C (A child), Re [2012] EWCA Civ 1477

[2012] EWCA Civ 1477Case No B4/2012/2039
IN THE COURT OF APPEAL (CIVIL DIVISION)
ON APPEAL FROM SHEFFIELD DISTRICT REGISTRY
HER HONOUR JUDGE CARR QC
SE12Z00226
Venue Royal Courts of Justice, Strand, London, WC2A 2LLDate 16/11/2012
Before
LORD JUSTICE MCFARLANERe: A (A child)
Hearing Hearing date : 1 November 2012
Mr Michael Shrimpton (instructed by Brendan Fleming Solicitors) for the Appellant
Mr Anthony Hayden QC and Mr Charles Prest (instructed by Rotherham Metropolitan Borough Council) for the First Respondent
Ms Jo Delahunty QC and Mrs Denise Marson (instructed by Howells Solicitors) for the Second Respondent
Judgment
[1]This is an application for permission to appeal which relates to a young boy, C, who was born on [a date in] 2009 and is therefore now aged just over three years. At the very beginning of his life, when he was only some four weeks old, it was discovered that C had sustained no fewer than twelve fractures of different types to different parts of his body. Expert evidence indicated at least two separate dates upon which the fractures had been sustained. In addition a week or so earlier concerning signs in his genital area had indicated either some form of infection or inflicted trauma.[2]Once the existence of the fractures had been discovered, C was not returned to the care of his parents and he became the subject of care proceedings. At the conclusion of a fact finding hearing on 5th July 2010, HH Judge Carr QC sitting in the Sheffield County Court concluded that all of the injuries to which I have referred were inflicted upon baby C by one or other of his parents. Following an assessment of the options for C’s future care, in a further judgment on 21st June 2011, Judge Carr ruled out the rehabilitation of C to his parents and made a full care order. The case returned for a third and final time before Judge Carr in June 2012. On that occasion the judge heard an application made on behalf of the parents by their solicitor for the fact finding process to be re-opened. In a reserved judgment dated 18th June 2012 the judge dismissed that application and granted the second application, which was by the Local Authority for an order authorising them to place C for adoption. By an application dated 8th August 2012 the parents applied to this court for permission to appeal the two determinations made by the learned judge in June.[3]A direction has been made that nothing is to be published as a result of this hearing which would seek to identify C as a child who is the subject of these proceedings or his parents as being the parents of such a child.[4]In order to establish the context in which this application is made it is necessary to descend to some detail. C was born on 3rd October 2009, apparently some ten to fourteen days beyond his expected due date. The delivery was assisted by forceps, but was otherwise unremarkable and baby C was described as fit and healthy.

(d) bruises to the perineum and left outer thigh

[5]On the occasion of that referral the doctors concluded that the signs were probably as a result of infection and C was discharged home with a prescription for antibiotics.[6]C was next presented at the hospital some four days later on 30th October 2009 at 22.14 hours with a swollen right leg. A subsequent skeletal X ray disclosed multiple fractures of ribs, fractures to his tibia and fibula which were metaphyseal in nature together with a transverse fracture of his right femur. There were twelve fractures in all which had been sustained by this four week old baby who was obviously not self-mobile.[7]The fact finding judgment of 5th July 2010 records that the parents were given full rein by the court to identify and instruct whatever relevant medical experts they considered might be able to assist the court in understanding how baby C came to manifest the injuries and symptoms that I have described. In particular Professor Bishop, who holds the chair of Paediatric Bone Disease at Sheffield Hospital, and who is regarded internationally as an expert in paediatric bone conditions, was jointly instructed by all parties to the proceedings. It is a feature of this case that at the fact finding hearing each of the respective experts were unanimous in their conclusion that the probable cause for the groin symptoms and the fractures was trauma inflicted on baby C at some time after his birth. On the basis of that expert opinion, but also on the basis that the judge, for reasons given in the judgment, found that the parents’ evidence indicated fault lines in their relationship and in their credibility when giving evidence to the court, HH Judge Carr made a very clear finding that baby C had indeed been injured in the period between birth and final presentation at the hospital and that the only possible perpetrators of the injuries were the mother and/or the father.[8]The parents’ application to the learned judge in June of this year was to re-open the whole fact finding process. The application was widely based and the skeleton argument on the parents’ behalf identified no fewer than twenty six factors which, it was submitted, now fell to be reconsidered in the light of suggested developments in medical understanding or which had not been given sufficient prominence at the original hearing. In a reserved judgment delivered on 18th June 2012 the judge reviews each of the points made to her on behalf of the parents and, in turn, rejects each one. Before doing so the judge noted that at the previous hearing “the court allowed the instruction of every expert/test requested by the parents, including, in particular – and contrary to medical opinion – genetic testing for possible bone disorder” and “even during the course of the hearing the court checked with those representing the parents whether there was any other expert evidence they sought – and was told ‘no’”.[9]During the course of the June hearing the judge was taken to two recent decisions, London Borough of Islington v Al Alas and Wray [2012] EWHC 865 (Fam) and A County Council v M and F [2011] EWHC 1804 (Fam). The first of these cases, which I will refer to as “Wray”, achieved national publicity. In the Wray case, Mrs Justice Theis held that bone injuries seen on a young child were the result of rickets rather than inflicted injury. HHJ Carr, in the present case, considered that neither of these two new authorities involved any new point of law, and did not necessarily assist her evaluation of Baby C’s case. She drew particular attention to the following caveat given by Theis J in the Wray judgment:
