Neutral Citation Number: [2011] EWHC 1804 (Fam)
Case No: 
IN THE HIGH COURT OF JUSTICE
FAMILY DIVISION

Date: 13/07/20110.

Before :

MR JUSTICE MOSTYN
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Between :

	A County Council	Applicant	
	
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	Mother	First  Respondent	
	
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	Father	Second Respondent	
	
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	The Children
(By their Children’s Guardian)	Third & Fourth Respondents	
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Mr S
(instructed by the Applicant)

Ms B QC & Mr A 
(instructed by Solicitors) for the First Respondent

Miss S QC & Miss M
(instructed by Solicitors) for the Second Respondent

Miss D QC & Miss R
(instructed by Solicitors) for the Third & Fourth Respondents

Hearing dates: 17 May 2011 – 28 June 2011
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Approved Judgment
I direct that pursuant to CPR PD 39A para 6.1 no official shorthand note shall be taken of this Judgment and that copies of this version as handed down may be treated as authentic.

.............................
Original Signed by
MR JUSTICE MOSTYN

This is the approved anonymisation version of the judgment. The anonymisation has been agreed between all the parties and approved by the court.  Significant parts of the evidence as recorded in the original judgment have been redacted.

The judge gives leave for it to be reported in this form as A County Council v M and F.

However, it is a contempt of court for any person to publish anything deriving from this judgment which may lead directly or indirectly to the identification of any person referred to anonymously.

Mr Justice Mostyn: 

1.	One bright morning M awoke at her home. By her were her husband, F and their two year old daughter D who had crept into their bed at about 4 a.m., as she sometimes did. After a few moments shaking off sleepiness M became concerned. The whole family had overslept, which was unusual, notwithstanding that they had had a late night after visiting her parents. More concerning was the silence from their seven month old son, S who slept in an adjacent room. He would invariably awake at around 5 a.m. and would need attention. D stirred and signalled that she had a wet nappy. M went to D’s room to fetch one. As she entered she saw S lying prone in his cot, prostrate with arms outstretched. She turned him over and knew at once that he was dead. She cried out and rushed to her bedroom, passing F on the landing, to call 999 in great distress. F attempted resuscitation as instructed by the emergency operator. The paramedics arrived very quickly – by 9 a.m. S was loaded into the ambulance where one of the crew inserted a Guedel tube into his mouth, administered oxygen, and worked on him. The ambulance arrived at Hospital at 9.15 a.m, where a team of seven doctors and nurses were waiting. S was worked on very forcefully; the work included the insertion (after a number of fruitless attempts) of intravenous lines into vein and bone. The effort was unsuccessful and at 9.40 a.m. the parents were advised that further efforts would be futile. They agreed that it should all stop and D was pronounced dead at 9.42 a.m. 
2.	Such is the account of M and F of that harrowing morning.
3.	At the autopsy the following afternoon no fewer than 23 separate injuries, some extremely serious, were observed on S’s body. It is agreed by all of the experts that none of the injuries either individually, or, taken collectively, caused S’s death, which is medically completely unexplained. An inquest held on returned an open verdict as to the cause of his death.
4.	This is a fact finding hearing as to (a) the cause of those injuries (and other earlier injuries observed to both S), and (b) the cause of death, ordered by the court within proceedings for a care order in respect of S2 (the child of M and F who was born after S’s death) under Part IV of the Children Act 1989 mounted by the local authority (“the LA”), (in relation to S2), and latterly (in relation to D).
5.	The LA alleges that M and F had, throughout S’s short life, periodically inflicted abusive violence on him, and neglected him. It further alleges that about 4 hours before S died at about 7 a.m., one or both of them meted out extreme violence to S of a nature that can only be described as savage, resulting in gross bruising to his hands, feet, arms, face and ears, and to a ruptured upper lip fraenulum that can only have been caused by a forceful punch or slap to his face. The injuries to the hands include almost uniquely rare bruising to both of his palms which could only have been caused by holding his hands open and by “repeated application of significant blunt force trauma”, likely by beating them with a weapon. The evidence relied on by the LA is primarily scientific evidence, which is said to be almost irrefutable, as well as additional evidence from photographs and from others as to observed earlier injuries. 
6.	In addition, the LA invites me to find that by virtue of the proximity of the time of causation of the injuries to the time of death, M and/or F later murdered S, probably by smothering him, which would likely leave no ascertainable evidential trace. 
7.	M and F strenuously deny that they abusively inflicted any injuries on S and they utterly deny that they murdered him. They are aghast that such allegations should be levelled against them. They assert that S was a much loved child, and was at all times adored and cherished by them. In respect of those injuries which occurred earlier than those arising around the time of his death they say that they were either the result of normal childhood bumps and scrapes; and, in respect of those arising at the time of death, as a result of (a) a natural disorder, and/or (b) post-mortem degeneration, and/or (c) of resuscitation attempts. These explanations are “vanishingly unlikely” says the LA.
8.	This fact-finding hearing, which all counsel agree has been exceptionally complex and challenging, has extended to 20 days in court. I have heard the oral evidence of 50 witnesses of whom 10 were experts (as opposed to treating clinicians) drawn from a range of disciplines. The dense written material occupies 13 lever arch files. The written final submissions from Counsel ran to 226 pages. All of this evidence and other writings I shall examine with care in this judgment (although for obvious reasons I will not summarise every single piece of evidence before me). Given the gravity of the allegations this judgment will necessarily be lengthy. By its nature the decision I have to make is as serious as any as any judge, in any field, is tasked to make. I adopt the variedly attributed apothegm used by Dr L in his addendum report “I am sorry for the length of my letter, but I had not the time to write a short one”. 
9.	I heard oral evidence from the following:
Jointly Instructed Experts 
Professor H Paediatric Haematology Consultant (by video link).
Professor S, Paediatrician (orally, and later on by telephone).
Dr L, Home Office Pathologist.
Dr K, Consultant Clinical and Forensic Psychologist.
Dr H, Consultant Histopathologist (orally, and later by telephone).
Dr G, Consultant Microbiologist (by video link).
Experts involved in the autopsy or the subsequent police investigation
Dr J, Home Office Pathologist
Dr W, Consultant Perinatal Pathologist
Dr C, Home Office Pathologist 
FS, Forensic Scientist
Medical professionals involved at or following S’s death 
AP1
AP2
Dr I, Consultant in Paediatric Intensive Care 
Dr R, Registrar 
Dr T, 
Dr K
 Dr P, Consultant Paediatrician
Sr T , paediatric sister 
S’s family 
M
F
PGM, paternal grandmother
MGF, maternal grandfather
MGM, maternal grandmother
F’s brother (by video link)
F’s sister (by video link)
F’s brother-in-law (by video link)
Primary medical carers of S
Dr D, GP
Dr F, GP
Dr M, GP
A, Midwife
B, Community nursery nurse
S’s nursery carers 
NC1 co-proprietor Nursery
NC2,  Senior Nursery Nurse
NC3, Senior Nursery Nurse 
NC4, Nursery Assistant 
NC5, Activity leader Nursery
Friends and neighbours 
F1 (friend)
F2 (friend)
F3 (M’s mentor at work)
F4 (friend)
F5 (friend)
F6 (friend) 
F7 (friend)
N1 (neighbour) 

N2 (neighbour)
N3 (neighbour)
N4 (neighbour)
N5 (neighbour)
N6 (neighbour)
N7 (neighbour)
10.	During the hearing a boxful of exhibits was collected which I list as follows:
Exhibit 1: CD containing the recording of the 999 call 
Exhibit 2: Two examples of Guedel tubes or airways, one type of which would have been used on S
Exhibit 3: A leaflet entitled “Child Death Review Process. Information for families and carers”.
Exhibit 4: Photographs of S.
Exhibit 5: Photographs of bib, grow-bag, and sheet produced by VT Forensic Scientist.
Exhibit 6: Three photographs of D taken at Centre Parcs
Exhibit 7: Photograph of M, D and S 
Exhibit 8: Google Map print showing who lives where.
Exhibit 9: Internet print of an example of Idiopathic Thrombocytopenic Purpura.
Exhibit 10: Original personal notes of neighbour.
Exhibit 11: Photograph taken during the proceedings of Sr T’s hand showing how she would have held the hand of S during resuscitation.
Exhibit 12: Three photographs (1) of F, (2) of D, and (3) of F7 and S 
Exhibit 13: Three photographs of the family taken at farm 
Exhibit 14: DVD of children in bike buggy 
Exhibit 15: Packet containing (a) an Intra-osseous infusion needle, (b) a Catheter Radiopaque and (c) an IV catheter. 
Exhibit 16: Album of family photographs produced by M.
Exhibit 17: packet of photographs taken by N6 (neighbour).
Exhibit 18: Service sheet for S’s funeral 
Structure of this judgment
11.	The structure of my judgment is as follows:
i)	The law
ii)	The scientific evidence: general
iii)	The narrative up to and immediately following S’s death 
iv)	Injuries sustained by D and S: the LA’s case
v)	Injuries sustained by S: the LA’s case
vi)	The subsequent events
vii)	The lay evidence
viii)	The expert evidence
ix)	Summary of the arguments of Counsel
x)	Conclusions
The law 
The burden and standard of proof
12.	The local authority must prove its allegations on the balance of probabilities. In Re B (Minors) [2008] 3 WLR 1, HL, Lord Hoffmann stated at para 2: 
“If a legal rule requires a fact to be proved (a "fact in issue"), a judge or jury must decide whether or not it happened. There is no room for a finding that it might have happened. The law operates a binary system in which the only values are 0 and 1. The fact either happened or it did not. If the tribunal is left in doubt, the doubt is resolved by a rule that one party or the other carries the burden of proof. If the party who bears the burden of proof fails to discharge it, a value of 0 is returned and the fact is treated as not having happened. If he does discharge it, a value of 1 is returned and the fact is treated as having happened.”
13.	Baroness Hale of Richmond stated at para 70:
“I would go further and announce loud and clear that the standard of proof in finding the facts necessary to establish the threshold under section 31(2) or the welfare considerations in section 1 of the 1989 Act is the simple balance of probabilities, neither more nor less. Neither the seriousness of the allegation nor the seriousness of the consequences should make any difference to the standard of proof to be applied in determining the facts. The inherent probabilities are simply something to be taken into account, where relevant, in deciding where the truth lies.”
14.	Earlier, at para 62, she had explained, definitively, the true meaning of a famous passage in the speech of Lord Nicholls in Re H and R (Minors) (Sexual Abuse: Standard of Proof) [1996] 1 All ER 1, HL,  sub nom Re H (Children):
“All of their Lordships in Re H were clear that there was one standard of proof, the balance of probabilities. But Lord Nicholls went on to say this at p.586:
“The balance of probability standard means that a court is satisfied an event occurred if the court considers that, on the evidence, the occurrence of the event is more likely than not. When assessing the probabilities the court will have in mind as a factor, to whatever extent is appropriate in the particular case, that the more serious the allegation the less likely it is that the event occurred and, hence, the stronger should be the evidence before the court concludes that the allegation is established on the balance of probability. Fraud is less likely than negligence. Deliberate physical injury is usually less likely than accidental physical injury. A step-father is usually less likely to have repeatedly raped and had non-consensual oral sex with his underage stepdaughter than on some occasion to have lost his temper and slapped her. Built into the preponderance of probability standard is a generous degree of flexibility in respect of the seriousness of the allegation.
Although the result is much the same, this does not mean that where a serious allegation is in issue the standard of proof is higher. It means only that the inherent probability or improbability of an event is itself a matter to be taken into account when weighing the probabilities and deciding whether, on balance, the event occurred. The more improbable the event, the stronger must be the evidence that it did occur…Ungeoed-Thomas J expressed this neatly in In re Dellow’s Will Trusts [1964] 1 WLR 451, 455: ‘The more serious the allegation the more cogent is the evidence required to overcome the unlikelihood of what is alleged and thus to prove it.’”
If he had stopped there, perhaps there would have been no difficulty, provided that lawyers and courts paid attention to the whole passage, including the words which I have italicised, rather than extracting a single phrase.”
15.	In Re S-B [2010] 1 All ER 705, SC, Lady Hale insisted that Re B did not represent a  departure from earlier authorities in the House of Lords, stating at para 13:
“ None of the parties in this case has invited the Supreme Court to depart from those observations, nor have they supported the comment that Re B “was a ‘sweeping departure’ from other authorities in the House of Lords in relation to child abuse, most obviously the case of Re H. All are agreed that Re B reaffirmed the principles adopted in Re H while rejecting the nostrum “the more serious the allegation, the more cogent the evidence needed to prove it” which had become a commonplace but was a misinterpretation of what Lord Nicholls had in fact said.”
16.	Thus the law sets a simple probability standard of 51/49, but the more serious or improbable the allegation the greater the need, generally speaking, for evidential “cogency”. In AA v NA and Others [2010] 2 FLR 1173, FD, I attempted to summarise these principles at para 24:
“Thus, it is clear that in all civil proceedings P cannot be set higher than a scintilla above 0.5. The various judicial statements that a more serious charge requires more clear evidence is not an elevation of P > 0.5. The requirement of evidential clarity is quite distinct from an elevation of the probability standard. Were it otherwise, and, say, an allegation of rape or murder of a child made in civil proceedings required P to be set at > 0.6 then one could end up in the position where a court considered that P in such a case was, say 0.51 but still had to find that it did not happen; when, as a matter of probability, is was more likely that not that it did. This would be absurd and perverse. P must always be set at > 0.5 in civil proceedings, but subject to the proviso that the more serious the allegation so the evidence must be clearer.”
17.	In para 2 of Re B Lord Hoffmann explained that sometimes the decision will be made by reference to the failure to discharge the burden of proof. In para 32 Baroness Hale made  the same point thus:
“In our legal system, if a judge finds it more likely than not that something did take place, then it is treated as having taken place. If he finds it more likely than not that it did not take place, then it is treated as not having taken place. He is not allowed to sit on the fence. He has to find for one side or the other. Sometimes the burden of proof will come to his rescue: the party with the burden of showing that something took place will not have satisfied him that it did. But generally speaking a judge is able to make up his mind where the truth lies without needing to rely upon the burden of proof.”
18.	A vivid example of the burden of proof coming to the rescue is the famous shipping case of The Popi M (Rhesa Shipping Co. S.A. v Edmunds, Rhesa Shipping Co. S.A. v Fenton Insurance Co. Ltd)  [1985] 1 WLR 948, HL. On 5 August 1978 the plaintiffs’ motor vessel Popi M sank in calm weather in the Mediterranean Sea off the coast of Algeria in deep water when laden with a cargo of bagged sugar. The plaintiffs, as assured, sought to recover, under two substantially identical time policies of marine insurance, against the defendants, hull underwriters, in respect of the loss of the vessel. The plaintiffs were entitled to recover under the policies if they could prove that the loss was caused by “perils of the seas.” The plaintiffs originally sought to explain the loss of the vessel in various ways prior to the trial but those explanations were all subsequently abandoned, and at the trial the plaintiffs finally advanced as an explanation for the loss a collision with an unidentified, moving, submerged submarine, which was never detected, never seen and which never surfaced. The defendants contested that explanation. Bingham J. made no finding concerning the seaworthiness of the vessel and although he regarded the plaintiffs' case as being inherently improbable he held nevertheless that the plaintiffs' submarine hypothesis had to be accepted, as, on the balance of probabilities, the explanation for the loss of the vessel. On appeal by the defendants, the Court of Appeal dismissed the appeal. The House of Lords allowed the appeal. Lord Brandon of Oakbrook stated:
“My Lords, the late Sir Arthur Conan Doyle in his book The Sign of Four, describes his hero, Mr. Sherlock Holmes, as saying to the latter’s friend, Dr. Watson: “How often have I said to You that, when You have eliminated the impossible, whatever remains, however improbable, must be the truth?” It is, no doubt, on the basis of this well-known but unjudicial dictum that Bingham J. decided to accept the shipowners' submarine theory, even though he regarded it, for seven cogent reasons, as extremely improbable.
In my view there are three reasons why it is inappropriate to apply the dictum of Mr. Sherlock Holmes, to which I have just referred, to the process of fact-finding which a judge of first instance has to perform at the conclusion of a case of the kind here concerned.
The first reason is one which I have already sought to emphasise as being of great importance, namely, that the judge is not bound always to make a finding one way or the other with regard to the facts averred by the parties. He has open to him the third alternative of saying that the party on whom the burden of proof lies in relation to any averment made by him has failed to discharge that burden. No judge likes to decide cases on burden of proof if he can legitimately avoid having to do so. There are cases, however, in which, owing to the unsatisfactory state of the evidence or otherwise, deciding on the burden of proof is the only just course for him to take.
The second reason is that the dictum can only apply when all relevant facts are known, so that all possible explanations, except a single extremely improbable one, can properly be eliminated. That state of affairs does not exist in the present case: to take but one example, the ship sank in such deep water that a diver's examination of the nature of the aperture, which might well have thrown light on its cause, could not be carried out.
The third reason is that the legal concept of proof of a case on a balance of probabilities must be applied with common sense. It requires a judge of first instance, before he finds that a particular event occurred, to be satisfied on the evidence that it is more likely to have occurred than not. If such a judge concludes, on a whole series of cogent grounds, that the occurrence of an event is extremely improbable, a finding by him that it is nevertheless more likely to have occurred than not, does not accord with common sense. This is especially so when it is open to the judge to say simply that the evidence leaves him in doubt whether the event occurred or not, and that the party on whom the burden of proving that the event occurred lies has therefore failed to discharge such burden.”
19.	The Popi M  was recently considered by the Court of Appeal in Alan Peter Ide v. ATB Sales Ltd; Lexus Financial Services T/A Toyota Financial Services (UK) PLC v. Sandra Russell [2008] EWCA Civ 424, CA, where Thomas LJ held: 
“2. It is necessary to refer to the trial judge’s decision in The Popi M [1983] 2 Lloyd’s Rep 235 as it contained what the trial judge described as a striking and novel feature of the expert evidence – all experts put forward explanations of the cause of the loss which were acknowledged to be highly improbable; each explanation was supported as the most likely explanation only because any other hypothesis was regarded as almost (if not altogether) impossible. . . .
4. . . . The Popi M was a very unusual case and as these two appeals demonstrate, the difficulties identified in that case will not normally arise. In the vast majority of cases where the judge has before him the issue of causation of a particular event, the parties will put before the judge two or more competing explanations as to how the event occurred, which though they may be uncommon, are not improbable. In such cases, it is, as was accepted before us by the appellants, a permissible and logical train of reasoning for a judge, having eliminated all of the causes of the loss but one, to ask himself whether, on the balance of probabilities, that one cause was the cause of the event. What is impermissible is for a judge to conclude in the case of a series of improbable causes that the least improbable or least unlikely is nonetheless the cause of the event; such cases are those where there may be very real uncertainty about the relevant factual background (as where a vessel was at the bottom of the sea) or the evidence might be highly unsatisfactory. In that type of case the process of elimination can result in arriving at the least improbable cause and not the probable cause.”
20.	Thus it will only be in a rare case where the burden of proof is the determinative element in the reasoning of the fact-finder.
21.	In the Popi M Lord Brandon explained that there was no pseudo-burden or obligation on the insurers to come up with alternative explanations as to why the ship sank. He stated:
“…although underwriters sued by shipowners for the total loss of a ship by perils of the sea are not under any obligation to plead in their defence, or to seek to prove at the trial, some alternative cause of loss against which the ship was not insured, they are perfectly entitled to do so if they wish. “ 
The same principle applies in fact-finding proceedings such as these. There is no pseudo-burden subtly shifted to the parents to prove a natural cause for S’ death. In Lancashire County Council v D and E  [2010] 2 FLR 196, FD, Charles J said:

