A & Anor v Northamptonshire County Counci & Ors

In April 2012 a child, E, then aged 7 weeks, was admitted to Northampton General Hospital. She was found to have sustained a number of fractures, which treating clinicians considered to be non-accidental injuries. In consequence, the Local Authority issued public law care proceedings.

In his judgment given on 27 September 2012, at the conclusion of a fact-finding hearing, Mr Recorder Hedley found that: (1) E had sustained four fractures, namely of her eighth left rib and a metaphyseal fracture of her left knee; a metaphyseal fracture of her right knee; and a metaphyseal fracture of her right elbow. (2) There was no underlying condition which predisposed E to suffer fractures. (3) They were all non-accidental injuries. (4) They were inflicted either by the mother or by the father.

The mother of E, A, has applied for permission to seek to set aside these findings. Her application is supported by E's father, B. The application is opposed by the Local Authority, Northamptonshire County Council, and by the Children's Guardian.

The parents have an older child, D, who is now 9 years of age. E is now 6 years' old. As a result of the findings of fact made, both parents accepted they could not care for the children. At the final welfare hearing in May 2013, both children were made the subject of Special Guardianship Orders in favour of the maternal grandparents, with whom they remain living to date.

The grounds of the application for permission to set aside the findings of fact are that there is evidence to suggest E was, at the relevant time: (a) vitamin D deficient; and (b) suffered from osteopenia which could lead to the conclusion that all four fractures resulted from an underlying condition which predisposed her to suffer fractures.

There is a broad consensus between counsel as to the law I should apply when determining this application to reopen the findings of fact made in 2012. In the case of Birmingham City Council v HH & S [2005] EWHC 2885 Fam, Charles J said at paragraph 55:

"In my view the approach of the family court to earlier findings has three stages: firstly, the court considers whether it will permit any reconsideration or review of or challenge to the earlier finding, here referred to by the parents as a review. If it does, the second and third stages relate to its approach to that exercise. The second stage relates to and determines the extent of the investigations and evidence concerning the review. The third stage is the hearing of the review, and thus it is at this stage that the court decides the extent to which the earlier findings stand, by applying the relevant test of the circumstances then found to exist."

This approach was endorsed by the President, Sir James Munby, in Re ZZ & Others [2014] EWFC 9, when he further described the three stages as follows:

"The same three-stage approach applies in my judgment whether the issue arises before the same judge or a different judge; whether in the same or different proceedings; and whether in relation to the same or different children. I do not, with all respect to Baker J's tentative comments, think that different approaches are called for in different forensic contexts. The attempt to create such a forensic taxonomy would, I fear, be productive merely of satellite litigation. Of course the application of the general approach in any particular case will reflect the circumstances of that case.

"So far as concerns the first stage, I agree with what Hale J said in Re B (minors: care proceedings: issue estoppel) [1997] Fam 117. In particular in the passage I have set out above, I add this: One does not get beyond the first stage unless there is some real reason to believe that the earlier findings require revisiting. Mere speculation and hope are not enough. There must be solid grounds for challenge, but for my own part, I would be disinclined to set the test any higher.

"I have misgivings about Macfarlane J's use in Birmingham (number 2) paragraphs 42, 55, of the words I have emphasised in paragraphs 16, 17 above. I suspect that in significant part, they reflect the approach of Lord Nicholls in Re H (minors: sexual abuse: standard of proof) [1996] 563. Be that as it may, I think, with great respect to Macfarlane J that that nuance is wrong.

"So far as concerns the second stage, the ambit of the review or rehearing, I doubt that one can sensibly be prescriptive. Much will turn on the forensic context, and the circumstances of the particular case. So far as concerns the third stage, the proper approach in my judgment, subject only to what I have said, is that spelt out by Macfarlane J in Birmingham (number 2). There is an evidential burden on those who seek to displace an earlier finding, in the sense that they have to make the running. But the legal burden of proof remains throughout where it was at the outset.

