A Local Authority v S

The application before the court is made by the A local for a care order under S.31 of the Children Act 1989 in relation to S, who was born on 17 ^th March 2006 and who has just turned three.

The children’s parents are N (the mother) who is twenty-five years of age having been born on 31 ^st January 1984 and F (the father) who is thirty-two years of age having been born on 31 ^st October 1976.

The proceedings arise out of the death of a second child of the family, Z. Z was born on 27 ^th July 2007. He collapsed at home on 29 ^th October 2007 when he was thirteen weeks old. He died on 1 ^st November.

Background

The mother speaks Puthwari, which is not a written language. She also speaks and reads Urdu. Her English is extremely limited and she has been wholly dependent upon the assistance of an interpreter.

This has been a case which not only has been lengthy, but during which the Court has heard a considerable amount of medical and technical evidence. I am grateful to the hard work, diligence and dedication of the interpreters.

The mother and father’s marriage was arranged by their respective families. It took place in Pakistan in 2003. They are distant cousins. The mother described having known the father’s family since she was a small child. Following the marriage, the mother and father lived for a period of about six months together in Pakistan in a property owned by the father’s family. At that time, the father’s mother was also living in the house in Pakistan. Shortly after the marriage an application was made for a visa for the wife. This application was turned down because the father was, at that stage, unemployed. The father thereafter returned to the UK in January 2004, which necessitated leaving the mother in Pakistan. The mother finally came to this country in March 2005 when her entry clearance difficulties had been resolved.

During the year they were apart, both the mother and father told me that they spoke regularly on the telephone. The father had previously bought a property in the UK which he had hoped that he and his wife would make their home. Unfortunately, he was unable to fund the mortgage and, as he put it, “handed back the keys”. As a result, when the wife came to live in this country, rather than living in her own home with her husband, they lived together with his parents and two brothers in a two-bedroom property.

During the time they were living in the home of the father’s parents, the father’s own father began to suffer from memory-loss. This tragically led to a speedy and distressing deterioration in his health, soon necessitating twenty-four hour care.

The father has a particularly close relationship with his father and, even after the young couple had a home of their own, the father would return each day to feed and assist in his care.

When asked how his wife had settled, the father emphasised that their culture is for the wife to move into the husband’s family home. He told me she spoke the same language as the rest of the family and, indeed, they were distant relatives. His father and his wife’s father had been good friends and so, therefore, the mothers knew each other as well. He described relationships within the family as “quite friendly”.

In March 2006, S was born. A few months later, in May 2006, the father, mother and S moved to live with the father’s sister and four other family members. They had moved out, the father told me, as there was not enough space and it was difficult with his father being ill. His sister, however, had an empty room which they were able to occupy. When asked about his wife’s relationships with his sisters he described them as being, “Okay, not over-friendly, no tensions”. Significantly, he said, his sisters were happy to have S in the house.

In July 2006, the father started to work as a bus driver. In October 2006 the parents moved to their own one bedroom flat, a privately rented property.

After they moved, the father told me that his father remained his responsibility and he went over daily (depending on which shift he was working) in order to feed and care for him. His wife went with him a number of times a week. At one stage, the father had to reduce his working pattern to four days each week in order to be more available to assist with his father. He explained in evidence that he still worked his full hours, but over less days. One can only admire the devotion to his father. The father described how it could take as much as half an hour to feed him one spoonful of food. In addition to that, he was responsible for changing his father’s nappy and bathing him because his father was more comfortable with him than anyone else. One cannot ignore the pressure this must have put not only on the father, but also on the mother setting up home in a foreign country with one tiny child and pregnant with her second baby.

Z was born by normal delivery in July 2007. No concerns were raised about the parents or either child by the health services, and the family were not known to Social Services. Upon the mother’s return home the mother, father and two children lived in the one-bedroom flat at M Road. The father slept with S in a double bed and the mother with baby Z in a single bed. S was sixteen months old when Z was born.

The father worked shifts and assisted in the care of his father. The mother stayed at home looking after the babies.

The father’s devotion to the mother cannot be questioned. He described in evidence how they were not just husband and wife, but also good friends and he hopes to keep it that way. He fought back the tears when he spoke of his love for her, and how she told him everything and confided in him if she felt sad, anxious or unhappy.

No matter how attentive the father may have been, and wished to have been, this young mother was on any view isolated. She spoke, and speaks, virtually no English even to the extent that she felt unable to call the emergency services for help when Z was in extremis . The father said that he encouraged her to be independent and, as he described it, “to fit into this environment”. He said he gave her money, but they shopped together. The problem was the language barrier. His sisters visited the mother when she was alone, but not much as they were busy with their own children. The mother had relatives in the UK, but she tended to speak to them on the telephone. The only example he could think of when she left the house alone was if he was on a break and she occasionally came to meet him in the town centre. On occasion she after Z was born she would also go to his mother’s house.

In addition to the isolation, both physical and occasioned by her inability to speak English, the mother and father both had the anxiety and responsibility of the father having to go daily to his parents’ home to help care for his father. This inevitably meant that the mother would spend long periods of time alone in their small flat with two babies.

On the morning of 29 ^th October 2007, the father left home for work at approximately 7.10am. On arriving at work, he was told that he was not required until later that day and returned home at about 8.50am.

The father told me he spent the remainder of the morning at home. Between getting home at about half past eleven he played with the children, he then went to bed and slept between 11.30 and 1.30pm - together with Z. He returned to work at about 2.15pm; his account is that Z was awake at that stage, although the mother said that he was asleep. The father came home at about 7.15pm for his break, had some supper and returned to work at 7.45. Z was asleep.

The father’s evidence, which I accept, was that during the course of that day Z was in good health. There has been some suggestion that a day or two prior to 29 ^th October, Z may have had a snuffle or a slight temperature. Neither parent has, however, referred to that in evidence. It is clear that both regarded him as a well baby on 29 ^th October.

Both babies, the father said, were normal. He described Z looking at him with a smile and following him with his eyes in a way that he described as “extra than normal”. It is common ground that this was the first occasion that the father had worked this late shift since Z’s birth.

According to the mobile telephone records, at 8.43pm the mother spoke to the father whilst he was at work driving his bus. As a result of that telephone call, a minute later at 8.44pm, the father rang his brother B. As a result of that telephone call, B in turn dialled 999 at 8.45. He told the ambulance control centre that his nephew was having difficulty breathing. He was conscious and breathing, but was breathing heavily and that an ambulance was required.

Meanwhile, at 8.45, the mother herself called F’s parents home where she spoke initially to her mother-in-law and then her sister-in-law, R. Shortly after that phone call one of the father’s other brothers, I, having been told that Z was unwell by his sister, immediately drove round to M Road. I arrived virtually simultaneously with the first ambulance crew, who it is reported arrived at 8.52pm. Meanwhile, B also headed for the house where he arrived to find I, the ambulance having just left. In a short time the father arrived and was told that he needed to go immediately to the hospital.

On the evening of 29 ^th October, a paramedic called Mr B was on duty. He was in the role of what is called “Fast Response”. As a result, Mr B was first on the scene. He was met by the mother crying hysterically with S next to her, also crying hysterically.

Upon examining Z, Mr. B could not feel any pulse, there was no sign of breathing and Z had pink frothy sputum running out of both nostrils and at the back of his throat. Mr. B started CPR at the house. He said in oral evidence that he was getting a chest rise which was a good indicator that air was getting in. He used suction to remove the pink froth once he had Z in the ambulance. He said there was no difficulty in clearing the froth so there were no obstructions to the airway that he could see either then, or when he was using the bag and mask. His feeling was that the suction had successfully cleared the sputum. He described the pink froth in the throat as being minimal and that it did not look like milk.

The ambulance arrived at the Accident & Emergency Department at 9.10pm, where CPR was continued. Eventually, at 9.16pm, a heartbeat and pulse were obtained. At approximately 3am that night (30 ^th October 2007) Z was transferred to Addenbrooke’s Hospital, Cambridge. At approximately 10pm that evening Z had another cardiac arrest (although, on this occasion, he was swiftly resuscitated). Z’s condition continued to deteriorate and he died at 5.20pm on 1 ^st November 2007.

I have to determine the facts of the case against the backdrop of the current law. The Local Authority brings the case and the burden of proving the facts rests upon them. The standard of proof is the balance of probabilities. I have in mind when considering these serious allegations, the judgments handed down by the House of Lords as recently as 11 ^th June 2008 in Re B [2008] (Children) UKHL 35. At para.70, Baroness Hale put it this way:

I adopt, with respect, the descriptions given by the Court of Appeal, Criminal Division, in its judgment on 21 ^st July 2005 in R v. Harris, Rock, Cherry and Faulder [2005] EWCA Crim 1980 paras.63-65:

The Court of Appeal, Criminal Division, then went on to consider the so-called unified hypothesis which arose out of a paper written by Dr. Geddes, known as “Geddes III”. At paras.66-69, the Court of Appeal said:

In Geddes III the unified hypothesis was summarised as follows:

In this present case not only are there a considerable number of experts, but I am asked specifically to make serious adverse findings in relation to two of those experts, Dr. Cohen and Dr. Squier. In Re LU &. LB [2004] 2 FLR 263, the Court of Appeal provided guidelines following the earlier case of R v. Cannings . At para.23, Butler-Sloss P. gave the following guidelines:

The cause of an injury or an episode that cannot be explained scientifically remains equivocal.

