A Local Authority v S

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:

“Such a diagnosis is a correlation of different features and though it is tempting to take each part separately, you have to take them collectively for a proper diagnosis/conclusion.”

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:

“Although you cannot see the difference between a re-bleed and trauma, we are looking the subdural haemorrhage down the microscope. If you take everything together, particularly the eyes and the history, you can conclude that, even if the subdural haemorrhage was a re-bleed, then it related to trauma/movement of the brain within the skull.”

And

“This diagnosis is affected by other findings, for example retinal haemorrhages in this case not only exist, but are of a distribution more likely to have been caused by trauma. Then, put all those matters together and the findings take a different interpretation, one that is more likely to be of trauma.”

And

“It is very important to remember that this is not a one-discipline diagnosis. You cannot rely on just what you see in the brain. It is suggestive and, with the other findings, it becomes a probability.”

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:

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:

“In the presence of subdural haemorrhages, if it was going to be said the primary event was a cardiac event there would have to be an explanation for the subdural haemorrhages.”

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:

“Subdural haemorrhages were associated with non-accidental head injuries and seen in any child of this age would make you concerned as to the possibility of a non-accidental head injury.”

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:

“Limited view, but there appears to be two haemorrhages in the left fundus close to the disc (pupils only about 3mm dilated).”

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:

“He has extensive bilateral multi-layer haemorrhages. These are most numerous in the posterior pole of each retina.

In excess of 10 deep retinal haemorrhages.

In excess of 50 superficial haemorrhages.

In excess of 5 subhyaloid haemorrhages - each eye pre-retina between the vitreous and the retina.

In the absence of metabolic or clotting, these findings are consistent with raised venous pressure caused by CPR or with shaking injury.”

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 βAPP i.e. Beta-Amyloid 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.

At the top of the spinal cord, at the cervical segment, Dr. Al-Sarraj found a heavy deposition. At the thoracic segment there was a focal deposit in a few

Due to the fact that these depositions in the spinal nerve roots are mainly in the posterior aspect and focal, rather than throughout the spinal cord, this raised the possibility to Dr. Al-Sarraj of the possibility of traumatic axonal damage. Although ischemia (which was seen throughout the spinal cord), could not be completely excluded as the cause of an axonal injury, it was, he said, also possible that it was the consequence of the movement of the spinal cord and stretching of the nerve roots in shaking. In other words, a hyper-flexion, hyper-extension injury.

βAPP examination in the cranial nerve roots of the brain was carried out. This is done routinely. Although there is no peer reviewed literature as yet published, this is an area of research in which Dr. Al-Sarraj’s department is engaged. Damage in that location would tend to favour ischemia and in Z’s case there was no evidence of axonal damage in the cranial nerve roots. When the cranial nerves are not involved and only local and posterior spinal nerves, whilst you cannot totally exclude ischemia as the cause, it is more likely, Dr. Al-Sarraj said, to be due to trauma.

Dr. Al-Sarraj concluded his report of 8^th February 2008 by saying that the

Dr. Al-Sarraj was of the opinion that shaking as the cause of Z’s injuries had been initially supported by the findings of SDH and the damage to the spinal nerve roots particularly the damage to the posterior nerve roots in the cervical snfd thorasic segments. Shaking as sthe cause of the primary event was now strengthened when put together with the evidence of Dr. Bonshek of virtual haemorrhages which had been observed early in the admission of the child which meant that they were not secondary to other causes.

When cross-examined, Dr. Al-Sarraj accepted that one relevant factor was the extent of the ischemia. He said, “I am always very careful and it is absolutely wrong to come a conclusion too soon”. He said that when he had done his first report:

“I had a brain in front of me with a small story. It would have been irresponsible not to allow for other possibilities. I did not have the eye pathology, only the clinical. If you want to judge my opinion, judge my final report”.

Dr. Al-Sorraj emphasised that his final diagnosis was affected by other findings, for example the retinal haemorrhages. He said, “It was of a distribution more likely to have been caused by a trauma”. Therefore, his findings take on a different interpretation, namely trauma.