“It is important to remember that my conclusions set out below are entirely related to this case. Despite their differences of opinion, all the medical experts agree this case is extremely complex. By their very nature, cases such as this are very fact specific and great caution should be adopted in using any conclusions I reach to support any wider view outside the very specific facts of this case…”
[10]Despite the fact that it is possible to summarise the June 2012 judgment in short terms, concluding as it did that each of the points raised on behalf of the parents took matters no further, it is right to record that the judgment itself indicates a significant amount of time and consideration given by the learned judge in which she traces each of the factors relied upon back to the evidence and conclusions that were current in the 2010 process.[11]The Notice of Appeal in support of the present application for permission to appeal was couched in similarly wide terms but, relying on the Wray case, argued that the development of medical understanding in relation to vitamin D deficiency, rickets and brittle bones justifies the Court of Appeal now considering whether or not the judge was correct in refusing to permit the re-opening of the fact finding exercise.[12]When the application for permission to appeal came before me for oral hearing on 19th September 2012 counsel for the parents, Mr Michael Shrimpton, was able to cast the parents’ case in a much more focussed manner. In the course of the judgment that I gave on that day I summarised the position as follows:
“6. What is the point that the parents seek to make? It can be put in very short lay terms. They contemplate, understanding as they and their advisors now do on the basis of medical knowledge, that it is possible for an unborn child to develop a deficiency in vitamin D to the extent that their bones are unduly soft, or otherwise be symptomatic of congenital rickets. The baby is born, and this was a difficult birth which may have been beyond term, although as I understand it the dates were not precise; and it is possible, say the parents, for the birth process, without any negligence or rough handling on the part of the medical team involved, to have caused the fractures in this case. The child is then born, no doubt it is postulated as at that moment deficient in vitamin D, but the child is then fed either entirely upon prepared milk or a mixture of breast and prepared milk, the prepared milk having vitamin D supplement within it. 7. Baby C was born on 3 October 2009, and his vitamin D was not measured at all until tests were undertaken in November, a month or more later. Those tests were normal. The argument on behalf of the parents is that it is not remarkable that the child’s vitamin D levels, once he ceased to be dependent upon the mother’s system, were up at normal levels because of the supplement he had been obtaining in the milk, and it does not prove one way or the other what his vitamin D level will have been at the moment of birth. I use the phrase “once he has ceased to be dependent upon the mother’s system” because it is a fact established on the medical evidence in the case that the mother herself has a modest -- and I think it is modest -- vitamin D insufficiency, and that therefore she may have been compromised in her ability to provide through the placenta an adequate supply of vitamin D to her unborn child. That is the synopsis of the parents’ case. 8. My concern on reading the papers was that, whilst it is possible to understand that process, it would be impossible now, three years after C’s birth, to have any firm clinical readings or tests which could prove one way or the other, or even indicate one way or the other, that what is put forward by the parents was anything more than an intellectual possibility. The way the case was put before the judge indicates that she was not given any firm clinical hook upon which to see that the parents’ case might hang. 9. This morning, on asking counsel, Mr Shrimpton, who represents the parents, whether there is any material that points one way or the other, I have been told of the abnormal liver readings which were obtained on 26 October, and, without now reading into this judgment the six different levels that I have been given, it is plain from what I have been told that two of those six indicate a modest low reading outside the “normal” range, one reading which is modestly above the range, but three which are quite markedly outside the normal range. The submission is made by lawyers to a judge, therefore between people who have no medical background, that the liver function is important in the sequence of production of vitamin D, and these abnormal liver readings may provide some base of clinical evidence to give support to the process that the parents now contemplate may have been involved. 10. Looking at HHJ Carr’s judgment, it seems that before her the point was not made in any way that is similar to that in which it is now made to me. At page 12 of her judgment, at (n) in the list of symptoms, the judge says this simply about C’s liver: “Abnormal liver function – this was well-known at the time of the Finding of Fact.”
And so far as the mother’s vitamin D insufficiency, she says this at page 13:
“(g) vitamin D deficiency – this was well-known at the time of finding of fact. It misses the essential point: [C]’s vitamin D level was normal.”