Recurrence is not in itself probative.

Particular caution is necessary in any case where the medical experts disagree, one opinion declining to exclude a reasonable possibility of natural cause.

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.

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.

The approach of the court to expert opinion must, it is submitted by Miss Cover on behalf of the children’s guardian, include the need to evaluate the witnesses and the soundness of each of their opinions. The mere expression, she submits, of a belief by a witness, however eminent, does not suffice. The court’s evaluation of the witnesses, Miss Cover submitted as Ryder J. said in A County Council v. XY& Z [2005] 2 FLR 129:

The judge must also examine:

In relation to the task facing the court, I have been reminded of the observations made in a number of cases where there is disputed medical evidence. It is not necessary to rehearse all the learning in relation to expert evidence for the purposes of this judgment, save perhaps to refer to two judgments. When considering the case of W v. Oldham MBC [2006] 1 FLR 543 in his judgment in Webster v. Norfolk County Council [2009] EWCA Civ 59;2009] 1 FLR 1378 , Lord Justice Wall stated that:

Ward L. J. considered the balance as between the Judge and experts in Re B (Care: Expert Witnesses) [1996] 1 FLR 670 (c)-(e):

Ms. Delahunty QC, on behalf of the mother, draws the attention of the court to a recent observation of Wilson L.J. in Re W (Children) [2009] EWCA Civ 59 where he said:

At about 8.30pm on 29 ^th October 2007, Z suffered a sudden collapse which proved to be fatal. The central factual issue in the case is the question of what it was that led to that collapse. This has been referred to during the course of the hearing as the “primary event”.

The Local Authority’s case is that there was a single primary event which provides a full explanation for every relevant observation. It all they submit, fits with a traumatic infliction of a shake or a shaking/impact event which led to Z exhibiting the classic triad of injuries. These injuries were, the Local Authority say, inflicted by the mother when she was alone in the flat.

The Local Authority seeks no findings against the father. They do not suggest either that he was present or that he was responsible for those injuries either directly or indirectly by having failed to protect Z from his mother.

The mother’s case is that she did not shake Z. A number of possible alternatives are advanced by the experts on her behalf, namely that there was a primary event occasioned by heart arrhythmia, a choking event or, hypothetically, some sort of SIDS event (Sudden Infant Death Syndrome). Those representing the mother do not submit that hypoxia is itself a trigger event, but it is suggested that the existence of what is agreed to have been an old subdural haemorrhage in Z’s brain created a vulnerable and ready area for a re-bleed which was triggered by a non-traumatic trigger with a cascade of consequences, including hypoxia, which exacerbated Z’s decline and clouded the pathology findings.

The suggested non-traumatic triggers were a choke, transient heart arrhythmia or failed auto-resuscitation. The cascade of consequences being:

Oxygen deprivation for excess of twenty minutes;

CPR for 24 minutes;

Hypoxia;

Coagulation impairment;

Reperfusion;

Re-bleed;

Ischemia;

The heart collapsing first as opposed to the liver and kidneys;

The second cardiac arrest with additional CPR;

Death;

Ischemic changes following death.

All of the experts accept that a non-accidental head injury is one of the possible causes of Z’s death and must be considered.

The court has heard extensive evidence in relation to the contentious issue of Non-Accidental Head Injuries (NAHI). Oral evidence has been heard from a number of experts in a range of specialities.

At all times during the course of the trial I have borne in mind that the parents do not have to prove anything. It is for the Local Authority to prove on the balance of possibilities that Z died of a non-accidental head injury and not for the parents to prove some other accidental mechanism leading to his death.

Dr. Janice Till was asked to assist the police in their investigations. Dr. Till is based at the Royal Brompton Hospital. She is a consultant there and runs a centre for the study of rhythm disturbances in children. Her particular interest is in sudden cardiac death in children. She sees between eighty and ninety children each year each of whom is at risk of, or suffers from, cardiac rhythm disturbances of one sort or another.

Dr. Nathaniel Cary is a Home Office pathologist. He initially specialised as a forensic pathologist at Papworth Hospital in Cambridge and is now a full-time consultant forensic pathologist. He carried out the forensic post-mortem examination on Z on behalf of the coroner.

Dr. Al-Sarraj is consultant neuropathologist at Kings Hospital in London. He was invited to examine the brain of Z following the post-mortem examination carried out by Dr. Cary.

Dr. Marta Cohen is a consultant paediatric histopathologist at Sheffield Children’s Hospital. Dr. Cohen has an interest in forensic pathology, but it is not her speciality. She frequently participates in post-mortem examinations acting as a paediatric pathologist together with a forensic pathologist. She hopes ultimately to practice as a forensic pathologist in her own right. Dr. Cohen has dealt with peri-natal work since 2003 when she came to work in the UK. She has done 100-105 peri-natal post-mortems of which 10-15% were suspicious. Her experience is, therefore, significantly less than that of the other experts. Dr. Cohen describes herself as an expert on Sudden Infant Death Syndrome (SIDS).

Dr. Waney Squier is a consultant neuropathologist at the Oxford Radcliffe Hospital, and an honorary clinical lecturer in the University of Oxford. Dr. Squier has written extensively on the triad.

Dr. Richard Bonshek is the consultant ophthalmic pathologist at the Manchester Children’s University Hospital Trust and a member of the NHS National Specialist Ophthalmic Pathologist Services. Dr. Bonshek is a member of the Ophthalmology Child Abuse Working Party at the Royal College of Ophthalmologists which published its findings in the Journal Eye in 1999 and again in 2004. Dr. Bonshek’s involvement in the case arose initially when he was requested to examine Z’s eyes following Dr. Cary’s post-mortem.

Professor Phillip Luthert is the Professor of Pathology at the UCL Institute of Ophthalmology. He was formerly a neuropathologist at the Institute of Psychiatry. Professor Luthert’s area of particular interest is specifically om relation to the retina. He has published over a hundred peer reviewed papers and he was a member of the 2004 Working Party. Professor Luthert was instructed on behalf of the parents. Professor Luthert looked at the photographs of the eyes taken under Dr. Bonshek’s direction, and at the slides and sections Dr. Bonshek had prepared.

Mr. Ian Chris Lloyd (known as Chris Lloyd ) is the consultant ophthalmic surgeon and paediatric ophthalmologist at the Manchester Royal Eye Hospital. Mr. Lloyd’s area of special area of interest is the eye in suspected non-accidental injury. He was also a member of the Working Party in both 1999 and 2004. He has examined over a hundred infants suspected of suffering non-accidental injuries. Mr. Lloyd was instructed by the children’s guardian. Mr. Lloyd also looked at the photographs of the eyes taken under Dr. Bonshek’s direction and at the slides and sections he had prepared.

Dr. Mark Peters is a consultant in paediatric intensive care at the Great Ormond Street Hospital for Children in London. Dr. Peters is the research lead for the critical care group within the department of Anaesthesia Intensive Care and Respiratory Medicine in the Institute of Child Health. Dr. Peters’ clinical workload consists entirely of the care of critically ill children within Great Ormond Street and across the North Thames region. Dr. Peters is involved in the care and treatment of more than 2,000 episodes of critical illness in children each year.

Mr. Peter Richards is a consultant paediatric neurosurgeon based at the Oxford Radcliffe Hospital NHS Trust. Mr. Richards practices predominantly in paediatric neurosurgery and he regularly assists the courts in cases such as Z’s. Mr. Richards was originally instructed to provide a report on the events surrounding the death of Z from a paediatric neurosurgical perspective for the police.

Drs. Cary, Al-Sarraj, Bonshek, Peters, Richards, Professor Luthert and Mr. Lloyd all regard non-accidental head injury as the most likely cause of all Z’s injuries and consider it improbable, or highly improbable, that the other suggested causes could have caused the triad and Z’s death.

Dr. Squier and Dr. Cohen regard non-accidental head injury as possible, but unlikely, in the absence of any other bony or soft-tissue injury, or other specific post-mortem evidence of trauma. Dr. Squier agreed that the triad seen in Z was also seen in cases of frank, inflicted trauma and in accidental trauma. Dr. Squier and Dr. Cohen consider the most likely cause of the primary event to be either a choking incident or a heart arrhythmia combined with the effects of prolonged CPR followed by resuscitation.

It is not suggested that Z sustained any accidental trauma has been described and no other cause of death has been suggested, save to the extent that Dr. Squier and Dr. Cohen advance the hypothesis of SIDS.

Drs. Cary, Al-Sarraj, Bonshek, Peters, Richards, Professor Luthert and Mr. Lloyd each hold what might be called the mainstream view of non-accidental head injuries as encapsulated in the judgments of the Court of Appeal in R v. Harris . None accept that hypoxia in the absence of trauma is a cause of subdural haemorrhages and retinal haemorrhages of the type seen in Z. Dr. Al-Sarraj summed up the approach which I find each of this group of experts regard as the proper approach in considering a case where the triad is present:- Dr. Al-Sarraj told the court that:

It was by the application of this correlation that Dr. Al-Sarraj concluded that the subdural haemorrhage found in Z’s brain at post-mortem was there as a consequence of an episode of trauma shortly before death. For example, he said that:

Each of the doctors I have enumerated are of the view that other injuries, such as grip marks, bruises or fractures, either seen externally or at post-mortem, (called during the course of the case as “external injuries”), are neither inevitable nor necessary in order to conclude that trauma is the cause of the triad in a child. Having said that, the presence or absence of such external injuries is evidence to be taken into account. Dr. Cary spoke of it as looking at each element and working them each individually before putting them all together. A number of the witnesses referred to the process as part of a jigsaw.