“[36] The exercise of identifying a perpetrator, or pool of perpetrators, forms part of the exercise of considering whether there was an inflicted injury. In my view, it is important to remember this because it removes or reduces an approach which considers the overall question from the standpoint that someone with the opportunity to injure a child has to show that he or she did not do so. Again, in my view, the approach of the local authority and the guardian, at times, came perilously close to this. The correct position is that a medical view as to the most likely cause of injuries is that that cause is clearly established as a real possibility that has to be considered, in all the circumstances of the case, together with the other possibilities, in determining whether a child was the victim of an inflicted injury.
[37] If the assertions of the parents with the opportunity to injure a child that they did not do so are true, a medical conclusion that the most likely cause is inflicted injury would be wrong and, therefore, in determining whether such assertions are true or false the decision-maker has to consider all the possibilities and circumstances of the case. On existing authorities, in these proceedings, the truth or otherwise of such an assertion by parents is determined by an application of the civil standard, and if the court concludes that it is more likely than not that either or both of the parents did not injure R by shaking him, then that is thereafter, as a matter of legal policy, treated as fact.”
22.	In similar vein HHJ Bellamy sitting as a Judge of the High Court stated in Re C and D (Photographs of Injuries) [2011] 1 FLR 990, FD, at para 203:
“There is, in my judgment, an obvious disadvantage to parents in an approach which requires that they provide an explanation for even the smallest bruise failing which there will be an automatic presumption that that bruise must have been an inflicted injury. Such an approach subtly changes the burden of proof and puts the onus on the parents to provide a credible explanation. As a matter of law, it is not for the parents to disprove the suggestion that the general bruising is non-accidental but for the local authority to prove that it is.”
The treatment of expert evidence
23.	There is important appellate guidance on the treatment of expert evidence in a case such as this. In Re B (Care: Expert Witnesses) [1996] 1 FLR 667, CA, Ward LJ stated:
“The expert advises but the Judge decides.  The Judge decides on the evidence.  If there is nothing before the court, no facts or no circumstances shown to the court which throw doubt on the expert evidence, then, if that is all with which the court is left, the court must accept it.  There is, however, no rule that the Judge suspends judicial belief simply because the evidence is given by an expert.”
Butler-Sloss LJ (as she then was) stated:
“An expert is not in any special position and there is no presumption of belief in a doctor however distinguished he or she may be.  It is, however, necessary for the Judge to give reasons for disagreeing with experts’ conclusions or recommendations.  That, this Judge did.  A Judge cannot substitute his own views for the views of the experts without some evidence to support what he concludes.”
24.	In Re U (Serious Injury: Standard of Proof): Re B [2004] 2 FLR 263, CA, Dame Elizabeth Butler-Sloss P stated at para 23:
“[23] …there is a broad measure of agreement as to some of the considerations emphasised by the judgment in R v Cannings that are of direct application in care proceedings. We adopt the following…
(i) The cause of an injury or an episode that cannot be explained scientifically remains equivocal.
(ii) Recurrence is not in itself probative.
(iii) Particular caution is necessary in any case where the medical experts disagree, one opinion declining to exclude a reasonable possibility of natural cause.
(iv) The court must always be on guard against the over-dogmatic expert, the expert whose reputation or amour propre is at stake, or the expert who has developed a scientific prejudice.
(v) The judge in care proceedings must never forget that today's medical certainty may be discarded by the next generation of experts or that scientific research will throw light into corners that are at present dark.”
25.	In an unreported decision of mine in July 2010 I suggested that a guide or tool for the treatment of expert evidence in care cases might be the standard direction given to juries in criminal trials. On appeal (Re D (A Child) [2010] EWCA Civ 1000, CA,) Hughes LJ rejected this as unhelpful and stated at para 24:
“At root the question in this appeal is whether the judge was entitled to prefer this empirical or factual evidence to Dr Gillett's prognosis derived from her psychological profile. The answer to that is yes. I do not think that it was helpful for the judge to embark upon a comparison with the direction which is given in criminal cases to jurors when they are dealing with expert evidence. Those directions no doubt are designed to remind jurors that the ultimate decision is for them, that the expert evidence must be evaluated and that if they disagree for a reason with the expert's conclusion they must do so, but that is to say no more than is the common coin of all litigation and jurors do not give reasons; judges do. In the context of a child care case, the judge is the decision maker, the expert is not. Where there is as here undisputed expert opinion evidence, the judge ought not to reject it without sound and articulated reason. This judge said at paragraph 171 that it was for him to weigh the evidence of Dr Gillett and the guardian in the context of all the evidence both oral and written in the case. To the extent that he parted company with the evidence or recommendations of Dr Gillett or the guardian, he recognised that he must give his reasons.” 
26.	While it is open to the judge to reject expert evidence, provided he gives good reasons, he must be very careful before he does so. In Re B (A Child) (Split Hearings: Jurisdiction) [2000] 1 FLR 334, CA, Dame Elizabeth Butler-Sloss P  stated (at 339):
“. . . This is a very experienced judge for whom everyone would have the greatest possible respect. But the judge does have an obligation to give reasons why he should set aside the medical evidence, which was strong, in favour of his view that, because the grandmother and the other witnesses were clearly not lying, the medical evidence could not stand. He did not, for instance, deal at all with the explanation given by Dr Hall as to why, on the evidence of early healing, the injury had to be at least 7 days old.
Mr Ames, in a valiant attempt to support the judge, has suggested that, because dating of injuries is an imprecise science, and that, in effect, is what both the radiologists have said, that the judge was entitled to prefer the impression of Dr Newson. I fear that will not do. In a case such as this where the expert evidence, and here the expert evidence of the radiologist was all one way, the judge is certainly entitled, if he has evidence that he can rely upon to the contrary, not to accept that evidence. In my view he did not have that evidence in this case. He did not, in particular, have evidence that made the uncontroverted medical evidence logically unsupportable. The judge failed to analyse the evidence and give any reasons. The credibility or otherwise of the lay witnesses on the facts of this case, in my view, cannot stand so high as to make the evidence of the two consultant radiologists of no effect.”
Otton LJ stated (at 340H):
“The circumstances when judges of the High Court can reject the evidence of a body of medical opinion are rare. This situation was considered by the House of Lords in Bolitho (Deceased) v City & Hackney Health Authority [1998] AC 232 … per Lord Brown-Wilkinson at 243:  
“In the vast majority of cases the fact that distinguished experts in the field are of a particular opinion will demonstrate the reasonableness of that opinion … But if in a rare case, it can be demonstrated that the professional opinion is not capable of withstanding logical analysis, the judge is entitled to hold that the body of medical opinion is not reasonable or responsible.
I emphasise that in my view it will very seldom be right for a judge to reach the conclusion that views genuinely held by a competent medical expert are unreasonable … It is only where a judge can be satisfied that the body of expert opinion cannot be logically supported at all that such opinion will not provide the benchmark by reference to which the defendant’s conduct falls to be assessed.””
Psychological evidence and assessment of credibility generally
27.	In Re CB and JB (Care Proceedings: Guidelines) [1998] 2 FLR 211, FD, Wall J (as he then was) considered whether psychological evidence had a role to play in the determinations of facts. He stated (at 217G-218D):
“(iv) Evidence which is relevant to the assessment of the parents or other family members if and when the threshold criteria are established should not be permitted unless for some reason it is of direct relevance to the factual issue being tried. It is the essence of a split hearing that assessments of the parties and their capacity to parent their children need to be carried out on the basis of the facts found by the court. Ex hypothesi that can only be done after the court has decided both that the threshold criteria have been satisfied and the factual basis upon which they have been satisfied.
(v) Evidence of propensity or a psychiatric or psychological assessment of one of the parties is unlikely to be of any assistance in resolving a purely factual issue. There will in any event be before the court evidence from the local authority and the parents relating to the history of the case and the backgrounds of each of the parents. A psychologist or psychiatrist instructed to undertake an assessment of a parent for the first stage of a split hearing is unlikely to have a complete knowledge of the facts.
(vi) Furthermore, such a witness may, as here express opinions as to propensity or as to responsibility for a child’s injuries which are both prejudicial and wrong. The assessment of adult credibility as to the responsibility for a child’s injuries (often the critical factual issue) remains the function of the judge. In my judgment, therefore, a psychiatric or psychological assessment of the parties should not be permitted at the first stage of a split trial unless the particular facts of the case demonstrate that such evidence is or is likely to be directly relevant to the factual issue to be tried.
(vii) Expert evidence as to the assessment of risk once the threshold criteria have been established is, of course, another matter. But the essence of such as assessment is that the psychiatrist or psychologist makes his or her assessment on the basis of facts found by the court and parental reaction to them.”
28.	However, in Re M (Residence) [2002] 2 FLR 1059, CA, Thorpe LJ stated the following approach as to expert evidence of a parent’s core personality:
“Of course the assessment of the father's credibility was primarily the judge's task. But the assessment of his core personality and the extent to which damage resulting from his early life experiences was disabling and permanent was primarily for the experts, whose professional training, qualification and clinical expertise equipped them for the task. In my judgment, given that the experts were unanimous on this vital aspect, it was not open to the judge to reject their conclusions, either on the basis of his own impressions of the father or upon the basis of the prejudice to the father's case caused by management decisions of the local authority and prison authority during the interlocutory stages. The assessment of the section 31 threshold could not admit of any redress to the father for that factor, nor could the assessment of considerations relevant to M's welfare.”
29.	The receipt of psychological evidence of a person’s core personality when making an assessment of credibility is the same territory as the judicial assessment of a witness’s demeanour, which has long formed an important part of the fact finding process, even if its numinous status has perhaps been overstated, as Lord Bingham of Cornhill pointed out in his essay The Judge as Juror: The Judicial Interpretation of Factual Issues (The Business of Judging OUP 2000):
“The ability to tell a coherent, plausible and assured story, embellished with snippets of circumstantial detail and laced with occasional shots of life-like forgetfulness, is very likely to impress any tribunal of fact. But it is also the hallmark of the confidence trickster down the ages.”
30.	As to the assessment of credibility generally I remind myself of the dissenting speech of Lord Pearce in Onassis and Calogeropoulos v Vergottis [1968] 2 Lloyd's Rep 403, HL, (referred to by Lord Bingham in his essay):
“‘Credibility’ involves wider problems than mere ‘demeanour’ which is mostly concerned with whether the witness appears to be telling the truth as he now believes it to be.  Credibility covers the following problems.  First, is the witness a truthful or untruthful person?  Secondly, is he, though a truthful person, telling something less than the truth on this issue, or, though an untruthful person, telling the truth on this issue?  Thirdly, though he is a truthful person telling the truth as he sees it, did he register the intentions of the conversation correctly and, if so, has his memory correctly retained them?  Also, has his recollection been subsequently altered by unconscious bias or wishful thinking or by over-much discussion of it with others?  Witnesses, especially those who are emotional, who think that they are morally in the right, tend very easily and unconsciously to conjure up a legal right that did not exist.  It is a truism, often used in accident cases, that with every day that passes the memory becomes fainter and the imagination becomes more active.  For that reason a witness, however honest, rarely persuades a Judge that his present recollection is preferable to that which was taken down in writing immediately after the accident occurred.  Therefore, contemporary documents are always of the utmost importance.  And lastly, although the honest witness believes he heard or saw this or that, it is so improbable that it is on balance more likely that he was mistaken?  On this point it is essential that the balance of probability is put correctly into the scales in weighing the credibility of a witness.  And motive is one aspect of probability.  All these problems compendiously are entailed when a Judge assesses the credibility of a witness; they are all part of one judicial process.  And in the process contemporary documents and admitted or incontrovertible facts and probabilities must play their proper part.”
Or as Lord Justice Browne put it, as recorded in Lord Bingham’s essay, “the human capacity for honestly believing something which bears no relation to what actually happened is unlimited.”
The scientific evidence - general
31.	The key (but not exclusive) scientific evidence is histological. Dr L confirmed to me that for most of the experts most (but not all) of the eggs were in the single basket of histology. Histology is the study of the microscopic anatomy of cells and tissues of plants and animals. It is synonymous with microscopy. It is performed by examining a very thin section of tissue encased in paraffin wax under a powerful microscope. Examination and identification of microscopic structures is frequently aided and enhanced by the use of histological stains. Of these Perls’ stain or positivity is relevant here, and will be examined by me a little later. Histopathology is the microscopic study of diseased tissue, often taken from a corpse.
32.	Among many things histology enables the examination of white blood cells. Most of us know that white blood cells fight infection, but our knowledge in this field usually stops there. White blood cells are technically known as leucocytes, the etymology being λευκό (white) and κύτταρο (cell).  There are several different types of leucocytes. One of these is the neutrophil granulocyte, known as neutrophils. A common synonym is polymorphonuclear leucocyte, or polymorphs (although, strictly speaking, polymorphs embrace all granulocytes, which include the eosinophil granulocyte and the basophil granulocyte). These leucocytes are called polymorphonuclear because their nuclear shape has a number of lobes which give the appearance of multiple nuclei.
33.	Polymorphs circulate in the blood and are the first to travel to, and accumulate at, a site of acute inflammation. They are phagocytic cells, which are cells capable of phagocytosis – i.e. ingesting (and then digesting or at least trying to digest) cellular and particulate debris anywhere in the body.
34.	Another type of phagocytic cell is the macrophage (μακρός (large); φαγευ (eat)). These also accumulate at a site of acute inflammation. Most of the macrophages involved in the inflammatory response are delivered by the blood circulation, and they tend to arrive rather later than the polymorphs.  They are capable of ingesting and digesting all forms of debris accumulating at the inflamed site, such as red cells, red cell fragments, haemoglobin and iron.  It is within these macrophages that the haemosiderin can be found.
35.	When red blood cells are broken down in the body (for whatever reason and in whatever location), the haemoglobin releases the iron component of its complex molecule.  In bruises, this haemoglobin is ‘digested’, largely by macrophages which enter the area as part of the inflammatory process, and the iron is converted into, amongst other compounds, haemosiderin.
36.	In 1867 Max Perls identified the eponymous method for staining ferric iron ions with potassium ferrocyanide and acid producing an insoluble blue compound (the so-called Prussian blue reaction).  A minor variant of his method is still in use, and is usually referred to as Perls’ stain.  Tissue deposits containing ferric ions are invariably haemosiderin, and, so, Perls’ positivity is considered to represent the definitive histological identification of haemosiderin.
37.	A crucial aspect of the histological evidence is the amount of time that it takes polymorphs and macrophages to travel to an injury site to commence reparative work. In his glossary Dr L stated: 
“[Polymorphs] probably start to accumulate within minutes of the onset of the inflammatory stimulus, but their arrival can not be appreciated histologically for several hours. “ 
In his report he stated:

“Injuries of all types initiate an acute inflammatory reaction as a means to try to limit the local spread of the causative agent and to try to repair any damage caused.  In the first instance, this involves delivery to the site of phagocytic cells; the first to arrive are the polymorphs (polymorphonuclear leucocytes), and they reach the affected area via the circulation.
Although the stimuli for the accumulation of polymorphs at the site of damage are produced extremely rapidly, it takes a finite period of time before the polymorphs begin to accumulate in histologically appreciable numbers.
It is said that polymorph accumulation at the site of an injury may be apparent on microscopic examination as early as two hours after the injury was inflicted, but most authorities believe that they are not usually seen until 4-12 hours post trauma.”
38.	As to macrophages (and the consequential production of haemosiderin) he stated in his glossary:
“Most of the macrophages involved in the inflammatory response are delivered by the circulation, and they tend to arrive somewhat later than most of the polymorphs.”
And in his report:

