on the fetus in utero. Although the evidence was that such pooling might disperse, it is certainly not noted on later scans performed on Mrs Hogg. Dr Rosenbloom, the Claimant’s expert neurologist, gave firm and compelling evidence – which I accept – that the musculature of the branches of the anterior cerebral artery is not present at 15 weeks. He also seemed unpersuaded by Dr Squier’s reliance upon the leptomeningeal collateral circulation system. He consequently ruled out the possibility of vasospasm, and felt unable to accept Dr Squier’s hypothesis as to primary mechanism at work. For those reasons, I too consider the mechanism inherently unlikely.
However, I accept that the Defendant’s case that the abnormalities were caused by some intrinsic (probably genetic) cause is also not without its difficulties.
The diagnostic chromosomal testing was normal. Higher resolution microarrays testing for mutations of genes HESX1, SIX2, SOX3 and OTX4 which have been reported as being associated with SOD was never done. Professor Patton suggested further testing in the conclusion of his report (paragraph 9.2). The reason for the failure to perform further tests is something of a mystery: I do not accept the suggestion made by Professor Patton that the Claimant (or, rather, his parents) had in some way refused to allow such a test. They clearly did no such thing. However, as I have indicated (see paragraph 38 above), the chance of one of those genes being implicated in SOD is in any event less than 5%. Dr Ogilvy-Stuart gave evidence to the effect that there is no known case of one of those genes being implicated where diabetes inspidus or any other defect in the posterior pituitary has been reported. Dr Reckless fairly accepted that that made it less likely that the Claimant’s diabetes inspidus or other abnormalities/conditions were caused by a mutation of one of those genes. I am satisfied on the balance of probabilities that the genes which to date have been associated with SOD are not implicated in the Claimant’s case.
Furthermore, Professor Patton (the Defendant’s genetics expert) was less than an impressive witness. In his report (paragraph 6), he gave four reasons for his opinion that the Claimant’s brain malformations are likely to be genetic, as follows.
Testing power has greatly increased since the general chromosome test was performed on the 1985. Further tests might reveal a genetic change associated with SOD. However, there is no evidence that the Claimant has any relevant gene mutation that would now be identified by further tests; and I have found that he does not (see paragraph 77 above).
The pattern of pituitary failure would be typical of genetically induced SOD. However, (a) endocrinology is outside Professor Patton’s expertise, and (b) for that proposition, he relied upon Webb & Dattani which, in cross-examination, he accepted did not support the proposition.
Professor Patton relied upon the fact that a relative of the Claimant had a brain malformation. However, he accepted in the joint statement of experts (paragraph 8) that that was not relevant.
He considered that more genetic mutations would be found to explain other cases of SOD; but, in the meantime, he accepted that there was less than a 50% chance that the Claimant’s abnormalities resulted from known genetic mutations. In fact, as I have indicated, general data and the joint statement of the genetics experts suggest the figure is less than 5%; and, for the reasons I have given, I do not consider that cause operative in this case.
The Defendant’s case was therefore not greatly advanced by Professor Patton.
Furthermore:
The Claimant’s experts (particularly, Dr Squier) were impressed by the fact that, although the abnormalities generally affect the mid-line structures, they are asymmetrical, focal and partial. For example, the corpus callosum appears to have formed properly, although the anterior part now has abnormalities. Further, some anterior midline structures (e.g. the sagittal sinus and falx) appear unaffected. Dr Kendall noted that the cingulate sulcus and cingulate gyrus are marked, and appear normal. The Claimant’s experts considered that, if the defect were genetically based, the abnormalities would more likely have been symmetrical and would have affected all (or more) of the anterior midline structures.
Dr Squier said that, if the problem had had a genetic origin, she would have expected to have seen other characteristic features (e.g. brain calcification, cystic cavities in the brain and heart malformations), not seen in this case.
