B e f o r e :
Sitting as a Judge of the Family Court
at the Royal Courts of Justice
ST HELENS BOROUGH COUNCIL
C (a child)
Andrew Loveridge (instructed by St Helens Borough Council) for the Local Authority
Frank Feehan QC and Janet Reaney (instructed by Berkson Family Law Solicitors) for the Father
Clive Baker (instructed by Morecrofts LLP) for the Child
Hearing dates: 6-10, 13-14 November 2017 Judgment date: 22 January 2018
Crown Copyright ©
Lord Justice Peter Jackson:
(1) On 12 September 2016, I directed that Professor Nussey should provide a report that identified his view more closely.
(2) On 30 January 2017, I considered Professor Nussey's further report and was satisfied (contrary to the submission of the local authority) that it constituted the necessary solid grounds for the original findings to be reviewed. As I said at the time, I would not have been satisfied of this on the basis of Dr Ayoub's evidence alone. I gave directions for an experts' meeting to be convened so that the medical issues could be understood and the scope of the rehearing settled.
(3) On 7 April, after a not altogether satisfactory experts' meeting on 28 March, I determined that the review of the findings should proceed by way of a rehearing of the medical evidence. I did not accept the submissions of the parents that there should be a rehearing of all the evidence, or that the rehearing should take place before a different judge. However, I left open the possibility that the parents might give further evidence if the medical evidence gave rise to a new issue on which they might be able to add to their earlier evidence. In the event, that did not arise.
(4) On 27 July, pre-trial directions were given. In fact, the court could have accommodated the rehearing locally in July, but the parents understandably wanted continuity of counsel which could not be achieved then.
Approach to fact-finding
(a) Particular caution is necessary where the medical experts disagree, one opinion declining to exclude a reasonable possibility of natural cause.
(b) The court must always be on guard against the over-dogmatic expert, or where the expert's reputation or amour propre is at stake, or where an expert has developed a scientific prejudice.
(c) The Judge in care proceedings must never forget that today's medical certainty may be discarded by the next generation of experts and that scientific research may throw light into corners that are at present dark.
"The moral I draw from this case and will never forget is that a hypothesis in relation to the causation of a child's injuries must not be dismissed only because such causation would be highly unusual and that, where his history contains a demonstrably rare feature, that the possible nexus between that feature and his injuries must be the subject of specialist appraisal at an early stage."
"28. … in some contexts a court or tribunal has to look at the facts more critically or more anxiously than in others before it can be satisfied to the requisite standard. The standard itself is, however, finite and unvarying. Situations which make such heightened examination necessary may be the inherent unlikelihood of the occurrence taking place (Lord Hoffmann's example of the animal seen in Regent's Park), the seriousness of the allegation to be proved or, in some cases, the consequences which could follow from acceptance of proof of the relevant fact. The seriousness of the allegation requires no elaboration: a tribunal of fact will look closely into the facts grounding an allegation of fraud before accepting that it has been established. The seriousness of consequences is another facet of the same proposition: if it is alleged that a bank manager has committed a minor peculation, that could entail very serious consequences for his career, so making it the less likely that he would risk doing such a thing. These are all matters of ordinary experience, requiring the application of good sense on the part of those who have to decide such issues. They do not require a different standard of proof or a specially cogent standard of evidence, merely appropriately careful consideration by the tribunal before it is satisfied of the matter which has to be established."
(1) My previous findings are the starting point. This judgment and its predecessor should be read together.
(2) The parents must present evidence to challenge those findings (the evidential burden).
(3) However, the legal burden of proving its case on the balance of probabilities remains on the local authority throughout.
(4) All the evidence, medical and non-medical, must be fully assessed.
(5) There is no priority as between evidence arising at the earlier and later hearings, nor between evidence that was given orally at the rehearing and evidence that was not.