Dr. Squier and Dr. Cohen have a very different approach in two important areas:

Dr. Cohen does not regard trauma as a proper diagnosis where the triad is present, but there are no external injuries such as bruises or fractures and /or a witness to the alleged shaking event.

Dr. Squier regards trauma as very important. She is of the opinion that the triad, in the absence of evidence of trauma, is simply “no evidence of shaken baby syndrome”. The triad of injuries may be due to many other factors that are not trauma. She does not accept that the triad is necessarily a strong indicator of shaken baby syndrome. In the opinion of Dr. Squirer, shaking alone may cause the triad, but the level of violence required is such that many people would be incapable of it and it would break the child’s neck. She said, in terms, that she would never advise the court that trauma was the probable cause absent external injury, either seen physically with the naked eye or found at post-mortem.

Both Dr. Cohen and Dr. Squier subscribe to the Geddes III hypothesis in one form or another. Put at its simplest, each are of the view that hypoxia in children can lead to subdural haemorrhages and retinal haemorrhages in the absence of trauma.

Upon his admission to the Luton & Dunstable Hospital, Z was cared for by Dr. Houston the paediatrician on call that night. During examination Z continued to make intermittent sustained gasping responses. Z was subsequently transferred to Addenbrookes in the early hours of 30 ^th October where he was cared for by Dr. Ross-Russell a Paediatric Intensive Care Unit Consultant. Dr. Ross-Russell that night, and at all times prior to Z’s death, thought that Z was suffering from a primary cardiac event - that is to say some form of heart disease. Dr. Ross-Russell, at the request of those representing the parents, had been given no updating material before giving his evidence. His oral evidence was confined to his observations and analysis in his role as the treating paediatrician at Addenbrookes.

Dr. Ross-Russell gave evidence that severe heart dysfunction will lead to rapid pulmonary oedema. Fluid accumulates in the lungs and the child becomes short of breath and begins to gasp. Dr. Ross-Russell was careful to emphasise that pulmonary oedema, of itself, is neutral as to providing assistance into the primary cause of collapse. The history given to him was that of choking, vomiting noises followed by apnoea and cardiac arrest. Z’s clotting abnormalities were he said mild - they were not abnormal in the context of the intensive care unit and of prolonged arrest - although they were slightly abnormal for a well child. The bedside ultrasound showed a poorly functioning heart. Dr. Ross-Russell was reinforced in his view that this was a primary cardiac disorder as the heart was more severely affected than the other organs, for example the kidney or liver. Advice on the ECGs of Z’s heart function was sought from Great Ormond Street.

At the time that Dr. Ross-Russell was treating Z , there was no apparent sign of brain injury or swelling, the anterior fontanelle was soft. These features, he said, though not definitive, make it very unlikely that Z was suffering from severe intracranial pressure. One of the key elements of Dr. Ross-Russell’s differential diagnosis was the comparative sparing of the liver, kidney and bone marrow. The amount of myocardial injury was he said very unusual. His working diagnosis therefore was that either myocarditis, a virus or a rhythm disturbance was the cause of Z’s illness. Non-accidental head injury was considered, particularly after Ms. Allen, the consultant paediatric ophthalmologist, reported widespread bilateral retinal haemorrhages.

Dr. Ross-Russell was unaware of the presence of subdural haemorrhages until he was in the witness box giving evidence. He told the court that had he known of them it would have impacted upon his differential diagnosis. Dr. Russell said:

He said that he would still feel the systemic features were very unusual. His primary impression had been of the cardiac problem, but he could not think of any cardiac problem which led to subdural haemorrhages. Dr. Ross-Russell concluded by saying that:

He felt, therefore, that one was looking at the possibility of a shaking impact injury which had led to a cardiac arrest. That being so, the features that he was seeing were still unusual because of the predominance of cardiac symptoms over renal and liver changes.

I bear in mind the importance of that, somewhat unusual, presentation as described by Dr. Ross-Russell.

Z’s eyes were examined twice while he was still alive. Initially, they were looked at by Dr. Brian Houston, the consultant caring for Z at the Luton & Dunstable Hospital. Dr. Houston examined Z at approximately 22.45 on the evening of his admission, 29 ^th October 2008. He examined the eyes with a direct ophthalmoscope without the pupils having been dilated. His note says:

In oral evidence he confirmed that he only had a limited view and that he could not see the whole of the retinal background.

Dr. Louise Allen, the Consultant Paediatric Ophthalmologist at Addenbrookes Hospital in Cambridge, was asked to examine Z some time before at 3.30 on 31 ^st October 2008. She said that she would, as a matter of routine, be called to see any infant who had been admitted with any type of apnoea. Z was heavily sedated at the time of her examination. His pupils were dilated by drops to allow a clear view and the examination was carried out by using an indirect ophthalmoscope (a more sophisticated ophthalmoscope than that used by Dr. Houston- it is worn on the head, has light magnification and a 3D view). Dr. Allen, unlike Dr. Houston, therefore had a good view of the whole of the retina.

Dr. Allen recorded her observations in a contemporaneous note, and expanded and refined it in oral evidence. That note reads:

In evidence, Dr. Allen explained that she said “caused by” CPR as at that time there was no clinical reason to suspect shaken baby syndrome. There were no CT scans and no external injuries.

When asked about Dr. Houston’s examination in A&E, she said that not much weight could be put on that examination, as to carry out such an examination in circumstances of resuscitation was difficult. She added that Dr. Houston was not an ophthalmologist and as the pupils were only 3mm dilated, he would have had a very limited view. She concluded by saying that Dr. Houston did very well to see the haemorrhages at all. Suggestions by the parents that Dr. Houston saw the whole picture of what were only very limited retinal haemorrhages and, that Dr. Allen’s examination revealed subsequent evolution of that haemorrhaging must be considered in the light of the contemporaneous note of Dr. Houston that he had a limited view, and the observations of Dr. Allen that I have just reported of Dr. Allen.

Dr. Allen said that once she became aware of the presence of subdural haemorrhages (after having written her note), she went back to the literature on CPR. Her reading of that literature is that subdural haemorrhages can be found following CPR, but that it is very rare especially in hospital settings and if found they are usually at the posterior pole. There is no evidence, she said, of anterior haemorrhages following CPR. Dr. Allen explained that where there has been trauma there is additional traction on the jelly in the eye, which is at the anterior of the eye and that traction seems to cause anterior haemorrhages. She described it as “shaking jelly tugging on the retina”. She took the view that there was a remote possibility that the haemorrhages she observed had been caused by CPR.

Dr. Allen regarded the possibility of retinal haemorrhages having been caused by hypoxia as “extremely unlikely”. Unlike the pathologists, Dr. Allen sees live babies with severe hypoxia. She said that, although a few may have mild retinal haemorrhages where they have birth haemorrhages, it is no more than that, even where there has been severe hypoxia.

Dr. Allen’s opinion is that the likely cause of the retinal haemorrhages she saw in Z’s eyes was a non-accidental injury such as a shaking injury. Hypoxia, she said, as a cause was extremely unlikely and CPR a remote possibility.

On 6 ^th November 2008 Dr. Flora Jessop, consultant paediatric pathologist at Addenbrookes Hospital, commenced a post-mortem on Z. During the course of that post-mortem she observed the presence of a subdural haemorrhage. The presence of that haemorrhage meant that she was no longer able to rule out non-accidental injury. She therefore followed a well established protocol. Dr. Jessop stopped the post-mortem and Dr. Nathaniel Cary, forensic Home Office pathologist, resumed the post-mortem on 8 ^th November 2008.

Dr. Cary found that Z had been a normal, healthy child and, in particular, there were no abnormalities of the heart. On examination of the brain, he saw blotchy subdural haemorrhages superiorly in relation to both cerebral hemispheres. There was also an area of haemorrhage in relation to the cerebellum, which may have been either subdural or possibly sub-arachnoid.

Dr. Cary sought the specialised opinion of Dr. Al-Sarraj as to the neuropathology arising out of the post-mortem examination and of Dr. Richard Bonshek in relation to the ophthalmic pathology.

Dr. Al-Sarraj examined a number of sections of the dura and also some free haematoma which he had found outside the dura. His examination of the dura showed evidence of a subdural haemorrhage several weeks old and more recent bleeding within the old haematoma in the sections of the dura from the midline, dorso-lateral side of the dura on the left side and lateral side of the dura as a large subdural bleed. This raised the possibility that the more recent subdural haemorrhage he observed could be from re-bleeding from an pre-existing subdural haemorrhage.

Dr. Al-Sarraj also examined the spinal cord. The axon is a nerve fibre which connects other nerve cells. They are generally in bundles. Protein comes down the fibres. One of the proteins is β APP i.e . B eta - A myloid Precursor Protein. If the axon is damaged for any reason, normal transmission will be interrupted and beads or swelling may be found along it. Such observations can be used as an indicator of damage, if deposition is seen in the spinal nerve roots it raises the possibility of traumatic root damage.

The identification of such damage does not in itself tell a neuropathologist whether the cause of the damage is due to ischemia or trauma. Multiple deposits were seen in the anterior horn cells (this is grey matter with nerve cells within the spinal cord itself) that is complimentary to a finding of ischemia. To Dr. Al-Sarraj of particular significance, however, is the βAPP stain deposition seen in the spinal nerve roots which are found outside the actual spinal column.

