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You are here: BAILII >> Databases >> England and Wales High Court (Queen's Bench Division) Decisions >> Hogg v The Secretary of State for Health [2015] EWHC 267 (QB) (12 February 2015) URL: https://www.bailii.org/ew/cases/EWHC/QB/2015/267.html Cite as: [2015] EWHC 267 (QB) |
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QUEEN'S BENCH DIVISION
Strand, London, WC2A 2LL |
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B e f o r e :
____________________
PETER LUKE HOGG (a Protected Party through his Mother and Litigation Friend CHERRYL DIANE HOGG) |
Claimant |
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- and - |
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THE SECRETARY OF STATE FOR HEALTH |
Defendant |
____________________
Margaret Bowron QC (instructed by DAC Beachcroft LLP) for the Defendant
Hearing dates: 19, 20, 21, 22, 23 and 28 January 2015
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Crown Copyright ©
Mr Justice Hickinbottom :
Introduction
i) Mr Myles Taylor (Consultant Obstetrician and Gynaecologist at the Centre for Women's Health, Royal Devon & Exeter Hospital)
ii) Dr Waney Squier (Consultant Neuropathologist at the John Radcliffe Hospital, Oxford)
iii) Dr Amanda Ogilvy-Stuart (Consultant Neonatologist and Endocrinologist at the Rosie Hospital, Cambridge)
iv) Dr Willie Reardon (Consultant Clinical Geneticist at Our Lady's Hospital for Sick Children, Dublin)
v) Dr Brian Kendall (Consultant Paediatric Neuroradiologist at HCA Wellington Hospital, London)
vi) Professor Alistair Fielder (Professor Emeritus of Ophthalmology at City University, London, and formerly Consultant Ophthalmologist at Hillingdon Hospitals, London) and
vii) Dr Lewis Rosenbloom (Consultant Paediatric Neurologist with Alder Hey Children's Hospital, Liverpool).
The following were instructed on behalf of the Defendant:
i) Mr Gerald Mason (Consultant in Feto Maternal Medicine)
ii) Dr Tom Jacques (Consultant Paediatric Neuropathologist at the UCL Institute of Child Health and Great Ormond Street Hospital for Children)
iii) Dr John Reckless (Consultant Physician and Endocrinologist with the Royal United Hospital, Bath)
iv) Professor Michael Patton (Professor Emeritus of Medical Genetics and Consultant Clinical Geneticist at St George's Hospital Medical School and Portland Hospital, London)
v) Dr Kling Chong (Consultant Paediatric Neuroradiologist at Great Ormond Street Hospital for Children)
vi) Mr John Elston (Consultant Ophthalmic Surgeon at the John Radcliffe Hospital, Oxford) and
vii) Dr Gayatri Vadlamani (Consultant Paediatric Neurologist at Leeds Royal Infirmary).
Medical Background
The Case History
The Relevant Anatomy
The Claimant's Brain Abnomalities
i) The septum pellucidum is completely absent.
ii) 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.
iii) 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.
iv) Posterior to the abnormalities in the left thalamus, there is a cystic abnormality to the right thalamus.
v) The posterior parts of the fornix appear to be normal; but the anterior columns and mammillary bodies are small.
vi) 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.
vii) 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.
viii) The optic nerves on both sides and the optic chiasm are small.
Septo-Optic Dysplasia
The Issues
i) Issue 1: Were the hospital staff negligent in estimating the Claimant's gestational age to be at least 16 weeks?
ii) 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?
iii) 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
"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.
i) 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[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.
ii) The second edition of Chudleigh & Pearce was published in 1992. Even the first edition was published after the relevant events[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[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.
iii) 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"[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.
Issue 2: The Ultrasound Scan
i) 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.
ii) 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.
iii) 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.
i) 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.
ii) 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[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.
iii) 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.
iv) 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.
v) 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.
vi) 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.
Issue 3: Causation
The Issue Identified
i) 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.
ii) 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.
iii) Neuronal migration damage, as a result of the damage to the germinal matrix.
Discussion
i) 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.
ii) 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.
i) 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.
ii) 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.
iii) 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.
iv) 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.
v) 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.
i) 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).
ii) 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.
iii) 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.
iv) 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.
i) 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.
ii) 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.
iii) 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[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[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.
iv) 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
i) 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.
ii) 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.
iii) 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.
iv) 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.
v) 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).
vi) 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.
vii) 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.
viii) 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"[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.
i) 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.
ii) 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.
iii) 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.
