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uncharted waters

The limits of current medical knowledge on fractures and rickets, discussed in the case of A Local Authority v M and Others 2013

 

http://www.familylawweek.co.uk/site.aspx?i=ed127031

 

This was a case where His Honour Judge Hayward-Smith had considered a fact-finding hearing about a child who had suffered multiple fractures, including a skull fracture. At that hearing, the medical evidence had been unanimous that the child had been suffering from rickets but that the injuries had been caused by the parents, and hence the findings were made.

 

Subsequent to that, the judgment in Al Alas Wray was published, and that obviously highlighted the possible connection between Vitamin D deficiency, rickets and fractures in children.

 

The case came back before the Judge, who authorised some fresh experts, to look specifically at whether the presence of rickets in the children might mean that the fractures were not caused deliberately by the parents.

 

The medical evidence here was not simple, and not agreed, and the Court had to not only address the conflict between the medical evidence, but also to address the fact that the issues in question were butting up against the edge of what was known medical science and attempting to extrapolate from that what might be learned in the future.

 In particular, it became clear that what was not known at this stage, and did not exist in the research was

 

(a)   Whether having rickets meant that a child could suffer fractures more easily or with less force than a child without rickets would require to cause the same injury; and

 

(b)   If so, how much more easily, how much less force?

 

(c) The extent to which rickets affected the healing speed of fractures, and thus the reliability of usual dating techniques to decide WHEN the injury happened where rickets is a feature.

 

On the first issue, the experts were agreed that the existing research on animals did strongly suggest that for animals there was a sufficient link between the presence of rickets and fractures occurring more easily or with less force to be confident that a causal relationship existed, and that this PROBABLY mean that the same was true of humans, and human children too.

 

On the second and third issues, there was no certainty at all and no research evidence yet to point clearly in either direction.  (Again, with animals, the research showed that rickets did impact on the healing rate of fractures)

 

One of the evidential issues that arose was whether, within the body of children who have rickets (and are known to have rickets) fractures and multiple fractures as in this case was a common feature, a fairly rare feature or an almost unheard of feature.

 

 The problem here was that although the Court had the benefit of two experts with a lot of experience on the issue, their experience differed, and neither had the raw data or research, just their own observations. One thought it was almost unheard of (and thus that with multiple fractures NAI was a more likely explanation for the injuries), the other felt that it was fairly rare but within his own experience.

 

Is the multiplicity of fractures significant?

33. As the evidence developed this issue appeared to me to lie at the heart of this case.  Professor Gardner went so far as to say that Professor Bishop’s experience in this area led him to conclude that this is a case of non-accidental injury.  There is no doubt that Professor Bishop is a very distinguished expert in this field.  He was described by one of the experts as knowing more about this field than anyone else in Europe.  Professor Bishop said during the course of his evidence:

“In Sheffield we see approximately 500 children in any one year.  The majority will have conditions leading to bone fragility, the majority being osteogenesis imperfecta [which is not rickets].  I have been involved in this area since 1987 with babies, including premature babies, and older children since mid-1990s.  I have seen cases of rickets and the number reaches three figures.  [He did not go further as to what he meant by three figures, but it is clearly a large number of children]. 

“Of the children that I have seen with rickets, as far infants are concerned and indeed older children, I have only had three or four with fractures and only one had multiple fractures.  The children, in my experience, with multiple fractures are mobile and not as young as M who would have been immobile, but in one case a child was so ill that the bones could hardly be seen on x-ray and there were multiple fractures; and in that child, indeed, the rib cage had fallen in, it was very severe de-mineralisation of the bones.” 

That evidence reflected what he had said at the experts’ meeting.  The transcript of what he then said reads as follows:

“My concern remains that I have seen a number of cases of rickets which are more severe than this where there has only been one fracture.  I have not seen any other child in my own clinical experience with this number of fractures with rickets or, alternatively, in the literature with a description of this number of fractures in the presence of clinically apparent rickets.  So to me, this is a disproportionate number of fractures and it was actually the reason that I agreed to take this case on in the first place because it was unusual and because I was expecting, when I reviewed the child clinically, to find evidence of some other underlying bone disease that would provide an explanation for the fractures not the rickets.” 

Professor Barnes then asked the question whether that reflected Professor Bishop’s experience in relation to children under the age of six and Professor Bishop said:

“Yes, certainly, it does reflect my experience that it is unusual to see this number of fractures in an infant with vitamin D deficiency, rickets, at this age and that is an experience that goes back over quite a large number of years.  Before I did bone disease I did a lot of neonatology for ten years and we did see from time to time infants in the premature baby unit who had fractures as well, although the aetiology there is quite different.  But this is a stand out from my perspective over that long period of time.”