Dr David Ayoub, radiologist, Springfield, Illinois
*Dr Jeremy Allgrove, consultant paediatrician and paediatric endocrinologist, Great Ormond Street Hospital
*†Dr Sze May Ng, consultant paediatrician and paediatric endocrinologist, Southport and Ormskirk NHS Trust
†Professor Nicholas Bishop, Professor of Paediatric Bone Disease, Sheffield Children's Hospital
Prof Stephen Nussey, Emeritus Professor of Endocrinology, St Georges Hospital Medical School
*†Dr Katharine Halliday, consultant paediatric radiologist, University College Nottingham
Approach to the medical evidence
- Dr A, treating paediatrician, describing C in the clinical note of an examination six days before admission: "a picture of health"
- Dr Ayoub, in written reply to questions in April 2017: "That C suffered from metabolic bone disease is beyond certain." [E378]
- Dr Allgrove, in reply to Mr Feehan: for a paediatrician to describe a child with so many fractures to normal bones as 'a picture of health' six days before admission is "unthinkable".
While vivid remarks of this kind have their place amidst the other evidence, they should not attract more weight than they deserve simply because they are memorable.
The expertise and approach of the medical witnesses
Dr David Ayoub
Ayoub D, Plunkett J, Keller KA, Barnes PD. Letter to editor: Are Paterson's critics too biased to recognize rickets? Acta Paediatr. 2010;99(9):1282-3.
Hyman CJ, Ayoub D, Miller ME. Letter to editor: Response to Taylor et al, Comments on Making the Diagnosis of Rickets in Asymptomatic Young Children. Clin Pediatr. 2010;50(5):474.
Hyman CJ, Ayoub D, Miller M. Response to Vinchon. Letter to editor: Hyman CJ, Ayoub D, Miller M. Childs Nerv Syst. 2011;27(2):201.
Ayoub D. Letter to editor: Fractures: Abuse or rickets? Radiology 2012. 264(2):614-5.
Ayoub D. Limitations of radiology in rickets. Letter to editor: Pediatr Dev Pathol. 2013 Sep-Oct;16(5):397
Ayoub D, Hyman CJ, Cohen M, and Miller M. A critical review of the classic metaphyseal lesion (CML): Traumatic or metabolic? AJR Am J Roentgenol. 2014 Jan;202(1):185-96.
Ayoub D, Hyman C, Miller M. Reply: To PMID 24370143. AJR Am J Roentgenol. 2014 Jun;202(6):W604.
Ayoub D, Miller M, Hyman C. Reply: SPR Child Abuse Committee Response Regarding Classic Metaphyseal Lesion. AJR Am J Roentgenol. 2014 Aug;203(2):W233.
Miller M, Ward T, Stolfi A, Ayoub D. Overrepresentation of multiple birth pregnancies in young infants with four metabolic bone disorders: further evidence that fetal bone loading is a critical determinant of fetal and young infant bone strength. Osteoporos Int. 2014 Jul;25(7):1861-73.
Paterson CR, Ayoub D. Congenital rickets due to vitamin D deficiency in the mothers. Clin Nutr. 2014 Dec 17. [Epub ahead of print] Review
Ayoub D. Letter to editor: Misinterpretation of birth-related growth plate injuries as classic metaphyseal lesions. Journal of Forensic Radiology and Imaging, 2015 in press.
(a) the court retains control of whether evidence will be admitted (at the outset in family proceedings, ultimately in criminal proceedings),
(b) the expert must give an opinion that is objective and unbiased, and
(c) where the expert propounds a controversial hypothesis, s/he must draw attention to the fact.
My previous findings in relation to the medical evidence
The initial x-ray on 16 June covered the right arm and shows the following fractures, with * indicating fractures that show no sign of a healing reaction:
1* Right acromion (upper part of the shoulder blade)2 Metaphyseal fracture of proximal right humerus3 Metaphyseal fracture of distal right humerus4* Comminuted fracture of the shaft of the right humerus occurring through the PR5 Fracture of distal right radius and ulna
The skeletal survey of 16 June shows the following further fractures:
6 Right middle metacarpal7* Left acromion8 Metaphyseal fracture of proximal left humerus9 Metaphyseal fracture of distal left humerus10 Distal left radius11 Metaphyseal fracture distal right femur12 Distal right tibial shaft13 Distal right fibula shaft14 Metaphyseal fracture distal left femur15 Metaphyseal fracture proximal left tibia16 Metaphyseal fracture distal left tibia17 Distal left tibia shaft18 Distal left fibula shaft19 Left 6th, 7th, 8th, 9th and 10th ribs laterally20 Right 6th and 7th ribs laterally
The skeletal survey of 16 June also shows quite florid PR at the following further sites where no fractures are seen: the clavicles, the ulnae, the first metatarsals and the scapulae. There are no wormian bones in the skull.