And of course, C’s vitamin D level was normal. The way in which the case is now put before me, as I have indicated, draws together the mother’s vitamin D insufficiency and the abnormal liver readings to indicate that there may be a possibility of concluding that the baby’s vitamin D level was insufficient at the time of his birth. 11. I am concerned now, having been exposed to the way in which the case is now put, that the conclusions reached in the fact-finding may be more susceptible to review than will have been obvious to HHJ Carr in the way that the case put to her. On enquiring why, as between June of this year, when HHJ Carr heard the case, and September, three months later, when I am hearing it, the matter is put in different ways, I am told that an expert, a Professor Nussey, who is an endocrinologist at St George’s Hospital in Tooting, who was an expert in the Wray case, has been instructed in another case in which the same solicitors who represent the parents here are instructed, and that between June and now Professor Nussey has produced his report in that case and given prominence to the liver readings for the child in that case, which leads to the more finessed and focused submissions that Mr Shrimpton has been able to make today.” “Abnormal liver function – this was well-known at the time of the Finding of Fact.” “(g) vitamin D deficiency – this was well-known at the time of finding of fact. It misses the essential point: [C]’s vitamin D level was normal.”[13]In consequence of the way in which the case was put in September, I adjourned the application for permission to appeal, gave permission to the parents to identify and instruct an appropriate expert, and directed that the case be re-listed as soon as possible after four weeks on notice to the Local Authority and Children’s Solicitor so that a balanced and informed view could be taken on the question of permission to appeal.[14]Fortunately the parents were able to instruct the expert of their choice for this purpose. He is Professor Stephen Nussey, who is professor of endocrinology and a consultant endocrinologist at St George’s Hospital in London. Following a letter of instruction which came from the parents’ solicitors alone, Professor Nussey produced his first report dated 2nd October 2012. He then responded to various email queries raised on behalf of the parents before producing an addendum report dated 23rd October 2012. This court is extremely grateful to Professor Nussey for undertaking this task within the very tight timetable that had been set.[15]The following would seem to be the important highlights from Professor Nussey’s reports. a) Blood results for baby C’s mother during the period of pregnancy demonstrate vitamin D deficiency in her system. Professor Nussey therefore states:
“thus, it is likely that C was subject to vitamin D deficiency for the majority of his inter-uterine life”; b) Haematology results for baby C’s mother indicate that: “she became progressively iron deficient during pregnancy though this was not confirmed by formal iron studies and it seemed to improve without iron supplements between August and October 2009.”
Professor Nussey explains that iron plays a role in collagen (the protein affected in osteogenesis imperfecta) synthesis and is an essential part of the enzyme that converts inactive vitamin D to its active form in the kidney. The professor knows of no studies examining the effects of combined vitamin D and iron deficiency during pregnancy and infancy; c) Whilst it is likely that C was born with vitamin D deficiency and low iron stores, it is clear that C was bottle fed with vitamin D and iron supplemented proprietary feed. By 6th November 2009 all readings relating to baby C reflected a normal serum vitamin D concentration. d) Professor Nussey concludes:
“Thus, whilst it is recognised that the quantities of vitamin D in formula feeds are calculated to prevent rickets rather than to optimise bone mineralization it is, on the balance of probabilities, unlikely that vitamin D deficiency played a significant role in bone fragility predisposing the fractures which C presented”; e) Later Professor Nussey also concludes: “There appears to be no medical condition linking the presentations due to fracture and its sequelae on 2nd November and 4th December 2009 to that on 26th October 2009.” (The latter date being the day that C was taken to A&E with symptoms around his genitals). f) The final question asked of Professor Nussey was “having considered the medical evidence available to you, please indicate whether or not you have sufficient material to conclude whether or not the child has a medical condition to account for his injuries and if not, what further evidence you would require to draw a conclusion”
. To which Professor Nussey replies:
“From the material available, within my expertise in endocrinology, I do not think there is a medical condition to account for C’s injuries. ” g) In relation to the liver readings which were given prominence at the hearing before me in September, Professor Nussey’s opinion is: “C’s recorded liver function tests were only mildly abnormal and not of a degree that was likely to affect the first activation step.”
Reference to “the first activation step” is to the first stage in any process whereby abnormalities in a baby’s system might affect the formation of bones.[16]On 1st November 2012 the application for permission to appeal was restored before me and was fully contested by leading and junior counsel instructed on behalf of the Local Authority and the child, respectively. In that regard it is of particular note that the solicitor and junior counsel for the child sought to instruct Miss Jo Delahunty QC who was brought into this case for the first time with the specific instruction of advising “if any areas in this case warranted further examination in the light of the science explored, and expert evidence given in, [the Wray case]”. The significance of this instruction is that Miss Delahunty was leading counsel for the parents in the Wray case and therefore likely to be fully aware of the scientific implications of that decision from the perspective of parents who have been accused of child abuse. The decision of the children’s solicitor and junior counsel to instruct Miss Delahunty was, in my view, both wise and responsible. The result has been a very thorough document produced in the form of a skeleton argument which expresses confidence in the safety of the findings made by HH Judge Carr in the present case and seeks to identify, for a number of specific reasons, why this case regarding baby C is in no manner one which falls to be reconsidered in the light of the Wray case.[17]Despite the fact that the opinion of Professor Nussey is almost entirely unsupportive of the parents’ position, Mr Shrimpton on behalf of the parents renews his application for permission to appeal at this hearing by relying upon the professor’s specific confirmation that baby C was vitamin D deficient at birth (see paragraph 15 (a) above). He describes this as the “key finding” in the professor’s report. He argues that this is at odds with the understanding held by the experts at the fact finding process and he regards it as therefore necessary for those experts to be now instructed to review their conclusion in the light of that finding.[18]Mr Shrimpton developed his submission by pointing to the fact that the use of forceps during the delivery provided a potential for trauma to the long bones through a pulling and twisting mechanism sufficient to produce metaphyseal fractures if the bones were weak. He also described the birth process itself, during which the baby’s body is squeezed, as being a sufficient mechanism for rib fractures to occur if the normal consistency of the baby’s bones is compromised by vitamin D deficiency. Mr Shrimpton accepts for the purpose of his argument that the X rays indicate that the fractures were sustained on at least two different dates, but he argues that the earlier set of fractures could have been sustained pre-birth when baby C was still in his mother’s womb.