“As part of the inflammatory process considered above, the phagocytic cells which arrive at the site of a bruise also start to break down the red blood cells which have been extravasated, and, as part of that process, they “digest” the haemoglobin pigment from within the red cells and convert it, inter alia, into haemosiderin.  The nature of the iron within the haemosiderin molecule is such that it can be stained, histochemically, by Perl’s stain.
Most authorities agree with Betz and Eisenmenger that approximately three days need to elapse after the infliction of a bruise before any haemosiderin can be demonstrated histologically by a Perl’s stain.”
39.	The other key aspect of Dr L’s evidence is that the migration of these leucocytes, whether polymorphs or macrophages, cannot occur post-mortem. In his oral evidence he stated in answer to questions from me:
Q. 	Can those polymorphs be on the move after death? ‑  A. Not really, not in the context that we see here. You sometimes see them in the stomach in relation to the acid which continues to do a bit of digesting, but in essence not in the context here no. They will cease their activities very shortly after death because they will run out of the essential nutrients that they need to derive from the viable circulation.
Q. 	That is their petrol is it? ‑ A. Yes, absolutely. That is exactly what it is. They need oxygen and they need various nutrients to keep going, which under normal circumstances in fact one of the things that happens at the site of inflammation is that the vessels do tend to dilate a bit, that is all part of the reaction, it is for that very reason you need the various nutrients to get in there and you need the oxygen to get those cells there to keep them alive, yes. 
… 
MR. JUSTICE MOSTYN:   Can I just get this right? If say a vet puts a horse down and immediately after the horse is dead a wound is inflicted on the horse the blood cells would not move in the body of that horse? ‑ A. They certainly wouldn't get, you certainly wouldn't see anything down the microscope. You may get a bit of bruising but that apart you wouldn't because there would not be enough time after death for the cells to start to accumulate before the cells die because they have run out of petrol.
Essentially it is said that on death, and the cessation of circulation, the migration of the leucocytes comes to an abrupt halt.
40.	Thus it is said that if sections or slides are taken from bruises on a corpse and those slides reveal polymorphs in one bruise and haemosiderin in another then the following conclusions may be confidently drawn:
i)	the bruises were caused in life, and were not pseudo or post-mortem bruises;
ii)	the bruise containing the polymorphs will have been caused 4 – 12 hours before death; and
iii)	the bruise containing haemosiderin will have been caused about 3 days before death.
41.	 Dr L described this science as “robust”. In his oral evidence he stated:
Q. 	And you conclude that answer it says, "Robust as you are likely to get."? ‑ A. Yes, I mean I think that is exactly right. The concept of inflammation has been around for two and a half thousand years or so and the microscopic correlates of that have been around a long time since the microscope was introduced and we started to develop microscope sections and staining with dyes and all of these sort of things when the macroscopic changes, which were well‑known, were correlated with microscopic changes and it is a well recognised sequence of events which has been well catalogued and well documented for, well certainly there are good descriptions in the 19th Century but certainly the 20th Century was associated with a proliferation of documentation and completed our understanding.
42.	Dr L accepted that the research which leads him to express the view that the science was “robust” had been largely performed on animals. Under cross-examination by Ms S QC this exchange took place:
Ms. S:   Then one comes to look at the histopathology of bruising. Once again the majority of the data has come from studies in mammals, has it not? ‑ A. Of course.
Q.	Because there is an inherent difficulty, one cannot carry out controlled studies of bruising in human beings? ‑ A. Well you can only do that in human beings who have died where there has been a known interval between death and the trauma, and it has been done in road traffic accidents and things like that. But yes, a lot of the experimental work was done in experimental animals for obvious reasons.
Q.	But you need to create a trauma and then observe what happens, so it is basically based in mammals? ‑ A. Yes, that's correct.
Ms. S:   And I suppose it is fair to say that you would still need to be sure you had a confident history of the type and time of trauma? ‑ A. Yes, although I think that could be arranged and could be organised even if the trauma were to be deliberately inflicted, yes.
Q.	But anyway it has not been done? ‑ A. There is not a lot of it been done, that is true.
Q.	And certainly not done at all with babies? ‑ A. That is also true.
Q.	Or young people or children? ‑ A. Again that is also true. 
43.	In similar vein, Dr J, the Home Office Pathologist who performed the autopsy, stated in reply to Ms B QC:
Q. 	So how good a science is the histology? ‑ A. The histology is a relatively reliable science in that people have done studies, it is not somebody having looked at a situation said oh yes well I have seen it therefore it is, which can be quite a lot of pathology science. The science of histology is actually done by causing an injury, typically to an animal, then causing the death of the animal so many hours later and looking at it. So it is actually reproducible science, as opposed to case report science.
Q. 	Albeit that for obvious reasons one wouldn't want to be doing this even to deceased people it is in animals rather than human beings. So one has to qualify it slightly? ‑ A. To some extent, yes.
Q. 	The reaction times might be somewhat different? ‑ A. Yes.
Q. 	So would you allow that there is possibility for misreading‑‑‑
MR. JUSTICE MOSTYN:   Well presumably there's some research on humans as well, in the sense that there must be instances where a known injury has happened and then someone has died and you are able to do the research on that unfortunate person? ‑ A. Yes, there is some work that is carried out.
Q. 	Someone in a car crash for example, and they knew the car crash was at such and such a time and they died 7 hours later and you can do that research presumably? ‑ A. Yes.
Q. 	The research isn't confined to animals? ‑ A. No, but most of the sitting down and coming up with a research protocol is done on animals because it is a more controlled situation. But yes.
MS. B:   One has individual cases where one might be able to work it out because one knows the timings, but the studies? ‑ A. The big studies are done on animals because you can have multiple animals and you can control things much more carefully.
Q. 	And the reason for animals is you need a large cohort in order to produce a reliable study because of variation between individuals? ‑ A. Yes.
Q. 	To get valid data? ‑ A. Yes.
MR. JUSTICE MOSTYN:   On rats yes? ‑ A. Or mice.
44.	As against this the histopathologist Dr H was able to say, based on her own experience:
THE WITNESS:   Can I just say, one instance where I have experience of very early wounds, I do a lot of cancer work when surgeons remove a tumour they like to sort of potter around for a while and they like to often take extra pieces of tissue from around the edge of the wound and send them to me to ask for an instant check to see if there are any cancer cells there. So I often get tissue taken within half an hour to say one hour of major surgery and I can confirm that they are often very much filled with polymorph neutrophils. So those cells do get there very, very quickly. They are a nuisance to me because they hamper my interpretation of that tissue. 
So here we have clear evidence of the early migration of polymorphs to a human wound, the timing of the infliction of which is exact. This is consistent with a table prepared by Betz in 2003 as part of an article or study of “Histological Parameters In Age Estimation Of Human Skin Wounds” which records the earliest appearance of neutrophils at 15 – 30 minutes (and of macrophages at 2 – 3 hours).
45.	That said, it is a remarkable fact that to the knowledge of the extremely experienced Home Office pathologist Dr L nobody in any court anywhere in any kind of proceedings, whether civil, criminal or coronial, has been found responsible for the infliction of wounds based on this science. He stated to me:
 Q.	In your experience, which is extensive, are you aware of any judicial case, whether it is an inquest, criminal case, civil case, care case where, and I am speaking slightly tautologically but you know what I mean, decisive decisions have been based on the presence of neutrophils or polymorphs in the wound? ‑ A. I can say that I have never been involved in a case where that has been so. I am sure there will have been cases.
Q.	I just wondered if you were aware of one? ‑ A. No I am not, I have not been involved in any case where it has hinged solely and exclusively upon that.
Q.	Or materially? ‑ A. (No reply).
Q.	Decisively is the word I want to use? ‑ A. I think the answer is, it has been discussed on many occasions that I have been involved with but in all honesty I don't think I can think of one where it has been decisive in the context in which I think you are implying by your question.
46.	Within the trial bundle are a number of pieces of medical literature. While they are supportive of Dr L’s position, they are not nearly as categorical in their findings of what appears now to have become in the realm of histology almost canonical. The first was published in 2001 in the Journal of Clinical Pathology by Dr. P Vanezis of the Department of Forensic Medicine and Science, University of Glasgow, entitled “Interpreting bruises at necroscopy”. The second was published in Forensic Science Medical Pathology in 2007 by Dr. Neil Langlois of the Westmead Department of Forensic Medicine, Westmead Hospital, New South Wales, Australia entitled “The science behind the quest to determine the age of bruises – a review of the English language literature”.  When weighing these pieces I bear in mind what Professor S told me about “publication bias”:
Q. 	I was asking about the latter? ‑ A. No I wouldn't conclude that because we are very aware of publication bias, which is a technical phrase I suppose. 
Q. 	Publication? ‑ A. Publication bias. People tend to go into print with the more extreme end and more dramatic end, I am not talking about the media now I am talking about in medicine, in science to get something published in the scientific literature it has to be eye‑catching for the editor and the journal readers. So you have this bias. So it is perfectly possible that people who are involved with fatal cases report them and write them up and then cases where it is still a very serious matter, please do not misunderstand me, but say the child has a few bruises and a torn fraenulum and nothing else that is very unlikely to get written up. Indeed if the child, as I explained in my experience, the child got a torn fraenulum from falling off a slide in a children's park that is definitely not going to be written up. So there is this inherent skewedness I think that one has just got to be aware of. All one can say is of all the cases published in the world they do a trawl of the whole English speaking world literature. 
47.	The first piece recorded this as to the timing of arrival of polymorphs at recent wounds:
“The earliest recorded leucocyte reaction was recorded at 20 – 30 minutes, although more recent observations give times in both haemorrhages and wounds varying between one and 24 hours.”
The piece includes a table which supplies a suggested schema for the histological estimation of the time interval from infliction of injury to death in open skin wounds and abrasions. This suggests that for the period 0 - 4 hours there will be no distinct signs of inflammation and the drawing of a histological distinction between ante and post-mortem wounds will not be possible; for 4 – 12 hours polymorphs will be visible and will predominate over macrophages; and for the period thereafter the macrophages will predominate.   
48.	The author also includes a section concerning the phenomenon of “pseudo bruising”. This is the “extravasation” of blood out of the vessels and into the tissues after death. He writes: 
“…as most pathologists will confirm, the distinction between bruising and pseudo bruising can sometimes be difficult if not impossible, both at necroscopy and even after routine histological and immunohistological examination. … Another area of practical difficulty for the pathologist is the differentiation of bruises from marks caused by resuscitation. Because in most instances resuscitation occurs around the time of death with some degree of maintenance of circulation, or at least intermittent forced movement of blood within vessels, there is every possibility of producing extravasation of blood to the tissues that is indistinguishable from true bruising. “   
49.	The second piece constitutes, as its title states, a comprehensive survey of the worldwide writings in English concerning the science of the age assessment of bruising. It is notable that the author is able to state that “published work on estimating the age of bruises was based on the observation of adults, with only seven subjects being aged under 16 years”, and suggests that studies be performed specifically on children. He also notes that “there is a lack of published histological studies of bruises of a known age”. He remarked that “probably one of the best [histological studies] was conducted on bruises on sheep”, and went on to state that “using Bayesian analysis of histological features it was concluded that bruises could only be aged as 0 - 20 hours or 24 – 72 hours with any accuracy”.  Dr Langois wrote:
“Other work in lambs and calves indicated that neutrophils were numerous at eight hours with blood and fibrin; macrophages and neutrophils were present in approximately equal numbers by 24 hours and macrophages predominated by 24 hours. However, data from animal experiments may not be applicable to humans. Neutrophils are not present in normal skin, thus the finding of any would be regarded as significant. Emigration of neutrophils within minutes has been reported in blunt trauma wounds in humans. “ 
50.	Later in his piece Dr Langois writes that: 
“An established infiltrate of neutrophils would be expected to imply that a bruise occurred during life, as neutrophils are not present in normal skin; however, it has been observed that neutrophils emigration can occur after death in response to cytokines – at least in mice.” 
51.	Dr L explained to me what cytokines were thus:
MR. JUSTICE MOSTYN:   What are cytokines? ‑ A. They are a collective group of substances ‑ and I am starting to get, we are getting into great detail here and I confess I am getting to the periphery of my knowledge. But they are the substances that are released under normal circumstances in the living tissues by whatever it is that initiated the inflammation. So the cytokines are amongst the group of substances which attract the polymorphs into the area.
MS. S:   Yes they are small cells, protein type molecules aren't they? ‑ A. Yes they are.
Q.	They are found in the immune system and they are very important in intracellular communication? ‑ A. Amongst other things yes, that is right.
Q.	And they can increase hugely in the presence of either trauma or infection, can they not? ‑ A. Of course, that is their role in that context. I suspect I don't know, that this is an experimental model in mice whereby cytokines have been introduced into the tissues immediately after death, which is a somewhat artificial circumstance.
MR. JUSTICE MOSTYN:   Well that is very artificial. You have got a dead mouse and you put some cytokines in and then you see if the neutrophils are on the move? ‑ A. Yes. Well they will be in the very early stages because the petrol has not run out, to use if I may the metaphor which you used yesterday, they will be under those circumstances.
MS. S:   Well we don't know if that is the case or not with this experiment, but in any event you do get do you not a cytokine release if you have a staphylococcal infection? ‑ A. Yes.
Q.	So if you have got a staph infection in your body that would have been likely to increase the cytokine production level? ‑ A. Yes.
Q.	And we do not have this paper but it may well be that certainly in mice it has been found that the cytokine level being raised has in fact led to neutrophil production post mortem, not ante mortem? ‑ A. Yes.
52.	Plainly, these opinions and conclusions give rise to a number of pertinent questions. Over-reaching all this is the warning given to me by Dr L concerning the certitude of this branch of science:
…the problem with biological systems is that they are not as predictable as, I don't know, physics where you can measure something and you know that if you repeat the experiment you should be able to measure exactly the same thing and get exactly the same result. The sort of thing I did for A level many years ago. That is predictable because it behaves in the context of various laws of physics. We do not have that here, we have biological systems and so therefore you cannot automatically assume that every one of us in this room will have exactly the same rate of accumulation of polymorphs at the site of inflammation it doesn't work that way, and there are other factors that may influence that. 
 I think the other point that I tried to emphasise yesterday is also relevant and that is that we are dealing with biological systems, we are not dealing with mathematics and physics and I think that is clearly implicit in what [Dr Langois] has said here, absolutely.
53.	I will state my conclusions as to the weight to be given to this scientific evidence as part of my overall conclusions below at paragraphs 226 to 261 of this judgment.
The narrative up to and immediately following S’s death 
54.	F is aged 39 years. He has a brother, and a sister. His father died suddenly. His mother was a witness before me.
55.	F was educated at Grammar School and then at University, where he graduated. 
56.	M is aged 34 years. She is an only child. Her parents were both witnesses before me. 
57.	M and F met in 2000. 
58.	M and F were married 2004.
59.	Their daughter D was born; then S was born. He died aged nearly 8 months. S2 is now aged 1 year old.
60.	At the time of S’s death M and F kept a large dog, now aged 9. Thus was the family at that time comprised.
61.	It is fair to say that F has involved his children from a very young age in vigorous outdoor activity. When D was very young, about 4 months old, he purchased from Halfords a “bike-buggy” which is an enclosed trailer for towing children behind a bicycle. F says that an instruction leaflet stated that the buggy was safe for children up to 6 months, and said nothing about the need for helmets. However, printed prominently on the back of the buggy are these words: 
CAUTION 
Not for use at high speeds!
Do not exceed 10mph!
Not for use with children under 12 months old!
Children must be able to support their own heads!
Each child must wear an approved safety helmet when riding in this product in trailer mode!
62.	These warnings are not visible when the buggy is folded up. F says that he never noticed these prominent inscriptions until very recently, which is, to say the least, surprising. He admits that, with M’s agreement, he would take D out in the buggy from a very young age, on Wednesdays, when he would be at home, and on one day at the week-end, and ride at speed, he said at up to 30 mph, over forest trails, bouncing over stones and tree roots. (Obviously, this asserted speed of 30 mph is exaggerated. It is the speed of a galloping sport horse. Professor S, who is a dedicated cyclist, has never been faster than 29 mph, downhill, on a light weight racing cycle). When S was born he would strap them both in, and I have seen a picture of S, aged 6 months,  slumped in his position in the buggy with the side of his head positioned against a hard(ish) fibre strut forming part of the canvas canopy, and with D’s head resting on his (within Exhibit 16). There is a video taken on a mobile phone (Exhibit 14) showing F preparing the children for a high speed ride in the buggy without helmets over forest trails punctuated by tree roots. F now admits that this was very careless on his part. The experts Professor S, Dr L and Dr H would go further and would characterise F’s conduct as seriously reckless and neglectful.
63.	M states that she too was unaware of the warnings and in any event rarely participated in these outings, although she did state in police interview that both she and F were always out with the buggy at week-ends.
64.	For the purposes of the history I should record at this juncture the following specific events, which are all relevant to the findings that are sought by the LA:
i)	M and F participated in a bike ride, towing D and S in the bike buggy. N7 took a photograph of S clearly showing a strikingly bruised left ear.
ii)	On Sunday the family attended an air show. Photographs were taken by M and F which clearly show S with a strikingly bruised left ear (Exhibit 4).
iii)	On Tuesday, at home F took a photograph of M, D and S – this photograph appears to show bruising to the backs of both of S’s hands (Exhibit 7). 
iv)	S was diagnosed by his GP Dr M as having an Upper Respiratory Tract Infection.
v)	The health visitor saw S (at D’s two year review), and observed that his left foot had a fungal infection: his big toe was inflamed and the skin was broken, and there were blisters under two of his toes. M was advised to take him to the GP.
vi)	S was seen by the GP Dr F. She noted lesions to both left and right big toes, and scabbed red dry skin. She was uncertain whether the problem was fungal or bacterial. She prescribed Timodine cream.
vii)	On a certain day M pointed out to NC4 at Nursery a bruise to S’s ear. 
viii)	S was taken by F to see Dr F who observed his bruised left ear, and a bruise behind the ear. Dr F was uncertain as to the cause or nature of the bruise and called in Dr D and also telephoned a Paediatric Registrar who speculated that it may be a haemangioma. F states that on this occasion the problem with S’s feet was also discussed; but there is no record of this.
ix)	In the following days M mentioned to the staff at Nursery her attendance at the GP about S’s ear.
x)	S was taken to see Dr F by M. He had been poorly the night before. An Upper Respiratory Tract Infection, and conjunctivitis, were diagnosed. Chloramphenicol eye drops were prescribed.
xi)	NC5 noticed a bruise to S’s left ear.
65.	I have described in my opening paragraphs the events up to 9.40 a.m. on the day that S died when resuscitation attempts at the hospital were discontinued. The resuscitation team comprised the Dr S Accident Consultant, Dr J, Sr T, Dr B Paediatric Anaesthetist, Dr R, Dr A, and Dr L. During the 25 minutes of resuscitation attempts the following things happened:
i)	Dr A was trying to access a vein to insert a line. Access sites included the back of the hand, which would have been held firmly for the purpose, the spine, both shins, the left ankle and the supra-pubic region. Eventually the right femoral vein was accessed, according to Dr J  and Sr T (it was the left one according to Dr F). Drugs (adrenalin) and fluids were ingressed, and blood samples were taken by 9.30 a.m., this being the time the earliest sample was received by the laboratory. I have seen examples of the IV catheters used, and they are sizeable indeed (Exhibit 15).
ii)	An endotracheal tube or laryngoscope was placed in the mouth with some difficulty as the jaw was stiff (this had earlier been noticed by the ambulance paramedic). S was ventilated.
iii)	Intra-osseous access was also gained on one of S’s shins. I have seen examples of the needle used, and it is even larger than the IV catheters (Exhibit 15).
iv)	Cardiac compression was performed forcefully.
v)	Blood samples were taken. Of these one sample reached the microbiology lab at 9.30 a.m; another at 9.35 a.m; another at 9.44 a.m; another at 10.30 a.m.
66.	After the resuscitation attempts had been discontinued, and S pronounced dead at 9.42 a.m., Dr R and Sr T conducted a full visual survey of the body, which was recorded in a workbook. A number of the injuries which were observed at the autopsy the following day were not recorded. The only injuries that were noted were:
i)	Healing laceration/scab left 1st toenail
ii)	Small scab left 5th toenail
iii)	Upper fraenulum torn
iv)	Swelling of left ear pinna 3 x 2 cm
v)	Bruise left forearm 3 x 2cm
vi)	Bruise right forehead 0.5 x 0.5 cm
vii)	Large left sided inguinal hernia 
viii)	Smaller right sided inguinal hernia
The body’s temperature was recorded at 33.6 C.
67.	Sr T then at 10 a.m. took forensic samples namely his pyjamas, his nappy, and moist and dry swabs from various sites. This required her to swab all bruised areas. She noted and swabbed only:
i)	Bruise to left ear
ii)	Wound to left big toe
iii)	Bruise to left forearm
68.	At this point M and F were allowed some time with S’s body in the resuscitation room; later they were joined there by PGM. At 2 p.m. his body was taken by Sr T and a mortuary technician, to the radiography department for a full skeletal survey. I have read [the mortuary technician’s] witness statement (she was not required to give oral evidence). She saw S’s naked body on the X-ray table, and observed no bruising or marks to his body other than to his feet which she said looked as though they had been “chewed”. She saw the radiographer massage open S’s hands in order to X-ray them. [The radiographer] also made a statement (she too was not required to give oral evidence). She confirmed that the hands were beginning to stiffen through rigor mortis and that she gently massaged them open. She states that as she was working on them she noticed dark blue colouration towards the centre of the palm which appeared to be bruising. She did not notice any bruising to the backs of the hands. She also noticed scabbing to the toes, bruises on either side of the forehead and a bruise to the left ear.
69.	At 2.45 p.m. a series of photographs of injuries to the left ear, right forearm and fraenulum were taken, I assume in the radiography department. No other part of the body was photographed, which is surprising given the observations that had been made of the feet, the forehead and palms, which I have set out. 
70.	Following this the body was taken to the mortuary and placed in the chapel. At 4 p.m. the body was transferred by undertakers to the RVI, where it was placed in the fridge. If S in fact died at 7 a.m. (as to which see paras 75 to 78 below), his body had been up to that point in ambient temperatures for 9 hours. 
71.	The results from the lab came through between the afternoon of [Day 1 and Day 3]. They revealed the following:
i)	Normal levels of protein in the blood.
ii)	A significantly and abnormally raised level of lymphocytes.
iii)	Severely abnormal times for thrombin and reptilase (these are aspects of blood clotting).
iv)	Staph isolated in a wound sample, and in a blood culture, although in the latter instance this was considered to be a probable contaminant deriving from the blood taking process.
v)	Staph aureus isolated in a wound sample.
72.	The following day, at 1.30 p.m., the body was removed from the fridge in preparation for the post-mortem, which was conducted by Dr J and Dr W. Nine other people, including police officers, and a representative of the Coroner, were present, together with a photographer. The body was photographed at all stages of the autopsy, and I have the dossier of prints. The body was fully anatomised and histological sections were, per Dr J, taken from only four sites, namely the fraenulum, the right palm, the left palm, the joint of the middle finger of the right hand, but it is clear that 14 sections were also taken from the ears.
73.	The record of observations made by Dr J is set out by me below.
74.	S’s funeral took place, following which his body was cremated. The order of service is Exhibit 19 and it has on the front one of the photographs taken at the air show (Exhibit 4). M and F held a reception afterwards which was attended by a number of the friends and neighbours who gave evidence before me.  N4 says she saw D in the hotel car park at the end of the reception and noticed that she had a split lip and a bruise on her face. N2 says she saw quite a nasty bruise to the side of her face. Earlier M had sent N2 a text saying that D had fallen out of bed and had a bruise on her face.
75.	An important question is when S actually died. Death in this context means the irreversible cessation of natural circulation and respiration. In the context of vigorous resuscitation there is obviously a grey area between life and death, as there is generally. Medically, the period of the death throes is referred to as the agonal period. This can go on for some time. Rigor mortis, the stiffening of the body’s muscles after death, is a biochemical change that can only occur after death. The ambulance crew noted stiffness in the jaw consistent with rigor mortis, as did Dr at the hospital.
76.	When M found S she knew at once that he was dead. Indeed at the beginning of her 999 call she says in extreme distress “my baby is dead in his cot”.  In contrast, F, who performed CPR on S, did not believe that he had actually died.
77.	In his evidence Dr L stated in answer to questions from Mr S:
Q. 	It is towards the bottom of the page just below the lower hole punch where you are noted as saying "I think S had probably been dead for at least a couple of hours and probably longer than that when found."? ‑ A. Right okay.
Q. 	And it may or may not be that things turn on this, but just so that we understand your expert opinion as best as possible. In your earlier evidence you said he had been dead for one or two hours? ‑ A. I think it is as vague as that.
Q. 	As vague as that? ‑ A. Yes it is. I suspect it is probably more than an hour, but if you said is that within the spectrum then I think the answer is yes. I think the maximum part of the spectrum is around a couple of hours or thereabouts which is what I was trying to say here and it could have been more. That was the other point I wanted to introduce into the discussion. It doesn't quite come over like that when you read the transcripts of what you said but that is what I was trying to say and trying to lead towards.
Q. 	So would it be fair to say that when found at 8.45, I appreciate of course it is very difficult to be specific, but that S had been dead for at least an hour? ‑ A. Oh yes, I think that that is a very reasonable and realistic conclusion and as I said before it could have been longer than that, but I think that that has to be a very, it has got to be likely he had been dead at least an hour.
MR. JUSTICE MOSTYN:   Does death in this context mean cardiac arrest? ‑ A. Yes, it means no circulation and no respiration, absolutely right. No oxygen. 
78.	To her final written submissions Ms B QC had an Appendix derived from internet research entitled “Postmortem Changes and Determination of the Time of Death”.  This states:
After death, a sequence of changes naturally occurs in the human body. Although these changes proceed in a relatively orderly fashion, a variety of external factors and intrinsic characteristics may accelerate or retard decomposition. Understanding common postmortem changes and the variables that affect them allows the forensic pathologist to more accurately estimate the postmortem interval (PMI) and to provide a time frame during which death occurred. Further, an awareness of common postmortem artefacts limits the risk of misdiagnosis at the time of autopsy. 
Postmortem changes begin soon after death and progress along a timeline. Two processes, putrefaction and autolysis, begin to alter the body; either one may predominate, depending on the circumstances surrounding death, as well as the climate. Putrefaction involves the action of bacteria on the tissues of the body. This process, prevalent in moist climates, is associated with green discoloration of the body; gas production with associated bloating; skin slippage; and a foul odour.
Autolysis is the breakdown of the body by endogenous substances. It proceeds most rapidly in organs such as the pancreas and stomach. It may predominate in more arid conditions and can eventually result in mummification.
In most circumstances, autolysis and putrefaction occur in tandem. In temperate climatic conditions, they can result in rapid degradation of the tissues. These alterations may eventually produce great distortion of the body after death, hampering the interpretation of the postmortem findings but not ameliorating the value of the autopsy.
Some of the more well-known postmortem changes, such as rigor mortis, livor mortis, and algor mortis, progress on a relatively set schedule; however, many external and intrinsic factors may affect their development. It should be remembered that the estimated period for the arrival and passage of these manifestations of the decomposition process is based on studies under very controlled conditions, including a temperate climate (i.e., 75° F). 
In reality, many deaths occur outside of these “ideal” settings, and additional confounding variables may be present (eg, layered clothing, obesity, fever). Further, the longer the PMI, the less accurate the PMI estimate becomes.
Postmortem changes may partially obscure ante-mortem trauma and disease or mimic their presence. It is essential that the pathologist recognize these findings for what they are. Despite the degradation the body undergoes during the postmortem period, a complete autopsy of a decomposing body often yields abundant information.
Although there is quite a lot of variability in the time schedule of common postmortem changes, all bodies eventually decompose to some degree. The physical and biochemical alterations, when considered in concert with a thorough medico-legal death investigation, may allow one to estimate the PMI. Estimation of the time of death is a critical component of forensic death investigations, but it is an imperfect science. Unless a death is witnessed, it is usually possible to provide only a time window during which death could have occurred. 	
79.	Although the evidence is, to say the least, inexact I conclude, on the balance of probability, that S died at approximately 7 a.m. The cause of his death is, as I have stated, medically unexplained. I do not however discount the possibility of post-mortem intermittent forced movement of blood as a result of resuscitation attempts, as noted by Dr Vanezis in his article. I shall call this phenomenon “false circulation”.
Injuries sustained by S: the LA’s case