There are no significant disagreements between the experts about the radiological appearances themselves. …
Dr Halliday considered the reports of the original radiologists that the bones on the June x-rays appeared osteopenic (white). She agreed that the right arm looked a bit osteopenic but says that this was a very subjective and inaccurate way of assessing bone strength and did not indicate a predisposition to fracture. It might be the result of disuse of the limb following fracture. Osteopenia of prematurity is common in premature babies but there is no generalised osteopenia in the skeletal survey.
On C's June x-rays, the PR is abundant at the fracture sites and also on bones that are not fractured, for example the clavicles and the 1st metatarsals in the arches of the feet. These appearances are extremely striking. The PR around each fracture is greater than usually seen and can be described as 'florid' or 'exuberant' in terms of the width of the reaction and the extent of the bones affected. Dr Halliday had never seen a case with so much PR on so many bones. She had seen PR this wide in isolated bones but not in so many bones. Its width and extent is unique in her experience.
The bones without PR are most of the unfractured ribs, most of the hand and feet bones, the spine, the pelvis and the bones at the base of the skull.
As to the fracture sites:
(1) Eight of the limb fractures are metaphyseal. These are associated with inflicted injury (pulling or twisting).(2) Metaphyseal fractures are not associated with bone disorders, where midshaft fractures are common. C had only one midshaft fracture (the upper right arm).(3) Fractures to the acromia are also associated with inflicted injury and can be caused by the arms being yanked.(4) The rib fractures are of a kind that would be caused by squeezing or squashing.(5) Fractures to the 1st metatarsals are also associated with inflicted injury resulting from the foot being twisted. Dr Halliday speculated that the PR on these bones might be associated with fractures that cannot be seen.(6) Fractures to the clavicles are also associated with inflicted injury. PR on the clavicles is an unusual appearance without an identified fracture, which Dr Halliday could not fully explain, unless it was the result of adult thumb pressure without fracture, or of rapid growth, or a combination of the two.
As to the extent of the PR, Dr Halliday thought it likely that this was the result of repeated handling affecting fractures that had not been immobilised, leading to much more PR in the area. This may explain why the PR is exuberant in the limbs, which are subject to twisting, but not on the ribs, where there are only blobs of callus at the fracture sites. Less likely as a cause of extensive PR is rapid growth, though this may contribute.
- Caffey's Disease
- Congenital syphilis
- Healing rickets
- I-cell disease
- Job Disease
- Osteogenesis imperfecta
- Temporary brittle bone disease (sic)
- Metabolic bone disease of prematurity
(1) C had normal bones.(2) The cause of the fractures was the application of excessive force to his limbs and torso.(3) The mechanisms described by Dr Halliday and Dr Ng (gripping or squeezing of the chest, twisting or bending of the limbs) would cause fractures of this nature.(4) The absence of external injury (bruising or other marks) is noteworthy but such injuries would not necessarily be expected unless there were blows to the body.(5) The eight metaphyseal limb fractures and the fractures to the shoulder blades are of a kind associated with inflicted injury.(6) C did not suffer from any of the numerous rare medical conditions considered by the specialists. There are no grounds for believing that the doctors have missed something.(7) The highly distinctive radiological picture provides a good reason to consider the possibility that C may have suffered from an as yet undiscovered transient metabolic bone disorder, but having considered the possibility in depth, I find that there is no good reason to believe that he did in fact suffer from such a condition.(8) The only reason for particular attention having been paid to Caffey's Disease is that it is a transient metabolic bone condition. In all other respects, C's condition is quite different from Caffey's, which affects whole bones in different parts of the anatomy and is not associated with fractures.(9) A diagnosis of "unknown cause" is a respectable one in any case when the cause of a medical condition is unknown, and will particularly arise in the context of controversy at the frontiers of medical science: the authorities referred to at paragraph 17 above arise from cases of baby deaths involving "the triad" of head injuries and possible Sudden Infant Death Syndrome.(10) In this case, I find that the cause of the fractures is not unknown, even in relation to the clavicles and the metatarsals. Given that the injuries to the other bones were the result of assaults, it is entirely possible that the PR seen on the clavicles was the result of force applied by adult thumbs that disrupted the periosteum without causing any identifiable fracture. Likewise, the PR seen on the metatarsals can be explained as being the result of an application of force, perhaps by a twisting of the feet, with or without fracture.