Old subdural haemorrhage of some week’s duration with superimposed areas of patchy more recent subdural haemorrhage, together with widespread ischemic changes.

Widespread fresh retinal haemorrhages involving all layers and occasionally extending anterior and under the retina, including ophthalmic nerve sheath haemorrhage.

No evidence of resolving grip marks or skeletal injuries to the body.

Dr. Cary concluded that the most likely explanation for the cardio-pulmonary arrest which ultimately led to the death of Z was that of inflicted injury of the shaking/impact type. He did not regard the absence of grip marks or skeletal injuries as affecting the likelihood of that diagnosis. For the purposes of his report to the Coroner’s office, Dr. Cary’s stated cause of death to be head injury. This was subject to Dr. Bonshek’s list of theoretical causes for retinal haemorrhage having been excluded by the other experts.

Dr. Till said she was “very hesitant to diagnose short QT from these ECGs”. She concluded: “you cannot rule out short QT, but it is very unlikely to be the case”. Dr. Till was also asked about retinal haemorrhages. She said:

Balancing together the totality of Dr. Till’s testimony as an expert of these extraordinarily rare Ion Channelopathy syndromes complied with their lack of association with retinal haemorrhages, I conclude that the primary event leading to Z’s collapse was not precipitated by a heart arrhythmia abnormality.

The court has had the benefit of hearing expert opinion from a total of nine experts on the issue as to whether or not the primary event was a choking/primary respiratory event or, alternatively, whether the primary event was precipitated by some form of head trauma.

Only the mother was present when Z collapsed. Her accounts of that evening given both then and more recently, together with the evidence the father can give, are of considerable importance in helping both the experts and the court in coming to a view as to the nature of the primary event and whether it was, indeed, a choking or respiratory event. Before moving on to consider the medical evidence in relation to a choking/respiratory event, it is necessary therefore to consider the accounts given by the parents.

By common consent, Z was a normal healthy baby at 7.45pm on 29 ^th October 2007. Just over an hour later he was in extremis .

The father told the court that the mother had told him when she rang to get help that S had cried when he was having his nappy changed. The father said that he had thought that that was because S had had to stop playing when it was time to change him and that his crying he had woken Z up. This account was the same as the one he gave to the police on 9 ^th November 2007.

Whilst the mother, father and B were at the hospital they were spoken to by, amongst other people, two police officers: W and M. PC M records in his Criminal Justice Act statement that the mother had told him:

PC M then says he spoke to Dr. Houston, the Paediatric Consultant, who told him the baby had been choking which had caused a cardiac arrest. Dr. Houston disagrees with the accuracy of this note.

The evidence of these two police officers, each of whom gave oral evidence, was little short of shambolic. Neither officer was able to give a consistent, or even coherent, account about who spoke to whom, when and about what. Mr W said that the relevant conversation took place in English between him and the father alone, however he seemed incapable of differentiating between the father and his brother. Mr. M said the same conversation was led by himself in the presence of Mr. W. Added to this each officer put together their Criminal Justice Act statements in reliance on the police log. This log was created by means of an oral report given to a Sergeant F who called the information in to an operator who then passed the information along to CID who entered it into the log. There is no paper trail of any of it and it is all by word of mouth. This is an example of the sort of “Chinese whispers”, that is wholly unacceptable in the early evidence gathering phase in a case of a serious injury to a baby which may have been caused by a parent.

The word “choking” has somehow found its way into the log and became the police version of events. That is not to say that the word “choking” was not used, simply that it is quite impossible to know one way or the other. Not surprisingly, neither parent claims it to be an accurate record of anything that was said by either of them.

In fairness to PC M, I should say that it was Mr. W, in particular, who presented as a very unsatisfactory witness and I understand that, whilst he was a probationary police constable at the time, he is no longer a police officer, but a community support officer. I place no weight on either the oral or written evidence of these two officers.

The mother gave an account of Z’s collapse to Dr. Houston at the Luton & Dunstable Hospital on the evening of his admission. The father acted as an interpreter. She said, as is recorded in the medical records,

This is the account upon which the mother now relies, save that she told me in oral evidence that he was in a baby bouncer not a cot and that he did not gasp for 5 or 6 minutes, but rather the whole incident lasted 5 or 6 minutes from beginning to end.

Regardless of whether this is essentially a true account, in that the mother did not by any act on her part cause or contribute towards the collapse of Z, it on any view omits crucial information. The clear impression given by the mother was that Z went from being a sleeping, well baby to ceasing to breathe all in a matter of moments and that the first thing to happen to alert the mother that all was not well was her hearing him making a noise as if he were trying to vomit. Nothing could be further from the truth.

The mother was interviewed by the police on 8 ^th November and again the following day. She made Children Act statements on 21 ^st November 2008 and, again, in February 2009. She gave the court an account from the witness box.

The m other’s first account to the police was that Z woke up and was crying. He would not stop crying even when she picked him up. She rubbed his back, but he still cried. She said: “While he was crying he took deep breaths [and she made the sound effect] like that. I phoned my husband”.

When questioned again the next day, the mother described Z as, “crying very badly”. She spoke of putting him on her shoulder and massaging his back, but he continued to cry “badly, then he was having some trouble breathing”. She said that while he was crying he “badly attempted to have some breath in himself”. Significantly she was asked if he was still crying at that stage and she replied, “Yes, he was”.

In the mother’s first statement, she expanded in this account. Having said that Z woke up and started to cry, she said she checked his nappy. He stopped crying for a little while and then started again. Mother said that she thought he was hungry so she made a portion of milk powder. When it was made she tried to give it to him, but he would not take it and forced the milk back out of his mouth. She said that he cried loudly and would not stop crying, so she walked around the room to try and make him stop crying. He was still crying when his breathing changed and he began to take deep breaths, “He was still trying to cry. He was in difficulties. He could not breath properly and was taking awkward deep breaths...I rang my husband”.

In the mother’s final statement, provided shortly before the start of this trial, she prefaced her account of the events of evening of 29 ^th October 2007 by saying:

Having set out as the backdrop to her statement her clear understanding of the importance of the history she was to give in her statement of what happened that evening, the mother said:

This was quite different from the history given to Dr. Houston. Far from the first thing to alert the mother to any problems being a noise “as if Z was trying to vomit” and, therefore, of him going from being asleep and a seemingly settled baby to collapsing all within moments, this was, a child who woke up and cried inconsolably, despite his mother adopting all the well known ploys used by any mother to pacify him. She changed him, she put him over her shoulder and walked around with him, she rubbed his back and tried to feed him.

In each account, she describes him continuing to cry after he has had difficulty in breathing. The initiation of those breathing difficulties were called “an attempt to vomit” as put to Dr. Houston or simply “breathing difficulties” as in her other accounts between then and her February statement.

In all his accounts, without exception, the father, for his part, is clear that he heard not just S, but Z crying when the mother telephoned him at work.

What the mother did not do in any account is describe how Z woke up. I am satisfied that, had the father not told the court of the account she had given him about S waking the baby, she would not have told anyone. This is very important evidence when trying to have an understanding about what went on in that house on that evening; without it the picture is of a three month old baby “being settled”, with it the picture is two children, one of nineteen months and one of three months, both crying, S having started when his nappy was changed and Z joining in when he was startled awake by the cries of his big brother.

When this was put to the mother, in oral evidence, she sought to play the scene down in a wholly unconvincing way. She described changing S’s nappy and said that she had “touched his thigh” and that he must have thought he was being “tickled” so he screamed, but it was “a happy scream”. He carried on, she said, screaming, but it was a “happy scream”. She accepted that that was what had woken Z and that she had told father on the telephone. But she said, again, it was a “happy scream” that had woken Z up.

It was put to the mother by the guardian, that the timescales must have been significantly longer than the 5-6 minutes she had previously suggested, given that she had changed, and tried to feed, Z, as well as to sooth and comfort him. When asked in this context whether she had made up the bottle for Z she said unconvincingly, and contrary to her statement, that she had already had it made up and it was sitting on the side to give him as she knew he would wake up. Initially she said, with unbelievable precision, that she had made up the milk at 8.05. She then altered this to sometime after 8 o’clock.

When the mother’s evidence was tested, she said the noise Z made was like sucking in and had not lasted as long as on the CD. (A noise all have listened to and was a matter of seconds). Z, she said, neither coughed nor choked.

After Z had forced the teat of the bottle out, the mother said he had carried on crying. After that he tried to vomit and nothing came out, She said in her oral evidence, “After that he did not cry”. When he had breathing difficulties she said in the witness box he stopped crying. She was adamant that after Z had attempted to vomit, he did not cry again. This was contrary to all her earlier accounts when she said that he had cried after he had attempted to vomit. The mother then said that she could not remember whether Z had been crying when she spoke to her husband, but that S had only started to cry when he saw her crying. She denies that both children were crying at the same time.

When the mother and the father gave their oral evidence to the court, the itemised telephone bills for their respective mobile phones were not available. Shortly after closing submissions, the relevant statements became available to the court and, accordingly, the mother and father were each recalled briefly in order to answer further questions about the telephone calls as between themselves and third parties on the evening of 29 ^th October 2008.

