AD & AM (Fact-Finding Hearing) (Application for Re-Hearing)

By this judgment, I set out my reasons for directing a re-consideration of findings of fact which I made within Part IV Children Act 1989 care proceedings in July 2013, following an investigation into the cause of life-threatening injuries to a 10 month old baby boy.

By my earlier judgment, I concluded that the baby’s mother had caused these injuries to her son (see Re AD & AM (Finding of Fact: Non-Accidental Injury) [2013] EWHC 4859 (Fam)) and that the injuries were non-accidental. However, more recent medical opinion on the cause of the injuries, centred to some extent on pathological analysis of a segment of the baby boy’s skull (which had, to all intents and purposes, been lost at the time of my earlier hearing), provide proper grounds on which this court should review its earlier conclusions.

The scope of the re-hearing is yet to be decided; that decision will be influenced by the outcome of an experts’ meeting which I propose should be convened as a matter of some urgency.

On 23 October 2012, AD (“AD”), a 10-month old baby boy was admitted by ambulance to Newham General Hospital, in a critical, life-threatening, condition. He was unconscious (registering 3 on the Glasgow Coma Scale – the lowest reading, indicating deep unconsciousness), moribund, and for a time immediately prior to the arrival of the emergency services had in fact stopped breathing. On investigation he was found to have a fractured skull, a subdural haemorrhage, and multiple fractured spinal vertebrae. He was transferred immediately to Great Ormond Street Hospital where he underwent surgery on the morning of 24 October for the release of pressure on his brain; his condition was stabilised, and after a period of recuperation, in early December 2012, he was discharged to the care of his grandparents. AD has been left permanently damaged by the injuries.

In 27 November 2012, the London Borough of Newham, the relevant authority in which AD, his older sister (“AM”) and his parents lived, issued proceedings under Part IV of the Children Act 1989, and sought a care order. The proceedings were listed before me for a fact-finding hearing in July 2013.

At the conclusion of the fact-finding hearing ([2013] EWHC 4859 (Fam)), I determined that the injuries had been caused to AD by his mother, and that the injuries were non-accidental. A welfare hearing followed in March 2014. In determining the futures of AD and his sister, I received social work analysis, a helpful report from the Children’s Guardian, and a comprehensive risk assessment from Dr. Cleo Van Velsen, Consultant Psychiatrist in Forensic Psychotherapy; at the conclusion of the welfare hearing (see Re AD & AM (Non-Accidental Injury: Welfare) [2014] EWHC 4899 (Fam)), I endorsed the Local Authority’s plan to rehabilitate AD and AM to the care of their parents, subject to a tightly drawn agreement between the family and the Local Authority, constant supervision of the mother’s care of the two children by family members, a shared residence order between the parents and the paternal grandmother, and a supervision order. I made plain that I contemplated that I considered it likely that the Local Authority would seek the renewal of the supervision order in early 2015.

The mother was, in the meantime, charged with criminal offences of assault (including a charge of inflicting grievous bodily harm with intent, contrary to section 18 Offences against the Person Act 1861) and child cruelty arising from the injuries to AD.

On 23 March 2015 the Local Authority applied for the renewal of the supervision order; on 7 July 2015 (having earlier indicated her intentions at an Issues Resolution Hearing before H.H.J. Atkinson at the East London Family Court), the mother cross-applied for a re-hearing of the findings of fact. In short, she asserted that evidence which had been obtained from reputable medical experts in the criminal proceedings cast doubt upon the findings which I had made in July 2013.

The mother’s criminal prosecution was brought to an end in October 2015, when the Crown Court judge dismissed the case for abuse of process, a determination brought about, so I understand, by repeated failures of the prosecution to be in a position to proceed to trial. Publication of my judgments in 2013 and 2014 has been deferred pending resolution of the criminal process.

I listed the mother’s application for determination on 11 January 2016. I heard argument over a day and a half. I reserved judgment. I set out my decision under the following headings below:

On an application for a re-hearing of a determination of facts, as in these circumstances, it is agreed that I should follow the approach advocated by Charles J in Birmingham City Council v H and others [2005] EWHC 2885 (Fam), and endorsed by Sir James Munby P in the case of Re ZZ & Others [2014] EWFC 9 at [31] (“Re ZZ”). There is a three-stage process, namely:

Munby P described characteristics of the three stages in Re ZZ thus:

Expanding on the first stage, Munby P referred to Hale J (as she then was) in In re B (Minors) (Care Proceedings: Issue Estoppel) [1997] Fam 117 in which she had said (at p.128-129):

I do not understand Munby P to be equating the test at ‘stage 1’ (“some real reason to believe that the earlier findings require revisiting”: [33] of Re ZZ, see [12](i) above) with the test which is 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 (see generally CPR 1998 rule 52.3(6)-(8) / CPR 1998 rule 52.9 and FPR 2010 rule 30.3(7)/(8)). 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 and others [2005] EWHC 2885 (Fam)), 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 [55]. This second policy consideration was further defined in Re K at [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”.

Interestingly, the Court of Appeal’s decision in Re K does not appear to have been cited to Munby P in Re ZZ. Had it been so, I suspect that it would have, in itself, provided a good illustration of a “real reason” for believing that “the earlier findings require revisiting”.

In reviewing this case, I have been invited to accept that scientific and medical knowledge and expertise may be further advanced than it was three years ago, and that research into the medical presentation of complex infant abuse continues to “throw a light into corners that are at present dark” (Re U, Re B (Serious injury: Standard of proof) [2004] EWCA Civ 567). Finally, it is argued that I should approach the case on the basis that the medical evidence should be considered ‘all of a piece’ together; it is not possible, or appropriate, that I should compartmentalise the opinions, viewing the 2013 reports separate from the 2015 reports. They need to be considered side-by-side: per Re T [2004] EWCA Civ 558:

“…evidence cannot be evaluated and assessed in separate compartments. A judge in these difficult cases has to have regard to the relevance of each piece of evidence to other evidence and to exercise an overview of the totality of the evidence in order to come to the conclusion whether the case put forward by the local authority has been made out to the appropriate standard of proof.” (Emphasis by underlining added).