(11) Such symmetry as exists in the distribution of C's fractures is not inconsistent with injury being inflicted during momentary losses of control. I do not accept that there would have to be a systematic approach. Each of the injuries could readily have been caused by sudden, momentary force applied by an adult who was holding the child's arms, legs or chest with both hands.(12) The wide extent and florid nature of the PR in this case is explained by the profusion of the fractures and the fact that they were not immobilised and will have been disturbed by repeated handling. It is not possible to know whether rapid growth played a part, but it may have done.(13) Even if C may have had a mild degree of osteopenia of prematurity, it would not have significantly predisposed him to fracture.(14) C suffered from gastro-oesophageal reflux which proved intractable. Medical personnel believed that this was his only complaint, and treated him accordingly. It is now clear that he was suffering from far greater difficulties, beginning at some point in the six weeks before his admission. This may coincide with the falloff in his weight gain shown by the growth charts, but that would be speculation. Nonetheless, the presence of so many untreated fractures undoubtedly affected his response to being handled, so that he has been described by his parents and grandfather as being "antisocial" or as wanting to be left alone. It is also very likely that the fractures made him even more difficult to feed.(15) The routine examinations by Dr O and Dr A did not cause fractures. I accept that iatrogenic fractures have been known to occur, particularly with extremely preterm infants, but, having heard from these doctors, I am satisfied that that is not the case here.(16) The investigations marshalled by Dr A were organised and thorough. There was no question of any bias towards a diagnosis of inflicted injury; on the contrary, he began from the working assumption that the cause might be an organic one. He took appropriate specialist advice from tertiary centres in reaching his clinical conclusions.
Overview of the medical evidence at this hearing
(1) Dr Ayoub fundamentally challenged the radiology assessment, arguing that C suffered from healing rickets, amongst other things. This view had little or no support from the other witnesses. Nevertheless, two particular aspects of the radiology received closer attention on this occasion: (a) the appearance of PR on the shoulder blades (scapulae), and (b) the appearance of the third metacarpal in the right hand. The latter led to a debate about whether C may have had secondary hyperparathyroidism (SHPT), the effects of which are often seen in the long bones of the hands, and if secondary to low calcium, can be in response to or evidence of vitamin D deficiency.
(2) Professor Nussey's theory that HVA may have caused or contributed to C's presentation was extensively considered and gained some qualified support from Dr Allgrove.
|On the balance of probabilities:||Ayoub||Nussey||Bishop||Ng||Halliday||Allgrove|
|The number of fractures has been overestimated||Agree||N/A||Disagree||N/A||Disagree||N/A|
|It is likely that C's bones were adversely affected by vitamin D deficiency in utero||Agree||Agree||Disagree||Disagree||Disagree||Disagree|
|C had rickets||Agree||Disagree||Disagree||Disagree||Disagree||Disagree|
|A reasonably possible alternative and/or additional diagnosis is that C had vitamin C deficiency/scurvy however it is not possible to establish this retrospectively||Agree||Disagree||Disagree||Disagree||Disagree||Disagree|
|A reasonably possible alternative and/or additional diagnosis is that C had copper deficiency||Agree||Disagree||Disagree||Disagree||Disagree||Disagree|
|C suffered from hypervitaminosis A leading to the radiological appearances of hyperostosis and contributing to fractures||N/A||Agree||Disagree||Disagree||Disagree||Equivocal|
|C has or had an undiagnosed metabolic bone disease||Agree||Equivocal||Disagree||Disagree||Disagree||Agree|
|The cause of C's fractures is inflicted injury||Disagree
Evidence of Dr Ayoub
Evidence of Professor Nussey
"A factor that has not been considered by Professor Bishop is the supply of calcium. It has long been recognised that the inhibition of gastric acid production reduces calcium absorption. Fibre within the diet may also reduce calcium absorption. Used as a feed thickener specifically for reflux, locust bean gum safety in neonates and young infants has been reviewed (Meunier et al. 2014). However, this is not been done in the context of other medications such as Gaviscon or Ranitidine used in the treatment of gastro-oesophageal reflux. In the case of C it is to be noted that its use is not recommended in pre-term infants (ibid). Studies in vitro have shown that locust bean gum reduces the availability of materials such as calcium and iron and this is likely to be exacerbated by a reduction in gastric acid production (Bosscher et al. 2001).