[19]Mr Shrimpton submits that the evidence before the judge in 2010 relating to the date of fractures was based upon an assumption of normal vitamin D levels and therefore now fell to be reconsidered. Mr Shrimpton argues that Professor Nussey’s finding is one that establishes that baby C had “congenital rickets at birth”. He told the court that “the clinical consequence of vitamin D deficiency is congenital rickets”. When asked to point to evidence in support of that latter comment, all that Mr Shrimpton could do was refer to page E 43 of the original trial bundle in which one of the specialists identifies as part of her CV that she is a specialist in “vitamin D deficiency (rickets)”.[20]Mr Shrimpton argues that once it has been established that the understanding of no vitamin D deficiency at birth is not sustainable, all the dating evidence is called into question. He points to Professor Barnes, an expert paediatric neuro-radiologist who gave evidence in the Wray case, as stating that the dating of fractures in infants is in any event problematic. Mr Shrimpton therefore submits that Professor Nussey’s finding “sweeps away the basis for the dating of the fractures given by the experts”. He argues strongly that all of those experts now need to re-evaluate their conclusion and he seeks leave to instruct a fresh expert, Dr Julie Mack, a paediatric radiologist based in America.[21]Separately Mr Shrimpton points to Professor Nussey’s identification of low iron level during pregnancy and a probable low iron level at the time of birth. This is relevant to bone formation for the reasons given by Professor Nussey. Mr Shrimpton then goes on to identify what he claims are six signs of congenital rickets. These are:(a) Some signs of soft dysmorphic features;(b) Hypertelorism(c) Two hernias(d) The identification of Professor Nussey of some sign of intracranial bleeding which might be the result of “birth trauma”(e) The October 2009 symptoms in Baby C’s groin, which Mr Shrimpton says are a result of infection.[22]Pausing there, it was not possible to understand how evidence of some intracranial bleeding or the fact that the child might have had an infection could be set up as positive signs of “congenital rickets”. In any event all six signs (the hernias being two) were features of the evidence at the original fact finding and have not been taken forward by Professor Nussey in his reports.[23]The judge was plainly impressed by the fact that the symptoms seen in baby C’s groin were separate and distinct manifestations unrelated to brittle bone disease. Mr Shrimpton seeks to challenge that position by submitting that a child with low vitamin D would be more vulnerable to infection. It is, however, of note that the groin injury occurred some three weeks after birth and at a time when, as the later readings show, it seems probable that baby C’s vitamin D levels were returning to normal or had already achieved normality.[24]In response to the application Mr Anthony Hayden QC for the Local Authority presents a robust defence for the process undertaken at the fact finding hearing and then earlier this year in considering the application to re-open the findings. He submits that a wide range of extremely experienced experts presented evidence to a seasoned specialist judge whose judgment demonstrates the conspicuous care that she brought to evaluating all of the relevant material. The findings are clear and, submits the Local Authority, nothing has changed. They argue that, far from undermining the process, the reports from Professor Nussey endorse the fact finding conclusion.[25]In particular Mr Hayden points to the prominence that the liver function tests of 26 October 2009 played in persuading this court to adjourn the case in September of this year so that Professor Nussey might be instructed. I have already set out Professor Nussey’s opinion on the liver function tests (paragraph 15 (g) above) and Mr Hayden submits that that opinion comprehensively erodes one of the central issues upon which the parent’s case had been based.[26]Although Professor Nussey is an endocrinologist, he offers a clear opinion as to the causation of the fracture, and concludes that they were not the result of a medical condition. At stages in his report the Professor is clear in indicating where opinion is sought which is outside his experience or expertise, but on this point he is prepared to offer a clear opinion and the court should give it weight.[27]The Local Authority submit that where, on an application for permission to appeal, an applicant seeks the court’s indulgence to obtain a fresh expert’s report, and where that report is delivered and is negative to the applicant’s case, the applicant asks further questions of the expert and receives a yet more negative response, it is an abuse of process for the court to consider further adjournment so that additional expert opinion can be sought.[28]At the core of the Local Authority’s case is a plea for the court to consider the impact of any further delay on this child, who has been in the public care system from the age of some four weeks and is now over three years old. He urgently needs, it is submitted, to move on to a permanent home.[29]The argument on behalf of the child is put in similarly robust terms by Miss Delahunty QC. I have already described how she was brought into the case to provide an informed and independent audit of the expert evidence. Her skeleton argument engages comprehensively with the central argument presented by Mr Shrimpton on behalf of the parents to the effect that, following the Wray case, this case, relating to Baby C, must now be reconsidered.[30]Miss Delahunty is rightly critical of the way in which this matter was presented to me in September. The 2010 fact finding judgment and bundle of expert opinion was not then made available to the Court of Appeal. In view of the need for urgency in resolving this issue I was persuaded to grant the adjournment sought rather than take further time seeking additional paperwork. However, Miss Delahunty argues that the fact finding judgment, which was plainly in the possession of the solicitors acting for the parents, would have demonstrated that HH Judge Carr had before her experts who had a particular expertise in bone disorders and vitamin D deficiency. These experts had been particularly asked to consider the very points now being made relating to the mother’s vitamin D deficiency and the possibility that the baby may have had vitamin D deficiency at birth and that that in turn may explain some or all of the fractures. The experts were also asked to consider if the birth itself could cause fractures and a neonatologist was specifically instructed to address the birth process.[31]Miss Delahunty took the court to the report of Dr Takon, a consultant paediatrician with expertise in rickets who confirmed (page E128) that “rickets does not resolve without treatment”. She also referred to the evidence of Professor Bishop (page E108) where he stated that “it would be difficult to see how C could have been severely deficient at birth, have normal-looking X rays and normal blood tests four weeks later without treatment-level intervention.”[32]Having looked at this matter in depth Miss Delahunty summarises the position as follows:
“From different specialism the same answers were given: birth could not account for the fractures. Neither could vit D or bone density disorders. The experts gave clear answers to clear questions. Vit D deficiency, even had it existed at birth, could not account for the type and age of the fractures identified upon admission.”