AD and his sister AM are the two children of MB (“the mother”) and FB (“the father”). The mother and father were both born in Nigeria, and are from the same area of that country; they were married there in 2008. They are professional people; the grandparents on both sides have professional backgrounds, the paternal grandfather being a professor of pharmacology. AD was born on 7 January 2012. He was breast and bottle fed, dietary supplement being offered by infant ‘formula’. The parents report that when only a month or so old, AD suffered “extreme colic”. When AD was only a few weeks old, question arose as to whether he may be vitamin D deficient. It was only when the mother subsequently arranged for her own vitamin D levels to be tested, that this revealed an abnormally low level. What is known is that by May 2012 AD was believed to have attained appropriate levels of vitamin D – the test in May 2012 shows normal levels of alkaline phosphatase (the only abnormal test being his haemoglobin levels).

On three occasions prior to 23 October 2012, AD was taken as an emergency patient to hospital:

The mother recalled that by the time of the key events (23 October), AD “could roll around at speed and was attempting to crawl. He was attempting to pull himself up, and could at least lift his bottom off the ground when an object was close to him”. When asked at the time about AD’s capabilities by the police, the parents are reported to have said that he could not pull himself up to stand.

On 23 October 2012, the mother left the home in the morning and was at work all day; the father was responsible for the care of the children. The day was apparently uneventful, save for an incident in mid/late afternoon.

The father recounts that at about 4.30pm he left AD and AM in the master bedroom while he went to fill a bucket in the bath to wash AM. He left AD sitting on the floor, propped up and surrounded by pillows. He was out of the room only long enough for the bucket to part-fill with water. He then heard AD cry – “not screaming, but quite a loud cry”. On returning to the bedroom, he says that he found AD lying on his right-hand side on the floor. He said that he noticed that a toy sit-on cart/scooter had moved; AD was lying close to the bed on his right hand side (facing away from the door), with his head about 12 to 15 inches from the table leg of the television table. AM (who had been sitting on the bed) was standing by the door. AD cried, the father said for “a few minutes”. The father said that he picked AD up, and carried him straight away downstairs; having left the bedroom he went downstairs without delay (AM following) and “by the time we were in the kitchen, he was not crying as loud; the crying stopped shortly after we got outside”. On this description I concluded that the crying was not likely to have lasted longer than 5-6 minutes.

Significantly, the father’s evidence at the hearing in 2013 contained the following comments:

Picking up that last comment, above, the mother herself first heard about the ‘4.30p.m. incident’ in the early hours of the morning of 24 October 2012 when she and the father were at Great Ormond Street Hospital. I commented in my earlier judgment that this may suggest of course that the father was trying to hide that something significant had happened while the children were on ‘his watch’; or conversely that the incident was of no great significance and has been magnified in the minds (and histories) of the parents since the discovery of the serious injuries, desperate to find an innocent explanation for the injuries with which AD was later to present at hospital.

At about 5.30p.m. the paternal grandfather arrived at the family home. When the father mentioned the ‘4.30p.m. incident’ to his father, the paternal grandfather said that he checked over AD’s head. The paternal grandfather told me that he thought that the right hand side of the head (which is the side the father said he had found AD resting on the carpet in the bedroom) felt “soft”, but in evidence acknowledged that (a) he did not compare it with the left side (which he did not in fact touch/feel), and (b) he was unsure that this was not just the ordinary feel of the baby’s skull at that stage of development. In any event, and importantly, he said that there was “no reaction” from AD when he touched the right hand side – evidence which I considered was likely to be inconsistent with AD having suffered a major skull trauma to the right parietal bone by that time, and is in contrast the position in the hospital later that day when AD reacted when the skull was touched.

The mother returned from work at about 5.45p.m. She said that the paternal grandfather was looking after AD when she returned. She assumed the care of AD at once and decided to make him some relatively instant food – porridge mixed with yoghurt. The mother described (witness statement) that he ate initially “enthusiastically” (this was also the father’s recollection), and “seemed to want several spoons” (in fact ate 6-8, even 10, spoonfuls before declining more). He had been, she said, “quite hungry” at first. The paternal grandfather told me that one of the parents (he could not recall which) had told him that AD had eaten “well” at that point. She then gave him a little Lucozade diluted with water, and separately some diarolyte which he sipped. He vomited a little when he was being winded. The mother said (and the father did not demur) that she took AD upstairs to start his bedtime routine at about 7p.m.

Shortly thereafter, the father saw AD upstairs and said that he thought that AD (then lying on the bed with the mother) “appeared more lively”. The father said that he believed that AD did not look so tired and attributed this to the fact that AD had recently eaten.

The mother told me that she ran AD a bath (a baby bath which rests on the frame of the ordinary bath). She told me that she undressed him and put him in the bath; she said that he “kicked” his legs and “splashed” as he was lowered into the bath, partly playfully and partly responding to the sensation of the water (he was not as playful as usual, apparently, but did splash). He was in the bath, she said for about 10 minutes or so, before she lifted him out, massaged him, and dressed him for bed. She gave him some more diarolyte, and he took 40-60mls. She then placed him on the bed surrounded by pillows (including, she told me a large ‘maternity’ pillow) to stop him rolling off the bed. She is sure that at no time did he roll off the bed. The mother said that at about 8-8.30p.m. AD fell to sleep. The mother acknowledged that over the course of the evening she “didn’t observe a deterioration” in him. The mother changed her own clothes, and then lay on the bed herself.

At about 21:30hs the mother said that she heard two distinct and “loud gasps” from AD; she told me that “they were quite deep”, she lifted him up and she described him as being limp and floppy: “his head was dipped; his head was loose”. She noticed that he was not breathing. She screamed for her husband, and ran down the stairs shouting for help. The mother put AD into the recovery position; she said that he was not breathing. She attempted resuscitation procedures, and could hear the air filling his lungs; initially she did not think he was breathing spontaneously, and then felt that his breathing was “really shallow”. She had been doing CPR for a couple of minutes “before he came round”. Her husband called the ambulance. The paternal grandfather began to pray. After a brief emergency admission to Newham General Hospital, AD was transferred to Great Ormond Street Children’s Hospital for specialist treatment, where he remained for several days.

The police interviewed the parents. Both denied responsibility for the injuries to AD. Both have continued to deny responsibility for the injuries.