"The judge has to consider the fresh evidence alongside the earlier material before coming to a conclusion in the light of the totality of the material before the court. I think that Charles J's phrase, 'a high test', is best avoided at this, as at previous, stages. I can well understand why in the particular circumstances of Birmingham (number 1) where there were concurrent findings of two High Court judges and the Court of Appeal, Charles J used those words, but to elevate them to a test, a legal principle, is unwarranted, unnecessary and potentially misleading. Indeed, I think with respect to Charles J that reference to 'a high test' at the third stage is simply wrong, essentially for the reasons given by Macfarlane J in Birmingham (number 2)."

In considering the approach of the court to the first stage, the President referred to the observations of Hale J, as she then was, in Re B (minors: care proceedings: issue estoppel) [1997] Fam 117 at pages 128 to 129 when she said:

"Above all, the court is bound to want to consider whether there is any reason to think that a rehearing of the issue will result in any different finding from that in the earlier trial. By this I mean something more than the mere fact that different judges might on occasions reach different conclusions upon the same evidence. The court will want to know whether there is any new evidence or information casting doubt upon the accuracy of the original findings."

The law relating to the reopening of findings of fact was recently summarised by Cobb J in Re AD & AM (fact-finding hearing: application for rehearing) [2016] EWHC 326 Fam. He endorsed the approach of the President in Re ZZ, and referred to the observations of Hale J in Re B. He continued as follows, at paragraphs 14 to 16:

"I do not understand the President to be equating the test at 'stage 1' ("some real reason to believe the earlier findings require revisiting" of Re ZZ) with the test which is to be applied on an application for permission to appeal. That is to say, I do not have to satisfy myself that the mother stands a 'real prospect of success' of disturbing the original findings, or that there is 'some other compelling reason' why the case should be heard. The test in these circumstances is not so exacting.

"On this application (and others like it, I am sure) there are at least two powerful public interests engaged, and in tension with one another: the strong public interest in finality in litigation (see Charles J in Birmingham City Council v H), in conflict (potentially at least) with the strong public interest in identifying accurately those who cause serious non-accidental injuries to children, wherever such identification is possible: see Re K (non-accidental injuries: perpetrator: new evidence) [2004] EWCA Civ 1181 at paragraph 55.

"This second policy consideration was further defined in Re K at paragraph 56: 'It is in the public interest that children have the right, as they grow into adulthood, to know the truth about who injured them when they were children, and why. Children who are removed from their parents as a result of non-accidental injuries have in due course to come to terms with the fact that one or both of their parents injured them. This is a heavy burden for any child to bear. In principle, children need to know the truth if the truth can be ascertained'."

I respectfully agree with the approach and/or the observations of Charles J, the President, Hale J as she then was, and Cobb J as set out above. The essential features of these four cases appear to me, when considering the application of the first stage of the process to be:

In the course of his judgment in Re AD and AM, when he referred to the strong public interests in identifying accurately those who cause non-accidental injuries, Cobb J had said, "I suspect that had Re K been cited to the President, it would have in itself provided good illustration of a 'real reason' for believing that 'earlier findings require revisiting'."

I do not consider that Cobb J intended by that comment to convey that the mere fact of a strong public interest in identifying accurately the perpetrator of non-accidental injuries to children would of itself provide a real reason for granting permission at stage 1. An applicant must go further, beyond relying upon this important public interest consideration, and demonstrate that there are solid grounds for mounting the proposed challenge to the findings of fact made, or that there is some real reason to believe that the earlier findings require revisiting.

When considering the application, whether I should admit the report of Dr Watt into these proceedings, I take account of the decision of the Court of Appeal in Re M (children) [2018] EWCA Civ 607, and in particular the judgement of Peter Jackson LJ. I also take account of the provisions of s.13 of the Children and Families Act 2014, in particular s.13(7), The Family Procedure Rules Part 25; and The Family Procedure Rules PD 25B.

As a result of E sustaining four fractures, and the issue of care proceedings, three medical experts were instructed to prepare reports. They were Dr Hislop, a consultant paediatrician; Dr Summers, a consultant paediatric radiologist; and Dr Fernley, an ophthalmologist. Further, a report was available from Dr Chapman, a consultant paediatric radiologist, who had provided an expert report to the police.