[33]In dealing with the oral submission now made by Mr Shrimpton, Miss Delahunty challenges counsel’s assertion that the clinical consequence of vitamin D deficiency is rickets. She accepts that vitamin D deficiency at birth may progress to rickets, but it does not equate to rickets. Miss Delahunty challenges Mr Shrimpton’s approach of cherry picking small parts of the expert evidence from the fact finding process when the total picture presented by all of the experts was entirely contrary to the argument now made.[34]Miss Delahunty characterises the mother’s vitamin D deficiency as “very minor” and therefore the potential for this factor affecting the child’s bones is remote. She describes the parent’s argument as “without hope” and the application for a further adjournment to disclose papers to experts as being totally unjustified.[35]The point made is that vitamin D could go from being down at birth but normal at four weeks, but weakened bones could not go back to normal in that time. It is submitted that Mr Shrimpton seeks to conflate the former, which is established by Professor Nussey, with the latter, which was the position of the experts at the fact finding hearing. The experts’ position is therefore unaffected by Professor Nussey’s insight into the intra-uterine vitamin D levels and that is confirmed by Professor Nussey’s own opinion that the vitamin D is, on a balance of probability, not related to the fractures.[36]I have been impressed by, and grateful for, the thorough process that Miss Delahunty QC and Miss Denise Marson, her junior, have undertaken. I propose to extract section E and F from their skeleton (pages 13 – 19) and publish them as an addendum to this judgment in order that both the thoroughness of the exercise and its clear conclusions can be understood.

Conclusions

[37]Plainly Professor Nussey’s contribution is insufficient to persuade this court to grant permission to appeal at this hearing. Mr Shrimpton accepts that this is the case but applies for an adjournment in order to canvass the opinion of the fact finding experts and to seek a fresh opinion from Dr Mack.[38]I am, as I was at the September hearing, profoundly aware of the impact of any further delay upon the welfare of this young boy. However, if I concluded that there was potential substance in the case as it is now put, I would sanction an adjournment for a further limited period, just as I did at the September hearing.[39]I have given anxious consideration to the matters now raised by Mr Shrimpton. I have done so because of the importance of the court keeping an open mind to the clarification of medical knowledge as it progresses over time. I also do so because I am well aware of the draconian nature of the orders made and the fact that they are entirely reliant upon the opinion of medical experts.[40]I have approached the evaluation of Mr Shrimpton’s arguments first of all as they have been made, which is by taking Professor Nussey’s confirmation that C probably had vitamin D deficiency at birth as the core starting point for his arguments and, at that stage, ignoring Professor Nussey’s overall conclusion, which is plainly adverse to the applicant’s application. Having done so I am totally unpersuaded that Professor Nussey’s vitamin D deficiency at birth conclusion supports the string of consequences that Mr Shrimpton seeks to extrapolate from it.[41]Firstly, no evidential basis has been put before the court for the assertion that low vitamin D establishes that C had congenital rickets at birth. Rickets is a systemic condition which, once established, continues to be present in the child unless and until it is treated. It arises from the inability of the child’s own system to produce vitamin D and is therefore not a condition which arises from the fact that a child may be under-supplied with vitamin D by his mother’s system whilst in the womb.[42]Secondly, no evidence has been put before the court to suggest, let alone establish, that this baby’s bone formation was detrimentally affected by a lack of vitamin D prior to birth. This was a matter that was thoroughly canvassed by the experts at the fact finding hearing, whose number included Professor Bishop, an expert in this field of international renown, and the conclusion was that this was not a factor.[43]Thirdly, and this to my mind is the crucial point, I agree with the Guardian’s submission, which I have already summarised at paragraph 35. Mr Shrimpton does indeed conflate the finding of probable vitamin D deficiency at birth, which can resolve without trace in four weeks, and, on the other hand, inadequate bone formation which would not. For the reasons given more fully in Miss Delahunty’s skeleton, the experts in the fact finding were justified in holding that the absence of any evidence of bone weakness at four weeks was conclusive as to the existence of weakness at birth.[44]Having summarised my main conclusions on Mr Shrimpton’s core submissions, without reference to Professor Nussey’s own overarching opinion, I look more briefly at Mr Shrimpton’s other points.[45]The “six signs of congenital rickets” that he drew attention to, were all known at the fact finding hearing and were not considered diagnostic, or even, it seems, indicative, of rickets by the experts then instructed. The fifth “sign”, namely the groin infection, is not in any event established as an infection. If it were an infection, that would take the case no further and could not possibly be a positive sign that the child had vitamin D deficiency at that stage which is mid way between birth and the discovery of the fractures. The sixth “sign”, relating to an apparent bleed in the brain, is not specific as to its causation, and is no more a “sign” that C had rickets than it is a sign of a number of other possible causations.