At the hearing in July 2013, I heard oral evidence from the mother, the father, the maternal grandmother and the paternal grandfather. Expert medical evidence was available in written reports from the following experts:

The extensive investigations and assessments which followed AD’s admission to hospital revealed that he had suffered the following injuries:

The injuries were further described as follows (paras. 44 and 46 of the original judgment):

“[44] There is general agreement (Dr. Anslow, Dr. Cartlidge, Dr Fairhurst and Mr Richards) that the skull fracture and brain injury are likely to have been caused by a hard impact with the right side of the head on an unyielding surface. The notion that the skull fracture may have been caused by focal impact was advanced (on paper at least) by Dr. Cartlidge; he was in my judgment, less sure about this when asked in oral evidence. The suggestion of a focal impact was discussed and rejected at the hearing by Dr. Fairhurst who indicated in her view that the presentation of the fracture was likely to have been caused by contact with a “completely flat surface or surface with some angle”. She went on to state that if the blow had been at a single focal point then she would have expected to see a depressed fracture with a “stellate” pattern of fractures radiating outwards, which she did not.

[46] Dr. Anslow, Dr. Cartlidge, Dr. Fairhurst and Mr. Richards all agreed that the thoracolumbar vertebral compression fractures could not arise out of normal handling and would have involved considerable force, and would have caused [AD] significant pain. The fractures probably occurred as a result of excessive flexion of the spine. When asked about this at the hearing, Dr. Fairhurst expressed the view that these injuries were “a different ‘kettle of fish’ from the skull fracture; they occur very rarely” (emphasis in the oral evidence) and that “a major event results in these fractures”. She postulated the circumstances in which an injury of this type might be suffered would be where a child was in a road traffic accident having being restrained in the vehicle only by a lap belt, adding that “we know that they occur where children fall from a great height onto their feet”. Whatever the event would be it would not be an event that “a parent would forget about”.

The experts considered whether the injuries had been caused in one or more than one event. My earlier judgment records ([47]) that Dr. Anslow, Dr Cartlidge and Mr Richards all agreed that the brain and skull injuries are likely to be caused by a single event on 23 October 2012, and likely to have been during the evening of that day. Mr. Richards specifically told me that it was “extremely unlikely that these occurred at different times”. Dr. Cartlidge too confirmed that the injuries were “likely to have been caused together”, although (it is noted – per Schedule of Agreement/Disagreement following the experts meeting) he had considered “that the spinal fractures cannot be dated accurately.” On the evidence before me, I concluded that it was unlikely that AD was subjected to two or more separate incidents of ill-treatment separated in time.

All the experts agreed that the force required to cause these injuries would be “substantial and considerable”. The experts were asked to consider whether it was possible that the skull/brain injuries were caused in a domestic fall. Dr. Fairhurst’s view was that “we know that falls of less than one metre are very unlikely to result in skull fracture”, and felt that “[AD] is not in a position to do this to himself”. Dr. Fairhurst added that the fracture to the vertebrae “can occur when a child is slammed down on a hard surface, or slammed against a wall”, and further that “a fall would have been highly unlikely to cause the skull fractures but would not have caused the vertebral fractures”. Dr. Fairhurst rejected the suggestion that the vertebrae injuries may have been caused in the professional resuscitation of the baby.

Reviewing the totality of the injuries, Mr. Richards opined that “I have not seen injuries of this severity from minor domestic accidents”. Significantly, the doctors were asked to consider whether these injuries may have been caused if AD had fallen from a standing position from the toy cart/scooter onto the metal table leg, and whether this would be consistent with the evidence of domestic falls causing injuries of this kind (i.e. 2 feet free-fall onto a hard surface). Dr. Cartlidge did not accept this: “this is getting nowhere near the 2’ free fall which is the minimum; most clinicians would suggest 3’”; he observed fairly that AD would not be 2’ tall, and a fall would not be a ‘free fall’. He added: “that wouldn’t be sufficient to cause the injuries. Velocity is virtually insignificant. Even if he was being pushed I don’t think the force would have been sufficient to cause the injuries”.

The researches undertaken around the evaluation of the key injuries include studies of the blood and endocrinology. It is not immaterial to observe that “[t]he tests performed in this case represent the most comprehensive set that I have seen in reporting upon over 200 suspected NAI cases.” (Per Professor Hann). I recorded the evidence as follows:

“[57] First, no clotting disorders or bleeding disorders which are relevant to the causation of these injuries were identified (Professor Hann and Dr Cartlidge agree). Further, Professor Nussey had concluded that there was no evident endocrine disorder relevant to the causation of the injuries and no demonstrable metabolic bone disease.

[58] Secondly, Dr. Anslow, Dr. Fairhurst and Mr Richards all agreed that the skull fracture would not be affected by any bone fragility, but that less force would be needed to cause the vertebrae fractures, if there was such a disorder. Professor Nussey and Dr Cartlidge opined that if there was generalised bone fragility, this would also affect the skull.

[59] When asked about this in evidence, Dr. Fairhurst commented that “if the child had a significantly reduced bone density then they’ll be more likely to suffer fractures.” (Emphasis in the oral evidence). She further indicated that there was “no radiological evidence of rickets. In the absence of this, we cannot say that there is an increased propensity to fracture.” She added that where there is a “sufficiently severe vitamin D deficiency, the child will be at a small increased risk of fracture, usually of other bones because they will be broken in falls. These are children with clear radiological evidence of rickets.”

[60] Professor Nussey concluded from his assessment that it was unlikely that vitamin D deficiency played a role in causing any, or any significant, bone fragility predisposing AD to fractures. The values for vitamin D, calcium, phosphate and alkaline phosphatase concentrations on 24 October 2012 were normal but were likely to have been affected by administered intravenous fluids. Dr Cartlidge agreed.

[61] At the hearing, Professor Nussey … confirmed that he did not believe that [AD] had vitamin D rickets, there was “no sign” of this (ibid.) – later adding that the “tendency to fracture is not measured in frank rickets, let alone subtle”.