During his initial oral evidence, the father has been asked about the mother’s telephone calls to him. He had also described those calls to the police when he was interviewed and in his two statements; the most recent being in March 2009, a matter of days before the trial began. In each account, and again in oral evidence, he described hearing both S and Z crying at the other end of the phone when the mother rang.

Although pressed on a number of occasions by Mr. Geekie QC on behalf of the Local Authority, the father insisted that he spoke to the mother only once, although there had been, he said, two missed phone calls when he was driving his bus and unable to take her call.

The mother, in her statement filed immediately prior to the hearing, spoke of ringing her husband until she could get through to him. The mother repeated this account in oral evidence. She too insisted she spoke to her husband only once only although before that had tried to ring him two or three times. Neither the account of the mother nor the account of the father tie in with the telephone records:

The clear impression given by the father was that immediately upon telephoning his brother, he had contacted his control centre to arrange to leave and go home to his wife and children.

Both were insistent that they had only spoken to each other once.

Neither spoke of any telephone calls after the father had spoken to his brother and the mother had spoken to her mother-in-law.

When asked about the itemised bill, the father said that, after speaking to his brother at 8.44pm, he had immediately driven off before stopping at the next bus stop, which was some distance away. At that stage, he said all the passengers alighted. At 8.54pm he listened to his voicemails and at 8.57pm spoke to his control centre to ask if he could go home as his child was ill – some fourteen minutes after speaking to his wife.

Not only does this not fit in with the impression given by his earlier evidence, but it completely ignores the fact that, between the father ringing his brother at 8.45pm and him listening to his answer service at 8.54pm, he had had a total of ten telephone calls from the mother. The husband says that he cannot actually recollect speaking to his wife on any of these calls, neither can he recollect whether there was one or more than one, or even any, voicemails from her on his answerphone. What we do know is that missed calls do not show up on the invoices and that his answer service took only nineteen seconds to relay his messages to him.

The father denies that he spoke to the mother when he had parked the bus . this, despite the fact that she rang him less than a minute after he spoke to his brother and again some two minutes later. The father finally rang the depot at 8.54, the ambulance having arrived at the family home at 8.52 and the mother having called him, undoubtedly completely hysterical by this time, twice at 8.53. The husband says the only time he spoke to her after the initial telephone call was when he rang her at 8.57pm, a telephone call about which the court would have been wholly unaware had it not been for the late production of the telephone bills.

Ms. Delahunty, in her submissions, urged caution upon the court when attempting to interpret the significance of these telephone calls. The point is well made. I accept that any mother in this mother’s situation would struggle to remember the precise number and duration of the telephone calls made. I also accept that it is easy forget who rang whom particularly as this couple (in common with many other couples) have a missed call ring system and arrangement between them. What I cannot accept, however, is that either the mother or the father would have forgotten a series of increasingly frantic telephone calls made by the mother to the father after her initial cry for help. It may well be that some of the very short calls did, indeed, go to voicemail. I do not accept that they all did. Not least because this father I am satisfied, is a kind and compassionate man who loves his wife. They were in the habit of speaking to each other very frequently on the telephone. There is a record of a telephone call lasting twenty-eight seconds immediately after the father had called his brother to get help. I simply do not accept that, having made the call to his brother on his wife’s behalf, this father would not have rung her back or picked up her telephone call to him in order to reassure that help was on the way. Even had he done such an inconsiderate thing, or the message had gone through to voicemail, it is, in my judgment, inconceivable that when he got call after call (from his account, going through to voicemail) he would have waited for so many calls before telling her that an ambulance was on the way.

I find that neither the mother nor the father is being frank about the telephone calls. Had the statements not been obtained after submissions were over, the court would have been left with the impression of virtually no telephone traffic between the husband and wife, and of the husband making arrangements to come home as soon as his wife got through to him.

Both of the father’s brothers gave evidence about the events of that evening. They were both evasive and reluctant to assist the court in any way. The father, when he gave his evidence, frankly and appropriately accepted this, saying that he could not understand why they behaved in such a way in the witness box as the questions they were being asked were very straightforward. At the time the father gave his oral evidence, I was prepared to conclude that the brothers’ evasiveness was simply reluctance to say anything in the alien court environment which might impact upon their brother. In the light of the new evidence, I believe these brothers may well have known more than they were willing to tell.

Prior to the mother and the father giving their additional evidence about the telephone calls, I was of the view that the husband was essentially a straightforward and honest witness who genuinely, whatever his suspicions may now be, did not know at the time what had happened on 29 ^th October 2008. I have inevitably had to re-visit that view, in the light of the misleading evidence I find he has given about his telephone calls with his wife at or about the time of Z’s collapse. The court is inevitably left with a suspicion that the father is doing all he can to protect his wife, even to the extent of actively misleading the court.

I found the mother’s oral evidence unsatisfactory in a number of ways. S, like any other toddler of his age, can be a handful. The mother described him as being stubborn, sometimes lying on the floor kicking and moving his head from side to side if he did not get his own way. The father was quite matter-of-fact in his evidence that S would start to cry if he was taken away from his toys to have his nappy changed.

Only the mother will ever know what happened on the evening of 29 ^th October 2008, I do not accept that S screamed a “happy scream”. I accept that the father is right when he says that the mother had told him that S was crying because he was having his nappy changed and in doing so woke Z. It follows, therefore, that I do not accept that only Z was crying or that his collapse came out of the blue.

I find on the balance of probabilities that S was crying and cross and woke Z, and that the mother could not pacify the two children. I do not accept that she had already made up a feed and it was sitting out of the fridge in preparation for Z waking up. I believe she told the truth in her statement when she describes trying to settle Z, making up a bottle, changing his nappy, rubbing his back, but that she was unable to console him and that he was crying loudly in a way that she had not heard before. It follows therefore that I do not accept that the whole incident from Z waking up to his collapse took only five minutes or so.

I am satisfied that this mother had two crying babies who she was completely unable to console and it was in that context and in that situation, that Z collapsed.

In order to conclude that the primary event leading to Z’s collapse was caused by choking, it would be necessary for the court to be satisfied on the balance of probabilities that:

Z, in fact, choked;

The choking was capable of causing each element of the triad, as identified at post-mortem.

The mother’s various accounts are set out earlier in this judgment. The mother does not claim a choking event. She describes a failed attempt to vomit and her baby gasping.

Dr. Mark Peters gave evidence that all the mother’s accounts were consistent with efforts on the baby’s part to breathe combined with loud crying. Dr. Peters and Dr. Ross-Russell gave clear, unequivocal, evidence to the court that, if Z was crying loudly, then his respiration was good. A choking event would not be consistent with that account as there would be no air flowing to pass over the vocal cords if he was choking. Dr. Peters said that if Z was choking he would be flailing around, making no noise at all and would turn blue and then white. In fact Z continued to make occasional gasping noises even after he was admitted to hospital. Dr. Peters added that the abnormal deep and struggling breathing described by the mother can be seen after both a head injury and heart failure.

Dr. Peters rejected the hypothesis that Z could have inhaled a quantity of vomit or milk so as to cause his airways to be obstructed. He told the court that a large volume of fluid would be required to cause such an obstruction as it would need to obstruct a significant area of lung tissue. When Z was intubated in hospital, there was no sign of fluid obstructing his airways. Pink frothy sputum, such was seen by the paramedics when they attended at the house, may develop for a number of medical reasons. Dr. Peters explained that there is a close association between neurogenic pulmonary oedema (“NPO”), of which the pink frothy sputum was evidence, and sudden catastrophic brain injury. Whilst not conclusive, Dr. Peters was of the view that the pink frothy sputem seen by the paramedic was consistent with shaking rather than choking and, indeed he observed its very colour indicated that it was not milk.

Dr. Peters explained that if a child is only fed on milk there is no question of an obstruction caused by food, for example a sweet or a peanut. What is necessary therefore, is sufficient obstruction in order to affect the gas exchange and none of the descriptions given by the mother fit.

On the basis of the clinical history and Z’s presentation, each of the clinicians considered the hypothesis of primary respiratory event/choking as unlikely or highly unlikely. Dr. Peters regarded it as physically impossible for Zaid to continue crying if he was suffering or had suffered a fatal choking event.

Dr. Cohen, whose evidence I shall refer in due course, placed significance on the mother’s description of choking. Dr. Cohen referred to a paper called “Sudden Infant Death Syndrome: Can Gastro-Oesophageal R eflux cause Sudden Infant Death? ” by Bradley and Thach. Dr. Cohen suggested that, where a baby is choking and has a gasping reflex which opens the airways, if there are any stomach contents in the larynx, the baby can gasp and tries to breathe and goes into apnoea and dies. She refers to a further paper called “Sudden Infant Death whilst awake” by Henry Krous and others. Dr. Cohen said she thought the SIDS could have caused Z’s collapse. She said that most SIDS cases are not resuscitated, but here he survived. Dr. Cohen said that she believed that if SIDS children were in fact resuscitated we would see subdural and retinal haemorrhages.

In support of Dr. Cohen’s hypothesis that Z had an inadequate response to apnoea, Dr. Cohen (wrongly) said that Dr. Till had referred to Z having an abnormal heart. Dr. Cohen said she plans to investigate SIDS in connection with Long QT syndrome . Dr. Cohen expressed the view that there was evidence of choking by virtue of the mother’s description. Vomiting was not necessary.