Conclusion
Note 1 Squier et al. Five cases of brain injury following amniocentesis in mid-term pregnancy. Dev Med & Child Neur 2000; 42: 554-600 (“Squier et al 2000”). The article reviews five cases of injury to the fetal brain following mid-trimester amniocentesis. [Back] Note 2 De Morsier G. Etudes sur les dysraphies cranio-encephaliques. III. Agensie du septum lucidum avec malformation du tractus optique: la dysplasie septo-optique. Schweiz Arch Neurol Psychatr 1956; 77: 267-292. [Back] Note 3 Hoyt WF, Kaplan SL, Grumbach MM, Glaser JS. Septo-optic dysplasia and pituitary dwarfism (letter). Lancet 1970; 1: 893-894. [Back] Note 4 See Barkovich A, Fram EK, Norman D. Septo-Optic Dysplasia: MR Imaging. Radiology 1989; 171: 189-192. [Back] Note 5 Raybaud C. The corpus callosum, the other great forebrain commissures, and the septum pellucidum: anatomy, development, and malformation. Neurology 2010; 52: 447-477 (“Raybaud 2010”). [Back] Note 6 Webb EA and Dattani MT. Septo-optic dysplasia. Eur J of Hum Gen 2010; 18: 393-397 (“Webb & Dattani”). [Back] Note 7 Patel H, Tze WJ, Crichton JU, McCormick AQ, Robinson GC, Dolman CL. Optic nerve hypoplasia with hypopituitarism. Septo-optic dysplasia with hypopituitarism. Am J Dis Child 1975; 129(2): 175-180. [Back] Note 8 McCabe MJ et al. Variations in PROKR2, but not PROK2, are associated with hypopituitarism and septo-optic dysplasia. J Clin Endocrinol Metab 2013; 98(3); E547-557. [Back] Note 9 Kelberman D and Dattani MT. Septo-Optic Dysplasia – Novel Insights into the Aetiology. Horm Res 2008; 69: 257-265 at page 258. [Back] Note 10 Lubinsky MS. Hypothesis: Septo-optic dysplasia is a vascular sisruption sequence. Am J of Med Gen 1997; 69: 235-236 (“Lubinsky”). [Back] Note 11 Stevens CA and Dobyns WB. Septo-optic dysplasia and amniotic bands: Further evidence for a vascular pathogenesis. Am J of Med Gen 2004; 125A: 12-16 (“Stevens & Dobyns”). [Back] Note 12 Chudleigh P, Pearce JM. Obsetric Ultasound: How, why and when. Churchill Livingstone. 2nd Edition; 1992. [Back] Note 13 Hadlock FP, Deter RL, Harrist RB, Park SK. Fetal biparietal diameter: a critical re-evaluation of the relationship to menstrual age by means of real-time ultrasound. Jour of Ultras in Med 1982; 1: 97-104. [Back] Note 15 Chudleigh P, Pearce JM. Obsetric Ultasound: How, why and when. Churchill Livingstone. 1st Edition; 1986. [Back] Note 16 Namely Campbell S and Newsman GB. Br J Obstet Gynaecol 1971; 78: 513. [Back] Note 17 Also at page 84. [Back] Note 18 E.g. Benacerraf BR and Frigoletto FD. Amniocentesis under Continuous Ultrasound Guidance: a Series of 232 Cases. Obs & Gynae 1983; 62: 760-763. [Back] Note 19 Bencerraf BR and Frigoletto FD. Amniocentesis under continuous ultrasound guidance. Obs & Gynae. 1983; 62(6): 760-763. [Back] Note 20 That is apparently derived from Squier et al 2000 (cited at footnote 1 above), to which I was referred, which relies upon data found in earlier papers, namely (i) Ron M et al. The clinical significance of blood-contaminated mid-trimester amniocentesis. Acta Obsterics and Gynaecologoy Scandinavia. 1983; 61: 41-43. and (ii) Williamson RA, Varner MW, Grant SS. Reduction in amniocentesis risks using a real-time needle guide procedure. Obs & Gynaec. 1985; 65: 751-755. [Back] Note 21 For this proposition, Dr Squier relied on Gilles FH and Nelson MD. The Developing Human Brain: Growth and Adversities. Clinics in Developmental Medicine No 193 2012 at page 186, which states that “By midgestation [i.e. 13-20 weeks], many leptomenigeal vessel walls have developed sufficient muscularis or collagenous adventitia to be recognisable as arteries or veins.” [Back] Note 22 Notably Rakic P and Yakolev PI. Development of the Corpus Callosum and Cavum Septi in Man. J Comp Neur 1968; 132: 45-72 [Back] Note 23 Raybaud C. The corpus callosum, the other great forebrain commissures, and the septum pellucidum: anatomy, development, and malformation. Neuroradiology 2010; 52: 447-477 at pages 456-457. [Back]