[62] Dr. Cartlidge opined that while AD was born vitamin D deficient, by May 2012 “he did not have rickets”; by 16 May 2012 he was on multi-vitamins and “I don’t think [AD] had rickets; his alkali phosphatase level was normal”. He has recently attempted calculations to demonstrate more scientifically the likely incidence of pre-injury vitamin D in the blood; these calculations tended to show some vitamin D “‘insufficiency”. Laudable though I find the attempts were to assist me, the results are necessarily imprecise given the absence of clear or comprehensive data.

[63] I note that the bone mineral density overall appeared somewhat reduced with “relatively poor bone mineralisation” on scan of 31 October 2012, but I accept the view of Dr. Cartlidge and Dr. Fairhurst that this is likely to be attributable to his relative immobility in the immediate and critical post-event / pre-scan period”.

In relation to timing of the incident my judgment recorded the following (paragraphs [65] to [69]):

“[65] Mr Richards gave important evidence on this [issue], confirming the following:

i)

the event occurred, according to Mr Richards “very recently before the child was admitted to hospital … compatible with a couple of hours, 3, 2, or 1; it would have happened after the child was last seen to be behaving normally”. He added later that after the incident there would not have been any “normal behaviour”;

ii)

He opined that after the agonal event [AD] would have been behaving “extremely abnormally”; he would not have been likely to have been conscious, but if so he would have been “crying and inconsolable, and gradually deteriorating into a coma”; on the mother’s account (see … above) there was no history of him generally deteriorating;

iii)

Mr Richards indicated that “I would consider it implausible that he would have fed after this injury”, and later “the account of bathing … not the actions of a child who had suffered the serious injury by then”.

[66] The Patient Report Form ... was examined. This revealed an entry as follows:

“O/A at Hosp. Slight swelling noticed on ® temporal area which started to grow while in resus”

The arrival at hospital was recorded to be 22:06, and the handover 22:08.

[67] Mr. Richards regarded this record to be of some significance. Although scalp swelling: “can occur within minutes but may take several hours…” Mr. Richards described this as a “rapidly evolving situation”, and (in answer to questions from me) indicated that “this [reference to ‘started to grow’] would put the timing [of the incident] nearer to the time of the 999 call than further”. The observation [in the patient report form] is consistent also with the comments of the anaesthetist who noted at 10.48p.m. that the “scalp swelling was increasing in size”.

[68] Dr. Cartlidge indicated that, in his opinion, the injuries occurred “very shortly” before the admission to hospital; he added that “as soon as the intra-cranial injuries were caused he would have displayed profoundly abnormal symptoms”. When asked [in oral evidence] about the possibility that [AD] had displayed behaviour consistent with a ‘lucid’ interval he said that there were three possible (albeit in each case “rare”) reasons for a lucid period. In this case he thought that the only one which could apply is where there is an expanding amount of blood in the cerebral spaces, and the amount of blood “squashes the brain causing deterioration in brain function and the child becomes unwell”. However, he added “the thing against this possible incident in the afternoon [followed by a lucid interval] is that he had eaten and drunk…he may not have been completely well, but had been not far off normal; then there was a catastrophic deterioration in the evening. That is not the pattern.” This is not the mother’s account – see … above.

[69] He added:

(a)

that after the skull fracture “anyone would have realised that he was severely unwell … I don’t believe that [AD] would have been reacting in any way like normal once he’d suffered these injuries.”

(b)

of the ‘4.30p.m. incident’ “there would be insufficient forces by any of the scenarios, and he was then feeding and playing in the bath … this is not consistent with severe head injury.””

Having considered the law, and applied it to the lay and expert evidence at the hearing, I concluded as follows:

It is relevant to note for present purposes that the parents responded to the findings (as I recorded their views in my March 2014 judgment) as follows:

“… while at one level they accept that I made the findings on the evidence, they do not accept that I was correct in my conclusions. Specifically:

The mother:

i)

The mother’s response to the judgment reveals that she “fully comprehend[s] why those findings have been made” but maintains that “I did not inflict these injuries”, adding that “I may not ever know what caused [AD’s] injuries” (ibid.); she denies that there were any tensions in the house at the time of the injury;

ii)

The mother told Dr. Van Velsen that she “wanted to work with the agencies concerned and accepted the Judgment, although felt that she could not say that she had hurt her son, because she had not”.

The father

iii)

The father accepted that the court had found that “it is unlikely that the 4.30pm incident was responsible for [AD]’s injuries” but later thought that there “was still some significance in the 4.30 incident” (Dr. Van Velsen); he has separately indicated (to the Guardian) that he thinks that Vitamin D deficiency and/or rickets may have played a part”.

The mother maintained her denial in the criminal proceedings, entering a plea of not guilty.

In preparation of her defence to the criminal charges, a considerable body of new medical evidence was collated, which the mother now wishes me to consider. It fills one lever arch file. The key evidence is as follows:

The expert evidence and its suggested relevance to the earlier findings have been summarised in a Scott Schedule to which all parties have contributed. The schedule is long and to some extent unwieldy, but it has overall been of assistance to me, and I am particularly grateful to Miss Bradley and Miss Townend for their considerable industry in bringing the various components of it together.

The mother points to six key aspects of the evidence now before the court, which she contends represent “solid grounds” (per Re ZZ) for challenging my earlier findings:

The father indicates his neutrality on the issue before the court. While anxious not to disturb the Court’s conclusion that he did not cause the injuries to AD, he does not oppose the mother’s efforts to mount a case that there may be a medical or unknown cause for the injuries. Mr. Feehan QC acknowledged in argument that it was possible that the finding of non-accidental injury would be undisturbed by the new medical evidence, but a different conclusion may be reached on the time-frame within which the most significant injury/ies were caused; if the time-frame were wider than previously identified, it may well draw his client (and possibly others) into a ‘pool’ of potential perpetrators.

The Local Authority resists the re-opening of the findings of fact of the court; while acknowledging that the significant developments in the case (specifically, the discovery of the piece of AD’s skull, the dismissal of the criminal prosecution, the collation of the extensive medial evidence) may tempt the court to embark on a review, it is necessary, argues Mr. Tughan QC, to look ‘below the headlines’, and to assess the true impact of these events on the findings made. Mr. Tughan points to the absence of any new evidence of an incident which injured AD; he further rightly points up the internally contradictory evidence of the newly obtained expert reports, including that of Professor Freemont, who (for instance) opined that while vitamin D deficiency can affect the skull, there is in fact no vitamin D deficiency in any of the skull sections.