Dr. Cohen, contrary to the evidence of Dr. Peters, was of the opinion that a small amount of liquid would be sufficient for Z to choke “Just a few mls” she said. She said, “Maybe” choking is a possibility, but Dr. Cohen said the most important thing is “hypoxia and that is the triggering event that leads to bleeding”. When asked whether or not the view of the paediatrician as to whether or not the child had in fact choked, was the view of the most assistance, Dr. Cohen said that she regarded herself as an expert in SIDS and one theory is that choking may cause SIDS and therefore she felt able to comment. She was most reluctant to defer to Dr. Peters. She said “Choking is a theoretical possibility”. She accepted that her view was controversial. She concluded by saying that she did not think there was any research to the effect that choking is not related to SIDS.

The court was left with theory on theory. Maybe Z choked and if he choked there is a theoretical possibility that it could have been a SIDS-type collapse. With respect to Dr. Cohen, her evidence was a stream of academic speculation and theorising rather than the rigorous forensic analysis necessary on the facts of this or indeed in any case.

The clinical evidence is clear and unambiguous.

The mother gave no description of the baby choking. The word may have been used, but does not tally with her description of the sound effects or her description of Z’s presentation.

If Z was crying after he had choked/attempted to vomit, then he had not choked and the gasping/attempt to vomit could not be a precipitating event which led to his collapse. Dr. Peters felt the gasping noises sounded like the classic gasping noises made by a dying child.

Dr. Cohen and Dr. Squier put forward various theories to account for the “choke”. In particular, some sort of awake SIDs (without any consideration of the fact that the child was crying lustily immediately prior to the event) and compromised auto-resuscitation resulting in the child choking (even though he had not been fed for several hours and had successfully spat out the milk his mother had tried to give him before carrying on crying).

I am satisfied that the mother understood perfectly the evidence given by Dr. Peters about choking and the significance of when Z did or did not cry. He gave straightforward evidence, expressed in common language without the use of any technical terms. As already mentioned, they had the benefit of a first class interpreter throughout the trial. Dr. Peters said that if Z had cried after the attempt to vomit, then he had not choked. I am equally satisfied that it was as a consequence of the evidence of Dr. Peters that the mother changed her evidence in the witness box, saying there for the first time that Z did not cry after he had attempted to vomit. The mother could not, however, get around the fact that not only in her very recent statements and interviews had she said otherwise, but her husband maintained his earlier evidence that both boys were crying when she rang him.

I accept the submission of the Local Authority that there is no evidence of a choking event in this case.

The court has therefore ruled out either a cardiac event or choking/SIDS as being the precipitating factor leading to Z’s collapse. In my judgment the compelling evidence points to the only probable explanation for the presence of the triad being found in Z’s case is that of head trauma This conclusion means that on one view it becomes unnecessary to examine the mass of medical issues raised in support of Ms. Delahunty’s cascade theory. Given the polarisation of the experts’ opinion, and the detail in which a number of these issues have been explored, I am of the view that it is important to consider a number of the aspects of this controversial topic in so much as it is suggested that they may provide alternative causes for Z’s subdural haemorrhages and retinal haemorrhages.

Dr. Squier, in seeking to support her theory of hypoxia following choking as a cause of subdural haemorrhage and retinal haemorrhages, said in her report:

I have had the benefit of hearing evidence from three of the country’s most eminent eye experts. (Four if one counts Ms. Louise Allen of Addenbrookes in Cambridge who is an expert in her own right, but gave evidence in this case as an examining specialist as opposed to a forensic expert.)

Dr. Peters explained that the hypothesis of hypoxia leading to subdural and retinal haemorrhages is based on pathological studies and not on clinical studies. He is unaware of any clinician who supports the hypothesis. An important piece of research that Great Ormond Street Hospital has been conducting is what Dr. Peters describes as “an audit of CPR”. About 77 children in intensive care who were being nursed sedated and could therefore be examined fully and easily were examined by ophthalmologists using retinal cameras following the administration of drops to ensure full dilation of the pupils. The ophthalmologists deliberately conducted their examinations blind, without the benefit of any history, in order to avoid any observational bias. (Although the photographs taken would obviously exclude it in any event). It goes without saying, that these children would be susceptible to reperfusion injury.

The point of entry for the GOSH audit has been:

The children are all over six weeks of age, so as to avoid birth retinal haemorrhages;

infections;

respiratory failure;

clotting that was consequential upon collapse;

trauma;

CPR – which represented eight cases.

Dr. Peters told the court:

The GOSH audit has been submitted for peer review. Dr. Peters told the court that it will be presented or published later this year (2009). It is planned, however, that the study will continue until a total of 300 cases have been examined.

This evidence is relevant to a number of issues in the cascade theory, namely reperfusion, coagulation and retinal haemorrhages. Dr. Cohen, for her part, was not of the opinion that CPR could account for the retinal haemorrhages seen. All her cases, she said, have prolonged CPR and they do not have florid retinal haemorrhages.

On 6 ^th March 2009, Dr. Bonshek, Mr. Lloyd and Professor Luthert had a lengthy telephone conference in which they addressed a number questions which had been previously agreed between the parties. A complete transcript of that meeting (as well as the subsequent meeting of the pathologists) is available and the substance of it has been reduced to a schedule. This is referred to as a “Schedule of areas of Agreement and Disagreement”, in fact so far as the Opthalmologists are concerned it should more properly be called “Schedule of Agreement” as there are no areas of significant dispute between the experts either as between themselves or with the views as expressed by Dr. Allen.

The combined opinion of the Ophthalmic experts can be summarised as follows:

Dr. Bonshek set out in his report his specific pathological findings. Mr. Lloyd and Professor Luthert agreed with his description. The only slight difference was as between Professor Luthert and Dr. Bonshek was as to what Professor Luthert called “calibration”, Dr. Bonshek described the retinal haemorrhages in the left eye as moderate and the right eye as mild to moderate. The left eye he said, was considerably more severe than the right eye; in the moderate/severe range. Professor Luthert for his part referred to the left eye as moderate and the right eye as mild. He said that his categorisation may be influenced by the fact that he tends only to deal with very serious cases. He readily accepted that Dr. Bonshek was in the better position to comment having seen the actual eyes microscopically, as opposed to photographs with all their inherent disadvantages. It seems to me that the shades of description matter not. What is significant is the type, position, depth and distribution, namely that the retinal haemorrhages were bilateral through all layers both posterior and anterior and that there was haemorrhaging at the optic nerve sheath.

There may well have been some progression in the bleeding in the eyes between Dr. Houston’s examination in A&E and Dr. Bonshek’s after death. This, however, does not detract from the fact that it is more likely that there were already extensive retinal haemorrhages when Z was first seen by Dr. Houston. In respect of their aetiology, it is immaterial whether they evolved or not.

Dr. Houston’s observations, or the full extent of them at that point in time, are highly unlikely to have been as a result of CPR or reperfusion.

Whilst the time frame for retinal haemorrhages is 1-8 days prior to Ms. Allen’s examination on 31 ^st October, it was likely to be nearer the one day end.

There is a very strong association between retinal haemorrhage and optic nerve sheath haemorrhage and cases of trauma. Resuscitation following cardio-respiratory arrest and cerebral oedema is a possible cause, but not a probable cause. Such retinal haemorrhages are usually extremely mild, even if there has been prolonged and unskilled CPR. In particular, Mr. Lloyd said that the majority of retinal haemorrhages in infants of this age are due to birth, and are very minor and clear quickly.

Choking/aspiration of milk is outside of probable cause. A simple choking aspiration would not cause optical manifestations of any kind. None of the experts are aware of any instances where an episode of choking or aspiration has led to collapse where the classic triad have been evidenced.

Raised intracranial pressure can cause retinal haemorrhages and optic nerve sheath haemorrhaging. The experts’ meeting did not favour it as a likely cause of retinal haemorrhage in Z’s case.

All the expert evidence in relation to retinal haemorrhages is that trauma is the probable cause of the retinal haemorrhages and the optic nerve sheath damage seen in Z’s eyes.

Each of the three ophthalmic experts gave careful and measured evidence. Time and again the importance of testing out each strand of the triad was stressed by them, as was the importance of keeping an open mind. At no time did the court feel that any of these experts were paying lip-service to being open minded whilst in reality the mere presence of retinal haemorrhage was diagnostic of trauma.

The limitations of the literature on this subject, were acknowledged but at the same time each expert was anxious to stress that their respective view was that the literature, insofar as it goes, supports the view they each individually hold as does their clinical experience. For example, Professor Luthert said in the experts’ meeting:

The Working Party guidance, to which each of these experts contributed, reviewed all the current literature. They are of the view that the guidance still holds good, even though it is some years old, and it ties in with their clinical experience. Amongst other things, the guidance says:

CPR alone is very unlikely to cause retinal haemorrhages, even if carried out by unskilled individuals.

Acute hypoxia, resulting from transient apnoea, has not been shown to result in the SBS picture (in particular subdural haemorrhage and retinal haemorrhage.)

A significant amount of time during the course of the trial was spent in the consideration of the old subdural haemorrhage which each of the experts agreed was present. They agreed also that:

the old subdural was at least a number of weeks old;

there was fresh blood at the location of the old subdural haemorrhage;

it is possible that the fresh blood was a consequence of a re-bleed at the site of the old subdural haemorrhage (although this is not the favoured explanation of all the experts).