Professor Bishop excluded the diagnosis of Caffey's disease because of the lack of associated clinical features. However, it is noteworthy that neither he nor indeed Dr Halliday included hypervitaminosis A in the differential diagnosis. Whilst I am not a radiologist, this is usually included in the textbook differential diagnosis of the characteristic exuberant periosteal hyperostosis. Furthermore, there are reports of hypervitaminosis A affecting the metaphyses of long bones.
Vitamin A is rapidly absorbed and slowly cleared. It is stored in the liver. In excess, it is the only toxic substance known in rats to lead to spontaneous fractures. Although vitamin A toxicity has been known about for centuries and characterised since the 1940s, there remain large lacunae in knowledge. It is recognised that toxicity is seen at lower doses in the young and elderly, and that there may be other factors exacerbating toxicity. Some of these may be genetic (Hathcock et al., 1990). In vulnerable groups such as children toxicity has been reported with doses of the order of 1500IU/kg/d (ibid). The presentation of toxicity varies with the dose and duration of exposure, as well as the age of the individual exposed. C was noted to have irritability, failure to thrive, persisting, anaemia, and by inference, bone pain and tenderness.
The Committee on Toxicity of the Food Standards Agency (CoT 2013) has recommended for infants, a Tolerable Upper Limit (TUL) for preformed vitamin A of 200µg RE/kg/day. Human breast milk contains circa 80µg RE/100ml; Cow & Gate Stage 1 55µg RE/100ml; human breast milk with fortifier contains 315µg RE/100ml (Cow & Gate; Reference). I am not a Neonatologist, and it is not possible accurately to calculate vitamin A intake in the SCBU from the available material, but it is to be noted that C received human breast milk with fortifier during this admission and after discharge until about the middle of April, when he was eight weeks old. At this time he was receiving 2500IU vitamin A in Dalivit and this was continued subsequently. Depending on the number of sachets of fortifier added to each 100ml of breast milk. It may be roughly calculated that he was receiving about fourfold the TUL and an amount of vitamin A that has been associated with toxicity in reported cases.
It is noted that the Dalivit dose was increased in June 2014 and yet the radiological appearances of C's bones were reported to have improved 5 months later. This may be accounted for by a number of factors. His growth meant that the dose of vitamin A per kg body weight was reduced. There may also have been maturation of changes in the liver. In addition, it is known that there is a potential antagonism between vitamins A and D. He was likely to have been born with a marked vitamin D deficiency and thus to have been more sensitive to vitamin A excess. As the vitamin D stores improved. He may have become more resistant to vitamin A. In addition, he was no longer taking any medication for reflux after discharge. As there is evidence that histamine has physiological effects on bone cells (both osteoclasts and osteoblasts) it is possible that histamine (H2) receptor antagonism may have played a role (perhaps idiosyncratically in C) in the effects on bone. This effect was removed when the ranitidine was stopped in June 2014."
(1) That C was born with bones adversely affected by vitamin D deficiency in utero, given the autumn/winter pregnancy and the lack of prescription of vitamin D supplements to his mother.
(2) That vitamin D deficiency and subsequent insufficiency may have created increased sensitivity in C to vitamin A excess.
(3) That C's calcium absorption may have been adversely affected by a 'polypharmacy' created by the acid neutralisers Gaviscon and Domperidone and the acid inhibitors Ranitidine and Omeprazole, breast-milk with supplements, formula feed, fortifier/feed thickener containing locust bean gum, and Dalivit.