There were no adverse clinical findings reported in E's eyes, and accordingly only Dr Hislop and Dr Summers gave evidence at the fact-finding hearing. During her admission to hospital in April 2012, E's vitamin D level was not tested, but she underwent a blood test, which was reported as normal, in particular, for her levels of calcium and phosphates.

In August 2012, the mother's, the father's and E's vitamin D levels were tested, and the results were respectively: 26.6 nano molecules per litre; 26.7 nano molecules per litre; and 25.8 nano molecules per litre. A result below 25 nano molecules per litre equates to vitamin D deficiency. E's test result indicated vitamin D insufficiency, for which she was prescribed Abidec, vitamin D drops.

The principle conclusions of Dr Hislop were as follows: she agreed with the radiologist's identification of the four fractures that I have just described. In her report she said:

"I would emphasise that in my opinion, and I also think that of the other experts, is there have been two separate episodes of bony injury. The rib fracture happened probably several weeks before the knee and elbow injuries, which may have occurred at the same time. Both these events are more likely that not to be inflicted non-accidental injuries based on the type of injuries seen, and the lack of any plausible explanation.

"There is nothing in E's medical history which suggests that she is more susceptible to bony injury than other children. There is no family history of susceptibility to fractures. She was not born pre-term, and her mother does not have any condition which would result in deficiencies in a new-born.

"The degree of hypermobility and blue sclerae shown by E when I saw her would, in my view, be within the normal range for a child of her age, and more severe hypermobility is something I see very frequently in my clinics. Those children do not have an increased risk of fractures, other than due to a tendency to fall more readily. E is not at an age where this factor would be relevant.

"There is no evidence to support a diagnosis of osteogenesis imperfecta. She is too young for most of the dietary conditions which would cause fractures; her bones do not have the appearance of a child with a metabolic disorder, such as rickets; and her blood tests do not support this, although I have not seen a test result for vitamin D level.

"The injuries found are not those that would be seen in a child with rickets. Given her age and feeding regime, this would only be likely to be present in any case in a child whose mother was significantly vitamin D deficient as she would have obtained her vitamin D from her mother. Given the pattern of fracture, and the absence of signs of bony disease, I consider that a medical cause of fractures is highly unlikely.

"In children with severe osteogenesis imperfecta, for example, there is almost always an explanation for the fracture. The difference is that a lesser degree of force is involved. The fractures also conform to a standard pattern of accidental fracture, shafts of long bones being common sites. Whereas E's fractures are typical of a non-accidental causation. Children with rickets who have bone fractures will always have other radiological evidence of rickets. Other mineral deficiencies do not occur in a full-term child of this age born to a healthy mother."

Dr Summers again confirmed the presence on the imaging of the four fractures previously described. In his first report, he made the following observations:

"Fractures to the metaphysis are highly specific for non-accidental injury, hence the term 'classic metaphyseal lesions' that is often applied. The mechanism for the injury is a torsional twisting force combined with a distraction pulling force. However, studies on infant pigs suggest the distraction force may be more important than the torsional force. Accidental rib fractures in infants and young children are extremely rare. They only occur in sever traumatic episodes, such as unrestrained child in a motor vehicle accident, or a crushing injury; and in such circumstances are associated with mortality rates of 40 to 50 per cent. Rib fractures may occur in children with metabolic or inherited bone disorders, for example, osteogenesis imperfecta. There is no evidence for that here."

Then, in a supplemental report, he said as follows:

"E is vitamin D insufficient. The test result is 25.8 Nano molecules per litre. The parents' levels are also insufficient. None are deficient in vitamin D. Vitamin D insufficiency, deficiency, may be caused by insufficient dietary intake, and low exposure to sunlight. In utero, the foetus obtains vitamin D from the mother via the placenta, and is therefore dependent on mother's vitamin D levels. Breast milk contains little vitamin D, and therefore a vitamin D deficient mother may not provide sufficient vitamin D in her breast milk to prevent insufficiency, deficiency in the infant. Formula milk is fortified with vitamin D, and therefore bottle-fed children are rarely vitamin D deficient.