The Guardian invites me to conclude that the evidence does not go far enough to establish any ‘solid’ basis for interfering with my earlier findings.

For the Re ZZ ‘stage 1’ exercise, I cannot undertake a detailed critique of the newly obtained expert evidence filed; it has not been tested before me. It is therefore not appropriate or indeed possible to make any meaningful comparison between the new evidence and that previously filed and considered in the 2013 fact-finding hearing. I focus on some aspects of the newly filed evidence, viewed against the backdrop of the 2013 findings which I have set out above.

The discovery, and subsequent analysis, of the skull section removed from AD in the surgery on 24 October 2012 is, in the view of some of the newly instructed experts (so argues the mother), highly material to the expert evidence as a whole. The picture which appears from pathological examination of the skull section renders it necessary, contends the mother, to re-examine:

Dr. Cohen identifies a “fresh fracture”, with “fresh haemorrhage”, and locates early neutrophilic infiltrates which suggest that the fracture is less than 48 hours old; she finds woven bone in the skull (woven bone is defined by the presence of bone mixed with partially calcified cartilage, which has poor tensile strength, as seen in the foetus), which at the fracture site is markedly thinner than elsewhere (0.1cm at the thinnest part), a finding with which Dr. Teas agrees. Woven bones, she explains, is a feature which may suggest vitamin D deficiency, and/or osteopenia; she considers it “anatomically plausible” that the fractured bones may have torn the dura in order to cause the subdural haemorrhage. Dr. Watt has commented on these new discoveries and identifies the presence of some radiographic features of a mild degree of osteopenia, which in the absence of any prior identified medical condition, is “very unusual in a child of this age”; he observes that signs of osteopenia have not, however, revealed themselves subsequently.

Professor Nussey, in his further report (2015), has also had chance to comment on Dr. Cohen’s findings of the skull section; he opines that:

“… it is possible that tensile strength was reduced.… The radiology reports indicating osteopenia and the histological finding of woven bone in the skull material examined histologically by Dr Marta Cohen would be compatible with vitamin D deficiency and would indicate that the post-natal supply of vitamin D was inadequate.”

This may be a material development from the evidence which he gave before me in July 2013 which I summarised at paragraphs [57]-[61] and [103] of my earlier judgment: see [36] above).

The new evidence on vitamin D deficiency, and/or its significance, is not all one way. For instance, Professor Freemont:

Dr. Hyman advances the view (though it is not clear whether he is deploying his own expertise or is relying on others) that AD “could have had weakened bones at the time of his injury. [AD] had several risk factors for diminished bone strength”, including “imaging changes of osteopenia” (which he later describes as “mild”), “which would be a significant factor in adversely affecting his bone strength and putting him at risk for fragility fractures”. He accepts that AD was probably not vitamin D deficient during October 2012 (per Professor Nussey), but challenges Dr. Fairhurst’s statement that reduced bone density would have only a negligible effect on the degree of force required to fracture a skull. He opines that the finding of reduced skull density at the point of the fracture “would be a risk factor for fracturing with low-force trauma"; he adds that evidence of woven bone in the skull and of cranial hypo mineralisation “could have adverse effects on cranial bone strength”.

I must remind myself that it is not vitamin D deficiency which causes an increased propensity to fracture, it is rickets. Moreover, as the Local Authority observed in submissions, even assuming that AD had an unidentified condition which caused his bones to be more vulnerable to fracture, such conditions still require an incident to cause the bone to fracture which has not (save for the ‘4.30pm incident’) been revealed.

Professor Ramsay is of the view that a short fall is:

“…seldom reported to cause a significant head injury but when they do the injuries include a scalp bruise and a linear skull fracture at or close to the site of impact, and epidural or subdural bleeding… In this situation, the infant may appear unharmed or minimally injured after the fall but then, minutes to hours later, becomes unconscious…”.

Specifically relating to [AD] he says:

“All other things being equal, I would not expect a simple fall from the seated position to have caused his injuries but I do not have the expertise to say whether the forces generated by a putative complex fall onto the various surfaces in [AD]’s vicinity… was sufficient to have fractured the skull especially if the skull was constitutionally weak (a possibility addressed by Dr. Cohen and Dr. Watt in their reports).” (Emphasis added).

Dr. Hyman goes on to express the view that the skull fracture is compatible with a short fall. Short falls can (he opines) in some circumstances generate enough force to cause skull fractures; “the history provided by the parent is compatible with the injury. It was an witnessed event (sic.) that caused [AD] to cry and attract the father’s attention to the situation"; Dr Hyman goes on to state:

“… his head possibly impacted into the wooden bed frame, metal table leg, or with a prominence on the toy trike; however, even an impact upon a flat surface can cause this type of fracture.”

Adding:

“… there is a myriad of biomechanical scenarios that could be associated with [AD]’s head impact, some of which – in my opinion – can generate enough force to cause all of [AD]’s head injuries.”

Dr Van Ee confirms judicial expectation that:

“… serious head injuries are unexpected and rare outcomes from short falls” even if not inconsistent; “severe head injury outcomes from domestic type falls are uncommon. In most fall cases, children will impact with feet, knees, arms, buttocks or shoulders first… it is in the relatively rare case where the head makes a primary impact”.

He specifically goes on to comment thus:

“… given the available data… It is not possible to exclude the scenario that [AD] suffered his skull fracture while in the room with his sister. I do find it to be an unexpected outcome but not necessarily an inconsistent outcome given the information available. To be clear, for a normal healthy child of this size tipping over from a seated position onto a flat firm surface I do not know of any scientific data that suggests that a skull fracture of this magnitude could occur. If however, the head impact surface presented an edge or some other localised feature, if [AD] had pre-existing bone abnormalities make skull weaker, and/or if [AD]’s sister interacted with [AD] lowering the head impact scenario then the biomechanical data is much less clear and this may very well represent a reasonable injury scenario explaining [AD]’s head injury.”