80.	In the schedule of findings sought the LA lists a number of injuries to S in respect of which they seek rulings that the injuries were abusively inflicted. A number of these injuries have already been noted above. 
81.	In respect of S the list is 
i)	S (then aged <4m) was found to have bruising to the back of his hands.
ii)	S (then aged 4½m) was found to have a graze on the back of his head.
iii)	S (then aged 5m) was found to have bruising to the right side of his forehead, both cheeks, the back of both hands and a large healing bruise on the back of his head.
iv)	S (then aged 6m) was found to have bruising to his right ear and right cheek.
v)	S (then aged 6½m) was found to have a swollen and bruised left ear.
vi)	S (then aged 7m) was found to have bruising behind his (swollen and bruised) left ear.
vii)	S (then aged <8m) was found to have bruising to the back of his hands.
Injuries sustained by S:  the LA’s case 
82.	In order to put the LA’s claims into clear context it is convenient to set out the list of injuries noted by Dr J at the autopsy conducted 2.30 and 4.30 p.m. As I have mentioned, the injuries were all photographed, and the dossier has been made available to me. This what she wrote in her police statement: 
RECENT INJURIES
Of the Head Neck
1. On the right side of the occiput, there was a scabbed abrasion 1 mm in diameter.
2. On the right forehead, 45mm above the outer angle of the right eyebrow, there was a purple bruise 4mm in diameter.
3. A similar bruise was present approximately 45mm above the outer canthus of the left eyebrow.
4. There were two purple bruises on the outer aspect of the inferior margin of the left orbit measuring 5mm and 4mm.
5. There was scabbing of the posterior margin of the right nostril.
6. There was a recent tear of the frenulum of the upper lip which was associated with a little erythema but no significant haemorrhage.
7. There was a red mark 2mm in diameter posteriorily in the midline of the hard palate.
8. Within the upper helix of the right ear, there was a purple nodule 7mm in diameter which on sectioning showed a little haemorrhage.
9. There was a fluctuant swelling 25 x 20 x 7mm with overlying purple discoloration of the skin within the left upper pinna. Sectioning revealed an organising cystic haematoma containing some liquid blood.
10. There was a well circumscribed area of superficial haemorrhage in the middle lower left lip measuring 3 x 2mm in the midline.
Of the Right Upper Limb
11. There were two purple bruises on the ventral aspect of the lower right forearm just above the wrist measuring 3mm and 5 x 3mm.
12. There were scattered blue bruises up to 7mm over the dorsum of the right hand and over the back of the index, middle and ring fingers of the right hand
13. On the centre of the right palm and the palmar aspects of the index, middle and ring fingers, there were similar blue bruises up to 7mm in diameter.
14. There were scattered abrasions on the back of the index finger 3 x 2mm and overlying the proximal interphalangeal joint of the ring finger measuring up to 2mm.
15. There was a red/purple bruise over the metacarpophalangeal joint of the middle finger of the right hand measuring 10 x 5mm.
Of the Left Upper Limb
16. At the centre of the left palm, there were similar blue bruises up to 7mm in diameter with at the base of the index finger, there was a transverse apparently post-mortem skin split.
17. On the back of the left hand and on the back of the left index, middle and ring fingers, there were similar blue bruises up to 7mm.
18. Over the metacarpophalangeal joint of the middle finger, there were small scabbed abrasions.
19. Over the proximal interphalangeal joint of the ring finger, there was an abrasion up to 2mm in diameter.
20. An abrasion 2mm in diameter was present over the proximal phalanx of the index finger.
21. There was a red mark on the proximal phalanx of the index finger.
22. There were two purple/brown bruises on the medial aspect of the left forearm measuring 12 x 9mm and 13 x 9mm separated by 10mm. The bruises showed yellowing at the edges.
Of the Lower Limbs
23. Over the 5th metatarsal of the left foot on the dorsal aspect, there was a purple bruise 5mm in diameter.
83.	The list of findings sought by the LA in relation to these injuries is framed as follows:
i)	S sustained the following injuries during the period of 4-12 hours before his death:
a)	A torn upper lip fraenulum;
b)	Bruising and abrasions to the palms of both hands.
ii)	S sustained the following injuries during the period of 24 hours before his death:
a)	Bruising and abrasions to the back of both hands;
b)	Bruising to his scalp (bruise to the right side of forehead; bruise to the left side of forehead; bruise within the left anterior temporal region);
c)	Two bruises to his left orbit;
d)	Bruising to his left foot.
iii)	S sustained the following injury at least 18 hours - and probably a few days - before his death: two bruises to the left forearm.
iv)	S sustained the following injury at least 3 days before his death a bruise over the major knuckle of the middle finger of the right hand; (please note: this may have been part of the bruising in finding no. [80.vii)])
v)	S sustained further bruising to both ears during the hours/days leading up to his death. 
84.	In addition to the above the LA seeks the following findings of neglect of S:
S was observed to have haemorrhage and crusting to both feet which was severely abnormal. This condition would have caused him pain and discomfort. It would have been apparent to any attentive carer that the appearances of his feet were severely abnormal and justified medical attention. M  and F failed to seek appropriate medical attention for S.
The subsequent events
85.	On the day of S’s death at 1 p.m. the police comprehensively photographed the interior of the property. They also removed certain items.
86.	From 10.30 to 10.58 a.m. M was interviewed by the police, and F was interviewed from 11.13 to 11.46 a.m. These were fact gathering interviews; neither parent was considered a suspect; neither was cautioned; and no solicitor was present. 
87.	Three days after the funeral, M and F were visited at home by Dr T, a consultant community paediatrician. She is part of a team of professionals overseen by Dr K2 that is activated whenever there is a Sudden Unexpected Death in Childhood. The object is to gather information ostensibly to help the parents to come to terms with their bereavement and to assemble data to see if the incidences of such deaths can be reduced. Her notes are recorded in a workbook. It is clear that if suspicious information were obtained it would be shared with the police although this was not made clear to M and F and no warnings were given. I have seen a leaflet which has come into being since 2008 (Exhibit 3) which seeks to explain the reason for the intervention. It states that “all of the information we gather will be treated with the deepest respect and in strictest confidence”, which is inexact inasmuch as suspicious information will be shared with the police.
88.	Dr J’s statement giving the result of the autopsy is dated, but it is likely that the results will have been known by LA before that date. The LA commenced a child protection investigation and an initial case conference formulated the child protection plan which prescribed no unsupervised contact between D and her parents. The arrangements were agreed by the parents, no doubt because they knew that if they did not agree them they would face an emergency application for an interim care order.
89.	The police started to take statements. Within the next 8 months they had taken no fewer than 82. I have read all those statements and many, but by no means all, of their makers have given evidence before me.
90.	The parents attended a police station for a second round of interviews. Although they attended with a solicitor, they had not been made aware that they were suspects. On arrival at the station, to their surprise, they were arrested on suspicion of child neglect, cautioned, and placed in separate cells. They were each interviewed for over two hours, and were released on bail.
91.	They re-attended for a final round of interviews. Again, they were arrested, cautioned, placed in separate cells, and interviewed for over two hours, apparently in freezing conditions (which later led to a complaint against the police, which was upheld).
92.	On the same day a review of the case took place in the Royal College of Pathologists. This is apparently routine (if cursory), and is a peer review procedure of autopsy work. The meeting speculated that the injury to the fraenulum may be an old injury (notwithstanding the polymorphic accumulation) and that the injuries to the hands and arms could be bite marks.
93.	The LA concluded its core assessment on M and F which was highly favourable to them. Its author was an experienced Social Worker.
94.	The CPS decided to take no further action against M and F. It explained that “there is insufficient evidence to establish a realistic prospect of convicting any identifiable individual for any criminal offence in respect of the “unexplained injuries” sustained by S prior to his death”. It was later explained that reliance was placed on the equivocal speculations by the Royal College of Pathologists. 
95.	I have described above how supervision of D was discontinued but how the régime was reintroduced after the birth of S2. 
96.	The LA applied for a care order in relation to S2. It later applied for a care order in respect of D. The court gave directions, including the fixing of this fact finding hearing. 
The lay evidence 
97.	For the purposes of my survey of the lay evidence I need first to record that in pursuing its case the LA argues that from 2006 onwards this was a family under considerable stress. It recognises that, generally speaking, extreme child abuse does not come out of a clear blue sky. 
98.	It is the LA’s case that these parents were beset by stress which led, or contributed, to a complete loss of self-control by one, or both, of them in the early hours of the night, as a result of which S was savagely and sadistically assaulted and murdered. It is the LA’s case, also, that these alleged stressors were contributory to the earlier alleged acts of violence administered to both D and S, which I have set out above.  
99.	It is fair to observe that no sign of the stresses postulated by the LA were detected by Dr K, or by its own social worker when preparing the core assessment.
100.	The evidence of Dr P falls, up to a point, into the category of psychological/character evidence. His role was to undertake the “care of the next infant” (CONI) a nationally recognised programme for the care of subsequent babies when a previous child has suffered a cot death. The CONI scheme recognises that for a minority of cot deaths there may be predisposing factors indicating NAI. Thus a paediatrician must exercise extreme vigilance in relation to the care of the next child. As such he participated in child protection review conferences held in relation to S2 and knew of the grave allegations made concerning S and D. He had also heard things from medical colleagues. In his evidence he stated that the parents were open about the background to S’s death; they were wanting answers. He was able to build up a reasonable picture as to what had been found in relation to S; it corroborated what he had been told by the parents. He understood the collective anxiety as regards unexplained injuries. D was extremely bright and responsive. The parents risked wrapping S2 in cotton wool. S2 was a happy lively normal baby; he had no concern about S2’s or D’s emotional or physical development.  The parents were still coming to terms with S’s death. They had good days and bad days. Nothing in the clinic concerned him; they did not appear avoidant, and he was looking very hard for that. They did not deny the existence of the injuries; or to seek to minimise them. He scrutinised them very closely.  He would be razor sharp as regards any injury to S2: “I have on each and every occasion been satisfied that his physical emotional and developmental care has been appropriate and of a high standard”. 
The evidence of lay witnesses of fact
101.	In analysing the evidence of fact I propose first to consider the evidence of S’s primary medical carers and his nursery carers. Dr D, while S’s GP only ever saw him once, when Dr F sought his advice concerning S’s left ear. In his oral evidence he stated that to the best of his memory it was just the fleshy outer part that showed bruising. There were no bruises to the scalp behind it. F, who had brought him in, did not know how it had happened. There was no mention about bruising to his right ear, nor was there mention of his feet. He stated that if there was any cause for concern this would have been recorded; there was no such record. It was not a suspicious NAI. He did not “take that away” from the consultation. In answer to questions from me he stated that in his opinion it was possible for a child sitting in his cot to fall and suffer this injury.
102.	Dr F was a GP Registrar at the Surgery. She saw S three times. What she observed I have already set out in the above mentioned paragraphs. She seemed to recall that the possibility of the injury to the ear being caused in the cot was mentioned by the F. Her notes record F stating that it happened 5 weeks earlier. (F later explained to me that this was a mistake on his part and when he told M that he had so stated she told him that it had appeared two weeks earlier). She confirmed that no mention had been made of bruising to the right ear. She could not remember if she was showed S’s foot on the last occasion – her notes make no reference to this, although F is adamant that this happened.
103.	Dr M is the designated family doctor for the family. He conducted D’s 6 week examination which was entirely normal. He saw S once for his 6 week examination, which was also entirely normal. As recorded above he diagnosed an URTI in S. This was in a telephone consultation. He stated that he had a very good relationship with M “who was a pleasure to deal with”. Similarly, F made a good impression on him.
104.	M’s midwife for both of D and S, although she in fact delivered neither. She described M and F as calm first time parents. There were no concerns whatever. There were no signs of any stressors. M was calm and relaxed; F was supportive of M.
105.	[A] community nursery nurse. Among other things she gave infant massage sessions. I have recorded above how she made certain observations of D. Although she states that she thought the scab a strange injury, and hard to get from the explanation given by M (i.e. rubbing her head on a play mat), this is not recorded in her notes. She explained that the scab was no bigger than a 5p piece. She confirmed that if there were child protection issues then certain procedures must be followed but she was not thinking NAI, then or at any time. She confirmed that M made no attempt to hide this scab.
106.	I now turn to the evidence of S’ nursery carers namely NC1, co-proprietor of Nursery; NC2, Senior Nursery Nurse; NC3, Senior Nursery Nurse; NC4, Nursery Assistant; and NC5, Activity Leader.
107.	NC1 produced a document completed by M entitled Child Personal Record which stated that S occasionally bled from the nose on sneezing, and that he had recently experienced an infection to his feet for which cream was used. She confirmed that she had no concerns in relation to any bruising or marks. NC3, who cared for S, recalled that she noticed bruising to S’s left ear. She spoke to M about it and was told that he would have to go back to the Doctor if it did not go down. She cannot recall any other marks or bruises to him.  NC4 was S’s key co-ordinator. She recalled M bringing a bruise to S’s ear to her attention, on an uncertain date.  She did not remember which ear, nor did she remember the exact date of the conversation.  She remembered M asking if she had noticed anything but said it was not there when S was previously picked up from nursery.  M told her she presumed S must have banged his ear in his cot.  She said S did not appear to be in distress and was his normal happy self.  She remembered the next time S came to nursery the bruise was still there but she could not recall if it was worse or better, nor could she recall whether the conversation took place on either a Monday or Friday, but the second time he had attended with a bruise he had apparently been taken to the doctor (although she had this information from another member of staff).
108.	The events were certainly dramatic in this small, close-knit, community and there was a deal of speculative gossip within it, fuelled by police involvement and the intermittent supply by them of information about the investigation. All this, it is said by the parents, fostered a climate of suspicion, which undermines the reliability of the evidence, which is said to be contradictory anyway,   and which should lead me to treat it with great caution. 
The evidence of the paramedics and the resuscitation team
109.	AP1 and AP2 comprised the ambulance team. AP1 could not remember that much. He could not remember which of them had inserted the Guedel tube. Of the two types that I have seen (Exhibit 2) it seems likely that the Medasil Airway (Guedel Type) Size 00 was used. The “stop” of this has distinctly sharp edges. AP1 thought that the tube could have caused the fraenulum to tear. He recalled difficulty inserting the airway due to the stiffness of S’s mouth. He saw no injuries to S but did observe a hernia. He administered CPR and oxygen. 
110.	AP2 did not notice any injuries whether to the fraenulum, hands, arms or legs. He accepted he might have torn the fraenulum; it was the first time he had intubated a baby. For him the most important thing is to save the baby’s life. When shown by me Photo No 476 (which shows S’s naked body with pronounced discolouration all over it), he was positive he had seen nothing like that.
111.	Dr I stated that they made desperate attempts to save the baby; but unfortunately the rate of saving children after cardiac arrest is dire. He noted difficulty putting an endotrachael tube into S’s mouth because of stiffness of the jaw.  He inserted a canula into the right femoral vein.  Dr A was trying to access a vein. When the medical team stopped working on S they noticed his fraenulum was torn; that both of his ears appeared bruised; the left ear was worse, like a cauliflower ear.  He had hydroceles and an umbilical hernia.    He thought Dr B told him about the torn fraenulum and they both thought it might have been caused by the airway.  He did not notice bruising on the arms, hands or forehead.  
112.	Dr B did not give oral evidence. Her statement records the attempts to insert a laryngoscope to view the windpipe but the jaw was quite stiff and it was difficult to open S’s mouth. She wrote: “Blood samples were taken including a blood gas which showed very severely metabolic acidosis and very high potassium consistent with a prolonged period of cardiac arrest”. She noticed significant purplish swelling on left ear and purplish discolouration to right ear.  There was evidence of a torn fraenulum which she thought could have resulted from the airway being inserted prior to arrival in A&E: “it was not bleeding”.  She noticed obvious swelling to the scrotum.  
113.	Dr A, a Consultant Paediatrician, did not give oral evidence. In his statement he noted that S was cold and in cardiopulmonary arrest on arrival.  He took a history from parents.  During resuscitation he found S had a torn upper lip Fraenulum, bilateral inguinal swelling, an abdominal hernia, swelling over left ear and he noted a bruise on S’s left forearm and right forehead.  
114.	Dr R was a middle grade Paediatrician. I have recorded above the results of his visual body survey. He also took a history from the parents, which is recorded in the workbook. In his oral evidence he agreed he had not recorded an injury to the right foot, the right ear, or the right hand; and that he recorded one bruise rather than two on the left forearm.  
115.	Sr T recalled attempts to put a line into S to administer drugs and fluids; that there were several attempts; and eventually access was achieved in the right femoral vein.  She recalled that access was attempted on both shins and on the left hand but she could not recall if this was in fact the back of the hand or not.  I have recorded above how she participated in the visual survey, and how she took samples from the body. She did not recall any marks of any nature to S’s hands. In her oral evidence she confirmed she had been with S throughout except when he was with his parents, when the nurse accompanying them was with S.  She described how to get a line in and demonstrated holding a hand to smooth the skin on the back of the hand to put the line in.  With children she said you would usually hold the wrist and it was unlikely that you would hold the hand although you may hold the fingers to extend the back of the hand.  She said it was to smooth the vein on the back of the hand and did not require a lot of pressure. A photograph was taken of how the hand would have been held (Exhibit 11). If using the feet you would hold just above the ankle.  She was shown the medical photographs of S’s ears and said she could remember the ear looking like that but could not specifically remember the other bruises.  In respect of the bruising to S’s forearm she said it did not look like it could have been caused by holding his arms during resuscitation as it was high up.  She looked at the photographs of S’s right foot taken at autopsy (Nos. 526-536) and in respect of 535 she said she could not remember if the backs of the toes were checked.  She could only remember the abrasion on the big toe and she certainly did not recall seeing the little toe. 
116.	I have recorded above the evidence of the mortuary technician and radiographer.
The evidence of Dr T and Dr K2
117.	I have recorded above the involvement of Dr T and Dr K2 with this family. Inasmuch as they offer opinions concerning the injuries to S I need only record that they are in line with those of Dr J (whose report they had read) and Dr L. Dr T’s notes of the meeting with the parents are in the trial bundle, as are the notes of Dr K2. Dr T stated that she did not see what she was doing as evidence gathering, which surprised me, as Dr K2’s notes record a telephone call between them where they discussed a “plan” which was to “try to establish any history for ear or arm injury”. Dr T’s notes record F saying to her “would see signs if strangled/suffocated?” which has distinctly sinister overtones, although it was not actually put to F in his evidence. 
118.	Dr K2 confirmed the uniqueness of the palmar injuries, and stated that because they were so unusual she assumed they could be post-mortem injuries.
The evidence of M and F 
119.	I am not going to attempt to summarise in any detail the evidence of M and F, each of whom occupied the witness box for two days. They utterly deny the allegations of abuse and murder. 
120.	I will, of course, within my conclusions set out my findings as to their personality and credibility and whether or not I believe them in their denials.
121.	M confirmed that theirs was a happy marriage and that F was loving, caring, honest and “crazy”. He was the nicest man and the best Dad, ever.
122.	M confirmed the factual background, which I have set out above. She confirmed that F would take the children out in the bike buggy two times a week. She asserted that she was not aware of the signage on the back of the buggy.
123.	When shown the photograph taken (Exhibit 7) M commented that S looked really poorly, pale and tired.
124.	In his evidence F described M as a trustworthy and excellent mother. The birth of D “really enriched their lives”. He was as involved as much as he could be after her birth.
125.	He was working at home. After the children had been put to bed, and M had retired he prepared the children’s milk and then went to bed. He cannot recall how long he worked in his study. 
126.	Although S suffered from a “hideous” cough at that time (which was confirmed by MGM, who described it as “frightening”) he did not cough that night. F stated that he awoke at 5 a.m. and could hear S making noises. This was after D had crept into their bed. He tried to give him his milk, three times, but he would not take it. He heard S breathing normally, if a bit snuffily; he was satisfied that all was well and went back to bed. His evidence thereafter is as described in my opening paragraph, although it should be noted that F stated, for the first time in his evidence in chief, that when performing mouth to mouth resuscitation he pinched and pulled at S’s upper lip in order to get his mouth open.
127.	Concerning the bike-buggy, this was bought when D was 4 or 5 months old. He understood from Halfords that it was for children aged 6 months or who could earlier hold their heads up, and D could do this at 4-5 months. He claimed that he had not seen the instructions until he brought the buggy to court on Friday; that he told M about the signage on that day and she was not happy with him at all. She was absolutely justified to be angry, but he did it with the best of intentions. He felt dreadful now.  
128.	Under cross-examination Mr S extracted the following statements and admissions from F:
i)	In an number of instances Doctors record statements by F which he either denied saying or could not recall saying.
ii)	He was not concerned that using the bike buggy would cause bruising; M had mentioned that D bruised easily.
iii)	Although S did have a number of ailments until his death that was not additional stress for him and M, at all.
iv)	When he stated in police interview that S’s ear had been inflamed for 5 weeks before he took him to the Doctor, that was wrong.
The expert evidence
129.	Dr J made three police statements and gave oral evidence before me. She also gave evidence to the Coroner and I have a transcript of that. In her first police statement she set out the list of 23 injuries which I have recorded above. She stated:
“Histology
Histological examination of the upper fraenulum shows fresh haemorrhage with a little associated fibrin. Neutrophils can be seen around adnexal structures. Within the bruise on the left palm there are similar changes with haemorrhages, oedema and neutrophils present around adnexal structures and within the fat. The tissue sample from the right palm is fragmented but confirms the presence of haemorrhage within the subcutaneous tissue associated with neutrophils. In a separate fragment neutrophils, blood and fat can be seen. Histological examination of the brown bruise on the back of the right hand showed further haemorrhage and neutrophils around adnexal structures. There is focal Perls positivity.
The lesion from the left ear shows numerous small vessels some of which branch and others have blood within them. There is fibrin and associated haemorrhage but no inflammation. Patchy iron deposition can be seen. Within the right ear a similar lesion is present. There is haemosiderin laden macrophages associated but no evidence of recent haemorrhage.
Microbiology
Please see the report of Dr W for full details of the microbiological results. However, in summary, there are no microbiological findings to account for death.
My conclusions are as follows:
The Cause of Death
Despite a detailed post-mortem examination including histological, microbiological, biochemical and toxicological analyses, no cause for S’s death has been determined. It is recognised that sudden and unexpected death can occur in infants for which a cause cannot be determined. Many of these deaths fall within the definition of sudden infant death syndrome. However, in this case S was older than the common age range for SIDS death and there were a number of injuries about the body which, although have undoubtedly not contributed to death, cause concern and therefore it is most appropriate to classify the death as unascertained. 
The Lesions in the Ears
Within the left ear there was a fluctuant swelling which on sectioning showed haemorrhage. A similar nodule was present within the right ear. Histological examination of these lesions showed underlying vascular lesions which have developed as a consequence of a developmental anomaly and are therefore hamartomas. Within the smaller lesion on the right ear there was evidence that there had been some bleeding in the past as there was haemosiderin within macrophages. The left ear showed haemorrhage with some iron deposition. This may be as a result of recent bleeding or may simple represent the lack of resolution of an earlier episode of bleeding. The presence of bleeding has occurred as a consequence of some degree of trauma to the ears although given the presence of the underlying leison this may be relatively minor trauma in nature. 
The Fraenulum
During resuscitation attempts in the Accident and Emergency Department, damage to the upper fraenulum was documented. At the time of the post-mortem there was an obvious recent tear with a little erythema evident macroscopically (injury 6). Microscopically the presence of fibrin and an acute inflammatory cell reaction with neutrophils which have migrated away from the vessel indicate that this injury has occurred during life and not as a result of resuscitation attempts. The histological appearances indicate that this lesion has not occurred around the time of death. These features have been described as early as two hours but it is generally held that these changes indicate that the injuries occurred four to eight hours prior to death. 
The Bruises
The post-mortem examination has documented a number of bruises about the body. Some of these injuries (injury 15 and injury 22) are undoubtedly older as they were brown in colour and, in the case of injury 15, from the right hand, histological examination has shown the presence of Perl’s deposition indicating some degree of resolution. The presence of Perl’s positive iron suggests that the bruise on the back of the right hand has been present for at least approximately 3 days. The most concerning bruises, however, are those to the palms of the hands (injuries 13 and 16). The palm of the hand is a difficult place to cause bruising and as such significant trauma would be required to lead to the damage to the blood vessels which leads to the bleeding. Histological appearances of these lesions again indicate that they have occurred during life and not in the time immediately leading up to S's death. The ageing of these lesions is similar to that seen in the fraenulum. As it stands, I am unaware of any explanations having been provided for these injuries and in the absence of such explanations these injuries strongly suggest non-accidental injury. It is likely that these bruises were not apparent during the earlier examinations of the body as they were relatively deep bruises which have developed over a period of time. On the left forearm there were two purple/brown bruises with yellowing at the edges (injury 22). The colour of the bruising indicates that it has been present for a period of time greater than 18 hours. The positioning on the arm is suggestive of being caused by a "nip" or pinch. There were a number of other bruises to the body including the head and around the eyebrows. Whilst these all were minor injuries in themselves, no explanation for these injuries has been provided to my knowledge 
Summary and Conclusions
S’s death remains unexplained. Although some features would suggest that S has died as a result of sudden infant death syndrome his age and the presence of the bruises around the body preclude its classification as sudden infant death syndrome and the death remains unexplained. A number of injuries has been documented with significant injuries to the hands and fraenulum which have undoubtedly occurred during S's life and most likely predate his death by a small number of hours. Whilst these injuries have not in any way caused S's death their very presence is seriously concerning.”   
130.	In her second statement Dr J stated:
“At the post-mortem examination a number of bruises were documented on the palms and backs of both hands. One of the bruises on the back of the right hand was red/purple in colour and histological examination suggests that this bruise had been present for at least three days based on the presence of Perl's positive material. The bruising to the palms of the hands is concerning. The palms of the hand and the palmar aspects of the fingers are an unusual place to see bruising as due to the nature of the tissues involved bruising to the palm is difficult to cause. Given that there were also bruises present on the backs of the hands, the most likely cause of the bruising to the hands is some form of compressive blunt force. Possible mechanisms of injury include stamping or standing on the hands and also the trapping of the hands between unyielding surfaces. The injuries themselves had no specific features to indicate which of these were the most likely.
The Injuries to the Fraenulum
At the post-mortem examination there was a recent tear of the fraenulum of the upper lip. The most common cause of injuries to the fraenulum include a tangential blow or forceful introduction of an item into the mouth such as a feeding bottle, dummy or finger. Although injuries to the fraenulum can be caused during resuscitation attempts in this case, the histological findings indicate that this is not the case as the injury shows attempts at resolution and healing.”   
131.	Towards the end of her evidence to the Coroner, Dr J was asked whether it was surprising that only a limited number of bruises were noted on S’s body at admission to hospital compared with those found during the post mortem examination. She replied: 
“Not necessarily, because the examination that we carry out is very different to the examination carried out immediately after death. And with the injuries to the palms we know that deep bruising develops over a period of time in the same way as if you bang your leg you might not see a bruise for a day or two, If you bang your shin for instance the bruise is much more obvious much quicker. So bruising can develop over a period of time. That can still happen after death so although bruising might not be evident when the initial examination of the child is carried out by the time of post mortem which is by definition a number of hours later the injuries may then be obvious.” 
She went on to confirm that she was confident that none of the injuries was caused post mortem.
132.	In her oral evidence to me she stated:
Within the fraenulum, which is a little bridge of tissue, and this was the upper lip that was affected, we could see fresh bleeding. There was also some fibrin which is part of the body's inflammatory response. What we could also see was white blood cells called neutrophils and these are the first blood cells that respond to something within the body. Sometimes it's infection but in this case it's trauma. 