Professor Barnes then asked him whether his experience had reached the literature and Professor Bishop answered: 

“No, it has not reached the literature because, as I say, it is a scattered experience over a long period of time and I have not kept the case notes of each individual child seen over that period so it is a cumulative experience.  I have talked as well with a number of colleagues about what their experience has been and the general agreement, I have to say, is that one fracture is not unusual in rickets, occasionally two, but, you know, more than that, four, no, we don’t see that.” 

He then said in further evidence:

“Even with that child that I referred to with very severe rickets, there were only three or four fractures.  The majority of rickets cases don’t have a single fracture.  Given the likelihood of multiple fractures in the context of rickets, it is more likely in this case that there has been a use of excessive extraneous force.”

He went on to say:

“There is no objective measure of force required to produce fractures.  In normal children, multiple fractures would indicate abuse.  Multiple fractures in rickets is not borne out on the evidence of my experience, but there is very little published evidence in relation to children under six months.  We x-ray babies all the time.  If rickets was responsible for a lot of fractures we would be seeing multiple fractures in children with rickets and we just don’t see them.  In some parts of the world many children have rickets and there are no reports of multiple fractures.  A fracture, and certainly multiple fractures, is uncommon in rickets.”

That is strong evidence from a distinguished source and I take it very seriously, as indeed I did at the last hearing.

34. There is no objective research and no literature to assist much in this field.  Professor Nussey told me that animal research indicates that rickets in animals greatly reduces the force required to break bones and all the doctors agree that that is likely to be so in humans.  Reference was made at this hearing, as at the last hearing, to the Chapman study, but it is of limited value because of the limited number of children involved.  Professor Nussey’s written report includes the following passages:

“The question as to whether the presence of several fractures rather than one is an indicator of abuse rather than general bone fragility is impossible to answer in the absence of any objective measure of the change in the tensile strength of bone in rickets.  Skull fractures are said to be unusual in rickets, but they have been reported.”

Professor Nussey said that he deferred to Professor Bishop’s experience in this area, but I did not take him to be wholly jettisoning his own evidence. 

35. Professor Barnes had much greater direct experience in this area than Professor Nussey.  In his hospital he treats approximately twelve children a year who have rickets, but in addition cases are referred to him and his unit from across the United States and he has seen a total of about thirty-six cases a year since 2008.  He is compiling a database of such cases.  Most of the children referred to him have fractures; that is usually why they are referred to him, as he put it, to sort out which are the cases of non-accidental injury and which are not.  He has a particular interest in children under the age of six months.  Most of them referred to him that he sees have multiple fractures, but by no means were all of them caused non-accidentally. 

36. Professor Barnes’ experience of children with rickets having multiple fractures differs from that of Professor Bishop. The reason for the difference in their experience is unclear, but it has been suggested that more x-rays are taken in the United States and so more fractures come to light.  In the United States most cases of rickets are referred to major centres, whereas in the United Kingdom they tend to be dealt with locally. 

 

 

 

In the concluding passage of the analysis of the medical evidence, the Judge said this:-

 

All experts agree that there has been little research into the nature of the issues in this case.  Rickets has been curable since the 1920s and there has, therefore, been no pressing need for such research.  All experts agree that the issues in this case should be approached with caution and that there were many unknown factors including the amount of force required to cause a fracture.  Professor Bishop said that he could not be sure to the criminal standard of proof that this was a case of non-accidental injury.  He put the balance of probability at about 75%.  Both Professor Nussey and Professor Barnes say that there is insufficient evidence to say whether or not non-accidental injury has occurred in this case and that the evidence is consistent with innocent parents. 

43. At the last hearing the medical evidence pointed inexorably to the findings I made.  This hearing has been very different.  I am now doubtful whether the parents would necessarily have noticed any of the fractures, apart from the humerus and the skull to both of which they reacted appropriately.  I have conflicting evidence as to the relevance of multiplicity of fractures.  I bear in mind that the parents have given no explanation for the injuries apart from a tight garment pulled over the head and a possible knock on the head in the car, but – given the nature of the rickets, the uncertainty of how bad it was prior to 2nd January and the lack of knowledge of how much force would be required to break a bone – it would, in my view, be wrong to draw the inference that a lack of explanation from the parents indicates non-accidental injury.  For all those reasons, I am not persuaded on the balance of probability that the parents did cause these injuries to M.  I do not find, therefore, that the section 31 significant harm threshold has been crossed. 

44. I add one final word about the medical evidence.  I have great respect for all the experts in this case. They are all very impressive.  I would not wish to be taken as criticising any of them or rejecting the expertise of any of them.  This case involves areas of scientific uncertainty where there has been a paucity of research for reasons I understand.  Medical experience differs and caution is required, as indeed all the doctors involved accept. 