Dr. Watt expresses the view that:

“… skull fractures do occur in children of normal skeletal strength with falls from a height of 1 metre or more, but are very infrequent. Fractures as a result of falls of less than this height are extremely rare… While it is difficult to be exactly sure how significant a force occurred in this case, the combination and number of features present suggest a severe force impact being the case rather than a simple fall in a child of normal skeletal strength. In my professional experience I have encountered similar injuries occurring from falling from an upper floor onto hard ground, or as a result of a high-speed road traffic accident with ejection of the child from the car, and it is reasonable to assume a similar degree of force would be required in this case if the child has normal skeletal strength.”

Significantly he opines that the severity of the injury “is inconsistent with [AD] appearing normal”.

Professor Freemont is of the view that:

“The skull bone appears normal other than where it is fractured and therefore the amount of force required to have caused this extensive fracture would have been considerable. In a child of this age accidental fracture is a possibility but unless there is a clear history of the child having fallen from a considerable height onto its head or equivalent, non-accidental injury must be considered, and is perhaps the more likely.”

There are six thoracolumbar fractures which (according to Dr. Hyman) demonstrate “two different patterns on imaging” indicating that “they could have occurred at two different times”. Dr. Hyman considers that they did not (contrary to my finding of a single incident) occur at the same time as the head injury. No further explanation is offered by Dr. Hyman for the circumstance in which there may have been “fracturing with low forces”. He comments that lumbothoracic compressions are the hallmark of osteoporosis in adult populations and can be seen in infants and children with certain medical conditions.

Dr. Watt expresses the further opinion (relied on by Mr. Storey QC) that:

“Vertebral fractures are extremely rare in young children… vertebral compression fractures are most commonly seen in this age group as the result of an underlying medical condition causing increased bone fragility resulting in fracturing with non-major trauma. The conditions include osteogenesis imperfecta and rickets… this type of injury is extremely rare in this age group in the absence of an underlying medical condition.” (Emphasis added)

He goes on to express the view that the vertebral fractures and the skull fracture were likely to have been caused in the same incident.

Dr. Watt concludes as follows:

“… [T]he imaging features suggested an impact or blow of significant force, incompatible with a fall from a low height such as out of bed in an infant of normal skeletal strength. Subsequent imaging studies identified multiple compression fractures of the spinal vertebrae, suggestive of a significant compressive or flexion force being applied to the spine, incompatible with a fall from a low height in a child of normal skeletal strength. Generalised vertebral osteopenia with compression fractures and mild osteopenia with metaphysical lucencies in the long bones were identified on the skeletal survey performed seven days after presentation.… This combination of findings is most commonly found to be the result of an underlying medical condition was not identified to be likely at the time. Blood tests not identify a nutritional deficiency but the reliability of the blood tests performed at the time has been called into question… If osteopenia from a medical cause was present in [AD] prior to his injuries, any assumptions as to the degree of force required to cause such skull and vertebral fractures would also therefore be unreliable.” (Emphasis added)

Interestingly, Dr. Van Ee refers to the vertebral fractures as “highly unusual traumatic injuries for healthy children”, and are “relatively uncommon”; he adds “as a biomechanical engineer all I can say is the vertebral abnormality identified for [AD] is very unique (sic.) And I do not have additional insight if it is the result of trauma, a physiologic bone condition, or a combination thereof.”

The new evidence poses a wide range of opinions on the timing of the critical injury:

If the critical injury occurred 10 days to 2 weeks (or more) before 23 October 2012, any ‘lucid’ interval would appear to be of a wholly extraordinary duration. Even if the incident which caused the significant damage is the ‘4.30 incident’ explanation has to be offered for the fact that AD ate his tea at least initially enthusiastically, been more “lively” lying on the bed, and was reported to have kicked and splashed in the bath. Although the potential for a 5-hour ‘lucid’ interval was considered, addressed, and rejected at the fact-finding hearing, the proposition that AD may have experienced such a lucid interval gains some momentum in the reports now before me.

Dr. Hyman interprets the evidence as indicating that AD was not “completely normal following the impact” at 4.30pm on 23 October; he points specifically to descriptions in the documents of AD’s behaviours which do not entirely square with my undisturbed factual findings (i.e. his “enthusiastic” eating of tea, “lively” thereafter). He added that:

“… latent intervals do occur in head trauma; accordingly, the family’s history should not be discounted.”

He goes on:

“A latent interval may occur before clinical signs and symptoms of extradural haemorrhages appear. After head trauma, the victim may recover and then relax into a deepening stupor or coma when intracranial pressure rises secondary to progression of subdural bleeding and or cerebral oedema. A lucid interval may persist for longer than the average four hours, which is commonly seen with epidural haemorrhage. In fact, there is no known upper limit to the duration of a lucid interval, as the acute subdural haemorrhage merges into a chronic condition that may recur after weeks or even months.”

Dr. Ramsay contemplates that AD would have suffered a “short-lived period of unconsciousness immediately after the event” and then “as the complications of the static injuries become apparent, the return of unconsciousness”. On the father’s evidence to me, there was no short-lived period of unconsciousness. Dr. Ramsay contemplates that it is “possible” that AD had a lucid interval.

As Mr. Tughan observed, this is the “high point” of the parents’ case on timing and symptoms. On its own, this new evidence is not particularly impressive.

This is an anxious case for the parents, as it is for the Court. The conclusions which I reached at the earlier fact-finding hearing in 2013 were the product of a wide review of the ‘wide canvas’ of evidence then available (Re U; Re B at [25]/[26]); the picture ultimately assembled at that time was sufficiently well-defined to allow me to make a confident finding of causation and identify the perpetrator of the injuries. The new evidence laid before the court only essentially affects one facet of that canvas (the expert medical evidence), but if it is accepted, it may (potentially at least) alter the final picture.

As will be apparent, I have found it necessary to examine the new evidence with some care, as I am conscious that I should not allow this case to proceed beyond ‘stage 1’ unless there are indeed ‘solid grounds’ for doing so. Even to embark on a limited ‘stage 2’ process without a proper basis, would be unfair to the parents (improperly raising their hopes), to the children (adding to uncertainty), and to the considerable number of experts involved (who would inevitably need to be re-engaged in the event of a review of some kind); it would of course be unduly burdensome to the Court system, unfair its other users, and wasteful of its limited resources.