The abnormalities affect parts of the brain which develop at different times. Dr Ogilvy-Stewart said (I believe, uncontentiously) that the hypothalamus develops at 4-6 weeks, and is fully formed at 14 weeks. Dr Kendall said that the thalami develop at (say) week 5, long before the corpus callosum. More controversially, reliant upon older papers (Footnote: 22), Dr Squier said that the corpus callosum develops between 11 and 17-18 weeks: although, as she accepted in her oral evidence, more recent data suggest that the lower margin of the septum is in place by week 10 and the corpus callosum is complete and easily recognisable by week 14 or 15 (Footnote: 23). Dr Kendall said that he found it difficult to envisage a gene that could cause a developmental abnormality to the thalamus in week 5, but then “go to sleep” and re-operate when the corpus callosum and septum were developing in, say, weeks 14-15. If, as Dr Chong suggested, the genetic defect operated in the hemispheres at the time the bundles of Probst were developing, that would be a third distinct operative time. Dr Kendall said that a gene mutation that caused different developmental abnormalities at different times, whilst possible, was very unlikely.
The obstetric experts were agreed that the umbilical cord would be so fine at 15 weeks, that it is unlikely that the blood in the samples would have come from it. Ms Nicholls noted “posterior placenta”. This makes it unlikely (they said) that the fetal blood would have come from the placenta, because it would mean the needle crossing more or less the entire diameter of the amniotic sac
Nevertheless, the expert witnesses (including both Professor Patton and Dr Reardon) all considered that other gene mutations associated with/causative of SOD will in due course be found, in explanation of some of the large proportion of SOD cases which, at present, have no known aetiology; and none considered the abnormalities in the Claimant’s case to be inconsistent with a genetic cause.
As I have already indicated, this issue is far from easy. However, upon particularly careful reflection, I have concluded that the Claimant has failed to prove that his abnormalities were caused by the amniocentesis procedure. In coming to that conclusion, I have taken into account all of the matters raised before me, including the above. I have particularly taken into account the following.
Whilst it is for the Claimant to prove on the balance of probabilities that his injuries were caused by the amniocentesis, he does not have to prove a particular mechanism. I have indicated above some of the difficulties faced in proving that any of the mechanisms he has put forward was operative; but his task is simply to prove that any mechanism triggered by the amniocentesis, individually or in combination, caused the abnormalities. That is how I have approached the matter.
I have found that none of the four genes which have been associated with SOD is implicated in this case – and so any genetic cause is, as yet, scientifically unidentified. Furthermore, I accept that cases of SOD are rare (1 in 10,000 live births) and cases of any fetal damage caused by an amniocentesis needle are also rare (so that a case of fetal damage causing SOD must, as a matter of statistics, be of compound rarity); but no case of SOD caused by a needle has been reported anywhere in the literature. Whilst technically possible – because of the diagnostic criteria to which I have referred – it is inherently very unlikely indeed.
Any theory must explain abnormalities to diverse parts of the brain, which develop at different times; and so any theory is dependent upon a mechanism that operates over time. Dr Squier suggested some form of vascular disturbance; but that may have an extrinsic or intrinsic cause.
Whilst uncommon – indeed, very rare – on the basis of current scientific knowledge, genetic mutations may affect development in an idiosyncratic way and even intermittently over a period of time. For example, homeobox genes act as “commanders”, and control other genes.
Whilst the abnormalities in this case could result from (or be consequent upon) traumatic damage, in my view the more likely explanation is that they have an inherent cause. Whilst not symmetrical, they generally affect midline structures. The literature shows that SOD may generally exhibit in less than a wholly symmetrical form; and Dr Chong said that asymmetric gene-driven abnormalities within the thalami are not unknown, with at least one (I accept, unrelated) genetic disorder of the brain (porencephaly) being asymmetric. It is being slowly discovered that genetics might be capable of identifying connections between apparently unrelated things. On the other hand, some lesions which are apparently classic encephaloclastic in form (i.e. appear to have a destructive cause) have been found to have a genetic basis (Dr Jacques report, paragraph 1).