 

 

The Judge could have done nothing other than this, I think. We have reached a point in determining non-accidental injuries where rickets is demonstrated to exist where we simply do not know, and are not likely to find out any time soon, whether it makes such a difference that injuries that appear deliberate are in fact caused by relatively minor trauma; and where such doubt exists, the benefit of it has to be given to a parent.

 

It is an invidious position for all involved to be placed in – for the parent who can’t find the definitive answer and might end up being separated from a child temporarily or permanently, for a social worker who is trying to make a decision about whether the risks mean that such a separation should be sought, for the doctors on the ground trying to reach a conclusion, and for Judges who are having to make a decision as to whether what on the face of it are awful and serious injuries may have their causes in biochemistry outside the parents control or responsibility.

 

One thing is for certain, in any case of suspected fractures to children, getting an answer as to whether rickets or vitamin d deficiency are a clinical feature and getting that answer early will be vital.

More on Vitamin D and rickets

 

A discussion of the Court of Appeal decision in Re C (A child) 2012  

 

The case can be found here – thank goodness for Bailii.

 http://www.bailii.org/ew/cases/EWCA/Civ/2012/1477.html

This was a case in which the parents sought to overturn findings made by Her Honour Judge Carr in relation to twelve fractures to a four month old infant, which she found to be non-accidental in nature and a result of trauma.  

 

  1. 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.
  1. 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.
  1. 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'”.
  1. 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…”

  1. 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.

 

 

The challenge in the Court of Appeal was interesting.  It is quite precise, so I won’t try to paraphrase it before you have read the judicial summary

 

  1. 12.   “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.

 

 

 

In terms, what is suggested is that it would be possible for an infant to have Vitamin D deficiency, which could lead to rickets, which could lead to susceptibility to fractures without trauma  – but that a test of Vitamin D at a later stage would not necessarily show a deficiency, because the Vitamin D levels can recover quite swiftly once the baby starts feeding.

 

The Court of Appeal immediately hit upon the problem with that:-

 

  1. 12.   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.

 

 The Judge also touches on the very interesting dynamic of a group of lawyers trying to persuade a Judge of the clinical and medical significance of some liver function tests, when none of them truly understand them.

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.

 

What happened thereafter was that the Court of Appeal allowed the parents to instruct an expert of their choosing  (Professor Nussey) to look at the totality of the clinical features and medical records, to see whether there was anything that pointed clinically to this child having – firstly a Vitamin D deficiency and secondly that this might have led to Rickets, and finally, that the rickets might have led to the fractures being caused non-accidentally.

 

Those representing the child simultaneously instructed Jo Delahunty QC to represent the child, knowing that she had at her fingertips, the wealth of information from Al Alas Wray about Vitamin D deficiency and fractures; to look at the case and advise on whether there was a problem here that needed resolution.

 

 

The conclusions of the expert are set out here

 

  1. 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. “

 

 

None of which is probably what the parents were hoping for, and it seems to get worse and worse as you go down the list.

 

The Court of Appeal were greatly helped by the involvement of Jo Delahunty QC, and set out her useful interventions here

 

  1. 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.
  1. 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.”
  1. 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.”

  1. 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.
  1. 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.
  1. 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.
  1. 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.

 

 

My reading of this is that there’s a risk in assuming that a possibility of vitamin D deficiency amounts to There was a vitamin D deficiency, the Vitamin D deficiency caused rickets, rickets caused the fractures; and one has to be careful in establishing that there is a clinical and medical case for advancing from each stage to the next.  Even establishing a Vitamin D deficiency does not establish that the fractures were caused by rickets, merely that this needs to be explored.

 

 

The totality of the conclusions, and the decision of the Court of Appeal was therefore that the findings made by Her Honour Judge Carr were not only robust and properly formulated, but not overtaken by medical developments that were more widely disseminated by Al Alas Wray.

 

[My broader conclusion is that you want to get on the phone to Jo Delahunty’s clerks at 4 Paper Buildings as soon as you can if you have a case where there’s a suggestion of Vitamin D deficiency, before anyone else beats you to it. It might be a stretch to suggest that she is the Perry Mason of family law – as he never ever ever lost a case, but I’d certainly suggest that having her on your team is rather like picking Lionel Messi to be in your five-a-side football team – you certainly would come to regret the other side having them instead of you.   If  Ms Delahunty wishes to use  “She is the Lionel Messi of the family bar” as a quote for Chambers Directory or the Legal 500, she would do so with my blessing]

 

 

The Court of Appeal felt that there were portions of her skeleton which warranted broader circulation, and annexed them to the judgment. I would agree, so here they are:-

 

 

 

  1. 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

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’.
  1. 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.
  1. 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 the

a. 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.

  1. 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).
  1. 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.

  1. 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)”;[1]
  1. 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)
  1. 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’
  1. 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.

  1. 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[2]. (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 QC
Mrs Denise Marson

Note 1   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).     [Back]

Note 2   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.    [Back]