[46]Finally, in dealing with the parents’ case as it is now put, Mr Shrimpton’s submission that the groin symptoms are probably an infection arising from vitamin D deficiency is based on the premise that the vitamin D level was still low at 26th October. There is no evidence to support that and, indeed, the evidence is that once the child was on a supplemented feed, his vitamin D level would rise, as indeed the later readings show that it did. All of the evidence at the fact finding hearing supported the judge’s conclusion that the groin signs were not as a result of infection and not related to vitamin D deficiency. This is now confirmed by Professor Nussey.[47]Thus far I have avoided all but a passing reference to Professor Nussey’s conclusions, but it is impossible to ignore the reasoned and entirely neutral opinion which this court now has from this eminent expert. I agree with the submission of Mr Hayden in this regard. Once a court has been persuaded to take the step of putting the previous court’s orders on hold so that the applicants are permitted to instruct the expert of their choice for the purpose of investigating and analysing the primary theory that is said to support their application for permission to appeal, and once the result of that process is a wholly adverse conclusion, which entirely knocks out one of the primary planks of the applicant’s case (the liver readings) and expresses a clear conclusion that, despite vitamin D deficiency being present at birth, there is not medical condition identifying a cause for the fractures, it becomes very difficult for the applicant to persuade a court to adjourn further so that additional investigation can take place. That position is compounded where, as here, the applicants ask the expert to re-consider certain aspects of the case and, for a second time and in more explicit terms, the expert confirms his opinion.[48]Having engaged in detail with all of the matters raised by Mr Shrimpton on behalf of the applicant, for the reasons that I have given I am entirely clear that there is no basis for now taking time to canvass the opinion of the fact finding experts or that of a new expert.[49]Before concluding I wish to acknowledge the genuine public interest which followed the Wray case and the reporting of the first hearing of the permission to appeal application in the present case. More generally the court is aware of sustained press comment to the effect that child abuse allegations which turn, as here, primarily upon medical evaluation, are conducted with superficial examination by the courts, reliant upon experts chosen and paid for by the Local Authority and where the evidence is not disclosed to the parents, who are not themselves permitted to instruct experts of their own choosing.[50]So that those who are interested in these matters may see what has occurred in this case and form their own view of the thoroughness and fairness of the process adopted by the Family court, an anonymised copy of the two key judgments in the case is to be released for publication alongside this judgment.[51]Those who take the time to read these judgments will note that at every stage the judge permitted the parents’ legal team to instruct experts on any aspect of the case that they, the parents, considered relevant and that the parents’ choice of expert was accepted by the court. In addition the court agreed to testing of the child whenever such was sought on behalf of the parents, even on one occasion when that testing was contrary to medical advice.[52]In the same context two factors stand out from this short process before the Court of Appeal: a) The parents have been permitted to instruct a nationally eminent expert of their choosing. This has occurred without even the knowledge of the Local Authority or the Children’s Guardian let alone the active involvement of those parties; b) The system, through the sense and wisdom of the solicitor and junior counsel for the child, has secured the introduction into the case at this stage of the very QC who represented the parents in the Wray case and established the existence of rickets. She was, quite properly, instructed to audit and evaluate the evidence in the case and to form her own independent view of the validity of the points now raised.[53]Drawing matters together, the application for a further adjournment so that further expert opinion may be sought is unsustainable. For the reasons that I have given the applicants have no reasonable prospect of persuading the full Court of Appeal to overturn HHJ Carr’s refusal of their application to re-open the fact finding process. In the circumstances permission to appeal is refused. ADDENDUM 54. EXTRACT FROM SKELETON ARGUMENT ON BEHALF OF THE CHILD FOR THE ‘PERMISSION TO APPEAL’ HEARING LISTED BEFORE McFarlane LJ ON THE 1ST NOVEMBER 2012 E THE MAIN ARGUMENT? VIT D DEFICIENCY AS A BENIGN CAUSE FOR THE INJURIES 55. This submission made on behalf the parents lacks a fundamental understanding of the interplay between Vit D Deficiency and rickets and ignores the following: 1). The skull is one of the first bones to lose bone density as its supply of Vit D and the formulation of calcium is sacrificed to the brain, blood and nerves. Vit D deficiency affecting the bones can manifest itself by wormian holes or craniotabes (softening or thinning of the skull). Baby C was delivered by Forceps. Dr Takon (Consultant Paediatrician with specific expertise in Vit D deficiency) advised that ‘rickets result from deficiency in Vit D which affects adequate bone formation. This is a disease of the growing bone and does not occur in utero. It can be caused by nutritional causes such as when there is a diet deficient in Vit D. Rickets does not resolve without treatment. Children with malabsorbtion and abnormal renal function which affects Vit D can present with rickets. C’s kidney functions, liver function and blood results were all normal. C had normal Vit D levels. The classic clinical signs of rickets are bone deformity. In infants the skull, the upper limbs and the ribs are the most affected due to the rapid growth of these bones during this period (Kruse). Deformity of the skull bones and bulging of the ribs are some of the bony changes that can be seen in addition to abnormal laboratory results. C had none of these biochemical or clinical features. He had normal Vit D levels’. 