On the material presented to the court at this hearing, I am amply satisfied that the mother is able to show more than “mere speculation and hope” of a potentially different result of the fact-finding determination on the evidence provided, but that is not enough. My more challenging task has been to establish whether there is some “real reason to believe that the earlier findings require revisiting”.

As indicated above, I have approached this application by applying the test most recently discussed by Munby P in Re ZZ; in this particular case, it gives rise to the following considerations:

While conscious not to say more than is appropriate to explain my reasoning at this stage given that there is to be more detailed review, I wish to record some reservations about the strength of some of the new evidence and its impact on the findings overall.

First, the evidence from a biomechanical engineer in a case such as this is likely to be, or certainly may be, of limited value. Dr. Van Ee’s expertise in the field of impact and orthopaedic biomechanics is well-known; however, his potential contribution to a factual enquiry in the family court in which non-accidental injury is alleged is more doubtful. Dr. Van Ee’s proposed instruction in a case involving alleged non-accidental injury was discussed in Re TG (Care Proceedings: Case Management: Expert Evidence) [2013] EWCA Civ 5, [2013] 1 FLR 1250 in which Sir James Munby P acknowledged:

“… that a biomechanical engineer will, in principle, be able to obtain values, whether by theoretical calculations and/or by experimental measurements, and in relation to a variety of postulated factual scenarios” [including the]… ‘tipping forces' and the ‘impact forces'.” [65]

But Munby P later went on to consider:

“… the more general question of whether, in other cases, biomechanical evidence might in future satisfy the ‘necessary' test. I would not wish to rule out the possibility, though I suspect that in the present state of the relevant science such cases will be at best infrequent in the family courts. As of today, it remains the fact that there is no case of which we are aware where such evidence has been found to be of any significant assistance. But I emphasise the qualifying words I have just used. We can only operate on the best and most up-to-date science available to us today. But we must always bear in mind that tomorrow may bring about a transformation of scientific knowledge so that, to use Dame Elizabeth Butler-Sloss P's words, new scientific research will throw light into corners that are at present dark. Whether and if so when this will come about in relation to this particular scientific discipline we cannot say” [68]. (Emphasis by underlining added)

I further note that he gave evidence in Islington London Borough Council v Al Alas, Wray and Al Alas-Wray (Through Her Children's Guardian) [2012] EWHC 865 (Fam), though this was said to be of limited value in that case: “His evidence both at the CCC and in this hearing made clear there is little data to be derived from experiment and the enormous difficulties in drawing conclusions because of the complexity of a baby's brain” (see [186]).

Secondly, I have some reservations about the content of Dr. Hyman’s two lengthy reports (>200 pages). Mr. Storey asked me not to be distracted by the unconventional report-writing style of Dr. Hyman given (what he asserts to be) the significance of the content. Mr. Tughan countered this invitation by submitting that the problems with Dr. Hyman’s report were as much an issue of substance as of style; Mr. Tughan made what appears to me to be the legitimate point that in expressing his views, Dr. Hyman may well have trespassed across a number of expert disciplines outside his own; there is reason to observe indeed that his report encroaches fairly substantially into judicial territory. Dr. Hyman’s (repeated) observation is that there:

“… are medical explanations for all of [AD]’s findings. None of his findings, alone or in combination, are pathognomonic or highly specific for child abuse”.

Pausing there, I understand by ‘pathognomonic’ in that context that he means “specifically characteristic or indicative of” abuse; if I am right in interpreting his language in this way, his observation on its own is not of great assistance. In other sections of the report, he equally unhelpfully encourages the reader to discount abuse as a likely cause of the injuries, given that the medical signs or presentation are not shown to be “diagnostic” or “highly specific” of the same. Unhelpfully, he does not state his opinion by reference to the likelihood of the validity of explanations for the relevant injuries, nor does he give good reasons for why he includes or rejects the explanations as reasonable (as opposed to fanciful or merely theoretical) possible causes (see Charles J again in A Local Authority v K, D, L at [89(ii)]). By way of example of some of his more frank assertions, his report includes (and repeats) the following:

“[I]t is my medical opinion that [AD] was not a victim of child abuse. The parents stated that they did not purposefully hurt [AD]. The parents support each other’s statements, as do their extended family… The most important consideration in why [AD] injuries were not abusive in nature is the fact that the parents – the only witnesses to some of his events – stated that they never purposefully hurt [AD]…. Discounting the parents’ history is tantamount to accusing them of lying. Since none of [AD]’s medical findings (alone or in combination) are pathognomonic of abuse, how can any of the evaluating physicians be certain that the family is lying or withholding a narrative of some traumatic event?” (Bold in the original)

Thirdly, Dr. Teas’ opinion that the skull fracture was at least 10 days to 2 weeks old “possibly weeks older” (with the minor injury “likely older than 24 hours”) is significantly outside the range of timings expressed by all other experts in this case (both historically and recently), and must accordingly be treated with very considerable caution. Had this been the only evidence before the court on this application I would have been disinclined to find that it represented a sufficiently ‘solid’ basis for a review. However, taken with the other evidence, it ought properly to be weighed in the review which I propose to direct.

Fourthly, I am alive to the finding of Eleanor King J (as she then was) in A Local Authority v S [2009] EWHC 2115 ([285]) where, in a case concerning non-accidental injury to a child, she referred to Dr. Cohen as having “fallen into that category of expert identified by Butler-Sloss P. in Re LU & LB, namely the expert who has developed a scientific prejudice” (see [71](iii) above).

Fifthly, although there appears to be greater support among the experts who have recently submitted evidence than those previously engaged (though precisely how much more is a moot point) for:

More generally, in my view the value of the newly filed material has been diluted by the fact that most of the reports have been written without sight of some (at least) of the earlier filed medical reports, and/or my judgment (see [71](vi)(a) above); only Professor Nussey would be likely to have seen and had the chance to take account of my earlier findings (assuming of course that he had been sent the findings &/or judgment, as he should have been pursuant to r.25.19 FPR 2010). The inconsistencies and contradictions between some of the reports further reduce their evidential value (see [71](iv) above). The contributions are inherently the weaker for that. Mr. Storey wisely did not pursue his case that ‘question marks’ hang over Dr. Fairhurst (see [43] (v) above). My own enquiry of the GMC reveals no record of any complaint against her (which I inferred from the submission), and Mr. Storey did not elaborate on what (if any) ‘question mark’ is being referred to. I am not in a position to form a view as to the relevance (if any) of this submission; indeed in the absence of any supporting evidence, I consider that the submission should never have been made. Nor, rightly, did Mr. Storey press hard the fact of the co-operation of the parents following the fact-finding hearing; to the parents’ credit, they did co-operate with the social worker to achieve the rehabilitation of their children and (so far as I know) thereafter, but this does not amount to a basis for challenging the earlier finding.