"In children, fractures occur in severe vitamin D deficiency in the presence of the bone disorder rickets. In rickets life is a radiological diagnosis. The absolute diagnosis is made histologically, but this is not feasible in life. There are typical changes within the skeleton, namely reduced bone density; widening and blurring of cranial sutures in infants, widening of the growth plates of the long bones; and cupping and fraying of the growth plates. Changes are most marked at the knees, wrists, skull sutures, and anterior ribs in young children. The present state of knowledge: Explaining fractures as being due to vitamin D insufficiency, deficiency in the presence of normal bones is not supported by the available evidence."

So, neither Dr Hislop nor Dr Summers considered there was an underlying medical condition which would account for E's fractures. As I have already mentioned, a fact-finding judgment was given on 27 September 2012. Thereafter, Professor Richardson, a consultant paediatrician at Great Ormond Street Hospital referred E for a further skeletal survey, which was undertaken on 10 October 2012. Dr Youssef and Dr Calder, consultant radiologists at Great Ormond Street, reported that the films demonstrated "mild diminished bone density", and that a mild form of osteogenesis imperfecta could not be excluded.

Accordingly, Professor Richardson referred E to Dr Saggar, a consultant clinical geneticist. In his first report of 31 October 2012, Dr Saggar considered that there was sufficient evidence to suggest this young girl has osteogenesis imperfecta, to warrant the testing of the COL1A genes. In his second report, of 30 November 2012, Dr Saggar advised that there was no mutation identified in either the COL1A1 or the COL1A2 genes, which most commonly account for mild forms of osteogenesis imperfecta, particularly where there is normal stature. He recommended discussion with the paediatrician to identify if any other metabolic tests were required. He concluded, "I am not able therefore to identify a specific gene mutation that would explain the fractures".

The matter came before King, J, as she then was, on 3 December 2012, when she directed that all further hearings, including the welfare hearings, would be heard by a judge of High Court level. The question of an application to reopen the findings of fact was raised before her, on behalf of the parents, in light of the conclusions of the radiologists at Great Ormond Street. King, J directed that any application by the parents to reopen the findings of fact should be issued and supported by skeleton arguments by 8 January 2013. No application was in fact ever made in the currency of the care proceedings.

In his third report of 17 February 2013, Dr Saggar recommended that the Great Ormond Street set of x-rays should be reviewed to ensure there was no loss of bone density, as a loss of bone density was incompatible with a conclusion of non-accidental injury. He concluded his report as follows:

"Osteogenesis imperfecta type 1 is characterised chiefly by multiple bone fractures, usually resulting from minimal trauma. Affected individuals have blue sclerae, normal teeth, and normal or near-normal stature. Fractures are rare in the neonatal period, up to the age of one month. Fracture tendency is constant from childhood to puberty, decreases thereafter, and often increases following menopause in women, and after the sixth decade in men. Fractures heal rapidly with evidence of good callous formation, and with good orthopaedic care, without deformity.

"E is growing well, and is not failing to thrive. She is not dysmorphic. Her development is normal as reported by Dr Hislop. In my opinion, E does not have any evidence for a metabolic condition that might predispose her to fractures, as seen on her x-rays. She has also been reviewed by Dr Shaw, an expert in metabolic bone diseases, who concluded the same.

"I am not able to assert that the injuries in E were caused by non-accidental injury as it is not my area of expertise. I can say, however, that I am not able to identify any other cause, such as osteogenesis imperfecta, or a metabolic condition, that would provide an alternative diagnosis. Hypermobility alone would not account for the fractures, although increased falling leading to fractures can occur. Since E is not ambulant, this is not a likely cause. I am not able to identify any other cause, such as osteogenesis imperfecta, or a metabolic condition that would provide an explanation for the fractures in E."