2). If baby C was born with congenital rickets derived from Vitamin D deficiency in utero, Vit D supply would have been its lowest at birth and from that point on would have robbed the bones of their supply before the Vit D supplements provided by the formula milk had taken effect. 3). The dating of the fractures, in any event, takes the point of infliction of them from after birth: the oldest was the 6th rib. Even if we reject the expert opinion that this was not birth related and assume it may be ( because of problems with dating the healing rate of calcium deficient bones ) that leaves thea. Posterior fractures of the right 10th and 11th ribs;b. 8 metaphyseal fractures of both distal and both proximal tibiae, left proximal fibula; both distal tibiae and right distal fibula;c. Transverse fracture of the right femur. 4). These were all dated at less than 11 days as at 2.11.09 i.e.: sustained on or after the 22nd October 2009, Baby C's date of birth being 3.10.09 (Dr Halliday Page E39 (paragraph 5.4). 5). It is significant a. that they were thus most proximate to the normal Vit D reading obtained from Baby C on 6.11.09. and b. That they showed signs of healing (see the well formed callus on the Right femur between 30.10.09 and 4.12.09 and the signs of healing on other fractures between the X rays of 2.11.09 and 12.11.09). The healing process demonstrates that Baby C’s bones were capable of utilising calcium to regenerate and form new bone. 6). This point was emphasised and addressed further by Professor Bishop (whose evidence was accepted by HH Judge Carr QC) at no. 7 page E108 “It would be difficult to see how he could have been severely deficient at birth, have normal-looking x-rays and normal blood tests 4 weeks later without treatment-level intervention (3000 IU vitamin D/day; milk formula contains 40IU/100ml)”; The jointly instructed expert , Prof Bishop , and his conclusions at E107: ‘ C underwent a number of blood tests including two bone profiles, and had his serum PTH measured twice and his serum Vit D level measured once. His levels of calcium and phosphate were at the upper end of normal range for age as is frequently observed following fracture. His serum alkaline phosphates was not elevated (272 and 260 IU/I) and his PTH was suppressed (&) probably because his calcium level was higher than average. His Hydroxyvitamin D level was very good (76.7 n/mol/l on 6.11.09: higher than is seen in infants at that age. These are normal responses following fracture in a Vit D replete individual; prior vitamin D depletion would be unlikely given the formula feeds he had been on ( which contain Vit D and his normal serum PTH and alkaline phosphates. His platelets were slightly elevated and on of the clotting test times were reduced, neither of these are associated with bone fragility. Maternal 25 Hydroxyvitamin D has also been measured and is sub optimal at 39 n/mol/l on 13.11.09 in association with a PTH is close to the upper limit of the normal range at 6.25 pmol/l; however this is not a particularly low level of Vit D for a pregnant mother and one would not expect it to impact on the Vit D status of the new born on transplancental calcium transfer (which is not dependent on Vit D). 7). Dr Takon agreed ‘calcium metabolism in the foetus usually involves transfer of calcium from the mother to the infant. The growing foetus does require increasing calcium requirements which continue to be derived from maternal supply through the placenta. During delivery , when the baby is born, there is an abrupt drop in the supply of calcium which then stimulates the baby’s calcium regulating hormones kicking in and gradual stabilization of the calcium levels in the new born. The calcium levels can therefore be low at birth and then trigger secretions of Vit D in the infant to help stabilize the levels’ ( E 128) 8). Prof Nussey agrees on this critical issue (@ CoA bundle 100) ‘whilst it is likely that (baby C) was born with vitamin D deficiency and low iron stores, it is clear that C was bottle fed with Vit D and iron supplemented proprietary feed. In a population study in Canada a small number of bottle fed children with rickets have been reported (Ward et al Ref 5). However, the serum 25 hydroxyvitamin D on 6.11.09 was 76.7nmol/l and the serum calcium, phosphate and parathyroid hormone were all normal reflecting this serum Vitamin Concentrate. This, whilst it is recognised that the quantities of Vit D in formula feeds are calculated to prevent rickets rather than to optimise bone mineralisation it is ,on the balance of probabilities unlikely that vitamin d deficiency played a significant role in bone fragility pre disposing to the fractures with which C presented’ 9). It is highly relevant that all bar one of the bony fractures were a. of the same age ( less than 11 days old) b. of which 8 were metaphyseal c. posterior re ribs The fractures (in position and type) were considered to be highly indicative of NAI It is not just that those fractures which were present were characteristic of inflicted injuries but the absence of others which might tend to suggest rickets that is relevant• No multiple fractures of multiple ages;• No fractures where the majority were the oldest and most proximate to birth (before the fortified milk had ameliorated any deficiency);• No fractures to the skull or the shoulders during the birth process and applied forces within it ;• No fractures thereafter to those parts of the body most commonly handled in bathing, changing nappies and dressing / undressing. We suggest that not only were the type of fractures sustained by Baby C most commonly associated with inflicted injury but he did not have those fractures which are suggestive of early onset of, and gradually resolving, bone fragility.