As I have indicated, Dr Chong’s evidence – which I accept – was to the effect that where the septum pellucidum attaches to the fornix, that usually forms a Y-shape; and that shape is maintained even where the septum is later destroyed, because it is an inherent part of the morphology of that part of the brain. Furthermore, in the Claimant’s case, the septum is entirely absent: despite the septum having formed (or started to form) by week 14-15, there is no vestige present. Dr Kendall accepted that, by that time, the septum would have started to form; but, after more than twenty years, he said you would not expect necessarily to see any remnant. However, I find the evidence of Dr Chong on this point compelling in evidencing that the septum never formed.
No bundles of Probst are present. Dr Kendall said that that is indicative of the corpus callosum having formed and being later damaged – because, if it did not form, then those bundles should still be found in the hemispheres. However, Dr Chong said – and I accept – that that might be so if there was complete agenesis of the corpus callosum (i.e. if it did not form at all); but, in the Claimant’s case, it did form, but only partially developed. In those circumstances, he said, it is more likely that the “missing” bundles were never formed. Again, in my view, this points to abnormality of the corpus callosum, despite its asymmetry, being the result of an inherent developmental problem.
SOD does not appear as a single homogenous entity. It has been said that “There is a wide variation in the severity of the clinical features found, and in their association with other diagnoses, which follows no clear pattern” (Footnote: 24). Dr Chong said that “the abnormalities are a mixture of missing parts, cavities, disorders of neuronal migration and disorders of neuronal organisation which relate to different times in brain development” (joint statement, paragraph 11) – and, when the abnormalities are looked at as a whole, there is more likely to have been an inherent cause. I found that evidence convincing.
Mr Havers submitted that the circumstances of the amniocentesis procedure themselves point to a traumatic cause. However, I do not agree. He relied upon the following matters:
He referred to the presence of fetal blood – in high concentration – in the samples (which also originally drove Mr & Mrs Hogg to the conclusion that the abnormalities were caused by the amniocentesis): but (a) as I have indicated, 25% of amniocenteses at that time resulted in bloody taps, and (b) no fetal tissue was found in the samples. Mr Mason says that the most likely source of blood was not the fetus, but the placenta (a highly vascular body), citing his own experience of (in very different circumstances) deliberately perforating a fetus and there not being significant amounts of blood. Although consistent with penetrating the fetus and damaging the fetal circulatory system, the source of the fetal blood in the samples is more likely to have been the placenta.
Mr Havers referred to the low volume of aspirated fluid, which suggests that the needle was not in a pool of free fluid. However, neither sample was a dry tap; so that the needle was, at some stage, in free fluid. The better explanation is that the needle perforated the placenta, resulting in a bleed into the fluid which was then aspirated. The needle appears to have moved during the second tap, to have been eventually outside the amniotic sac, resulting in a very small sample.
Mr Havers referred to the reference in Ms Nicholls’ note that the placenta was “posterior”; but Mr Mason said that that does not rule out the placenta extending laterally round the side wall of the sac. The notes often record only where the majority of the placenta lies. Indeed, although not relied upon by Mr Mason (nor is it relied upon now by me), it is noteworthy that on the 10 December 1985 scan of Mrs Hogg there was noted: “Posterior placenta onto rt lat wall”.
In my view, on all the evidence, it is likely that the amniocentesis needle perforated the placenta at the lateral side of the amniotic sac, and Dr Robinson aspirated fluid with blood from the placenta in both samples, withdrawing the needle during the second aspiration so that it exited the sac before completion.
For those reasons, Mr Havers – who could not have put the Claimant’s case more forcefully or effectively – has failed to persuade me that it is more likely than not that the Claimant’s abnormalities of the brain were caused by the amniocentesis.
Conclusion
I have every sympathy with the Claimant, and his parents who have contested this claim moderately and with fortitude over many years. As I hope I have already emphasised, I am in no doubt that Mrs Hogg has brought the claim on her son’s behalf with sincerity of purpose. However, for the reasons I have given, despite those efforts, she has failed to persuade me that the condition from which her son suffers was caused by the amniocentesis at the focus of this action.
Consequently, I must dismiss the claim.