The court subsequently approved the instruction again of Dr Summers to provide an overview of the radiological evidence. In his report of 3 April, he concluded as follows:

"The determination of bone density on x-rays is a subjective and qualitative assessment. With high quality radiographs, the assessment that bone density is normal is usually straightforward. However, the assessment of reduced bone density is more difficult. In adults it is believed that approximately 40 per cent of bone mineralisation needs to be lost before it becomes obvious on x-ray. There is no comparable data in children. In addition, poor quality x-rays or variations in technique and/or post-processing of digital x-rays can lead to a false assessment of reduced bone density.

"The quality of the radiographs from Northampton in this case appears not to be an issue, however the x-rays from Great Ormond Street are qualitatively different. Several of the images, particularly of the hands and feet, demonstrate quantum mottle. This is a type of image noise, and produces a grainy image. It is often caused when the x-ray dose is reduced excessively. It can also result from poor optimisation of the imaging system for small children. The images of the long bones also appear to have higher contrasts than I am used to seeing, possibly with the post-processing technique called edge enhancement.

"The overall effect as reported by Great Ormond Street Hospital is an impression of reduced bone density, osteopenia. This may be real or the result of imaging techniques used as described above. The imaging department at Great Ormond Street Hospital should be able to provide information on the x-ray dose and post-processing techniques employed, but no reprocessing of the x-rays will now be possible. In conclusion, I believe it would be impossible to determine whether the reduced bone density reported is real or due to technical factors. Osteopenia is not a diagnosis and does not indicate the cause for reduced bone density.

"I can say there are no Wormian bones in the skull; there is no radiological evidence for a metabolic bone disease such as rickets or scurvy or copper deficiency which may cause osteopenia. At the time of the skeletal survey, blood tests including calcium, phosphate and vitamin D were all normal, thus excluding any possibility of rickets. There is no definitive test for bone density in children. The most commonly-used techniques in adults is dual-energy x-ray absorptiometry. This is not widely accepted as a useful technique in children.

"Bone density at the time the fractures occurred was normal radiologically. There is no evidence at that time for any abnormality that might have resulted in an increased tendency to fracture. In October, when she is reported to have reduced bone density, she had no fractures, and had not sustained fractures since, to my knowledge, the time of writing. However, as stated above, if E does have osteopenia, it will affect her long-term risk of fracture."

Prior to the final welfare hearing in May 2013, the parents had already accepted that they could not care for either of their children. At that hearing, the mother said in a statement dated 15 May 2013, with which I am told the father was in complete agreement, that:

"I confirm that at the hearing on 7 May, I confirmed that I accepted there are no other medical explanations for E's fractures. I came to this view after going back over all of the medical evidence. On the medical evidence which is available to me, I do accept that the injuries are non-accidental injuries. I cannot explain how the injuries occurred, or when they occurred, but I do know that I have not knowingly injured E in the normal course of caring for her. I do however accept that I do now have to draw a line under the medical evidence, and I am not seeking any further medical assessment or tests on E regarding the court's findings.

"I do also have to acknowledge that if I haven't injured E, there is a potential risk of B, my husband, having done so, and I have to acknowledge that it is possible he could have caused the non-accidental injuries to E. I also accept that it is not going to be possible for the children to come home. I would dearly like for that to happen, but I know it is not possible."

When I enquired why these concessions had been made, I was told by leading counsel for the mother, and counsel for the father, that they had been advised/decided to focus on the welfare outcome. I do not understand why concern about that outcome should have deflected them from challenging the findings of fact, but there we are.

Thus, the final welfare hearing concluded with the children being made the subject of Special Guardianship Orders in favour of the maternal grandparents. In 2015 as a result of a GP referral, reports were provided by Dr Saggar; Dr Bailey, a consultant paediatric rheumatologist; Professor Graham, a consultant rheumatologist; and Dr Ridwan, a consultant paediatrician: all concerned with whether E suffered from hypermobile Ehlers-Danlos syndrome.

In his report of 21 December 2016, Dr Ridwan concluded there was no evidence of E suffering from any form of hyper-extendibility. Meanwhile, in early 2016, the parents made contact with Dr Watt, a consultant paediatric radiologist. In an email to him of 6 February 2016, the parents asked him to review the April 2012 x-rays and the October 2012 x-rays. The email reads as follows:

"We have recently been in contact with Rachel Carter from Wollen Michelmore, who highly recommended yourself. We were wondering if you could view two sets of x-rays that we have, as there are inconsistencies between them. The first set of x-rays were done at Northampton General in April 2012 when E was 7 weeks' old. The second set was done at Great Ormond Street Hospital in October 2012 when E was 8 months' old. Also, when she was at Great Ormond Street, blue sclerae was seen, and mild diminished bone density was reported. We had vitamin D testing done in August 2012. My result was 26.8, my husband was 26.9, and our daughter was 25.8. At this point, E was being supplemented with formula milk."

On 27 October, Dr Watt responded to the parents by email, attaching his report of even date. I was given no explanation as to why the report from Dr Watt in the bundle is dated 7 February 2017, albeit in identical terms to the earlier dated report. Furthermore, counsel for the Guardian reminded me that I had in February 2018 directed the parents to file and serve every communication they had had with Dr Watt.

In response to my enquiry of what questions of Dr Watt had been asked to be respond to by the parents, I was surprised to be provided with, on the afternoon of the first day of this hearing, Dr Watt's email and report of 27 October 2016; and an email of 1 November 2016 from the parents to Dr Watt, asking and him responding to supplementary questions. No explanation was forthcoming as to why these documents had not previously been disclosed in compliance with my order of February 2018.

In his substantive report, of whichever date, Dr Watt agreed with the identification of the four fractures that E had suffered. His report contained the following opinion:

"In respect of the CD from Great Ormond Street Hospital, skeletal survey dated 11 October 2012, seven months, 25 days' old, 24 images of technically-adequate quality. No abnormality in the heart, lungs or abdominal bowel gas pattern. There is mild deformity of the right distal humerus in keeping with a previous fracture. The long bones of the lower limbs appear subjectively slightly osteopenic, but no local pathology is evident."

The questions asked in the email that I have just referred to, and Dr Watt's responses, are as follows:

"Question 1: The bone density which has reported at GOSH by several professionals now: any reason why the bone density was not seen on the Northampton x-rays as E's vitamin D deficiency and serum calcium levels was a lot lower as they introduced supplements after these had been done. Answer: The possibilities here are (a) it was not present; (b) it was present, but not visible on the Northampton radiographs; or (c) there were technical differences in the radiographic acquisition in the two hospitals that would account for the differences. Radiographs are poor at assessing bone density in young children.

"Question 2: How long would it take a bone fracture to remodel and completely heal to be unrecognised on an x-ray with someone who has been diagnosed with EDS type 3? [That is hypermobility EDS]. Answer: Bone healing and remodelling usually takes up to three to six months, depending on the fracture type. I am unaware of EDS type 3 having any impact on this.

"Question 3: Great Ormond Street Hospital noted one fracture on the full skeletal x-rays and no previous or current fractures. Elsewhere, fracture sites had been done a couple of times; regard to these discrepancies between the two sets. Answer: The other fractures sites had healed to completion by the second set, and were therefore not visible. This would be expected given the time interval.

"Question 4: The GOSH x-rays: in your professional view, why would there be one fracture seen and not others? Answer: See the answer above."

The view expressed by Professor Graham in his letter of 29 March 2016, that E had ‘clear phenotypic features of EDS type III’ which should be reviewed in 2 years’ time, led, in this application, to an agreement between the parties to the joint instruction of Dr Irvine, a consultant clinical geneticist. She had available to her all relevant materials, including all of the experts' reports, to which I have referred, save of course to Dr Watt's report of 27 October 2016, and his answer to the parents' supplemental questions of 10 November 2016.