[9]Not only were the fractures not those of the type, distribution and multiple ages suggestive of rickets but there were also no radiologically evident signs of rickets For example see Dr Halliday @ E 119 just as an example: who had looked at the x rays for signs of oesteopenia (where the bones appear less white on an x ray) and wormian holes (small bones within the sutures of the skull). Nor were there visible signs of widening and splaying of the growth plates or widened periosteal reactions. By itself, it may be that this was not conclusive evidence of the absence of rickets, BUT it is to be seen in conjunction with the point above and the points below.[10]Bone Density/ Appearance. Baby C’s scans and x rays were examined by treating medics and experts for signs of any bone abnormality. This included the skeletal X rays and CT skull imaging. None were found. Again, by itself it may be argued that this does not conclusively rule out rickets but it is highly relevant when considered in conjunction with the other matters in this section. Dr West (Const Paed):
‘no radiological of any underlying bone abnormality’ (E3) Dr Halliday (Neuro Rad) ‘there is no evidence of abnormality of C’s bones on the radiograph which make him particularly susceptible to fracture. In particular there is no evidence of osteogenesis imperfecta or brittle bone disease (E38) and again @ E119 ‘rickets is also associated with osteopenia. Together with widening and splaying of the growth plates (cartilaginous strips at the end of the bone) and some times a wide spread perisosteal reaction. These features were not present on C's films’
Prof Bishop (Prof Paed Bone Disease) ‘the size and architecture of the bones looks normal to me. There is no evidence of loss of bone mass’. and then @ E108 ‘there is no evidence of any bone abnormality or bone fragility. The pattern of fractures is characteristic of non accidental injury rather than bone disease. In my opinion C’s bones are normal and he has been the victim of non accidental injury.[11]Vitamin D deficiency affects the whole of the central nervous system of a baby’s body, it is essential to feed the nerves and brain cells, it follows ( as Al Alas explored at length) that its absence makes the baby - 1. vulnerable to seizures ( prone to hypocalcaemic fits) 2. with an increased susceptibility to infection and 3. with a decreased ability to recover from infection These are the clinical signs of Vit D deficiency. (see Dr Takon @ E47) Baby C exhibited none of them either at the time of his admissions or on report of the parents between them. He did not have an infection. (see Dr Takon @ E48/ E 50/ E 55/ E 126)) If he did have an infection he had been able to fight it off. Clinically Baby C did not show signs of Vit D deficiency Conclusion: In Baby C’s case all the multiple ways of detecting rickets and Vit D deficiency pointed in one direction and away from it being a causal factor in the fractures he sustained:• The absence of the type, number and age of fractures more likely attributable to rickets• The presence of fresher fractures close to the normal Vit D testing and their type• the lack of radiological evidence of rickets• the lack of biochemistry results indicative of Vit D deficiency• the lack of clinical indicators of Vit D deficiency These factors, individually and collectively demonstrate that whatever condition Baby C may have been born with, rickets and on going Vit D deficiency does not provide a benign cause for the fractures he sustained. This is not news . Dr Takon in her report @ E 60 considered and pulled together the significance of the mothers Vit D levels, her bone density scan and concluded that baby ‘C does not show any physical, biochemical or radiological features of Vit D deficiency’ . As did Prof Wyatt @ E 100 and Prof Bishop @ E 107. Moreover, Baby C did not only suffer from fractures found to have been inflicted, he also sustained genital injuries which were found to have been inflicted. There is no link identified by Prof Nussey between the genital presentations and the fracture related presentations. F THE GENITAL INJURIES Whilst baby C’s genital symptoms (injuries) seen by Mr Roberts on the 26.10.2009 were initially diagnosed and treated by him as an infection for which he prescribed antibiotics, there is in fact, no objective evidence of infection. There were no clinical signs of infection, C’s temperature was normal, C’s blood test results were normal It is of significance that the blood was taken from C whilst at Rotherham District Hospital (RDH) this was prior to antibiotics being prescribed at Sheffield Children’s Hospital (SCH), see F23 from the original care proceedings bundle re discharge from RDH, and F173 – F174 re admission to SCH. See also further reference at page 98 of Prof Nussey’s report. The lack of infection ‘markers’ was NOT as a consequence of antibiotics having been prescribed. . (see Dr Takon @ E56) . Baby C had no other treatment or diagnosis for infection in the first four weeks of his life. The conclusion of those experts who considered Baby C’s genital injuries were that they were ‘unusual and worrying’ and the result of traumatic injury where no accidental explanation had been given by the parents (e.g.: see Prof Wyatt @ E 93) With no evidential base for rickets/vitamin D deficiency and no evidential base for infection, there is no underlying reason why C should present with injuries to his genitalia. Prof Nussey agrees and can see no linking cause between the presentations. Ms Jo Delahunty QCMrs Denise Marson

Cited in 1 later judgment