Q. 	And in relation to the fraenulum can you just explain the findings there please? ‑ A. The findings indicate firstly that the injury didn't occur around the time of death and that the body has had time to mount a response. Secondly, it gives us some indication of how long the injury has been present. They have, the neutrophils having moved, have been described as early as 2 hours but it's typically considered that these changes are 4 to 8 hours old. …
Q. 	In relation to the palm bruises you set out similar observations in your report and again in your oral evidence to the inquest, is there anything that differentiates the histological findings in relation to the palm bruises from those in relation to the fraenulum? ‑ A. No.
Q. 	In relation to the palm bruises just one further matter please at page 12 of your report. Towards the bottom of the page just level with the lower hole punch, a little lower you say "It is likely that these bruises were not apparent during the earlier examinations of the body as they were relatively deep bruises which had developed over a period of time." Can you expand upon that please and perhaps bring into that your own experience of the development of certain bruises? ‑ A. It is not uncommon for an initial examination to not document a bruise. That is not to say the injury wasn't present, it is just that it is not evident at the skin surface. So often for instance if you bang your thigh you might not see a bruise initially, you know it's sore but the bruising develops over time and it comes to the surface. And that part of the process does still continue after death, so we do still see some bruises that were not present at the initial examination. So for in this case for instance in Accident and Emergency in a child being resuscitated that are evident at the post mortem. Again we see it sometimes between two different post mortem examinations, we may see further bruising having come to the surface as it were. In other areas of the body, such as to say the shin, you would expect the bruise to be evident immediately simply because the damage is so close to the skin. So typically we do not see, some of the bruises that don't come out are the ones that are actually in the deeper tissues as it were. 
MR. S:   The process of iron building up, does that process end at death or can it continue after death? ‑ A. No, these processes essentially stop at the time of death.
Q. 	You say these processes, do you include in that the distribution of neutrophils? ‑ A. There is a little distribution of neutrophils but not to the extent that we see here.
Q. 	You set out at page 11 your views at the time of your report in relation to S's ears and the underlying‑‑‑
MR. JUSTICE MOSTYN:   If a patient is being resuscitated and being given adrenaline and CPR and intubation does that keep these processes going, even though a person may be dead. I mean are you artificially alive for these purposes? ‑ A. It very much depends how quickly after death resuscitation takes place. So if you have resuscitation taking place for instance in a hospital setting where you have been seen to collapse so resuscitation is almost instantaneous then yes to some extent you will get a little bit of continuation. In most situations in the community we do not see somebody collapse, and therefore the body has already effectively shut down before resuscitation starts and resuscitation will not restart the process. …
MR. S:   In relation to S's ears your views are set out at page 11? ‑ A. Yes.
Q. 	You have since had the opportunity of considering Dr. L's views and then the views of Dr. H, the histopathologist. Can you tell us please how if at all they have affected your approach? ‑ A. Dr. H is an expert in this area of the body and looking at these changes down the microscope so her experience will be far more tailored than mine is. Therefore, if her opinion is that these are trauma related I think that is most likely the case. Dr. L again has a great deal of experience and I would agree that if he believes that they are trauma related, purely trauma related then I wouldn't argue against that. I looked at them, I was concerned that there was a natural component underlying it, but that I have said that the bleeding was trauma related.
133.	Under cross-examination Dr J accepted the following propositions:
i)	She was not able to estimate the time of death.
ii)	The science of dating bruises by their colour is inexact, although less inexact where the bruise looks yellow, where it might be possible to say that it is at least 18 hours old.
iii)	Pseudo-bruises, caused by pressure after death by, say, resuscitation, may have the appearance of real bruises, but the bruises here did not look like bruises caused by resuscitation.
iv)	The photographs (Nos. 508 and 513) of bruises to the knuckles of the middle fingers of both hands appear to show puncture marks suggesting IV entry sites, although no such marks of medical intervention were listed in the autopsy. She was reasonably sure that these were not medical intervention sites.
v)	Although ventilation at resuscitation might cause the movement of neutrophils the “changes in the fraenulum and the changes in the hands show more extensive more advanced changes than I would expect for merely something which has occurred during resuscitation”.
vi)	Before she had the histology results she certainly held as a possibility that the injuries to the palms and the fraenulum had been caused by resuscitation.
vii)	The histology science is largely based on animal research. There is no good study base in humans, let alone babies.
viii)	She was not aware of any studies about the timing of bruises coming to the surface post-mortem.
ix)	In relation to the ears both she and Dr W felt there was an underlying medical cause – a harmatoma – where much less trauma, indeed normal handling, could give rise to the bruises.
x)	She had seen nothing pathologically which would suggest a clotting disorder, but she had not ever conducted an autopsy on a child with a clotting disorder.
xi)	Although she thought it unlikely, it was possible that bacteria had entered the blood-stream and had moved within the blood after death. The raised lymphocyte count recorded by the microbiology lab may signify a serious infection which the body was fighting.
xii)	If S had been ventilated for an appreciable time then the histological findings in relation to the fraenulum may be consistent with the attempts at resuscitation; but in her opinion he had not been ventilated for long enough for this to be the case. She accepted that there was very little published work about this.
134.	Dr W, Consultant Perinatal Pathologist, who attended the autopsy, made a police statement and gave evidence before me. He also wrote a letter in which he stated that studies had shown that perhaps 10% of deaths labelled as SIDS were in fact deaths caused by covert homicide or maltreatment. In his oral evidence he stated that he was not in a position to comment on Dr J’s opinions concerning the histology. As to the possibility of bacterial infection of the blood he stated:
Q. 	Yes, all right. In relation to the cause of death I wonder if we could look first of all at the findings in relation to the blood count. We know, it is right isn't it, that there was indeed a very high lymphocyte count? ‑ A. There was. Apparently as I saw from the report from Professor H it was interpreted as a high lymphocyte count. My experience is that interpreting blood counts post mortem is very difficult to do because of changes that occur after death, and in fact some of the cell counters in my experience will interpret other cells that may have been shed after post mortem as actually lymphocytes. 
MR. JUSTICE MOSTYN:   Lymphocytes, I am speaking from a position of quite slender knowledge here I hasten to add, when lymphocytes go into action, they are white blood cells when there is a problem they charge into action, so why wouldn't they go and attack the bacteria? ‑ A. Because the white cells that attack bacteria in the initial phase are the neutrophils. So on the haematology report you will also see a neutrophil count.
MS. S:   So would you get increased neutrophils in a child who was combating a bacterial infection? ‑ A. Yes.
Q. 	Within the bloodstream? ‑ A. Yes. Very often you would. …
Q. 	Dr. W, is a raised lymphocyte count adequately explained by the presence of an upper respiratory tract infection? ‑ A. It could do, but I think it goes back to what we were saying before, you are probably best to get interpretation from a haematologist in something that is related to the blood in that case. All I can say is that the usual response to a viral infection will be to elevate the lymphocyte count, because the lymphocytes are the white cells in the body responsible for attacking viruses.
135.	Dr C, Home Office Pathologist, had been asked by the police to give a further opinion as to S’s injuries. He made a police statement and gave oral evidence before me. In terms of pathology his evidence was consistent with that of Dr J and Dr L, being firmly based on the histological science. In his report he stated:
“Summary and Conclusions
S appears to have died early on (date) . His body was examined at post-mortem by DR. J and DR. W and a variety of pieces of tissue were retained for histology. I have been asked to comment upon the possible causes of the injuries to the hands and fraenulum and the timing of these injuries, in particular in relation to the point of death. 
The Injury to the Fraenulum
This has occurred shortly prior to death. It has not occurred after death or during attempts at resuscitation. It could have been caused by the rough insertion of something such as a bottle into the mouth, or alternatively by a blow to the area of the central part of the upper lip, possibly a slap. The histological appearances suggest that it probably occurred at least a few hours prior to death. 
The Bruising on the Hands
In relation to the bruises on the back of the hands, these have again undoubtedly occurred in life. They were generally blue in colour suggesting they were recent and quite possibly had occurred around the same time as the injuries to the palms of the hand. One, however, was subjected to histology (Dr. J’s injury 15) and there does appear to be a little haemosiderin present although the quantity is small and the staining not of the very best quality.    
The presence of haemosiderin is said to indicate that the injury occurred generally a small number of days prior to death and it would therefore appear that this bruise at least is rather older than those on the palms of the hands (see below). 
The naked-eye and histological appearances of the bruising on the palms of the hands indicate that it has occurred during life, not during resuscitation and not after death. The histological appearances suggest that it only occurred a few hours prior to death. It is in general very difficult to bruise the palms of the hands because of the nature of the tissue which is relatively fibrous. It is not something that is easily done and does not occur after any sort of trivial traumatic event. The sort of forces involved would make any event which produced this bruising memorable to witnesses. It is possible that the bruising was caused by the hands being bitten but the only part of the injury which has appearances to particularly suggest this is the row of three small blue bruises on the back of the right hand. The other bruises do not in any way show any specific type of pattern to indicate a particular cause. It is possible that they were caused by biting but if so a little surprising that the skin on the back of the hand was not broken. 
In my opinion it is more likely that some or all of the bruises were caused by the palm of the hand being hit forcefully whilst the back of the hand was resting against something, or alternatively the hands being trapped and squashed in something like a door. Bruising to the palms of the hands in infants is distinctly unusual. The absence of any memorable accidental explanation and the presence of bruising on the palms of both hands rather than simply one are both highly concerning features which make it extremely likely that these injuries were deliberately inflicted.” 
136.	In cross-examination he agreed that the dating of bruises by visual observation was an inexact science. He postulated that the most likely mechanisms for the palmar injuries were either direct blows or the hands being trapped. The histology was not pursued with him in the light of my indication that it would be merely repetitious of the evidence of Drs J and L.
137.	Dr L is an experienced Home Office Pathologist. He was jointly instructed and made three reports: his main one; his first addendum dealing with the report of Dr H; and his second addendum dealing with the “bike-buggy theory”. I have set out above in my section concerning the key scientific evidence the general parts of his report dealing with the science of histology. There is also to hand a transcript of the telephone meeting he held with Professor S. 
138.	In his main report his first conclusion was as follows: 
“Despite a careful and detailed joint post mortem examination, no cause for death was identified; specifically, nothing was found morbid anatomically, histologically, biochemically, microbiologically, virologically or toxicologically to account for, or even to contribute to death.
I would add that, in my opinion, none of the injuries considered below, either singly or in combination, contributed to death.”
139.	As to the injuries identified on S at autopsy his conclusion was as follows:
“I have listed above, at pages 4-7, all the injuries identified at post mortem examination.
In my opinion, ALL were sustained prior to death, and I am entirely satisfied that NONE was sustained after death, including during resuscitation attempts, particularly as I believe that the finding of a “stiff jaw” during the latter points towards death a while before the body was found.  (his emphasis) 
It would, I think, be easiest if I were to consider S’s injuries under the headings and in the order used above:-
A) Scalp
The forehead bruises were relatively small (both 0.4 x 0.4 cm), but each clearly required significant local blunt force trauma for its production, especially as both involved the full thickness of the scalp.  It is important to point out that bruises are invariably non-specific – i.e. they give no clue(s) as to their cause.  Nevertheless, bruises of this size do tend to suggest to me that they may have been caused by finger tips – as in poking, prodding or firm gripping.
In contrast, the bruise within the substance of the scalp in the left anterior temporal region was significantly larger (1.5 x 1 cm), suggesting that a greater amount of force is likely to have been involved in its production, and that something larger than a finger tip (for example, a thumb during gripping) is likely to have been responsible.
As far as age is concerned, I do not think that any of these bruises was subjected to microscopic examination.  As stated above, it is notoriously difficult to estimate ages of bruises from photographs, but I note that all were described as being purple/blue in colour, with no evidence of any colour change.  Consequently, I think that it is likely that they probably occurred within 24 hours of death, and it is worth noting that this could, at least in theory, have been within a few minutes.
I am entirely satisfied that these bruises were not caused during resuscitation or in any other way after death.
B) Left Orbit
These are small purple bruises (0.5 x 0.5 and 0.4 x 0.4 cm), and, as such, attract very similar comments to those seen in the forehead and considered immediately above.
Consequently, I think that they too could have been caused by finger tips and that they are likely to have occurred within 24 hours of death.
C) Upper Lip Fraenulum
This was recently torn and, histologically, there is minimal but, I think, definite accumulation of polymorphs at the site of recent bruising.
The microscopic identification of polymorph accumulation, even if minimal, is an extremely important observation, because it indicates, quite unequivocally, not only that this injury must have occurred before death, but also that it must have occurred several (at least two, and probably 4-12 hours) before death.  In other words, this injury did NOT occur at or around the time of death, and it could NOT have happened during the resuscitation attempts. 
Tearing of the upper lip fraenulum usually follows an oblique or tangential blow (often a punch or a forceful slap) to the mouth which forces the upper lip to one side – thus stretching and, if sufficient force in involved, lacerating the fraenulum.  Clearly, a significant amount of force is necessary to produce such an injury – far more than associated with the normal handling of an infant.
It is said that deliberately forcing something into the infant’s mouth – for example, a bottle, a dummy or even a finger – can tear the upper lip fraenulum, but I agree with the comment in the document reporting the meeting that “work being undertaken in Cardiff seems to have gone against the bottle as a cause”.
In the absence of any acceptable accidental explanation for this injury, I can only conclude that it must have occurred non-accidentally.
D) Lower Lip
Unfortunately, this bruise is not seen clearly on the photographs provided, and Dr. J has not given its colour in her statement.
Consequently, I am afraid that I can offer no helpful comments about this injury, although I do wonder whether it could have occurred at the same time as, and during the same incident as, the upper lip fraenulum injury.
E) Ears
Both showed nodular changes with purple discolouration (left more than right).
I am aware that, on the basis of the histological appearances here, Dr. J considers that the sections “showed underlying vascular lesions which have developed as a consequence of a developmental anomaly and are therefore hamartomas”; for my part, I admit that I am uncertain as to the exact nature of the histological changes, and whilst I can appreciate Dr. J’s interpretation, I feel unable to exclude completely the possibility that all the changes seen have resulted from repeated local trauma.
Whether there are underlying haematomas present or not, there is evidence of bleeding into both ear flaps; the left showed considerable haemorrhage which appeared to be recent, and both showed collections of haemosiderin-laden macrophages which must reflect one or more previous episodes of bleeding.
Any bleeding, past or recent, into either ear must have resulted from localised blunt force trauma, and although I accept Dr. J’s point that “given the presence of the underlying lesion this may be relatively minor trauma in nature”, I believe that there would have had to have been significant local trauma.
I have to say that I find it very difficult to imagine how both ears of an infant can be subjected accidentally to sufficient trauma to produce significant bruising.
Had I thought that sufficient time was available, I would have suggested that a further opinion may have been helpful with regard to the histological appearances of S’s ears.
F) Left Forearm
Here, there were two separate purple, brown and yellow bruises (1.2 x 0.9 and 1.3 x 0.9 cm) which were approximately 1.0 cm apart.
These bruises were not subjected to histological examination, but the identification of yellowish discolouration around the edges indicates that they must have been at least 18 hours, and probably a few days, old at the time of S’s death.  Clearly, they did not occur during resuscitation.
These are quite sizeable bruises and, in my opinion, they must therefore reflect significant local blunt force trauma.  I agree with Dr. J that “the positioning on the arm is suggestive of being caused by a ‘nip’ or pinch”, and I would add the adjective ‘forceful’ if a ‘nip’ or a pinch had been responsible.
I note that in the documentary record of the meeting it states that “the bruise to the arm could also be a less clear bite mark”.  Whilst I can not exclude a bite as being responsible for these two bruises, I would have expected a bite producing this amount of bruising also to have penetrated the skin, and I therefore would have expected to see one or more individual injuries produced by the teeth.
As with the torn fraenulum, I would conclude by adding that, in the absence of any acceptable accidental explanation for this injury, I can only conclude that it must have occurred non-accidentally.
G) Hands
Above in this report, I have attempted to identify and to describe every one of the various injuries present on S’s hands – partly for the sake of completion and accuracy, and partly because I find the totality of the injuries on both hands very significant.
Thus, on the RIGHT hand, there were 13 injuries, comprising 10 blue bruises, one red/purple/yellow bruise and two abrasions (one with a probable associated bruise); on the LEFT hand, there were eight injuries, comprising five definite blue bruises and three probable bruises, together with five associated overlying abrasions.
Three of these areas of bruising were subjected to histological examination (v.s.).  Sections from both palms show local recent haemorrhage and some extravasation of polymorphs, but staining for haemosiderin is negative; in contrast, sections from the red/purple/yellow bruise on the back of the right hand show well established extravasation of polymorphs, and staining for haemosiderin is focally positive.
Consequently, histological examination has identified not only that bruising occurred during life but also that there is evidence of bruising of at least two separate ages.  The palmar bruising appears to have occurred several hours (probably 4-12) before death, whereas that on the back of the right hand must have been several days old (at least three) at the time of S’s death.
Given that all the bruising apart from that on the back of the right hand looks similar on the photographs, I think that it would be reasonable to presume that it all could (but not necessarily must) have occurred at the same time or during the same incident, and, as Dr. J points out in her first statement, it is also possible that the more recent hand bruising could have occurred at the same time as the injury to the upper lip fraenulum.
Although it is common to see bruises on the backs of hands, it is very uncommon to see bruising to the palms of hands and the palmar aspects of fingers, and it must be extremely uncommon for this bruising to be bilateral; I have never seen anything like this in an infant in over 30 years of forensic pathology.
It is said that the main reason why bruising only rarely involves palmar surfaces is that in these areas, dense fibrous tissue and restrictive fascial planes prevent the accumulation of blood, and that, as a consequence, and in order to create significant bruising, considerable blunt forces are required.  In contrast, the tissues over the back of the hand are much more lax, and, therefore, relatively easier to bruise.
It consequently must follow that, in order to produce the totality of the injuries on S’s hands, there must have been the repeated application of a very considerable amount of blunt force.
I find these injuries to S’s hands entirely non-specific – in other words, I can see nothing here which, in any way, helps to determine the mechanism(s) for their causation; indeed, I readily admit that I find it very difficult indeed to imagine how they may have been caused, especially as there is more bruising on the palmar aspects of both hands than on the backs.
In her second statement, Dr. J says that, in her opinion, “the most likely cause of the bruising to the hands is some form or compressive blunt force.  Possible mechanisms of injury include stamping or standing on the hands and also the trapping of the hands between unyielding surfaces”.  I can not disagree, but my professional experience of stamping on hands (albeit in adults) is that the resulting bruising is more severe over the backs of the hands, and that the bruises are not as discrete as those seen here.  In the same way, and for the same reasons, I would have though that trapping of the hands would also produce bruising which was more severe over the backs.
I note that the minutes of the meeting say that “the injury to the hands displays a circular appearance that could be explained by a bite mark.  In particular, three bruises to the palm of the palm of the right hand [sic] seemed to be tooth marks”.  Again, I can not disagree with this suggestion, but I think that if these palmar injuries had been produced by biting, the amount of force required for their causation would also have produced overlying abrasions and/or superficial lacerations from the edges of the teeth.
Dr. C, in his statement says “it is possible that the bruising was caused by the hands being bitten but the only part of the injury which has appearances to particularly suggest this is the row of three small blue bruises on the back of the right hand.  The other bruises do not in any way show any specific type of pattern to indicate a particular cause.  It is possible that they were caused by biting but if so a little surprising that the skin on the back of the hand was not broken”.  I agree.
Dr. C then continues by saying “in my opinion, it is more likely that some or all of the bruises were caused by the palm of the hand being hit forcefully whilst the back of the hand was resting against something, or alternatively the hands being trapped and squashed in something like a door”.  Again, I agree, but my thoughts about trapping of the hands are as above.
Despite my considerable difficulties in trying to explain these hand injuries, I can say that under no circumstances can I accept that they could have been caused by S’s older sibling (D aged 2 years and 5 months at the relevant time) – whether whilst playing “row, row, row the boat”, whilst in the “bike buggy”, or in any other possible context.  It is my opinion that they needed considerable more force for their causation than could be generated by a young child of this age.
The more I think about these hand injuries, the more I am inclined to the use of some form of blunt weapon as a means of inflicting them.  If so, then it would mean that, as far as the bruises on the palmar surfaces are concerned, the hand would have had to have been held open whilst the injuries were inflicted.  Under these circumstances, it is at least possible that a single, forceful blow with a weapon could produce bruising in more than one location – thus, for example, a blow with a linear weapon could have caused the bruising on the palmar aspects of the proximal phalanx of the right index finger, the proximal phalanx of the right middle finger, and the middle phalanx of the right ring finger.
In the absence of any acceptable explanation for these hand injuries, I can only conclude that they must have occurred non-accidentally.
H) Feet
As far as injuries are concerned, there was a purple bruise over the dorsum of the left foot overlying the 5th metatarsal (0.5 x 0.5 cm), and I think that photographs of the left foot also show apparent bruising over the dorsal aspects of the distal parts of the 3rd and 4th toes, and the proximal part of the 5th toe.  In addition, there was what appeared to be fungal infection of several toes of both feet (L>R).
It is unusual to find bruises on the feet of infants, and, as with bruises anywhere else, they must reflect local blunt force impact trauma.
The unequivocal bruise (over the dorsum of the left foot) is non-specific – i.e. there are no clues as to its possible cause – but it has clearly resulted from some form of local trauma.
I must say that the apparent bruising which I think that I can see over the left 3rd, 4th and 5th toes reminds me somewhat of that seen on S’s hands (v.s.), and so I think that consideration of all the same possible causative mechanisms must apply.
All the bruises which I can see on the photographs are blue/purple in colour – appearances suggesting that they were probably less than 24 hours old at the time of S’s death.  If so, I think that they could have occurred at or around the same time as most (but not all) of his hand injuries (v.s.).
In the absence of any acceptable accidental explanation for the definite bruise (and the other three bruises if the Court accepts that they exist), I can only conclude that it/they must have occurred non-accidentally.
The apparent fungal infection does seem to me to be somewhat severe, but this is outside my field of expertise.”
140.	In his first addendum he essentially defers to, and agrees with, the opinions of Dr H. In his second addendum he admits the possibility that conveyance in the buggy might have caused the ear injuries but considers this to be unlikely. In his oral evidence, when recalled, he stated, having seen the actual buggy, that he considered this possibility to be very unlikely. He did say, however, that he thought it likely that some injury would be caused, probably to the head.
141.	In his evidence-in-chief and under friendly cross-examination from Mr S he confirmed his findings, which were, to say the least, categorical. Under adverse cross-examination on behalf of M and F the following statements, admissions and concessions were made:
i)	The resuscitation attempt could be described as aggressive.
ii)	Such attempts could cause widespread pseudo-bruising, but not, in his opinion, the actual bruising here.
iii)	If S had a significant bleeding disorder then he would have expected to have seen even more bruising than was present.
iv)	Polymorphic migration could be a reaction to either injury or infection. The presence of neutrophils does not enable one to tell disease from trauma.
v)	The high lymphocyte count here was a sign of the body fighting infection.
vi)	The high thrombin and reptilase times noted by the microbiology lab could be features of a clotting derangement. 
vii)	He had not undertaken any post-mortem examination on an infant who suffered from disseminated intravascular coagulation (DIC).
viii)	The commonest cause of DIC is infection.
ix)	He had possibly been over-dogmatic in the conclusion he drew from the evidence of the forensic scientist.
x)	The punch or slap needed to tear the fraenulum would not necessarily leave outward signs.
xi)	The injuries to the palms were very mysterious, and even the hypothesis of being beaten with a weapon like a ruler or cane did not really fit with the appearance of the bruises.
xii)	The bruises to the ears could in his view really only have derived from repeated punching to each of them.
xiii)	The wounds were only consistent with repeated sadistic treatment of a tiny baby.
xiv)	All biological science is inexact, in contrast to the laws of mathematics and physics.
xv)	(as I have recorded earlier), almost all the eggs are in the basket of histology.
xvi)	(as I have recorded earlier), there is a huge dearth of histological evidence on babies and infants.
xvii)	(as I have recorded earlier), a staph infection would seriously increase production of cytokines.
xviii)	(as I have recorded earlier), to his knowledge nobody anywhere has been held responsible for the infliction of wounds by reference to this histological evidence.
xix)	While he maintained that the conveyance in the bike buggy was “very unlikely” to have caused the wounds to the ears he accepted that as a matter of mechanics the faster the bike went the more vertical and lateral movement there would be of the buggy with increased scope for damage to the ears either by contact with the strut or the wheel, or with D’s head. 
142.	Professor S, was jointly instructed to report on both children. He wrote a main report and an addendum about the bike-buggy theory. I also have the transcript of his meeting with Dr L. He has been a busy general paediatric consultant for 20 years. He has published a wealth of articles, including three on the ageing of bruising in children.
143.	In his report he states:
“I have not met the parents or examined either D or S2 myself and I was not involved in any of the care of S prior to his death or at the time of his death. Everything I know about this family is from the documents I have been sent. I have not discussed the case with any of those involved.”
The same is true of Drs L, H, G, and C, and of Professor H. Drs J and W did not care for S in life.
144.	 From his lengthy report I extract the following passages:
“Features of injuries in children which give rise to suspicion that they are non-accidental:
a.	delayed presentation
b.	injuries on parts of the body which are not easily explained by a single accident
c.	injuries which appear to be of different ages
d.	injuries which occur at unusual sites for accidental injuries. Research has shown that non-accidental soft tissue injuries occur more commonly on the areas of the face, head, neck and trunk whereas genuine accidents more often injure the limbs.  Injuries to the pinna of the ear are almost never seen as a result of true accidents but are not an uncommon site of non-accidental injury. 
e.	injuries in a pre-mobile infant
f.	inadequate explanations
g.	changing or different explanations
h.	there are a few injuries which are particularly suggestive of non-accidental injury. Petechial (pinpoint) haemorrhages rarely arise due to accidents.  Symmetrical petechiae on the cheeks can arise from vomiting, crying or choking.
Petechiae
There are a few injuries which are particularly suggestive of non-accidental injury. Slap marks sometimes cause petechial (pinpoint) haemorrhages whereas petechial haemorrhages associated with bruising rarely arise accidentally.  In contrast, symmetrical petechiae on the cheeks can arise from vomiting, crying or choking.
Pinprick or petechial haemorrhages can be a sign of a clotting disorder or indeed of meningococcal infection but if neither of those are the case, patechial bruising on the cheek of child who was fifteen months old at the time is most likely due to a slap.  If there were petechial bruising on both cheeks and around the eyes and the child was unwell it could be due to strenuous vomiting or choking and is sometimes seen after very strenuous paroxysm of coughing.  There is no indication that any of these applied to D at the time. 
Petechiae appear soon after trauma, within minutes or a few hours, not days.  My experience from petechiae due to all four recognised causes (infection, coagulopathy, coughing or retching, and non-accidental injury) is that they fade and disappear rapidly.  They always disappear within a week and sometimes they are fading by a few hours and disappear by a day.  This sequence can therefore be faster than for larger bruises.
Harmatomae
It would be extraordinarily unusual in my experience for a child to suddenly develop a hamartoma overnight, a developmental abnormality, at the age of seven months quite spontaneously.  I am not a pathologist but I wonder whether it is possible that the numerous small blood vessels which were seen under the microscope by Dr. J and which led her to conclude that these were a hamartoma could have developed as a consequence of the healing process following a trauma or some other problem giving arise to the ear swelling at seven months of age?  