(4) That the absence of pathology five months later may be explained by improvements in C's vitamin D levels alongside a maturational process.
Evidence of Dr Allgrove
Evidence of Dr Ng
Evidence of Professor Bishop
Evidence of Dr Halliday
The parties' submissions
- C did not suffer perinatal fractures.
- The two February x-rays do not show any abnormality in his bones.
- All the fractures were sustained in the seven-week period between 2 May and 16 June 2014, a time spent entirely in the parents' care.
- If C had a metabolic bone disorder, it manifested itself only then.
- Specifically, if he had a hypersensitivity to vitamin A, it did not display itself at any other time or in any other way.
- There is no cogent evidential basis to support the hypothesis of vitamin A toxicity. A hypothesis that might raise doubt in the minds of a jury must be carefully analysed in these proceedings.
- Any hypothesis must account for both the fractures and the PR, and their symmetry.
- The only hypothesis that explains (i) the symmetrical raised PR; (ii) the raised PR in non-fractured bone; (iii) the noted osteopenia; (iv) the unusual bone texture; and (v) the lack of observable external symptoms; is that of Professor Nussey. The failure to account for all of the above is a real problem for those who assert abuse.
- The existence of PR in apparently uninjured sites, notably the scapulae, shows that something must be wrong with the bone.
- Transient conditions do exist – osteopenia of prematurity, rickets and Caffey's.
- Sensitivity to vitamin A may be temporary, due to the effects of maturation.
- The court should be cautious before placing too much weight on the February x-rays. They did not include the lower limbs, which may have been fractured.
- Further, the November x-rays, if abnormal, as suggested by Prof Bishop, show that there may have been further fractures at some time after admission.
Conclusions on the medical evidence
The number of fractures
Vitamin D deficiency
Hypervitaminosis A (HVA)
(a) The appearance of the PR is suggestive of a systemic difficulty.
(b) HVA does come within the rare differential diagnosis of generalised PR.
(c) C's vitamin A consumption was above 'normal' at periods after his birth due to the supplementation.
(d) If Dr Ayoub's evidence is accepted, Professor Nussey's view of the biochemistry and Dr Ayoub's view of the radiology may be considered mutually supportive.
(e) Rarity does not exclude possibility.
(a) None of the research papers referred to comes close in terms of dose of vitamin A, time of exposure, or age of the child.
(b) None of the research papers referred to shows an association with fractures in humans.
(c) HVA is not associated with fractures.
(d) No other presenting symptoms are asserted as being consistent with excess vitamin A reaction.
(e) It appears universally accepted that such a condition is very rare indeed.
(1) Such testing as was carried out was sufficient to allow a fair appreciation to be gained of C's biochemical status at the time of his birth and his later admission. The available data shows a relatively mundane picture, indistinguishable from any number of newborn babies. This does not exclude the presence of HVA, but is nonetheless of significance.
(2) The radiology in February was entirely in keeping with that of a normal premature baby. The possibility that C, who had no upper limb fractures, may at the same time have been carrying lower limb fractures outside the x-rays is so improbable that it can be discounted.
(3) Similarly, the biochemistry and radiology following C's admission to hospital in June, showed an essentially normal metabolism at work.
(4) Insofar as Professor Bishop identifies a minor abnormality in the November x-rays (irregularity of the distal metaphyses of the left forearm bones), I prefer the evidence of Dr Halliday to the effect that these were normal. Professor Bishop is a specialist in metabolic bone disorder, not radiology.
(5) It is an indispensable element of Professor Nussey's theory that C should have had a unique, transient, and possibly genetic hypersensitivity to vitamin A, and that he should then have recovered from it, perhaps as a result of maturation. Though nothing is impossible in medicine, there is no dependable theoretical foundation for this conjecture and no primary evidence of a pathology which causes vitamin A toxicity with such devastating results, and then abates.
(6) It is not an indispensable element of the theory that there should have been an interplay of polypharmacy arising from the anti-reflux medication, but I nonetheless find that this relatively common form of medication cannot have contributed significantly to the catastrophic condition of C's bones. Dr Ng has particular experience and expertise in relation to premature babies, and I accept her evidence on this issue.
(7) There were no clinical signs of HVA, such as a bulging fontanelle.