It is important, in considering the old subdural haemorrhage to bear in mind that even if re-bleed provided a complete explanation for the new blood, it could not provide an explanation for the sudden catastrophic collapse of Z so as to provide an explanation for the “primary event”. A re-bleed causes collapse through the build up of pressure on the brain due to the space occupying nature of the bleed. Such a bleed would lead to deterioration in condition prior to the collapse and show as a large space occupying subdural, not the thin film of blood that was seen in Z.

Dr. Peters said, “Such irreversible loss of consciousness was not as a result of the bleeding itself, but of the injury which also led to the bleeding”. In as much as one could tell from Dr. Squier’s evidence which seemed to move around from hypothesis to hypothesis, her favoured causation for the fresh subdural haemorrhage found in Z’s brain was that it resulted from hypoxia having caused a re-bleed in the old sub-dural haemorrhage rather than extensive CPR or reperfusion having caused the alleged re-bleed.. She said:

All the pathologists agree that the old subdural haemorrhage could date back to birth. It is accepted by each of them, that there is a possibility that this creates a vulnerability which would lead to a lesser amount of force being required in order to cause a rebleed than that which would be required to cause a fresh subdural haemorrhage.

In evidence, Dr. Cary said: “If it was suggested that only minimal trauma was necessary for there to be a fresh bleed, the evidence in the eyes would be against minimal trauma” . In his experience, the nature and extent of the retinal haemorrhage were typical of the trauma seen with fresh subdural haemorrhage. The assessment of force should, in his view, be related to the eye damage and not the subdural haemorrhages. Dr. Al-Sarraj is of the same opinion. He said that whether or not it was a completely new subdural haemorrhage or a re-bleed does not take the matter much further. If it is the result of a re-bleed, it is related to an episode of trauma or movement of the brain within the skull. It was the second episode, he said, which led to Z’s collapse.

Reperfusion injury was suggested by Dr. Squier as one of a number of possible causes of Z’s retinal haemorrhages (as well as his subdural haemorrhage) although, as already noted, it does not seem to be her preferred causation. Reperfusion occurs after a relatively long period of cardio-respiratory arrest. The surge in pressure against the damaged cells, once circulation is re-established, can render those cells more likely to bleed. The ophthalmic experts do not accept this to be a cause of the retinal haemorrhages, although, as explained by Professor Luthert in his report, it is one of a number of factors which could have caused some evolution of the retinal bleeding between the primary event and death. In relation to the aetiology of the retinal haemorrhages, it was immaterial Dr. Luthert said whether they had or had not evolved. In the same way that re-bleeding gives the court no assistance as to the cause of the primary event, neither does reperfusion which, after all, is one of the consequences of resuscitation, not a cause for a child requiring resuscitation in the first place.

Dr. Al-Sarraj observed nerve root damage predominately to the posterior nerve roots he regarded this as an indication in favour of trauma. Whilst he was cautious about the interpretation of this finding, which although in the presence of ischemia can be difficult to interpret, he regarded the presence of nerve root damage in this case as an indicator in favour of trauma. Dr. Squier accepted that nerve root damage may occur in trauma. Indeed, she said in evidence, that some years ago she would have regarded such damage as having been an extremely strong indicator of trauma.

Dr. Squier, distributed some photographs by email to the experts after the beginning of the trial. They purported to show cases in which she had been in volved which had resulted in her changing her view. She said that they demonstrated by photographic evidence examples of nerve root damage in the absence of trauma. Dr. Al-Sarraj was somewhat scathing at the production of such photographs accompanied, as they were, with nothing more than the briefest case history. He said:

Dr. Cary also expressed his disquiet at Dr. Squier’s photographs being taken into account without the cases having been thoroughly considered.

I do not regard Dr. Squier’s photographs as helpful, produced in the way they were, without the neccessary information being made available to allow a proper and detailed forensic analysis of the cases to which she referred.

Dr. Al-Sarraj was clear that this is an area which is expert understanding developing and, given the presence of significant ischemia in Z’s case, I draw no conclusions one way or another as to the relevance of the presence of the axonal damage.

Both Dr. Cohen and Dr. Squier regard as highly significant the absence of any external injuries, such as grip marks, In the experts’ meeting, Dr. Squier said that, in the absence of any evidence of trauma such as fractures and bruises and where there were no eyewitnesses but there was evidence of hypoxia, she would conclude that a hypoxic event would have been the cause of the subdural bleeding. The subdural bleeding itself she said was most likely a consequence of Ion-Channelopathy or choking.

Dr. Cary responded in that meeting by saying that, from a forensic pathological point of view, in cases in which the triad is seen, the examining doctor does not by any means always see bruises or skeletal injuries. Significantly, he said:

In her oral evidence, Dr. Cohen, when pressed, said that she “requires” external trauma such as grip marks before she is satisfied that the presence of the triad is an indicator of trauma. Dr. Cohen noted that only the mother was present when Z collapsed and that there was no witness to any trauma.She said in elaboration “there is evidence of heart failure when we look at the ECG”. When challenged about her assertion that there was evidence of a heart abnormality, Dr. Cohen retreated by saying that there may be a “possibility” of there being a “problem” to the heart. She said, finally, that she had to leave it to Dr. Till, as she was not a cardiologist. Unfortunately, that fact had not prevented her from either misreading or failing to read the notes showing that Z had a normal heart This failure as was clear from her oral evidence, resulted in her belief that Z had a specific heart defect upon which she then relied to support her theory.

Dr. Squier, for her part, has a similar reluctance to put forward trauma as a likely cause for a primary event in the absence of external injuries (by which she means bruises, grip marks and fractures, whether visible externally or only visible at post-mortem). Dr. Squier went further than Dr. Cohen, suggesting that the nature of the force that would be required for a shaking injury would result in the child having a broken neck. In the event that the child had been subject to a so-called shake/impact injury, she would, she said, expect to see bruises and marks. She does not accept any theory that suggests that such children are often thrown down onto soft surfaces such as a bed or a sofa –with the consequence that there are no external injuries.

The cascade effect put forward by Ms. Delahunty has as a key element, hypoxia as a potential cause of the subdural haemorrhages (if they were not caused entirely by re-bleed) and of the retinal haemorrhages. It is necessary, when considering this aspect of the matter, to consider the approach of both Dr. Cohen and Dr. Squier towards this difficult and controversial area of medicine.

Dr. Cohen believes that hypoxia alone can cause subdural haemorrhages (Geddes III). This is rejected by Drs. Peters, Cary, Al-Sarraj, and Mr. Richards. Dr. Squier, in the experts meeting of the pathologists held on 13 ^th March 2009, said that it is difficult to establish a causative link between hypoxia and bleeding from the dura. The association between the two is she says “well documented and very significant” That opinion led her to conclude that the bleeding in Z’s case was the result of an hypoxic, ischemic injury.

All the experts accept that this case is unusual in that the period of time in which Z was in cardiac arrest and, therefore, to which he was subject to CPR was unusually lengthy. As already discussed, the heart seemed to be affected first rather than Z’s other organs. This does not mean, however, said Dr. Bonshek, that the presentation overall is atypical of shaken baby syndrome. I have to bear in mind the words of Lord Justice Wall when considering these unusual features of Z’s presentation.

All the experts are in agreement that the literature relating to each element of the triad has its limitations both as to its extent, and, as more than one expert pointed out, the intrinsic impossibility of experimenting on babies.

The trial bundle contained more than fifty research papers relating to various aspects of the medical issues raised during the course of this trial. The experts agree that often the evidence base upon which the papers rely is poor and in certain areas there are only a small number of studies. Time and again, when giving evidence, experts spoke of their own experience. It seems to me that the experience of these eminent clinical experts, acquired by them day after day in practice, is highly relevant, particularly where there is a paucity of top quality research to assist the count.

In considering the evidence of Dr. Cohen and Dr. Squier, I have in my mind the guidance of Butler-Sloss P. in Re LU v. Re B (set out above), and in particular:

That the court must be on guard against the dogmatic expert... who has developed a scientific prejudice and:

A judge in care proceedings must never forget that today’s medical certainty may be discarded by the next generation of experts.

The latter is of importance in the present case where it is accepted by all that there is much to learn and much which is not yet understood about so-called shaken baby syndrome and the triad. Dr. Cohen and Dr. Squier each agree with Geddes III. Dr. Cohen and Dr. Squier each believe that in the absence of additional external injuries, such as grip marks or fractures, there is no reliable evidence of shaken baby syndrome. Dr. Squier does not accept the triad to be a strong indicator of shaken baby syndrome.

These views are, undoubtedly, controversial. They go against the mainstream of current thinking and the analysis of the Court of Appeal in R v. Harris . Dr. Al-Sarraj told the court that his views are in line with mainstream opinion. Mainstream opinion in all the other specialities is the same as his, that is to say that hypoxia cannot cause subdural haemorrhages. Al-Sarraj told the court that there are 40-44 neuropathologists in the country of whom a maximum of 10 or 12 are forensic neuropathologists. To his knowledge, the only neuropathologist in the UK believing that hypoxia can cause subdural haemorrhages is Dr. Waney Squier. In addition, he said there are two or three other people who share her opinion who are working in different, but related, specialities, of whom Dr. Cohen and Dr. Scheimberg (Dr. Cohen’s co-author) are presumably two. Dr. Al-Sarraj said:

I found Dr. Al-Sarraj to be a very impressive witness. He was fair, measured and rigorous in his analysis. He is an exemplar of the process. He analysed the information available to him within his own speciality. He then put it together with the views of the experts in the other relevant specialities before reaching a conclusion. I did not think, contrary to what was put to him in cross examination, that he was seeking to back away from his observations in his first report where he had said that the “findings are difficult and hard to interpret”. It was simply that, only as he received the input the additional expertise of Dr. Cary and Dr. Bonshek, was he able to put the picture together to reach his concluded view, a view shared not only by Drs. Cary, Bonshek and Al-Sarraj, but also Dr. Peters and Mr. Richards.