Dr Irvine in her report of 15 June 2018 excluded E as suffering from hEDS. Further, she gave the following opinions:

"E herself has not sustained any fractures since those detected in infancy. Fracture susceptibility in the mildest form of osteogenesis imperfecta, namely type 1, usually manifests when infants become toddlers, and fall over. On the occasion when E fell frequently prior to having her glasses, she did not fracture any bones. A previous assessment through clinical genetics led to a genetic testing of two genes most commonly associated with OI type 1, namely COL1A1 and COL1A2. The results shared with me in the case bundle show no mutations were found, although there was note made that larger changes within these genes, accounting for 2 per cent for those with OI, might not have been detected through this test. There were no grounds indicating a clinical need to pursue further testing.

"I understand therefore that further testing was not arranged, a clinical decision with which I concur. E does not have clinical or molecular evidence of being affected with OI. Indeed, there is no clinical evidence that she has an underlying genetic predisposition to be more susceptible to fractures. As there does not appear to be any evidence that E has a genetic predisposition to being more susceptible to fractures, no further genetic testing is indicated.

"In taking into consideration the necessary evidence, I conclude that E does not have a genetic predisposition to increased susceptibility to fractures. The necessary evidence includes my own clinical assessment of the family history, medical history and physical examination, as well as reviewing additional information in the results provided to me in the case bundles. Although E did not allow me to conduct a hands-on physical examination, I am satisfied the scope of this information has allowed me to accurately draw this conclusion."

In consequence of Dr Irvine's report, the parents did not pursue the submission that there was evidence that E was suffering from, or had suffered from, hEDS. Dr Irvine was available to attend this hearing to give evidence. No party, however, required her attendance, and she was stood down. As Mr Peddie, QC, said in his oral submissions to the court, he could not gainsay her opinions and conclusions.

In light of the decision of the Court of Appeal in Re M above, and the approach adumbrated by Peter Jackson, LJ, I had to consider whether I should accede to the application of the mother to admit into evidence the report, be it that dated 27 October 2016 or 7 February 2017, of Dr Watt, and his answers to the supplemental questions asked. Although his substantive report contains the required statement of compliance, in light of the parents' failure to disclose, or disclose in a timely fashion, communications with Dr Watt, I had real reservations about whether I had, even now, been given all communications between the parents and Dr Watt.

Once again, for the avoidance of any doubt, I do not suggest that any responsibility for this state of affairs lies with Dr Watt, nor do I make any criticism of him whatsoever. At one stage, because of these reservations, I was minded to refuse to admit the report and the answers into evidence. Ultimately, I concluded that because of Dr Watt's considerable experience as an expert witness, and his probity, I should admit his report in evidence.

I am immensely grateful to leading and junior counsel for the comprehensive and immensely-helpful skeleton arguments and schedules which, with the benefit of their oral submissions, have greatly assisted me in considering the issues in this complex matter.

The mother and father are as one in the way they have put their respective cases in support of the mother's application. Ms Storey for the father adopted the submissions made on behalf of the mother. I trust Mr Peddie, QC and Mr Bailey on behalf of the mother will forgive me if I summarise their principal submissions in the following manner: (1) The parents were, prior to April 2012, unknown to social services or the police. (2) Their care of E was observed to be good and gentle. (3) D had suffered no physical harm in the care of his parents. (I interpose to say I accept and take account of all of those matters). (4) The conclusions of a loss of bone density in respect of the October Great Ormond Street Hospital x-rays raises a real issue in respect of the findings of fact made in September 2012. (5) These conclusions are supported by the opinion of Dr Watt, that the x-ray films appear subjectively slightly osteopenic but with no local pathology. (6) The features of blue sclerae, the various descriptions of the absence or presence of Wormian bones, and the question of diminished bone density raise the possibility of a rare form of osteogenesis imperfecta, or other underlying medical condition which may account for E's fractures. (7) In the premises, it is significant that an unknown course for E's fractures was not considered at the fact-finding hearing. (8) The failure not to test E's vitamin D levels in 2012 was an unfortunate omission, and leads to the real possibility, given that she was tested as vitamin D insufficient, with borderline deficiency, that in April 2012 she was in fact vitamin D deficient which may have disposed her to fractures with no, or far lesser, force than normally expected or predicted.