(8) There is no indication that C's vitamin D status was so compromised that it would have had a knock-on effect on his vitamin A levels.
(9) HVA is only associated with extensive PR if vitamin A is administered in very high, prolonged doses. That was not remotely the case here.
(10) HVA is not associated with fractures.
Undiagnosed metabolic bone disease
Ranitidine (H2 receptor blocker) 14 April-6 May (3 weeks)
Domperidone (H2 receptor blocker) 25 April-16 June (8 weeks)
Omeprazole (Protein Pump Inhibitor) 10-16 June (1 week)
It was Prof Nussey's evidence that PPI medication was more likely to affect calcium absorption than H2 receptor blockers, and that in this case Omeprazole (PPI) had been prescribed for too short a time to have any effect. I would add that its prescription also postdates many of the fractures.
(1) I am unable to accept that C's condition resulted from an identified metabolic cause. Specifically, for the reasons given above, I find that hypervitaminosis A does not offer an explanation.
(2) The other conditions that were ruled out in 2015 remain ruled out now. They are listed at  above. In particular, I confirm the finding that C did not suffer from rickets or from vitamin D deficiency of such significance that it could have set in train a demineralisation in his bones that might explain the medical picture.
(3) The investigation has been exhaustive and I am satisfied that no other known condition has been overlooked. Having considered the possibility that testing at other times would have revealed radically different biochemical information, I reject it as overwhelmingly improbable
(4) There are consequently only three realistic explanations for C's condition: that it is the result of a pathology that is beyond our present knowledge or the result of force inflicted by an adult, or both.
(1) The condition would have to have had devastating effects on C's metabolism without leaving any concomitant biochemical markers.
(2) At the same time, it would leave him (on any view) with multiple fractures of a kind that were bound to be accompanied by significant PR: it is the extent of the PR, not its presence, that is so unusual.
(3) It is particularly problematic to envisage a condition that could cause so many fractures with normal handling, but which has nonetheless escaped detection by medical science.
(4) Such a condition would need to be transient in order to fit with the reliable medical information. In this regard, I found the evidence of Professor Bishop about the nature of transient conditions to be particularly helpful. He explained that we understand the reasons for transience in the few transient conditions that are known to exist. As he put it, fragility does not simply go away. The likelihood of there being an unknown transient condition of such severity that it caused appearances of this kind and then disappeared is extraordinarily unlikely, and cannot in my view be plausibly explained by normal maturation.
(5) I accept that the lack of the PR on the scapulae and clavicles is a finding that tends to point the other way. However, one has to look at the evidence as a whole, and in a complex case of this kind it is not unusual for there to be some anomalies. In this case, the absence of a ready explanation for the anomaly does not in my view invalidate the hypothesis.
(6) Lastly, there is no dispute among the domestic experts that the medical findings could be the result of inflicted force: what divided them sharply was the assessment of probability.
The other evidence
As to pain, at :
… I find that an adult was undoubtedly in the closest proximity to him whenever the injuries occurred and that he will have cried in pain when his bones were fractured. The inability of either parent to describe a single occasion when he reacted in this way is highly suspicious. The only incidents that they have offered for consideration occurred in doctors' surgeries.
As to C's environment, at :
… it is not difficult to envisage how one of the parents might have lost control for the first time, quite possibly in exasperation at his slowness or inability to feed, and how this led to a vicious circle in which C's injuries made it harder for him to feed, and so on.
As to the parents' credibility as witnesses, at :
There are cases where a witness's evidence is of such quality that it outweighs all other evidence and the court is able to accept it unconditionally. That is not the case here. The parents are no doubt credible narrators of normal life events. However, with regard to the specific issue of C's injuries, I did not consider that I could rely on the evidence of either of them.
As to opportunity, at :
I accordingly conclude that there was plainly the opportunity for C to suffer injury from one or both of his parents, despite the level of surveillance and the protective factors.
As to perpetrator, at :
If it was possible to identify one parent as the perpetrator, that would be desirable for C's sake, but unfortunately neither has been fully forthcoming. As matters stand, it is possible that either of them caused his injuries and at this stage I cannot say that one is more likely than the other to be responsible.