Dr. Cohen and Dr. Squier support Geddes III, even though Dr. Geddes herself in Harris withdrew from her own unified hypothesis. Dr. Cohen and Dr. Squier maintain their position that in the absence of external injuries trauma cannot be established despite the Court of Appeal’s conclusion that:

In considering the evidence of Dr. Cohen and Dr Squier, I remind myself that four years have passed since Dr. Geddes accepted that her unified hypothesis could no longer credibly be put forward. Dr. Cohen and Dr. Squier regard themselves as having built on her work. I remind myself also that the next generation of experts and scientific research may, as Butler-Sloss P. said:

I have to consider whether or not these experts have “developed a scientific prejudice” or whether they are in the vanguard of research and learning.

In the context of the evidence given by Drs. Cohen and SquierI have to consider whether their respective beliefs in:

Geddes III

That trauma may only be regarded as likely causation where there is a triad plus additional external injury (or alternatively a witness) has led to their conviction in respect of SBS overwhelming their forensic analysis of the case.

Having read the careful submissions of the Local Authority and the children’s guardian, it seems to me there are three areas which the court should consider in relation to each of Drs. Cohen and Squier in order to determine that issue namely:

Their use of research material;

Their willingness to defer to the experts in another field and as part of that their acceptance of the importance of confining their respective opinion to their own expertise and;

The importance in any forensic examination of factual accuracy and in this case, in particular:

In Dr. Cary’s opinion there is no clinical evidence, from a clinical point of view, that hypoxia causes subdural haemorrhage. He has extensive pathological experience of resuscitated children with severe hypoxia and has seen no evidence in any case that he has ever dealt with that a hypoxic injury causes subdural haematomas.

In 2007, a paper was published called “ Lack of evidence for a causal relationship between hypoxic - ischemic encephalopathy and subdural haemorrhage in foetal life , infancy, and early childhood ”. Roger Byard, a forensic pathologist from Australia, was the lead author of six authors, all of whom are forensic pathologists, from five different countries from around the world. The cohort was 82 foetuses, infants and toddlers with proven hypoxic ischemic encephalopathy and no trauma (but including four cases of aspiration of food/gastric contents). In no case was there microscopic evidence of subdural haemorrhages. The study concluded that no support could be given to the hypothesis that hypoxic ischemic encephalopathy in the young, in the absence of trauma, causes subdural haemorrhages.

In their conclusions, the authors expressed the view that their results accorded with the judgment in the Court of Appeal in Harris that: “The unified hypothesis can no longer be regarded as a credible alternative cause of the triad of injuries”.

Dr. Cohen together with one of the co-authors of Geddes III, Dr. Irene Scheimberg, published a paper in 2009 called “ Evidence of occurrence of intradural and subdural haemorrhage in the perinatal and neonatal period in the context of hypoxic ischemic encephalopathy. An observational study from two referral institutions in the United Kingdom ”. The examination included 25 foetuses and 30 neonates who lived for between one hour and nineteen days. The stated finding of the paper was that subdural haemorrhage on the convexities of the cerebral hemispheres is not an unusual finding in the setting of intrauterine, perinatal or neonatal deaths.

Dr. Cary had read and considered the Byard research and Dr. Cohen’s recent papers. He was critical of both papers in so far as he was of the opinion that foetuses should not have been included in either cohort, Despite that criticism, he confirmed that the important factor was that the Byard paper showed no evidence in any of the 82 children included of a causal connection between hypoxia and subdural haemorrhage.

Dr. Cohen’s recent paper looks at different circumstances and a different age group. Dr Cary says this article simply shows that it is not uncommon to get “a bit of intradural and subdurals at birth”. This is not either new or surprising as asymptomatic birth subdurals are seen, he told the court, in approximately 46% of all live births.

Dr. Cary says that hypoxia in the brain is “incredibly common” in these circumstances. It does not prove causation. In any event, he says, the cohort examined were foetuses, fresh still-births or neonatal deaths. It is necessary therefore to take into account that there has been recent labour and the effect of that on the brain of hypoxia and or the circulation, and therefore the potential for a rise of venous pressure. It is deeply disappointing, Dr. Cary said, that there is a press campaign, in which Dr. Scheimberg has given interviews, (although not Dr. Cohen), that suggests that the Cohen / Sceimburg article gives valuable insight into shaken baby syndrome. Dr. Carey is adamant that it is of no assistance whatsoever.

Dr. Al-Sarraj agreed with Dr. Cary’s conclusions. He said that hypoxia alone cannot cause a solid subdural haemorrhage seen with the naked eye, as in this case. He bases his views on a number of matters:

Dr. Al-Sarraj was critical of Dr. Cohen’s conclusion that the analysis of the data in her paper was, “confirmatory of Geddes III”. Dr. Al-Sarraj looked at the data relating to the newborn babies, (as opposed to the foetuses). He referred to the fact that there were ten cases which had pathology other than a hypoxic ischemic injury. In effect he regarded the research as “lightweight”, referring specifically to the fact that:

He understood that the paper had been peer reviewed, but felt that the paper was being used to support a hypothesis far beyond its findings.

Dr. Al-Sarraj concluded by saying that even if the cases examined were “¾ per cent pure”, there was no information as to whether or not there were retinal haemorrhages present, no information as to how many cases in total were reviewed and the inferences drawn go wholly against his clinical experience. He concluded his remarks by saying that the paper creates many issues and he anticipated seeing many people writing against it. Al-Sarraj was unequivocal in his view, that he did not regard the paper as credible if it purported to say that hypoxic injury leads to subdural haemorrhages.

Dr. Cohen explained that, as per her paper, she frequently sees subdural haemorrhages in young babies with no suspicious circumstances. She and Dr. Scheimberg believe the subdural haemorrhages are caused by hypoxia. Put as best I can it would seem that the theory is that the dura is highly vascular and the hypoxia ruptures a transmembrane protein called Claudin – 5 causing bleeding. I feel unclear as to whether I have accurately recorded this hypothesis. It was touched on in Dr Cohen’s report but she elaborated on it in other experts or of the court.

Dr. Bonshek says that Dr Cohen’s paper is very similar to Geddes III. Similar he said to Dr. Geddes’ paper in terms of speculation made about materials not examined. In saying this he refers to an observation in Dr. Cohen’s paper that the findings indicate that hypoxia may also play a role in the aetiology of retinal haemorrhages.

Dr. Cohen accepts that the Byard paper comes to a different conclusion from her. She notes that all the authors are forensic pathologists, whereas she and her co-author are paediatric pathologists. She does not believe that authors of the Byard paper have the “practice to sustain what they say”. Dr. Cohen does not, however, explain why, if her hypothesis is correct, none of the clinicians (clinicians, in the position of Dr. Peters), the forensic pathologists or the neurosurgeons, are seeing subdural haemorrhages in cases of pure hypoxia.

Dr. Cohen said that her paper is “confirmatory” of Geddes III and is, she says, “more scientific”. Dr. Geddes, she said, had said that subdural haemorrhages can be caused by hypoxia, but what Dr. Cohen’s paper says is that hypoxia can cause intradural haemorrhages and resulting in a thin film of haemorrhage. Such is Dr. Cohen’s confidence that she says it is not merely a theory, rather, she said “we have developed a close association that hypoxia leads to intradural haemorrhages leading to subdural haemorrhages”.

I have grave concerns about Dr. Cohen’s paper being used in any way to support a proposition that suggests that it has been scientifically established that subdural haemorrhages are caused as a result of hypoxia (direct as in Geddes or indirect by intradural haemorrhages, as suggested by Dr. Cohen).

It has long been established that a significant number of babies (46% is the agreed figure for the purposes of this hearing) are born with small subdural haemorrhages. These haemorrhages are largely asymptomatic and resolve on their own. What limited research there is suggests that they are largely gone by the time the baby is a month old, but they can linger on for as long as three months. It is for that reason that despite the view of some of the experts that this related to an earlier episode of trauma, it would have been wrong of this court to discount the possibility that the old subdurals found in Z’s brain dated from his birth.

Dr. Bonshek, Dr. Cary and Dr. Al-Sarraj are all of the view that all Dr. Cohen’s paper does no more than confirm what is already known, namely that a number of tiny babies have subdural haemorrhages following the birth process which is, by its very nature, traumatic. I regard it as impossible to draw any further conclusions from this paper.

The cohort of children were foetuses (which the preponderance of medical opinion suggests do not provide the court with useful data given the fundamental differences between a child in the uterus and a live child) and babies up to nineteen days old, the later covering the very period when one would expect to see birth subdural haemorrhages.

It became clear in the course of her evidence that Dr. Cohen and Dr. Scheimberg had been selective in respect of the inclusion of children in the study. In other words, unlike Dr. Peters’ study at GOSH, not all babies who matched the entry criteria were included in their study. This must inevitably undermine the value of the study. This does not, however, mark the limit of my concern in respect of use being made of this paper in support of the proposition that Z’s subdural haemorrhages were caused as a consequence of hypoxia following choking: