SITTING AT NOTTINGHAM
Nottingham NG1 7EJ
B e f o r e :
| (1) A
- and –
|(1) NORTHAMPTONSHIRE COUNTY COUNCIL
(2) MR & MRS C
(3) D & E
(via their Children's Guardian)
1st Floor, Quality House, 6-9 Quality Court, Chancery Lane, London WC2A 1HP.
Telephone No: 020 7067 2900. Fax No: 020 7831 6864 DX 410 LDE
MS A STOREY-REA (instructed by Helen Fitzsimons Family Law) for the Second Applicant
MS H MARKHAM QC and MR B MANSFIELD (instructed by LGSS Law) for the First Respondent
MR M BROOKES-BAKER (instructed by Family Law Solicitors) for the Third Respondent
Crown Copyright ©
This judgment was delivered in private. The judge has given leave for this version of the judgment to be published on condition that (irrespective of what is contained in the judgment) in any published version of the judgment the anonymity of the children and members of their family must be strictly preserved. All persons, including representatives of the media, must ensure that this condition is strictly complied with. Failure to do so will be a contempt of court.
MR JUSTICE KEEHAN:
"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."
"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)  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)  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)."
"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."
"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)  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'."
(1) Whether the court will permit a reconsideration or review of, or challenge to, the earlier findings.
(2) Whether there is any reason to think that a rehearing will result in a different finding from that in the earlier trial: is there any new evidence or information casting doubt upon the accuracy of the original findings?
(3) The test is not whether the applicant stands a real prospect of disturbing the original findings.
(4) Rather, there must be some real reason to believe the earlier findings require revisiting. Mere speculation and hope are not enough. There must be solid grounds for challenge.
(5) The recognition of the tension between the powerful public interest in finality in litigation and the strong public interest in identifying accurately those who cause serious non-accidental injuries to children, wherever such identification is possible.
(6) The court must have regard to whether, if at all, medical knowledge and expertise may have advanced in the years between the original findings and the application to reopen the findings.
"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."
"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."
"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."
"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 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."
"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."
"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."
"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."
"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."
"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."