Irrespective of possible causation, suffice to say that all the research shows that children under six months are very unlikely to sustain bruising and this is worth noting as part of the overall picture.
It does not seem likely, in my experience of hundreds of children with vascular birth marks (hamartomas) that a bruise behind the ear could be due to a hamartoma of the pinna of the ear.
Bruises 
In the body of my report I have set out that most of contemporary descriptions were either bruise or cauliflower ear. In my own personal experience over 25 years, I have only seen the kind of swelling and discolouration described in the photographs following traumatic injuries in older children and adults as a result of contact sports.  I describe my experience now of two medico-legal cases when either the child concerned or a sibling had a skull fracture and where very abnormal appearances of the ear as described in this case were seen. One of these case were attributed to something called a pseudocyst of the auricle, a condition which neither I as an experienced paediatrician nor an experienced ear, nose and throat surgeon nor an experienced dermatologist had seen or considered. Given the appearance of blood at the time of post – mortem within the lesion within the ear, I think this idea of pseudocyst is even more implausible in the case of S. Dr J has raised a possibility of hamartoma but it does not seen to me that would fit either the temporal sequence or the appearances. 
Ageing of soft tissue injuries is notoriously difficult, even from colour photographs.  I have personally published research demonstrating this.  Contemporaneous ageing (ie from the appearances observed at the time, rather than from photographs) of genuine accidental injuries of known age is also difficult.
Nevertheless, relative ageing in loose time frames is probably easier. Eg bruises containing yellow, brown or green colouration are likely to be older than bruises which appear red, blue or purple. This is due to changes in the colour of the haemoglobin pigment in red blood cells as it is broken down.
Fraenulum
In such a young infant the most likely cause of the torn fraenulum is force feeding. Dr J is clear that the injury was caused not at the resuscitation but before death.  I have at one occasion seen a torn fraenulum in an older child who fell off a slide in the park. The torn fraenulum was associated with bruising of the lip and it was not an isolated finding.
The degree of force required would be excessive and not that involved in normal feeding of a child. It is likely to be the result of a spoon or some type of cutlery or a feeding bottle being forced up between the top gum and the upper lip. This is a type of injury which is most classically seen in a boxer.
Nosebleeds
Nosebleeds in young infants are very rare.
Mobility
Between 2 ½ and 4 ½ months he would acquire the ability to be able to push himself up for from a prone position using his arms (but it is rather like a press up with his legs remaining on the bed) and this would be the greatest height which his head could fall at this age unless he was dropped by someone else.
Few infants start crawling before 6 months. The earliest I have seen is 4 ½ months. About 50% of all infants can crawl at 7 months; 75% can do so at 10 months and 90% of all infants have mastered it at 11 months. 
25% of infants can bear weight on their legs by 2 months and 90% by 4 ½ months; 25% of infants can roll over by 2 ½ months and 90% by 5 ½ months;  25% of infants can stand with support by 6 ½ months; 25% of infants can be pulled to a standing position by 8 months;  25% of infants can stand for 2 seconds by 9 months;  25% of infants can walk well by 11 ½ months..
Feet
If some of these samples were from foot lesions, given no fungi were isolated but staphylococci were, it is possible that he did in fact have impetigo which could explain crusting, scabbing and bleeding and would not respond to antifungal treatment.
This is the second case I have been involved in where a child under 8 months of age has presented with marked swelling and reddening of the ear and on both occasions the swelling contained blood. On one occasion the presenting child incurred a skull fracture and in this present case, the sibling had a skull fracture. I have never seen this appearance in any other children of this age. Everyone who has given contemporaneous descriptions in both cases described what appeared to be bruising or a cauliflower ear (typical of that seen from trauma in contact sports such as rugby). Expert witnesses in both cases have concurred that they have never seen such appearances other than due to trauma. However, in the first case, the court eventually attributed the appearances to a rare cause due to pseudocyst of the auricle (which itself may be a consequence of repeated slapping) and in this second case the possibility of a hamartoma has been suggested. I am concerned that I have never seen such appearances in my whole career in an infant due to natural causes, nor have I met or heard from anyone else who has. In contrast, in both of these two cases, there were other reasons to be concerned about trauma.
I have seen some fairly bad cases of fungal foot infections in my time but nothing like this with such a degree of haemorrhage, certainly not in an infant. 
All I can say I have never seen such a severe fungal infection of the feet in a young infant and I have never seen such an infection accompanied by haemorrhage to this degree.
Injuries to S
At the time of his death, S had sustained 53 separate injuries. It is probably not going to be fruitful for me to go through each of these and state whether they are organic, accidental or non-accidental and likelihood of each possible cause. 
I set out at A to H above features of injuries in children which give rise to the suspicion that they are non accidental. All of these features are present at one time or another in relation to S.”
145.	In his evidence in chief Professor S confirmed his report but made this important observation:
Q. 	… Professor (H) opines that the raised lymphocytes found probably reflects very serious illness maybe indicative of infection. And he continues by referring to the possibly infected feet in positive cultures and suggests that the experts on infection in children be asked to specifically exclude this as a causative factor in the death. Now is that a question you can answer? ‑ A. I believe I can assist the Court, yes.
Q. 	And what is the answer? ‑ A. I think I am the only person in the proceedings that I have read who has raised the possibility that the foot infection is not solely a fungal infection, but the appearances could be consistent with a bacterial infection. That then leads to the hypothesis that if those bacteria got from the feet into the bloodstream they could cause an overwhelming illness and death. I think that is possible but not probable for the following reasons. 
Q. 	Yes please? ‑ A. The first is that the pathologists found no evidence of a cause of death and indeed would probably have ascribed this by exclusion as a cot death had they not found injuries which they could not explain. They didn't find evidence of the cause of death. The second is that a high lymphocyte count whilst probably a sign of stress in this case, if it was an infection would suggest a viral infection. Whereas bacteria would cause the white cells to be raised. I think the third reason and least compelling of the three actually is that S by all accounts appeared to be well when put to bed and not overtly ill when seen at 5 a.m. I say least compelling because it is plausible that bacteria getting from his feet into his bloodstream could cause a fever and we know that fever can contribute to cot deaths but wouldn't explain the other features found in the case and children can deteriorate very rapidly. And in a dark bedroom at 5 a.m. and brief cursory contact with the child it might not be apparent to a parent that the child had developed a fever, an infection.
Q. 	So what, if any, conclusions do you draw? ‑ A. On balance of probability there are really no features in life or in death that suggest this child had an overwhelming septicaemia, blood infection. I think it is no more than a possibility.
Q. 	There are of course degrees of possibility can you attempt an estimate of the degree of possibility? ‑ A. I don't think it's getting close to balance of probability, it's not marginal. If that helps, my Lord. 
…
Q. 	[Impetigo] Can be anywhere? ‑ A. Can be anywhere. So these samples I can't identify where they come from, but I list them by page number. One was thought to be by whoever reported it the microbiologist, one is staphylococcus, typical skin bug which if it got in the blood stream would be extremely serious. 
146.	Under cross-examination by Mr S, Professor S stated:
Q. 	Professor S, I am asking questions on behalf of the Local Authority. Just following on in relation to these tests. Having explained them in more detail does your view remain that in terms of the likelihood of there having been a severe infection here it is unlikely and, as you clarified earlier, not marginal not close to a balance of probabilities? ‑ A. Let me be absolutely clear what I am saying. I do not think anyone has suggested that a cause of death has been found in this case, and I am quite clear I think in my mind that had the injuries not been found I suspect, it is for you to ask them, but I suspect the pathologist would have said that this was a cot death. Rather older than the average and it's summer which is unusual, but it happens. It is possible that, we know that cot deaths can be precipitated by overheating and we know I think from reading their evidence that S probably had a cold or upper respiratory tract infection running up to this night, that in itself could be enough to cause a temperature and to cause overheating. If in addition he had some blood poisoning easy to imagine a high fever coming on in the middle of the night and leading to a cot death. That is going towards cause of death. To my mind it does not explain the unexplained injuries that were found at post mortem and clearly it does not explain the torn fraenulum or the other injuries in the other two children which is for his Lordship to decide whether they were fact or not, not for me. So I want to be absolutely clear that I am trying to assist the Court as to potential mechanism and cause of death.
Q. 	But leaving that topic for the moment is it fair to leave it on the basis that infection as a cause of death your view remains marginal in terms of probability or likelihood? ‑ A. Marginal in terms of explaining these other findings. It may have been a contributory factor to what otherwise would have been a cot death, sadly.
Q. 	Then in relation to as an explanation for the injuries, and not going over the evidence you have already given in terms of the distribution and the clusters, it is very unlikely. Is that a fair summary of your evidence? ‑ A. Yes. I will not repeat it, I gave 3 reasons why I think it is unlikely that there was an overwhelming septicaemia, but I accept it's a possible precipitant of a cot death. I have said that even if that were the case it doesn't explain these other findings. The idea of a what we call a coagulopathy or bleeding diathesis it is a terminal event of an overwhelming infection and this doesn't look like this in my experience. …
MR. JUSTICE MOSTYN:   This is something I asked you a little while ago. Can blood poisoning or septicaemia be present for an appreciable period? ‑ A.. No.
Q. 	One is reminded of Rupert Brooke being bitten by a mosquito and being dead the next day from septicaemia. I mean it happens, doesn't it. It can't just exist in a low grade way for an appreciable period? ‑ A. Well there are a small minority of conditions which are incredibly rare, subacute bacterial endocarditis, SBE, is a condition that you can be walking around for weeks. You are not well, you are unwell, but you don't drop dead and die. But leaving that aside blood poisoning in children tends to be overwhelming and they deteriorate very rapidly and become ill incredibly quickly and are very, very ill, I would say within 24 hours. … And just to be absolutely clear for the record, if S had had SBE that would be something that would be very apparent on post mortem.
I just want to be absolutely clear. To be absolutely clear it is possible for both things to be true, it is possible that S had a genuine SIDS cot death, albeit rather older than average at an unusual time of the year but all of that happens. It is possible for that to be true and also to be true that he had unexplained inflicted injuries. The two can both coexist as I am sure you are aware, I was not trying to link them.
147.	He made this observation about parents in general:
As a generalisation my experience is that parents are rather assiduous observers of their children, particularly young children. We teach medical students to listen to the parents, they are telling you the diagnosis. The basis of that maxim is that no‑one knows their child better than their own parents. So we listen carefully to what they say. They dress their children, they bathe them, they feed them, they are in intimate contact with a young child if not quite 24/7 almost so. So they tend to be good witnesses of what is going on in their child's life, yes
Q. 	The bruising shown to the right ear we know was not presented for medical attention. It ought to have been presented for medical attention, is that your opinion? ‑ A. Well let me answer that in three ways. My experience would suggest that most parents, this is a generalisation, would present a child with unexplained bruising to the ear, or at least ask advice. Not least because it might betoken some of the underlying diseases that we may come back to and we have been discussing in these other reports. Secondly, they might not seek attention if they witnessed and knew how it was caused. So if they saw a sibling strike that baby on the side of the ear with a cricket bat and saw the injury caused, no they might not seek attention because they might quite legitimately say well he has got a bruised ear and we know how it was caused and do something to stop it happening again. The third thing would be that they did behave like most parents in my experience, come July they did seek medical attention for something that was clearly troubling them. That would be my experience of most parents, in a young infant they wouldn't ignore this. 
148.	Under adverse cross-examination on behalf of M and F the following statements, admissions and concessions were made:
i)	It is not for him to make any judgment as to whether a report of anything by a third party was or was not accurate.
ii)	“It is actually incredibly difficult to ascribe any one bruise or injury to a cause or mechanism. So if you go back to the photographs I was shown with the bruising on the cheek, I cannot say that that was caused in such and such a way, all I can say is that it is very unusual in young premobile infants to have these injuries but I can't say how they were caused.”
iii)	The medical profession has cautioned against ageing of injuries from photographs.
iv)	These children were very much out in the community and were not hidden away.
v)	Older children do cause injuries to their smaller siblings. There may be a deal of under-reporting of this.
vi)	As to the injury on S’s forearm, it could be a nip but “actually what was done I have no idea really”.
vii)	Caution had to be exercised in positing a causative reason for the torn fraenulum.
viii)	The appearance of the ear was so extraordinary that the GP should have sought expert opinion as it could well be indicative of some major bleeding disorder. He has never seen bruising of this nature in abused children. Similarly he had never seen anything like the palmar bruises, neither in children who had been resuscitated, nor in abused children, nor in dead children. 
ix)	He did not want to speculate on possible mechanisms for the bruising to the feet, or in fact on any of them.
x)	He allowed for the possibility of a bleeding disorder here. The record by M at the nursery of occasional nosebleeds when sneezing is possibly consistent with a bleeding disorder. Nose bleeds are “extraordinarily uncommon” in infants.
xi)	An overheated environment is a really big risk factor for cot death.
xii)	Medical science is always moving on and may have answers in the future where we do not have them now.
xiii)	A microbiology test of blood will not identify the scale of any problem, just its presence.
xiv)	As a mechanism the insertion of the Guedel tube is a possible explanation for the broken fraenulum. 
149.	In his addendum Professor S wrote:
“Having seen the video and the photos, it does seem to me plausible that a child being carried at speeds of up to 25 miles per hour off road in such a buggy at S’s age without a cycle helmet could sustain significant trauma to his head and ears.  Indeed, now almost three years after the event, this is in keeping with what I postulated throughout my report which was that I had only seen such traumatic injuries to the ears in older children who had been involved in contact sports or who had been struck on the ear.”
However, he was extremely critical of F for doing this. He wrote:
“…were a parent to cycle at even 10 to 15 miles per hour with a child of a few months in a buggy without a cycle helmet over rough terrain against the manufacturers’ recommendations and all common sense, as a paediatrician I would consider this reckless in the extreme and well below the standard of care I would expect any reasonable parent to deliver to their child.  It would amount to the adult putting their pleasure and excitement and love of speed and sport over the most basic human duty to care appropriately for a young child.  If such behaviour were to cause injury to a child and the adult were to continue or repeat the process on a number of occasions, that would be even more serious in my view but I would wish the court to be clear in my opinion as a paediatrician, even to do so once would amount to significant neglect.”
150.	Professor H is a Paediatric Haematology Consultant. He provided a report and gave oral evidence by video link. 
151.	Professor H provided a helpful summary of his conclusions which I set out in full:
“1.	I was able to identify definite petechial haemorrhages on the face in the post mortem photographs and periumbilical bruising in an unusual linear pattern. 
2. Blood samples taken from the parents and sibling of S were normal apart from an irrelevant finding of low iron stores in his sister D. 
3. The blood results from S are grossly abnormal but extremely difficult to interpret.   Blood taken during asystole is subject to defibrination which is the probable cause of the extremely abnormal clotting tests. 
4.	The raised lymphocyte count in S probably reflects very severe illness but may be indicative of infection.   In view of the possibly infected feet and positive cultures, the experts on infection in children can be asked to specifically exclude this as a causative factor in the death. 
5. The blood tests rule out causes of bruising due to low platelets.   The family studies make it very unlikely that von Willebrand disorder was present.   They also make it unlikely but not impossible that the commoner albeit relatively rare severe disorders of clotting factor protein deficiency e.g. Haemophilia A & B were present in S. 
6. The blood tests do not rule out the very rare disorders of platelet function, factor XIII deficiency and alpha 2 antiplasmin deficiency which are very unlikely due to rarity and lack of family history and lack of prior serious problems.   If the Court decides to pursue these very unlikely possibilities, then parental testing could be carried out.   These disorders can lead to very easy and sometimes spontaneous bruising.”  
152.	In her final written submissions Ms B produced a helpful summary of the oral evidence of Professor H which I am satisfied corresponds to the transcript, and which I now draw on, with some editorial changes.
153.	He explained by reference to his report and to the article by Dr Leisner and Kate Khair commissioned by him the difficulty in differentiating whether bleeding or bruising is normal or abnormal. Professor H made clear that there is a huge range, from normal bleeding to grossly abnormal bleeding with a large grey area in between.  He confirmed that, even in severe disorders, one would not necessarily see signs of bruising from a very early age. 
154.	As regards testing, it was possible to test for congenital disorders, although they would not always show up on testing. Testing for acquired disorders was far more complicated.
155.	With regard to haemophilia, Professor H confirmed that the mother might be a carrier, who had passed the disease on to S, without her tests being abnormal. The majority of haemophiliacs present only once they are toddling. Haemophilia remains a possibility in S’s case.
156.	With regard to blood disorders which remained possible in S, despite the results of the testing of the parents, Professor H said that the only acquired disorder which could be excluded was a platelet disorder, since S’s platelet count was normal. The rest of S’s results, in particular the lymphocyte count, were grossly abnormal and, although likely to be artefactual changes (due to the dying process) they were also consistent with the possibility that S had developed one of the acquired blood disorders (other than a platelet disorder). There was a range that was possible on the results seen, in particular consumptive coagulopathy or disseminated intravascular coagulation (DIC). Severe illness and severe infections are the commonest initiating facture in these conditions.
157.	While he was aware that the pathologists considered that a blood disorder should be discounted, Professor H was clear that it remains a possibility. 
158.	Whilst it was very unlikely that S had a severe congenital bleeding disorder, this could not be ruled out. A more minor bleeding disorder was unlikely but possible.
159.	Professor H would not accept that S would necessarily have had a severe bleeding disorder for this to explain the bruising to his palms. But he had seen such appearances only twice in a long career, both times in patients with bleeding disorders (one a severe disorder).
160.	Professor H emphasised how quickly a baby may become desperately ill and that the problem in S’s feet and the upper respiratory tract infection from which he was suffering might be relevant here. He recommended that this issue be raised with the paediatricians. As to DIC, Professor H was clear that there is no gold standard test on histology or pathology. DIC needs to be diagnosed in the light of the haematology clotting tests and could not be ruled out in this case.
161.	Professor H declined to defer to the pathologists in relation to injuries resulting from bleeding disorders and their causation. He pointed out that it has more often been the case that children in whom non-accidental injury has been suspected have turned out to have a blood disorder than vice versa.
162.	In summary his evidence was that both congenital blood disorders of certain types and/or an acquired blood disorder (such as DIC) are unlikely but possible in S’s case. 
163.	Dr H, Consultant Histopathologist, prepared a report, and an addendum and gave oral evidence. She was jointly instructed and was asked to consider the histopathological findings relating to the ear lesions of S.
164.	In her report she wrote:
“Auricular haematoma and cauliflower deformation of the ear are most often observed in contact sports (boxing, wrestling and rugby). Artistic descriptions of damaged ears exist from 500BC. In the 19th century, questions were raised as to whether some cases of this condition had a non-traumatic cause. Several authors at that time commented on the occurrence of this condition in the so-called “insane”. By the onset of the 20th century however, it was agreed that these lesions were indeed trauma induced and that the frequency of auricular haematoma in the insane was in direct proportion to the agitated behaviour of these patients and their numerous traumas. Two papers from the 1970s regard auricular haematoma as arising due to blunt trauma. 
One instance in which I can find reports of cauliflower ear without a clear cut history of trauma is in individuals with opium addiction. This association is described in a couple of historical papers discussing elderly Chinese men who have heavy opium dependency who spend prolonged periods of opium induced slumber while lying on beds with hard wooden pillows, common to the opium dens at that time. 
In terms of the cause of the ear lesions, the histopathological features fit entirely with a diagnosis of auricular haematoma / cauliflower ear. There are no features to suggest a diagnosis of any of the other listed possible causes of ear lesions. Specifically, there is no pseudocyst and the vascular proliferation is neither hamartomatous or neoplastic, and is entirely in-keeping with reparative vascular granulation tissue. 
In terms of the cause, the literature pertaining to this condition states a clear association with blunt trauma. The degree of impact / trauma is best compared to that suffered by boxers, wrestlers and rugby players when participating in their respective sports, since these are the only groups of patients whom suffer with this type of lesion with any frequency. … “
165.	Her review of the 14 histological slides from the two ears was highly technical and was  as follows:
“Right ear (smaller tissue piece)
This is a piece of pinna, consisting of non-ulcerated surface epidermis, underlying dermis and deep to this, a cartilaginous plate. 
There are significant abnormalities. A prominent finding is the presence of separation of the dermal connective tissues from the underlying cartilage with formation of a cleft. This is in the tissue layer referred to as perichondrium. Within this, there appears to be some deposition of fibrin which is the result of coagulation of extravasated blood. 
Adjacent to this, there is a proliferation of blood vessels embedded in cellular fibroblastic connective tissue. The arrangement of the vessels is fairly haphazard, they show some mild variability in size and they are predominantly of thin-walled capillary type. The type of fibrous tissue in which they are embedded, is consistent with that of immature scar tissue being formed by haphazardly arranged plump fibroblasts that are separated by immature non-fibrillary collagen.  There is minimal (and no significant) active inflammation although quite large numbers of macrophages which contain finely granular pigmented material consistent with haemosiderin (breakdown products of red blood cells, occurring 3 days or more after damage and leakage of blood vessels) are present. 
The degree of vascular proliferation, size, type and arrangement of blood vessels and type of fibrous tissue within which these are embedded are typical of reparative granulation type tissue. Below and also when answering question 1, I will explain why I don’t believe that this vascular proliferation is the result of a vascular hamartoma or neoplasm. I have considered carefully whether this degree of vascular proliferation could represent an underlying lesion. Reactive vascular proliferations (either due to injury, trauma or inflammation) are very common findings in routine diagnostic histopathology I believe that the degree of vascular proliferation seen in this ear lesion is in-keeping with that. Today, just prior to reviewing this case, I reported several biopsies from a patient with excessive healing / scar tissue removed from the site of a recent operation and found a comparable degree of vascular proliferation with that seen in this ear. 
A point worthy of note is the phenomenon of zonation. The predominantly vascular proliferation is seen more obviously adjacent to the perichondrial cleft. As we move away from the cartilage, the tissue becomes less vascular and more fibrotic with the fibrocartilage seen at the most peripheral aspect of the lesion.  This phenomenon of zonation, central immaturity merging into peripheral maturity, is characteristic of a reactive (therefore non-hamartomatous and non-neoplastic) process and well described in many basic textbooks of pathology. 
An additional and highly significant finding is the presence of some regenerative tissue with appearances that are hybrid between scar-like fibrous connective tissue and cartilage. This tissue is regenerating fibrocartilage. 
The EVG elastin stain shows presence of a fine network of elastic fibres within the normal dermis. Within the fibro-cartilaginous tissue and also the scar tissue, there is no evidence of elastin fibres. This would suggest that this is not yet a fully matured scar. 
The Perl stain confirms that the pigment within the macrophages is indeed iron derived, and therefore, that of haemosiderin. The immunohistochemical stains for CD31 and CD34 which are both markers of vascular differentiation highlight the prominent network of vessels which are variable in size and highlights the zonation. 
Left ear (larger tissue piece)
This is skin of pinna including intact, non-ulcerated epidermis and underlying dermis. There is also some deeper tissue, formed by a plate of cartilage. The most prominent abnormality at this site is that of a large sub-perichondrial haematoma. This is in the form of collections of fresh haemorrhage with detectable red blood cells, and also large masses of pink material, in keeping with fibrin. This then merges with a layer of highly vascular tissue. The vascular tissue contains predominantly small capillary sized vessels that are rather haphazardly distributed and variable in size. There is then merger of this highly vascular tissue with a zone of cellular fibroblastic tissue resembling immature scar tissue. Again, the zonation described above is conspicuous. 
In some of the slices examined, there appears to be destruction of the cartilaginous plate by this highly vascular reparative tissue. 
Within the reparative tissue, there are detectable plump spindle shaped fibroblastic cells and also some plump, more rounded cells which are highly suggestive of immature chrondroblasts. This would suggest colonisation of the wound by both fibroblasts and chrondroblasts, although no distinct reparative fibrocartilage is identified at this site in the tissue examined. 
On the opposing cartilaginous surface, i.e. that not containing the haematoma, there is a prominent proliferation of small capillary sized vessels. These are located within the perichrondrium. This presumably represents an attempt at increasing the vascularity of the cartilage in an attempt to prevent loss of vitality due to loss of perfusion on the haematoma containing side.
The EVG elastin stain again shows a network of fine lasting fibres in the normal dermis and absence of these in the cellular fibroblastic tissue meaning that this is not yet a fully mature scar. 
Perls stain confirms presence of haemosiderin laden macrophages as above and the CD31 and CD34 again decorate the prominent vascular proliferation. 
In summary, tissue from the left and right ear show slightly different histological features but the appearances are those of a continuum seen in a reactive healing or regenerative process. The healing process can be triggered by tissue damage as a result of infection, trauma or surgical intervention. There are no features of infection here (a lack of any significant inflammatory cell population) and there is nothing in the history provided to suggest any surgical intervention at this site. The only remaining explanation is that of trauma and the presence of a haematoma would also greatly favour trauma over infection. 
The presence of the haematoma in a perichrondrial location is significant. The formation of regenerative fibrocartilage is also significant. 
The histopathological findings correlate with the descriptions of auricular haematoma evolving into cauliflower ear type deformity (see below). I can see no evidence of any pre-existing or underlying lesion.”  (Her emphasis)
166.	In her oral evidence she confirmed her findings but under cross-examination the following concessions and qualifications were established:
i)	She acknowledged that it was a mystery that, despite the appearances on histology, no injury had been seen to the right ear when S’s body was examined. 
ii)	She could entirely see why Drs J and W had considered the lesion to be a possible harmatoma because of the degree of vascularity seen and the fact that it was very florid, and of a very peculiar appearance.
iii)	The long-standing changes were difficult to explain if this was a harmatoma, although it was quite possibly the case that this had resulted from a previous knock.
iv)	She only had a snapshot to look at within the samples she had.
v)	(As I have recorded earlier) in relation to the early appearance of neutrophils in response to injury, she put this as a matter of minutes, typically receiving the samples from theatre within 30 minutes. She similarly recognised that infection would produce a similar reaction.
vi)	She contemplated a clashing of heads as a possible mechanism. She said she could “see no reason why one solitary incident couldn’t set it off”.
167.	In relation to the bike buggy, Dr H accepted that the mechanism envisaged by S riding next to D in the buggy, moving at some speed over bumpy terrain would fit with a traumatic cause for the ear lesions.
168.	Dr G, Consultant Microbiologist, was jointly instructed during the course of the case. He wrote a short report and gave rather indistinct evidence by video link. I set his report out in full:
“Baby S had a short (8 month) life with several visits to his doctor for various ailments including upper respiratory tract infection (URTI), ear swelling, and possible fungal infection in a foot. Other skin breaks/abrasions had been noticed, but none apparently infected.
16 days before death he presented again with an URTI, probably viral.
He presented moribund at Hospital but could not be revived. Post mortem was not conclusive. Ante mortem and post mortem microbiology culture results did not reveal any suggestion of bacterial infection.
In particular, nasopharyngeal secretions and nose swab, collected grew Staphylococcus aureus. This almost certainly  represents colonisation in the absence of post mortem findings of respiratory tract infection, most commonly pneumonia. E coli, also grown from nasopharyngeal secretions is of unlikely significance. Blood cultures showed clear contamination at collection (a common problem) and no evidence of infection. Two wound swabs (?site) were reported as growing nothing of clinical significance and in the absence of post mortem signs of infection, were unlikely to be a source of systemic infection. Finally, a throat swab grew coliforms and post mortem lung tissue  grew E coli, both  of doubtful significance. The latter is a common post mortem finding and the former could reflect recent antibiotic treatment. 
There was, however, a mild systemic lymphocytosis and the CSF gram stain also suggested a lymphocytosis, raising the possibility of viral meningo encephalitis, possibly related to the prior URTI. It would be interesting to know whether the post mortem examination of the brain and meninges revealed any abnormality consistent with this. I note that limited pre mortem virology of conjunctiva, and post mortem virology of lung tissue was negative. I cannot comment further on this as I am not a Virologist.
In conclusion, none of the microbiology cultures are suggestive of infection, so it is unlikely that his death was due to bacterial infection. This seems to be confirmed by the non-specific post mortem findings. Up to 20% of children carry Staphylococcus aureus in their noses as a normal commensal. While this can, and frequently does, become pathogenic and cause infection, there is no evidence this happened here. The only evidence of possible infection is the lymphocytosis which would, I believe, be compatible with a meningo encephalitis. Such a diagnosis is a possible cause of death but should have been obvious at post mortem. I am not a virologist, so cannot comment further on this aspect of the case.
Finally, I don’t believe that the absence of ante mortem samples is a problem in trying to refute or confirm bacterial infection in this case.”
169.	In his oral evidence the following qualifications and concessions were established:
i)	He agreed (with the strong caveat that he is not an expert in such cases) with the findings of the paper “Difficulties in interpretation of post mortem microbiology results in unexpected infant death: evidence from a multi disciplinary survey", from Great Ormond Street and the UCL Institute of Child Health London. He stated that the abnormal microbiology results here arose because of the microbes which inhabit the surface of any person and which are essential to healthy human life. He discounted the evidence of infection in S’s upper respiratory tract on the basis that 20-30% of the normal population carry staphylococcus aureus in their noses.
ii)	He doubted that the findings of E-coli were of significance since this is ‘usually’ due to post mortem artefact. Based on what he regarded as no ‘obvious’ sign of bacterial infection pre or post-mortem, he said it was very unlikely that bacterial infection caused S’s death. 
iii)	He acknowledged that there are cases where bacterial infection which is fatal is not seen in the blood. He could not exclude the possibility that sepsis caused death but was not seen in the microbiology.
iv)	Whilst stating that it was beyond his expertise, he allowed for the possibility that the URTI developed into encephalitis and resulted in death, although he said (despite it not being within his expertise) that he would have expected to see evidence of this in the meninges.
v)	Asked by me to clarify whether, absent contaminants, the abnormal microbiology results were part of a disease process, Dr G agreed that this was so.  
170.	A Senior Forensic Scientist examined the bottle, bib, sheet and grow-bag in S’s cot on the day of his death. She made a police statement and gave evidence before me. She made the following observations:
i)	Milky staining mixed with blood staining were present on the front and lower back of the bib. She opined that this blood may well have originated from S’s mouth as a result of wiping.
ii)	Light smears of blood were detected on the lower inside back of the grow-bag. In her oral evidence she said that this could relate to a small weeping injury
iii)	Blood staining overlaid with saliva staining was detected on the top right hand corner of the sheet.
Summary of the arguments of Counsel
The argument on behalf of the LA
171.	Mr S, for the LA, argues that the expert medical evidence before the Court is, in all significant respects, agreed; it is cogent and compelling; whilst the burden of proof remains squarely on the LA it is nonetheless a striking feature of the case that there is no counter pathological or paediatric opinion to support - by reference to the balance of probabilities - any of the parents’ assertions. Inasmuch as the Court could properly conclude that, notwithstanding the weight of the expert medical evidence, the injuries were caused accidentally, there would need to be a heavy investment in the credibility of the parents; such an investment is not justified here where the parents’ accounts and oral evidence have been characterised by inconsistency, contradiction and implausibility.
172.	As to the law he emphasises the following points derived from the authorities:
i)	The standard of proof is the simple balance of probabilities.
ii)	If the perpetrator of NAI cannot be identified, it is still important to identify the pool of possible perpetrators by reference to whether or not there was a real possibility that a particular person was involved.
iii)	This case is not a ‘Popi M’ case: non-accidental injury as a causation of injury is not improbable; on the contrary, here, it is supported by cogent medical evidence.
iv)	The authorities emphasise the importance of expert medical evidence, particularly where such evidence is agreed, and confirm that if the court is to depart from expert opinion, then it must explain its reasons for doing so.
v)	The judge in family proceedings invariably surveys a ‘wide canvas’.
vi)	In those cases where the court is considering a number of suspicious episodes, whilst each episode has to be judged in isolation, a judgment on all of the episodes in their sequence and pattern is no less important. Indeed, any other method would probably invite error.
vii)	In split hearings, a psychological assessment undertaken before facts are found by the court is unlikely to be of assistance. 
173.	Mr S argues that the medical evidence is balanced, measured and compelling. In all significant respects, it is agreed. There is no basis for any suggestion of dogmatism (let alone ‘over-dogmatism’). Far from it: the key experts have been demonstrably fair in their approach, and have readily acknowledged - where appropriate - the limits of their own particular expertise. As the Court knows, clarity, authority and even robustness do not equate to dogmatism.
174.	As to the experts evidence he makes the following submissions: 
i)	Dr L was jointly instructed with a CV reflecting considerable experience and expertise. He identified the need for a histopathologist in relation to the possibility of an underlying natural cause for the bruising to S’s ears. He moderated his position when appropriate (for example in relation to the extent to which he could be categorical in his opinion that the blood on the bib came from the torn fraenulum). He accepted as ‘fair comment’ when it was put to him that it was significant that he was unable to fit a mechanism to the palmar bruises (though this did not cause him to change his opinion as to their likely non-accidental causation).
ii)	Professor S was jointly instructed with a CV reflecting considerable experience and expertise. In advocating the holistic approach, it was clear that this was in no way a broad-brush approach: rare things do happen, and it was accompanied by a plausible explanation. He raised the possibility of bacteria getting into S’s blood stream through a bacterial infection in the feet and then causing septicaemia and overwhelming illness (and then discounted it after careful consideration). He was clear that he had taken into account the observations of positive interaction between parents and children.
iii)	Professor H was at pains to point out in his written and oral evidence that he is not an expert in (a) post mortem changes, or injuries or their causation; he defers to Professor S and Dr L in relation to injuries and their causation (with the caveat that he has greater experience of looking after children with bleeding disorders) or (b) diagnosing severe infections in young children.
iv)	Dr H and Professor G both brought obvious expertise to the discrete issues on which they were asked to comment; both were careful to acknowledge the limits of their expertise. 
175.	As to the key histological evidence Mr S unsurprisingly argues that this is the conventional and accepted wisdom in the field of pathology and the science is robust. Histology is an essential component of being a pathologist. There is no significant difference between children and adults in terms of the arrival of polymorphs, within the wide spectrum described. The science is supported by respected research. Although the research is largely animal based, it is reproducible science rather than case report science. It accords with the approach and evidence of Dr J, Dr W and Dr C who bring further expertise and experience to the case; as Dr C said: “ [Neutrophils] are the most definite evidence that it occurred in life yes. The presence of fibrin, the presence of necrotic tissue are supportive evidence”.
176.	In relation to the references in research as to the emigration of neutrophils within minutes of blunt force trauma, and as to emigration of neutrophils after death Mr S argues, by reference to the expert evidence:
i)	It is the accumulation of neutrophils which is significant, and – as confirmed in the paper “Nonetheless, traditionally, neutrophils would not be expected to be numerous until several hours have elapsed from the time of injury”;
ii)	Dr L was cross-examined about this; the ‘mice’ article was not available at the time but Dr L’s response was balanced and robust;
iii)	During her evidence in chief, Dr J said: “There is a little distribution of neutrophils [after death] but not to the extent that we see here.”
177.	Mr S argues that it is important to emphasise that Drs L, J, W and C were not simply applying received wisdom in a vacuum:
i)	They all had the opportunity of looking down the microscope and bringing their own independent expertise to bear;
ii)	Dr J and Dr W had the macroscopic advantage of looking at S himself;
iii)	Dr L was able to consider the histology in the context of the other available information including the post mortem photos;
iv)	Dr C also had sight of the photos of the palms and fraenulum.
178.	Mr S concludes in this central area that mindful of the authorities in relation to the proper approach to expert evidence, that in relation to an issue such as this - which is so clearly within the province of the pathology experts - there is in reality little if any scope for the Court to gainsay the agreed evidence.
179.	On the expert evidence Mr S argues that it is highly unlikely that S was suffering from any sort of bleeding disorder, whether inherited/congential or acquired. Even if he was, it would not explain the bruising and torn fraenulum.
180.	The histology rules out the possibility of the fraenulum having been torn during CPR (whether by F at 8.45 a.m. or by the paramedics). But even leaving the histology to one side:
i)	In conceding it as a possibility, Professor S indicated that he had never come across it before  and that it would not explain the blood on the bib;
ii)	Insofar as the stiffness of the mandible is being relied upon as a reason why more force was needed during this particular CPR, that does of course support the contention that S had been dead for some time;
iii)	Although F, during his evidence in chief, appeared to be suggesting that he may have accidentally torn the fraenulum – through his demonstration and somewhat florid description (saying, apparently for the first time, that he had been “pinching and pulling to get S’s mouth open”) – he was adamant in cross-examination that he did not cause it, even accidentally.
181.	The histology further rules out the possibility of the following bruises being caused during CPR:
i)	The palmar bruises (minimum 2 hours before death);
ii)	The bruise to the major knuckle of the middle finger of the right hand  (minimum 3 days before death).
182.	The observation of yellow in the 2 bruises to the left forearm (which can be seen in the photo) indicates that it was at least 18 hours old at death, and so rules out the possibility of those bruises having been caused during CPR.
183.	Having regard to the expert evidence given, even without the histology, it is submitted by Mr S that CPR as a cause for any of the injuries (beyond the marks of intervention noted by Dr J) would have been an unlikely possibility. Bringing the histology back into the equation, it can be excluded as a possible cause.
184.	While relying on the generalised empirical paediatric evidence of Professor S it was submitted by Mr S that Dr K’s assessment is of no assistance to the Court at this stage. 
i)	His assessment was based on a completely unsure factual footing; he himself highlighted the need for a fact-finding hearing;
ii)	He was not in a position to challenge the parents about their accounts;
iii)	He did not have the benefit, which the Court has now had, of hearing all of the relevant medical and factual evidence;
iv)	Leaving to one side the disputed factual allegations, the Court may well ask itself how Dr K’s assessment might have been affected had he heard F’s account in relation to the bike buggy and read the observations made by Professor S as to how that reflects upon F as a parent.
185.	Thus I was invited simply to determine the facts and leave to one side, at this stage, what psychiatric label (for example ‘sadist’) might or might not be attached if findings are made.
186.	As to the evidence of the parents generally Mr S asserts that there was a high level of inconsistency. There were differences in accounts given at various stages:
i)	The notion that the parents were naïve participants at police interviews is undermined by:
a)	Their obvious knowledge of the concerns held by the police, medical professionals and Children’s Services following S’s death (eg the restrictions placed upon them accessing their home; Dr T’s discussions with them about a range of injuries found on S;
b)	The discussions at the case conference: the Court may consider it curious that F could not recall DS B’s comments at G53, and his own comments at G55 (adverse to his case in that they clearly reflect a knowledge of heightened suspicion) but could clearly recall the production of the photograph at G53 (which might be thought to be favourable as a reflection of co-operation); 
ii)	Taking the bike buggy as an obvious example, there is simply no good explanation for the inconsistency between the accounts now being given in relation to the bike buggy, compared to those previously given;
187.	There is a high level of contradiction between the parents’ accounts: 
i)	M was, and still is, sure that S was dead at 0845; F, apparently, is not;
ii)	F was apparently aware of the unusual appearance of S’s testicles, whilst M was not; though F subsequently, and implausibly, went on to deny that he was aware.
This completely undermines the way in which the parents have presented their relationship as one of openness and closeness.
188.	There is a high level of implausibility:
i)	Despite the stressors mentioned, neither felt any stress whatsoever;
ii)	Obvious bruises were not noticed;
iii)	Significant events (including certain bruises and certain conversations which might be thought to have been memorable) could simply not be recalled; 
iv)	As to accidental explanations for injuries: hard toys, other children, row row the boat and so on; 
v)	Former friends (including two nurses) have gone to the trouble of giving untrue  police statements, Children Act statements and oral evidence, though no good reason can be put forward for any of this;
vi)	The nursery, despite their diligence and procedures, failed to note an incident involving another child;
vii)	Medical professionals have failed to note important events (including Dr F/Dr D) or have noted certain events with complete inaccuracy (including Dr T);
viii)	Neither M nor F (two intelligent professionals, noticed – (when the buggy was bought) until the evening before the bike buggy was to be produced at Court (at the request of the Court)  – the warnings emblazoned on the back of the buggy under blocks of red and yellow.
Thus says Mr S there is a pervading sense that both M and F, when they think it suits them, will seek to pull the wool over the eyes of family members, friends, professionals and the Court. This is exemplified by the advancement by them of a number of ‘red herrings’ namely:
ix)	That M and F bruised easily as children:
x)	That D bruised easily:
xi)	Child A as cause of bruises to D/S:
xii)	D as cause of bruises to S
xiii)	The bike buggy
189.	Mr S invites me to accept the evidence of the neighbours as straightforward and honest. They gave their evidence in difficult circumstances, with arrangements tailored to ensure fairness for the parents. They did not deny that there had been discussion between them (in certain respects), but were all clear that these discussions had not influenced their evidence. I am invited to reflect upon why these professional people would go to the trouble that they did if they were other than concerned to provide information which might be relevant. The parents have been unable to suggest any basis for a malign motive.
190.	Those lay witnesses called on behalf of the parents, with respect to them, offered little assistance in relation to the factual issues. It is clear that to most observers, the parents presented as respectable and decent parents. However the LA invites me to consider what actually happened, factually, ‘behind closed doors’.
191.	Thus the LA seeks the finding that one or other or both of the parents deliberately inflicted the injuries I have listed above. As to S’s death Mr S submits: 
“The LA invites the Court to consider the findings sought in relation to S’s death and to make such findings as it considers appropriate in the light of the expert and lay evidence.”
This does strike me very much as being willing to wound but not to strike. Frankly, the LA must nail its colours to the mast. Given the findings that its seeks as to deliberate violence it would be a strange thing, on the LA’s case (notwithstanding Professor S’s evidence) if by an extraordinary coincidence a few hours after being meted exceptionally brutal violence, S suffered a cot death. I will deal with this further in my conclusions.
192.	The LA further seeks findings that the non-perpetrator(s) failed to protect S. He says that the evidence in this regard is overwhelming. This was a family living together in close quarters. As discussed above, the injuries were obvious and explanations given by both parents have been inadequate. Each parent maintains, even now, that they have not asked the other whether they caused any injury to S.
The argument on behalf of F 
193.	Ms S QC and Ms M argue that this is a highly unusual case. The allegations are of the gravest kind. They involve the infliction of very serious injuries to a young child, and, indeed, include an allegation of causing that child’s death. The nature of some of the injuries which the court is being asked to consider is exceptional. The injuries to S’s ears and palms are outwith, or virtually outwith, the experience of the medical experts who have given evidence in this case.  Moreover, the allegations are made against parents who have been very highly regarded by those who have known them or assessed them. They have been seen to be loving, caring and committed parents. Non accidental injury, particularly the cruel and vicious nature of some of the actions of which they are suspected, appears to be starkly out of character. 
194.	If the injuries to the fraenulum and palms were inflicted in the way the LA seeks to prove, they would have caused acute pain. The other parent must have known. Thus one parent must have inflicted cruel and repeated injury, and the other parent must be colluding. Neither the infliction of such injuries, nor collusion in hiding them, fits with anything that is known about either parent.
195.	As to the law Ms S QC emphasises the following:
i)	The burden of proof rests squarely upon the LA. The standard of proof is the civil standard; that is the balance of probability.
ii)	With respect to any fact alleged by the LA, the court is not entitled to come to the conclusion that, on the one hand, the local authority has failed to establish that fact on the balance of probability but that, on the other hand, the possibility that the circumstances may be as alleged by the local authority cannot be discounted completely. Suspicion is simply not enough.
iii)	Expert medical evidence has been one part of the evidence in this case. But it is only part of the evidence in the case. All the evidence, both medical and non-medical, has to be considered in assessing whether the pieces of the jigsaw form into a clear convincing picture of what happened (Re B (Threshold Criteria: Fabricated Illness) [2004] 2 FLR 200, Bracewell J).
iv)	It is open to the court to conclude that the threshold criteria had not been met, notwithstanding the concurrence of medical opinion that a non-accidental injury was more likely than not, where the parents had impressed the court as credible witnesses and the medical experts acknowledged that there was a real possibility (as opposed to a fanciful one) that the injury did have an unknown accidental cause (Lancashire CC v D and E [2010] 2 FLR 196, Charles J).
v)	I need to be aware of the danger of a shift in the burden of proof onto the parents.
196.	Ms S QC highlights the character of these parents. They are described as a warm hearted and sociable couple, and there is a mass of positive comment about the quality of the care of their children and the close and loving relationship between the children and them. These observations were reflected in the observations of the nursery staff. The quality of the parents’ care was professionally assessed by social workers in the aftermath of S’s death, and has continued to be assessed. The quality of their care was described in glowingly positive terms and remains so. It has received nothing but praise.
197.	In similar vein strong reliance is placed on the assessment of Dr K.
198.	The marks or injuries were noted because D and S were babies who were in the public view. Neither was hidden from sight. If these parents had been seeking to avoid scrutiny, or had something to hide, it is unlikely either child would have been presented with injures. The pattern frequently seen in non-accidental injury cases is of children who are kept away from the public gaze; routine appointments with health visitors and the like are missed; and public scrutiny is avoided. This is not such a case.
199.	In relation to the injuries to the ears and palms Ms S QC highlights the remarkable feature of this case namely that none of the experts  had ever in the course of extensive careers seen injuries like this before (save for Professor H in relation to the palms and then only twice in cases of severe bleeding disorders). 
200.	Thus, if the cause of the injury to the ears were non accidental, it would suggest a blow or blows being inflicted to both ears of a small baby. As an inflicted injury to a baby, it would be of a serious and cruel kind.  This type of inflicted injury simply does not fit with all that the court knows about the parents from a welter of sources. It does not fit with the social workers’ observations of them.  It does not fit with Dr K’s assessment of them. However, it does fit with the wholly inappropriate use of the bike buggy. 
201.	As to the injuries noted at the autopsy Ms S QC highlights those that were not surveyed 27 hours earlier. Strikingly, at that survey there is no note of any marks or injuries to either hand, either on the front or the palms (in stark contrast to the post mortem photographs); there is some limited scabbing on the feet which is very different from that which appears in the post mortem photographs; and only one bruise on the head was seen (on the right forehead). The bruises observed by Dr J by the left eyebrow and to the orbit of the eye were not recorded.
202.	There is no clear non accidental cause to the injuries to the fraenulum and the hands. Nothing fits. It would be wrong to approach a case where something is so unusual simply on the basis that because there is no explanation from the parents it must be non-accidental injury. The resuscitation attempts may well have led to forceful compressive forces on the palms and outside of the hands as a line was attempted to be introduced. Later there were also attempts to unfold S’s hands (which were beginning to stiffen with rigor mortis) for the purposes of the radiological survey of his body. Neither should be excluded as a possible cause.
203.	Ms S QC then sought to meet the challenge of the histological evidence. First she raises the question concerning the time of death. I have already, with some diffidence, made my finding about that. But she nonetheless asks the pertinent questions: is it possible to say whether or not S was dead and when he died? Or whether he was still in the grey area between life and death?  
204.	Ms S QC states that S was ventilated from shortly after the arrival of the ambulance technicians at 8.53 until CPR was stopped at 9.36 (thus he was ventilated for 43 minutes). Would that have an effect on the production of neutrophils? 
205.	Ms S QC challenges the soundness of the science being deployed against the parents, although it is noteworthy that neither she nor Ms B QC has called a dissentient expert. She acknowledges that the key premise of the pathological evidence is that neutrophils are not produced post mortem.  Yet, upon scrutiny, she says, it can be seen that there has been little scientific examination about the production of neutrophils, and none in young children or babies. She relies upon the limited and less than categorical writings that I have referred to in my section on the histological science. She says that there is a possibility that S died as the result of an overwhelming infection, either bacterial or viral. If so, it is not possible to exclude the possibility that increased cytokine production may have caused post mortem production of neutrophils.
206.	As to the allegation that the parents murdered S Ms S QC states that there is no evidence that either of these parents caused S’s death. It is a terrible allegation for these parents to have had to face. On the Local Authority case, one of them would have had to have been up in the night and have inflicted very serious and cruel injuries (in some unknown manner) to each of S’s hands, caused the tear to his fraenulum and other injuries, and then after at least two hours one or the other parent in some other assault would have had to have killed him. It is a wholly improbable scenario to say the least, given what this court knows about these parents, although, as I have pointed out, if the parents did in fact commit the gravest form of GBH on this tiny baby then it is a remarkable coincidence that a couple of hours later he should have suffered a completely unconnected cot death.
207.	Ms S QC argues that there is a real possibility that S may have had some infection which led to his death. The microbiology is, she submits, ambiguous. There certainly is evidence of staphylococcal infection in two blood samples which if genuine would represent bacterial infection in the blood. The view is expressed by the lab that they are probable contaminants, but there is no way that can actually be established one way or the other. It is simply a matter of inference. Dr G is not an expert in microbiology relating to babies or in sudden unexpected death in infants (SUDI) and thus was unaware of the recent paper “Difficulties in interpretation of post mortem microbiology results in unexpected infant death: evidence from a multi disciplinary survey", from the highly respectable sources of Great Ormond Street and the UCL Institute of Child Health London. This paper points to the fact that whilst post mortem microbiological investigations are recommended in SUDI cases, there are no current evidence based guidelines for the interpretation of the results. It points to the fact that data suggests that there may be an underlying infection related systemic process in a proportion of cases despite the absence of histological evidence of infection. Their findings emphasised that, at present, interpretation of microbiology results varies amongst specialists and is based on opinion rather than objective criteria. There is at the moment no gold standard test. Dr G also drew attention to the possibility of S having a serious viral infection because of the high level of lymphocytes. 
208.	A bleeding disorder, either before death or as a result of DIC following severe infection, remain possibilities which cannot be wholly excluded. It is a curious feature than the only expert who has ever seen such bleeding to the palms is Professor H whose specialism is blood disorders. That factor in itself makes it impossible to dismiss the idea of bleeding disorder.
209.	Ms S accepts that F should not have taken S in the bike buggy and should not have travelled at speed in it. He accepts that. He should have made himself aware of the instructions and followed them. He accepts that. In truth, the appearance of the ear was puzzling. It went up down and then up. It did not cause S any pain or discomfort. S was taken to the doctors about it after it had increased in size again. F was told advice would be sought from the hospital. He was then told it was a haemangioma.   In other words, there was a natural cause. Once the parents had received that advice, it is not surprising that they did not look for an accidental cause of the appearance of the ear thereafter. They would not have had to think about it again until the question of non-accidental injury to the ear was raised following S’s death.  Then they became aware of Dr J’s’ view that it was a harmatoma. In reality this father is never likely to use the bike buggy for such a young child or in such a way again. Nor would M let him. 
The argument on behalf of M
210.	Ms B QC and Mr A argue that this is a highly complex case on a number of levels. In particular:
i)	any case involving the sudden death of a baby in circumstances in which no cause of death is ascertainable is of itself highly unusual and complex.
211.	Two of the three major alleged injuries to S, those to the palms and to his ears are universally regarded as highly unusual. Only Professor H has seen similar appearances before and then only twice in a career spanning over thirty years. Both patients had blood disorders. No other expert had ever seen similar appearances, whether as a result of an accident or as a result of trauma; similarly Drs J and W and numerous clinicians.  
212.	At post mortem, the macroscopic appearances of S’s upper fraenulum were considered by Drs J and W to be consistent with an injury sustained in the course of resuscitation. Importantly, both paramedics involved in the insertion of the Guedel airway considered that the injury may have been sustained in this process, as did the anaesthetist, who saw it in situ and replaced it. Only the histology as interpreted suggests otherwise. 
213.	Numerous injuries to S found at the post mortem examination carried out some 28 hours after his death were not apparent on close examination of his body following resuscitation. 
214.	As to the law Ms B QC emphasises the following propositions:
i)	The LA’s approach has been that, unless the parents can provide an explanation which fits an alleged injury, that lesion must be found to have been caused non-accidentally. This is a reversal of the burden of proof and wrong in law. 
ii)	A medical conclusion to the effect that inflicted injury is the most likely cause of an injury or finding establishes no more than that this is a real possibility that has to be considered. It does not mean that the court must make such a finding unless the parents are able to show that there was an organic or accidental cause. The court is in the unique position of hearing and reading all the evidence and of observing the parents in court during a lengthy hearing. 
iii)	The truth or otherwise of the parents’ assertions that they did not injure either child is to be determined on the civil standard. If the court concludes, on a balance of probabilities, in relation to either M or (as M would submit is appropriate) both parents, that they did not injure their children, that ‘as a matter of policy is treated as fact’ and they are entitled to be exonerated. 
iv)	Photographs need to be approached with a high degree of caution as it is impossible to know what the role of the light conditions and shadows played in the appearance of what is shown. The approach of the local authority, however, has been to assume that what is shown is an entirely accurate representation as to how the appearances looked at the time and ask the parents a number of years later to account for what appears in the photographs. The Court is then invited to draw an adverse inference from any difficulty in recollection. The risk of a subtle change in the burden of proof that results from such an exercise was highlighted in Re C and D (Photographs of Injuries) [2011] 1 FLR 990. This decision also considers good practice in relation to photographing possible injuries and warns as to the difficulties which arise if photographs are not taken as soon as practicable and clearly timed. In the context of a case involving alleged sex abuse, the same warning note was struck in Re Y (Evidence of Abuse; Use of Photographs)[2004] 1 FLR 855.
v)	The onus is and remains on the local authority to prove its case on the balance of probabilities. The propositions set out in the decision of the House of Lords in The Popi M [1985] 2 All ER 712 in relation to a conclusion on the balance of probability are applicable here.  M’s primary submission is that she has told the truth and that the Court should be satisfied as to this (at least on a balance of probabilities). On this basis the local authority has not proved its case against her.  If the Court is against M on this primary submission, she submits that the improbability of what is postulated means that the Court is not bound to make a finding either way but may properly conclude that the local authority has not discharged the burden of proof.
215.	Ms B submits that M’s accounts of events have been clear and consistent. This is apparent from her police interviews, her Children Act statements, her discussions with professionals and her oral evidence. Her inability to remember certain events or the detail of others is unsurprising. 
216.	It is submitted that anyone listening to the recording of the ‘999’ call cannot fail to be affected by it. The mother is incoherently hysterical and it is submitted that it is inconceivable that this was not genuine. The mother’s immediate reaction, as recorded, is clear evidence that she:-
i)	had just discovered S in an unresponsive state;
ii)	knew nothing as to how this had happened; 