In response, Ms Markham, QC on behalf of the Local Authority submitted as follows: (1) There is in reality no new or fresh evidence. (2) The concerns raised by the radiologist at Great Ormond Street in respect of the October 2012 x-rays were comprehensively dealt with by the opinions of Dr Saggar and Dr Summers in 2013. (3) There is in fact no real difference between the opinions expressed by Dr Summers in 2013, and Dr Watt in 2016, especially as clarified by Dr Watt in his answers to the supplemental questions raised by the parents after his first report of 27 October 2016. (4) That any outstanding issues between them, i.e. the subjective assessment of slight osteopenia in the long bones were decisively resolved by the opinions and report of Dr Irvine, who was not required to attend and give evidence at this hearing.

Mr Brookes-Baker on behalf of the Guardian agreed with and adopted these submissions. He also helpfully reminded me of the conclusions of Dr Saggar in his report of 30 November 2012 and 17 February 2013.

The original expert reports of Dr Hislop, Dr Summers, and Dr Chapman, before Recorder Hedley in 2012, were agreed about the fact that (a) E has sustained the four identified fractures; (b) There was no underlying disease or organic process which would predispose her to suffer fractures; and (c) They were all non-accidental inflicted injuries.

I agree it is unfortunate that E's vitamin D levels were not specifically tested in April 2012, but the test results undertaken in August 2012 demonstrated that she was not vitamin D deficient but only vitamin D insufficient. Her blood test results undertaken in April 2012 were reported as being normal, especially her calcium levels and phosphates. There was nothing in these test results to suggest any clinically significant issue in respect of her vitamin D levels. In any event, Dr Hislop considered a breast-feeding mother would have to be significantly vitamin D sufficient before E was at risk of suffering rickets, and the mother was not.

Dr Summers was of the view that bone fractures only occur in the presence of severe vitamin D deficiency. There is not a scintilla of evidence, or even a reasonable basis to posit, that E ever had a vitamin D deficiency, still less one that might be described as significant or severe.

In the premises, I am satisfied that in the totality of the medical evidence disclosed there is not a scintilla of evidence that (a) E was ever vitamin D deficient or still less (b) that any such insufficiency could have ever been described as a significant deficiency or severe deficiency such as to have had a material bearing on the causation of E's fractures.

In light of Dr Watt's answers to the supplemental questions asked by him of the parents in November 2016, I can discern no material difference between his conclusions and those of Dr Summers given in April 2013. Dr Watt has reported a subjectively mild osteopenia in the lower limbs, but did not opine, because no doubt he was not asked, whether this was a clinically significant or relevant finding in relation to the fractures suffered by E. He agreed with Dr Summers that there were various possible interpretations of the Great Ormond Street October 2012 x-rays.

Whether or not there was a subjectively slight osteopenia seen on the Great Ormond Street films, I am persuaded by Dr Irvine that they provide no evidence that E was suffering from, or had ever suffered from, a disease or organic process that would predispose her to suffer fractures. I take account and attach weight to the fact that (a) neither the mother nor the father required Dr Irvine to attend this hearing to give evidence; (b) the parents abandoned any submission that E had suffered a form of hEDS which might explain her fractures and (c) Dr Irvine's unchallenged opinion that E had no evidence of a disease or organic process that would predispose her to fracture.

In the premises, I am entirely satisfied that the parents have not established a solid ground for challenging the previous findings of fact, nor some real reason that the earlier findings require revisiting. I regret to conclude that the parents' case is built on smoke and mirrors, and not on anything of real substance. Dr Saggar and Dr Summers have comprehensively dealt with the issues raised by Great Ormond Street in 2012, and Dr Irvine has, without challenge, dealt with any continuing or outstanding issues raised by Dr Watt in his report.

I should make clear that my finding is that there is no material, clinical or forensic difference between the opinions expressed by Dr Summers in April 2013 and those that Dr Watt expressed in October 2016 and/or February 2017. I have reached the clear conclusion that the mother's application for permission to reopen the findings of fact made by Recorder Hedley in September 2013 should be dismissed.