I am conscious that the expert evidence on which I relied was provided nearly three years ago; nothing I have read causes me to believe that scientific advances or greater understanding of bone structures or subdural injury requires a review of the earlier conclusions; however, I remain always alive to the possibility that more contemporary opinion may have the effect of throwing light into certain less well-defined quarters of any case (Re U; Re B at [23]).

However, in spite of those reservations, as I indicated in paragraph [1] above I have reached the view, on balance, that there are sufficiently ‘solid’ reasons to permit, as the next step, a limited reconsideration or review of the earlier findings. I am not persuaded at this stage that the new material is likely (i.e. more likely than not) to alter the original findings; I do not need to be persuaded of this, any more than I need to be satisfied that the mother has a real prospect of success, or that there is some other compelling reason why the case should be heard. It is sufficient for her to demonstrate that there is at least “doubt” around them (per Re B Hale J above), and I am sufficiently persuaded that there is.

In so concluding, I have been particularly influenced by the following four factors.

First, in October 2012, the treating clinicians at Great Ormond Street Hospital were plainly of the view that it was of significance to their investigations into the cause of AD’s catastrophic injuries that the segment of AD’s skull, removed during surgery on 24 October, should be analysed by a histopathologist of national renown. Regrettably, as we now know, it was not so tested at the time. The results of pathological analysis of the skull performed much more recently (2015) reveal clinical findings of potential interest and significance to our understanding of AD’s vulnerability to bony injury. Specifically, while the skull thickness and its bony characteristics were not known at the time of my original findings, the evidence now available reveals features which may indicate material weakness. While there is a difference of opinion (Cohen / Freemont) as to (a) the findings, and (b) their significance, the evidence could impact directly on some of the earlier evidence, specifically that of Dr. Fairhurst and Dr. Cartlidge.

Secondly, and linked with the point above, Professor Stephen Nussey, on whose evidence I placed considerable reliance at the fact-finding hearing, has now had the chance to express further opinion on the issue of bony fragility in light of the results of the skull sample testing (see [36] above). I have set out his earlier opinions above (including notably his comment that vitamin D deficiency “was not of such a magnitude as to have played a significant role in bone fragility predisposing AD to any of the fractures (including the vertebral fractures) [60] of my original judgment), but his earlier opinion was moderated by a degree of frustration at the lack of adequate information, and the “limited reliable information” (see his Third Addendum Report: 11 June 2013: my emphasis). It is fair to observe that there is now more information, and I cannot confidently say that it would not make a difference to his view. Indeed, from the material I have seen, I detect a possible shift in his assessment of the case. Guarding myself against the possibility that the shift may be more perceived than real, and conscious that any such shift may makes no material difference to his ultimate opinion, these are issues which ought legitimately to be revisited.

Thirdly, I am satisfied that aspects of the newly obtained medical evidence (some of which is summarised in the paragraph above) cast a sufficiently fresh perspective on the evidence previously adduced as to warrant review. Dr. Cohen’s findings of woven bones materially suggests vitamin D deficiency, and/or osteopenia in AD (a finding which Dr. Watt considers is “unusual” in a child of this age); her discovery that the skull was particularly thin at the fracture site, while not uncontroversial, may be material in understanding causation of the fracture. There is greater scope for the argument that a short fall (such as described in the ‘4.30p.m. incident’) may have been sufficient to cause the injury (see [54-58] above). I would be assisted to know the views of Mr. Richards and others on Dr. Cohen’s opinion that it is “anatomically plausible” that the fractured bones may have torn the dura in order to cause the subdural haemorrhage (see [49] above); this scenario was not previously considered. Dr. Hyman’s view (see [59] above) that the vertebral fractures show “two different patterns on imaging” (indications of fracture at two different times) is inconsistent with my earlier finding of an isolated incident, and is worthy of reconsideration.

Fourth, and finally, it follows that if some or all of the newly obtained expert opinion is accepted, specifically concerning (a) the number of incidents, (b) the timing of injury/ies (and the greater likelihood that we are considering the ‘4.30p.m. incident’, and (c) the presentation (and inherent fragility) of the skull and vertebrae, it may have any one of a number of implications for AD and his parents:

Having satisfied myself that the case satisfies the ‘stage 1’ threshold, I have considered carefully the ambit of ‘stage 2’. I have allowed the parties the opportunity to address me on this aspect, and if necessary I shall list the case for directions for that purpose. But my provisional views are these.

Stage 2 must be conducted expeditiously, fairly, and proportionately in order to comply with the overriding objective of rule 1 FPR 2010. I believe that the “forensic context” of this particular case (see [12](ii) above), requires an urgent experts’ meeting (to include as many of the experts from both rounds of litigation: 2012/2013 and 2015/2016) as an important next step. I am not prepared to be drawn on the extent of the shape or extent of any enquiry following such a meeting; I will be guided by the outcome of the meeting and a consideration of the combined / informed views of the experts. I consider that for the meeting, the experts should immediately have available to them:

I propose that a ‘nominated professional’ (per PD25E FPR 2010) responsible for convening and arranging the meeting shall be selected by agreement between the parties; in default of agreement, I shall invite the children’s solicitor to undertake the task. The arrangements for the meeting shall faithfully follow the discipline of rule 25.16 FPR 2010 and PD25E FPR 2010 (adapted to reflect (i) the fact that the expert reports have already been filed, and (ii) a more generous allowance in days for the circulation and approval of agenda and responses). The experts should be invited to consider a focused agenda which shall be drawn by the nominated professional, in consultation with the parties and to be approved by me, which should focus on:

Only in light of the experts’ opinion will it be possible to establish the extent of any further hearing, and specifically, whether (as Mr. Storey contended) there will be a need for the parents to furnish the court with further evidence themselves.

That is my judgment.