iii)	was not involved in any ‘cover up’ – it is noted that this possibility was not even put to her in cross-examination. 
217.	Ms B QC then addressed the pathological and medical evidence in relation to the alleged injuries and as to a possible bleeding disorder. I do not do her exegesis justice if I simply summarise her submissions in conclusion thus:
i)	that real caution is necessary in interpreting the results in S. There is a substantial risk that evidence of infection has been too easily dismissed as artefact.
ii)	In light, in particular, of the difficulty in determining when S dies, what is seen as the beginnings of the extravasation of neutrophils may have been wrongly interpreted or may be present but due to:-
a)	S not being actually dead when resuscitated (either by the father or by the paramedics or resuscitation team).
b)	Resuscitation as a cause
c)	a reaction to infection
iii)	It is submitted that it would be unsafe to draw any conclusion adverse to the parents based on the post mortem results. 
218.	Ms B QC placed reliance on the assessment of Dr K. She relied strongly on the highly positive character evidence. Finally in her section entitled “piecing the picture together” she submitted that as is so often the case, the approach of the medical experts (and pathologists) is that, unless parents can establish an accidental cause for an injury which may have been inflicted, a conclusion should be reached that the injury was non-accidental. In this case, the approach of the local authority has been similar, despite this being contrary to the legal position.
219.	The reality is that medical evidence, however superficially compelling, is only one piece of the jigsaw. In this case a number of questions remain unanswered by the experts. The area of interpretation of the extravasation of neutrophils is particularly difficult and the science underdeveloped; it is likely to be an area in which further light will be shed in years to come.
220.	She argues that I have the enormous advantage of seeing, hearing and reading all the evidence, including the parents giving evidence for many hours and observing them in court during the hearing. Many witnesses have praised the mother’s ability to carry on and provide superior care for her children despite the stress she has for so long been under arising from S’s death, the involvement of the police and social services and the supervision requirements which have for so long been in place.
221.	I am ideally placed to consider the allegations in the context of all the other evidence. In this case the positives about the mother are in very stark contrast to the allegations of serious and repeated cruelty to her very young children. The conclusions reached by Dr L and Professor S in particular as to what is most likely are completely at odds with everything which is known about the mother. It is submitted that it is inconceivable that the mother would either have:-
i)	behaved in any of the ways alleged; and/or
ii)	covered up for the father had he so behaved.
222.	The injuries to S’s hands and ears are extraordinary and exceedingly rare. Nothing like the appearances in his palms has been seen by way of inflicted injury by any of the experts or clinicians despite their collective vast experience. The combination of the palmar bruising and that to the backs of the hands is impossible to reconcile by any postulated mechanism.
223.	It is very rare that paramedics admit to the likelihood of a torn fraenulum being caused during ventilation. Here it is very significant that the anaesthetist who saw the Guedel airway in situ and removed it considered that it had caused the tear. This and the high degree of improbability (in light of all that is known) that this was an inflicted injury leads to a conclusion that:-
i)	S was not dead when the paramedics commenced their efforts to resuscitate him, or
ii)	The ventilation he received was sufficient to give rise to neutrophils in response to injury, or
iii)	The extravasation of neutrophils (indicating an injury in life) has been wrongly interpreted or had a different cause (such as infection), or
iv)	There is some other innocent explanation 
224.	I am invited to conclude that this is an extraordinary case involving science which is far from certain and that it would be wrong ‘blindly’ (sic) to follow the science in reaching a conclusion adverse to the parents, in particular in light of the devastating consequences for this family which would flow from such a conclusion.
225.	M and F have given evidence that neither caused S’s death. M submits that this is entirely credible evidence and ought to be accepted. The mother respectfully invites the Court to conclude that S’s death resulted from an unknown natural event. Such a conclusion would give the family much needed closure and assist them to move on with their lives.
The argument on behalf of the guardian of D and S2
226.	Ms D QC and Ms R represent the litigation guardian of D and S2, Ms S. In her written final submissions Ms D QC wrote: 
“In this hearing the Children’s Guardian takes a neutral and objective position.  It is not her role to argue for or against any of the other parties.  
Ms S has had the benefit of hearing most although not all of the evidence throughout the hearing.  She has had the benefit of the transcripts of the experts and medical witnesses provided.  She was represented throughout.  She has had the benefit of reading the documentary evidence filed and she has met with and had discussions with the parties.  She has met the children.  If the Court makes any findings against M or F the Children’s Guardian will be in a good position to consider and formulate her recommendations to the Court for the welfare of the children. 
To that end the Children’s Guardian has considered the oral evidence heard, the written evidence submitted and the expert opinion received in the context of the LA’s Schedule of Findings.”  
227.	I was surprised to read that. Given that the outcome of this hearing could have a most far-reaching effect on her clients D and S2 I would have thought that I would be offered at least a steer as to what findings I should make. But no, I was firmly told that this is not the practice, and with my slender experience of this kind of work I am not in a position to argue. That said, approaching the matter with an open mind uncluttered by years of experience of this kind of work I would have thought that at the very least the role of the Guardian and those representing her should be akin to Counsel to a Statutory Inquiry, assisting the court in exploring complex scientific evidence and making suggestions to the court as to what findings should properly and tenably be made. The practice of sitting with an assessor has fallen into disuse (notwithstanding that the procedure for appointing an assessor has recently been reiterated in FPR 2010 r25.14), and thus the role of the representative of the Guardian in a case such as this cannot be overstated.
228.	In keeping with her position of strict neutrality Ms D QC produced a very helpful summary of the evidence given, which I have drawn on in preparing my account of it above. She was however prepared to submit that there is no evidence upon which the court can rely in support of the allegation that S’s death was the result of further physical abuse. Thus far she was prepared to go, but no farther. 
Conclusions  
229.	The business of judging in this case is peculiarly difficult. 
230.	Yet, if I accept Mr S’s submission that there is little, if any, scope for me to gainsay the histological evidence, which must lead me inexorably to find that in the early hours of the morning these parents, acting together, meted out the most extreme sadistic violence to S which involved thrashing his little hands and punching him in the face with sufficient force to snap his fraenulum.
231.	The same point is to be made in relation to the allegations in respect of S when the photograph at Exhibit 7 was taken. Standing alone all the allegations suffer from obvious evidential weaknesses, but when viewed through the prism of the histological evidence they present an altogether different image.
232.	But I do not believe that I should judge the histological evidence in isolation. It is part of a wider canvas. This is a recurrent theme from the authorities. I must weigh it against my assessment of the credibility of M and F and the (im)probability, judged from a non-scientific stance, that this ghastly event actually took place. So as regards the components of the evidence the court is, up to a point, in a chicken and egg situation. 
233.	 What I therefore propose to do is to make judicial observations on:
i)	The credibility, character and personality of M and F.
ii)	The use of generalised empirical statistical paediatric evidence.
iii)	The use of photographic evidence.
iv)	The reliability of ageing bruises by visual observation.
v)	The reliability of the lay evidence from the neighbours.
vi)	The histological evidence.
I shall then stand back and pull all the threads together and make my findings applying the law as I have set it out above. 
The credibility, character and personality of M and F
234.	The evidence of Dr K, the social worker and Dr P is unequivocal and points only one way. To the same effect is the character evidence. The core personalities of the parents have been closely anatomised, not only by the givers of testimony but also by the trial process where they have both been subjected to the test of close, searching, cross examination.
235.	I am wary of judging people by reference to their demeanour in the witness box for the very reasons mentioned by Lord Bingham in his essay, but demeanour is nonetheless relevant. I found M and F to be very straightforward, decent, fundamentally honest, and above all loving and caring  parents. Mr S has set out a number of instances where he says that their evidence has not only been inconsistent but also demonstrably false. 
236.	I do not believe that in relation to the penumbra of circumstantial or peripheral matters M or F were either materially inconsistent or dishonest. This conclusion is derived from my impression of them as they gave their testimony and on observing them carefully in court, from the evidence of Dr K, (the social worker) and Dr P, and from the character evidence. It is also importantly bolstered by the content of the 999 call. The overt distress evidenced by M is obviously authentic; she would have to be a phenomenally good actress to feign that. Equally, while F was more controlled, his distress was palpable. This sits most uncomfortably with the case of LAwhich is, of course, that both of these parents (or one with the complicity of the other) were meting out savage violence to S a few hours earlier.
237.	Of course, if the account of the parents in all its great detail had been entirely consistent then it would have been said that they had carefully mapped out their stories.
238.	In judging the truthfulness of the parents as to the events of the night one has to reflect on the implausibility of what the LA seeks to prove. Although the LA did not explicitly challenge all the elements of the parents’ account as set out by me above, it should not be taken as accepting any of it, save where it is incontrovertible. Its case is that for the crucial period only M and F can say what actually happened, and they say that they should not be believed. However, stripped to its core elements the sequence that they posit is this:
i)	At about 3 a.m. one of the parents inflicted extreme injury to S’s palms by repeatedly thrashing them in some way with some weapon. S was also punched in the face with such force that his fraenulum snapped. This would have caused S to suffer extreme pain, and he would have been screaming very loudly. The other parent, if not participating in this awful act, was present and complicit.
ii)	D either heard all this, but never mentioned anything to anybody, or slept through the whole thing, even though her bedroom is next to S’s in a very compact area.
iii)	None of the neighbours heard anything in this compact estate.
iv)	At 7 a.m., as I have found, S died. Either one or both of the parents smothered him, or, by an extraordinary coincidence, he died a cot death.
v)	At 8.50 a.m. M dialled 999 and seemingly in great distress told the emergency operator that her baby was dead in his cot.
239.	Obviously, improbable things do happen, but this sequence of events seems very unlikely. It is against this unlikelihood that I have to judge the truthfulness or falsity of the parents’ denials. 
240.	The injuries to the palms, which are the most serious of all, and which can be regarded as a touchstone, are shrouded in mystery. The surface area of the palm of a seven month old infant is very small indeed. No-one, apart from Professor H has ever seen anything like these bruises. He has only seen them twice in people with bleeding disorders. Although Dr L posited that they might have been inflicted by a ruler or cane he admitted that their appearance did not really fit with that hypothesis. In argument I pressed Mr S to advance a likely mechanism but he just fell back on “repeated application of significant blunt force trauma” and declined to be drawn into specificity. So I am being asked to conclude that the parents inflicted with some mystery weapon, which no-one can visualise, repeated beatings on these tiny palms causing bruising the like of which none of these experts,  Professor H aside, has ever seen before.
The use of generalised empirical statistical paediatric evidence
241.	In his report Professor S referred to and relied on a deal of generalised empirical statistical paediatric evidence. I have set some of this out above at para 141. Specifically Professor S relied on published research, empirical data, and personal experience as follows:
i)	In relation to soft tissue injuries in children:
a)	Jean Labbé and Georges Caouette. “Recent Skin Injuries in Normal Children” PEDIATRICS Vol. 108 No. 2 August 2001, pp. 271-276, where 2,040 examinations were done on 1,467 youngsters in Canada from 0 to 17 years of age.
b)	Carpenter RF “The prevalence and distribution of bruising in babies” Arch Dis Child 1999, 80, 363-366, where 177 babies were reviewed between the ages of 6-12 months to look for bruises.
c)	Mortimer, PE & Freeman, M. “Are facial bruises in babies ever accidental?”. Archives of Disease in Childhood 1983; 58: 75-76, where the authors carried out 620 examinations of a random sample of babies attending clinics.
ii)	In relation to nosebleeds in young children:
a)	Neil McIntosh, Jacqueline Y.Q. Mok and Adrian Margerison “Epidemiology of Oronasal Haemorrhage in the First 2 Years of Life: Implications for Child Protection.” PEDIATRICS Vol. 120 No. 5 November 2007, pp. 1074-1078 (doi:10.1542/peds.2007-2097), which examined 77,173 accident and emergency department attendances with 58,059 admissions during the 10 year study period in children <2 years of age.
iii)	In relation to skull fractures in infants:
a)	Helfer et al, 1977, a review of 246 children under the age of 5 years who fell at home or in hospital.
b)	Nimityongskul et al, 1987,  a review of 57 children under 5 years old and 19 children aged 6-16 years who fell from a bed, crib or chair (heights of 1 - 3 feet).  
c)	Warrington SA et al. “Accidents and injuries in premobile infants”. Archives of Disease in Childhood  2001; 85: 104-107,  a review of data from 3,202 reported falls in infants under 6 months of age.
d)	RA Williams “Injuries in infants and small children resulting from witnessed and corroborated free falls” The Journal of Trauma 1991; 31(10): 1350-52), a review of 398 consecutive falls.
iv)	In relation to petechiae, on his experience of seeing thousands of bruises, accidental and non-accidental.
v)	In relation to infant mobility on statistical evidence, the source of which he does not state.
242.	Obviously, in a fact-finding hearing where NAI is alleged paediatric evidence of a generalised empirical statistical nature is relevant in aiding a determination of whether the parents actually inflicted the injuries. But it must always be remembered that it is not specific to the facts of the case, and in a way is even less specific than the psychological evidence that authority has said is likely to be generally unhelpful. That research shows that petechiae can be seen on the cheek, ear and trunk of children who have been deliberately slapped or struck, does not prove of itself that petechiae on this child was caused by a slap. That all the research shows that children under six months are very unlikely to sustain bruising does not of itself prove that this child sustained bruising non-accidentally. That research shows that nosebleeds in young infants are very rare does not of itself prove that this child did not suffer from nosebleeds, and that M was lying about that. This empirical evidence is what it says it is, empirical, no more no less. It is part of the jigsaw puzzle, and is not determinative. 
The reliability of ageing bruises by visual observation
243.	This is a notoriously inexact technique. The experts are agreed that bruises of any colour other than yellow signify nothing as to the age of the bruise, and this is backed up by the paper by Dr Langlois. There are however here two bruises to the left forearm which are described as yellow. The presence of the yellow colour led Dr J, Dr Land Professor S to say with some confidence that these bruises are at least 18 hours old, and therefore must have been inflicted on a separate earlier occasion  to the injuries inflicted to the hands and fraenulum.
244.	In his paper Dr Langois is not nearly so categorical. He states
“If yellow is seen in a bruise, then that bruise is not recent …There are a number of important points to this statement. … Yellow means bright yellow, not orange or brown. … The observer has to be able to perceive yellow. Tests have demonstrated a wide variation in the threshold for yellow perception in the population and sensitivity for yellow decreases with age …It has not been rigorously established when yellow appears in a bruise. The published study stated that yellow was not seen in a bruise that was less than 18 hours old….The study lacked rigour as it was based solely on the observations of the author, with no formal testing of inter-observer or intra-observer variation.” 
245.	I have seen the photographs taken of these bruises at 2.45 p.m. For what it is worth I would say that they do not look yellow to me. Of the three photos taken at the autopsy the following day (Nos. 518 – 520) there is, to me, a faint circumferential tinge of yellow on No 518 but none in the others.
246.	Again, this evidence is relevant and admissible but must be treated with great caution. It would not be safe to form any conclusions based wholly or mainly on the alleged colour of a bruise. 
The histological evidence
247.	I have set out above at some length:
i)	The scientific evidence generally.
ii)	The conclusions drawn by Dr J.
iii)	The conclusions drawn by Dr C.
iv)	The conclusions drawn by Dr L.
v)	The conclusions drawn by Dr H (paras 160 to 164).
248.	The injuries from which sections were taken and which were the subject of histological examination were (as taken from Dr J’s list of 23 injuries):
6. There was a recent tear of the fraenulum of the upper lip which was associated with a little erythema but no significant haemorrhage.
8. Within the upper helix of the right ear, there was a purple nodule 7mm in diameter which on sectioning showed a little haemorrhage.
9. There was a fluctuant swelling 25 x 20 x 7mm with overlying purple discoloration of the skin within the left upper pinna. Sectioning revealed an organising cystic haematoma containing some liquid blood.
13. On the centre of the right palm and the palmar aspects of the index, middle and ring fingers, there were similar blue bruises up to 7mm in diameter.
15. There was a red/purple bruise over the metacarpophalangeal joint of the middle finger of the right hand measuring 10 x 5mm.
16. At the centre of the left palm, there were similar blue bruises up to 7mm in diameter with at the base of the index finger, there was a transverse apparently post-mortem skin split. 
249.	I will examine each injury and summarise the histological evidence for each:
i)	The tear to the fraenulum. “There was minimal but definite extravasation of polymorphs. Staining for haemosiderin was negative” (per Dr L).
ii)	The right ear. There was haemosiderin within macrophages. As Dr H put it “There is minimal (and no significant) active inflammation although quite large numbers of macrophages which contain finely granular pigmented material consistent with haemosiderin”.
iii)	The left ear showed haemorrhage with some iron deposition. As Dr H put it “Perls’ stain confirms presence of haemosiderin laden macrophages”.
iv)	The palms. “Within the bruise on the left palm there are similar changes with haemorrhages, oedema and neutrophils present around adnexal structures and within the fat. The tissue sample from the right palm is fragmented but confirms the presence of haemorrhage within the subcutaneous tissue associated with neutrophils. In a separate fragment neutrophils, blood and fat can be seen.” (per Dr J). “Sections from both palms show local recent haemorrhage and some extravasation of polymorphs, but staining for haemosiderin is negative” (per Dr L).
v)	The right middle knuckle. “Histological examination of the brown bruise on the back of the right hand showed further haemorrhage and neutrophils around adnexal structures. There is focal Perls’ positivity.” (per Dr J). “Sections from the red/purple/yellow bruise on the back of the right hand show well established extravasation of polymorphs, and staining for haemosiderin is focally positive.” (per Dr L).
250.	This evidence leads the four experts to conclude, as confidently as they can, that, by reference to the telos of this science as set out by me at para 40 above:
i)	All of these injuries were caused in life and not after death; 
ii)	The injuries to the ears and knuckle were caused about 3 days before death; and
iii)	The injuries to the palms and fraenulum were caused about 4 – 12 hours before death (most likely around 4 hours). 
251.	In judging these powerful conclusions, at this stage without reference to the wider body of evidence I have sought to set out and comment on above, I would make the following general observations:
i)	This science is forensically untested. The reason that I have not been given any medico-legal papers detailing the results of legal cases where responsibility for injuries has been found based on this science is because there have not been any, apparently anywhere.
ii)	The science is based largely on research conducted on animals. There is almost no published scientific research in this field performed on humans, and none at all on babies. While it is said that the cellular and vascular features of all mammals are identical, this is mere assertion. I do not have any scientific evidence that tells me that neutrophil and macrophage migration is the same in mice, sheep, human adults and human infants.
iii)	Biological science is not nearly as certain or predictable as the science of physics or the laws of mathematics. As Dr L accepted “we have biological systems and so therefore you cannot automatically assume that every one of us in this room will have exactly the same rate of accumulation of polymorphs at the site of inflammation -  it doesn't work that way, and there are other factors that may influence that”.
iv)	Science is always moving on. Scientific certainties of a past age are often proved conclusively wrong by later generations. In an address to the British Association for the Advancement of Science in 1900 Lord Kelvin, one of the greatest of all scientists, stated that “there is nothing new to be discovered in physics now. All that remains is more and more precise measurement” and in a 1902 newspaper interview he predicted that “no balloon and no aeroplane will ever be practically successful.”. Thus the warning of the President in Re U, Re B at para 23(v) that “the judge in care proceedings must never forget that today’s medical certainty may be discarded by the next generation of experts or that scientific research will throw light into corners that are at present dark”.
252.	I make the following more specific observations:
i)	The research of Drs Vanezis and Langois show that the categorical stance of the four experts here is not universally shared.
ii)	The distinction between bruising and pseudo-bruising can sometimes be difficult if not impossible, both at necroscopy and even after routine histological and immunohistological examination. 
iii)	In most instances resuscitation, which includes CPR, injection of adrenalin, and administration of oxygen by tube, occurs around the time of death with some degree of maintenance of circulation, or at least intermittent forced movement of blood within vessels. There is thus thereby every possibility of producing extravasation of blood to the tissues that is indistinguishable from true bruising.    
iv)	There is some evidence of neutrophils arriving at wounds within 15 – 30 minutes and of macrophages at 2 – 3 hours, although this is said to be rare, although not so rare that Dr H had not made such observations of neutrophils from time to time.
v)	It has been observed that neutrophil migration can occur after death in response to cytokines, at least in mice. 
vi)	A staphylococcal infection would give rise an increase in the cytokine production level. 
253.	In relation to S’s medical condition at the time of his death we know the following:
i)	S was diagnosed by his GP Dr M as having an Upper Respiratory Tract Infection.
ii)	S was seen by the GP Dr F. She noted lesions to both left and right big toes, and scabbed red dry skin. She was uncertain whether the problem was fungal or bacterial. She prescribed Timodine cream.
iii)	S was taken to see Dr F who observed his bruised left ear.
iv)	S was taken to see Dr F by M. He had been poorly the night before. An Upper Respiratory Tract Infection and conjunctivitis were diagnosed. Chloramphenicol eye drops were prescribed.
v)	In her evidence M observed that in the photo of S (Exhibit 7) S looked really poorly, pale and tired.
254.	According to Professor H, the blood results from S were grossly abnormal but extremely difficult to interpret. Blood taken during asystole is subject to defibrination which is the probable cause of the extremely abnormal clotting tests. Although likely to be artefactual changes (due to the dying process) they were also consistent with the possibility that S had developed one of the acquired blood disorders (other than a platelet disorder).
255.	The grossly raised lymphocyte count in S probably reflects very severe illness, but may be indicative of infection. There was a range that was possible on the results seen here, in particular consumptive coagulopathy or disseminated intravascular coagulation (DIC). Severe illness and severe infections are the commonest initiating feature in these conditions.
256.	As to congenital disorders the family studies make it very unlikely (but not impossible) that von Willebrand disorder was present. They also make it unlikely (but not impossible) that the commoner albeit relatively rare severe disorders of clotting factor protein deficiency e.g. Haemophilia A & B were present in S.  The blood tests do not rule out the very rare disorders of platelet function, factor XIII deficiency and alpha 2 antiplasmin deficiency which are very unlikely due to rarity and lack of family history and lack of prior serious problems. These disorders can lead to very easy and sometimes spontaneous bruising.   The mother might be a carrier of haemophilia, and had passed the disease on to S, without her tests being abnormal. The majority of haemophiliacs present only once they are toddling. Haemophilia remains a possibility in S’s case. He had seen bruising to the palms such as this only twice in a long career, both times in patients with bleeding disorders, one a severe disorder. In his experience, it has more often been the case that children in whom non-accidental injury has been suspected have turned out to have a blood disorder than vice versa.
257.	In summary his evidence was that both congenital blood disorders of certain types and/or an acquired blood disorder (such as DIC) are unlikely but not impossible in S’s case. 
258.	According to Professor S there was a possibility (but not a probability) that the foot infection was not solely a fungal infection, but also a bacterial infection. That then leads to the hypothesis that if those bacteria got from the feet into the bloodstream they could cause an overwhelming illness and death. 
259.	Although Dr G thought it most unlikely that this was a case of sepsis he acknowledged that there are cases where bacterial infection which is fatal is not seen in the blood. He could not exclude the possibility that sepsis caused death but was not seen in the microbiology. He allowed for the possibility that the URTI developed into encephalitis and resulted in death. While firmly of the view that the abnormal microbiology results were the result of contaminants, he accepted that were this not so they would signify a disease process.  
260.	On this evidence it is possible (and I do not at this point use any adjectival description of the possibility) that some or all of the following applied:
i)	Throughout his short life S was a sickly baby. Indeed this is positively asserted by LA. 
ii)	He periodically suffered from URTI, which is viral. 
iii)	He suffered from a nasty foot infection that was both fungal and bacterial. 
iv)	He suffered from a congenital bleeding disorder.
v)	Alternatively, he just bruised easily.
vi)	On the night of his death microbes from his foot entered his blood stream causing sepsis, which in turn led to an acquired bleeding disorder.
vii)	This infection raised the production of cytokines, but nonetheless overwhelmed him.
viii)	From 9 a.m. he was the subject of 42 minutes of full resuscitation which involved aggressive physical actions including CPR, the prising open of his hands and the holding of his feet, the insertion of IV lines into veins and bone, and intubation/ventilation.
ix)	All of the injuries apart from the bruises to the forearm, the knuckle and the ears were in fact pseudo-bruises caused by resuscitation. For this reason the bruises to the hands and feet were not noted at the visual survey at 10 a.m. The fraenulum was broken by the sharp edge of the Guedel tube.
x)	The severity and frequency of this bruising is accounted for by the presence of a congenital or acquired bleeding disorder.
xi)	The forced circulation caused by the resuscitation attempts gave rise to neutrophil migration to the fraenulum, and palms. They arrived within minutes, not hours.
xii)	The injuries to the ears, knuckle and forearm, and those injuries seen on the backs of S’s hands by N2 and in Exhibit 7, were caused by S being thrown about in the buggy during a reckless bike ride. As Dr L stated it would be surprising if he were not thereby injured. The ears had been repeatedly injured by this means.
My very final conclusions 
261.	I conclude:
i)	Based on my survey of the lay and psychological evidence it is extremely improbable that these parents have ever deliberately inflicted injury on either of these children. It is, however, possible. I do not accept the neighbours’ evidence as to observations of marks or bruises save as to the marks seen by N2 to the backs of S’s hands on the week-end before he died.
ii)	However, I believe that injuries to S, were caused by F recklessly taking both children out in the buggy in disregard of plain safety warnings. M would have been complicit in this, up to a point. There was nothing malign in this. It was just stupidity born of an over-enthusiastic and over-energetic immaturity on the part of F, and, up to a point, M. Obviously, it must never happen again, and I do not believe that it ever will. 
iii)	Based on my survey of the scientific evidence it is extremely improbable that an innocent explanation for S’s injuries is furnished by the eventuation of those things mentioned above. It is, however, possible.
iv)	The paediatric evidence from Professor S does not alter my conclusion in (i) above. Nor does the photographic evidence. It is consistent with my conclusion in (ii). The forensic evidence of FS does not alter my primary conclusion. There are perfectly innocent explanations for blood on the sheet, bib and grow-bag. We know that S suffered from nose-bleeds, that he had an erupting tooth, and had bleeding feet.
v)	Although the orthodox histological evidence is powerful I am not prepared to rely on it to displace my conclusion in (i) above for the reasons set out by me above. I would venture to suggest that there needs to be consideration within the medico-legal community as to reliance on histological evidence such as this in the forensic process where there is such a dearth of research on humans, and, particularly, babies.
vi)	I am not prepared to find that the parents neglected S in relation to his feet. They sought appropriate medical advice for what was certainly a fungal and possibly also a bacterial infection. It is clear to me that there had been a significant postmortem degeneration in S’s feet by the time the photographs of them were taken at the autopsy.
262.	I am therefore left with two improbable explanations namely that S was brutalised and murdered by his parents; alternatively, that he suffered a sequence of pathologically unlikely events that gave rise to his injuries and overwhelmed him. This is a Popi M case. Just as the decision of the House of Lords left no-one knowing why the vessel plunged to the bottom of the Mediterranean Sea, so we are left here with no explanations for the injuries and death of S, other than those I believe were caused in the bike buggy. This is one of those very rare cases where the burden of proof comes (as Baroness Hale put it) to my rescue and so the parents are entitled to the return of Lord Hoffmann’s value of zero, namely that they will be treated in law as if they did not deliberately inflict violence on and to these children.
263.	This is not to say that there is not the possibility, even the real possibility (to use the language of Lord Nicholls in Re H and R when discussing the test under the second limb of s31(2) Children Act 1989), that these parents did indeed so grossly mistreat their children. But a suspicion or a risk is not enough on a fact-finding hearing, as the House of Lords so emphatically confirmed in Re B.
264.	I appreciate that the parents, and indeed the LA, want definite answers and I am sorry not to be able to supply them. I am only prepared to find on the 51% balance of probability test, having surveyed all the evidence holistically as the authorities mandate I must do, that I am not satisfied that these parents deliberately abused their children (as opposed to treating them recklessly in the buggy), or neglected or murdered S. Thus far I am prepared to go, but no farther.