Dr. Bonshek set out in his report his specific pathological findings:

“The eyes showed widespread bleeding in, and associated with, the retina and the optic nerve sheath. In particular there were widespread retinal haemorrhages in the eyes, more so in the left than the right. The haemorrhages involved, primarily, nerve fibre layer, ganglion cell layer haemorrhage, especially posteriorly. There were a number of microscopic foci and intra-retinal haemorrhages involving the layers extending up to the periphery of the retinas in both eyes. Posteriorly there were so-called pre-retinal haemorrhage, especially in the left eye and there was vitreous detachment with sub-hyaloid haemorrhage present. In the left eye a small amount of blood was present in the anterior chamber. The haemorrhage was most extensive in the subdural location, although there was bleeding in the sheath and bleeding in the orbital tissues adjacent to the optic nerve. The retinal tissues and the tissue of the optic nerve heads showed secondary oedema.”

Dr. Bonshek in his report indicated that the bleeding associated with the retina and the optic nerve sheath were of a distribution and type which is consistent with a traumatic origin, in particular due to a non-accidental injury or shaking impact. He said, however that other causes should be considered.

Dr. Bonshek, accordingly, provided the police with a list of in excess of thirty causes of retinal and associated haemorrhages ranging from the relatively common to the rare to the vanishingly rare.

At an ophthalmic expert’s meeting held prior to the trial, Dr. Bonshek added to his list an additional couple of potential causes. Each one of the possible causes appearing on Dr. Bonshek’s lengthy list has been painstakingly considered. The work involved in order to exclude each possible cause no matter how remote has led to a delay in the hearing of this case. It is, however, an indicator of the rigour to which Dr. Bonshek has approached his consideration of Z’s death and the open mind with which, it seems clear to me, he comes to each and every case upon which he is invited to report.

Having received the reports of Dr. Al-Sarrarj and Dr. Bonshek, Dr. Cary filed a further report dated 19^th May 2008. He identified:

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. Cary’s opinion as to the cause of Z’s death is not accepted by the parents and other possible causes were explored at the trial on their behalf.

Given that all the experts are agreed that some primary event caused a sudden and catastrophic encephalopathy, it is necessary to examine the likely alternatives.

Given that the early view of Addenbrookes Hospital was that the primary cause of Z’s collapse was related to his heart, the police asked Dr. Janice Till to assist them in their investigations. She concentrated on rhythm abnormalities given that, at post-mortem, Z’s heart had been found to be normally formed and there was no evidence of cardiomyopathy.

Dr. Till is an expert in Ion-Channelopathy, a group of rare diseases that affect the electrical functioning of the heart without affecting its structure. This means they can only be detected in life and not at post-mortem. A fault in the heart in these conditions can be seen only by looking at ECGs and is usually identified by looking at what is known as the “QT intervals”. QT interval is a measure taken from the ECG waves - from the Q wave to the end of the T wave, each corresponding to an electrical systole - that is to say the time at which the ventricular contraction occurs.

In relation to Z, the only relevant Ion-Channelopathy is known as “Short QT syndrome”. This is an extremely rare condition which has only been recognised within the last decade. Approximately one in a thousand individuals present with a sudden cardiac arrest. Of those, approximately 4% will suffer from an Ion-Channelopathy. Of these about 10% is made up of Short QT and another similar syndrome. The extreme rarity of the syndrome is best illustrated by the fact that Dr. Till, despite specialising in Ion-Channelopathies, has never seen a case of Short QT in a child and only once in an adult. The ambulance ECG did show a short QT reading, but it is however important, Dr. Till said, when assessing the length of the QT interval, to have a normal heart rate (sinus rhythm) as the QT intervals lengthen and shorten according to heart rate.

A mathematical formula called Bazett’s Formula is designed to smooth out the differences of the very low heart rate, but the formula does not hold good at the extremes of the very high and the very low, both of which Z was subject to from time to time during the course of this illness. Even without the effective use of Bozell’s formula.Dr. Till feels that whilst in the ambulance the heart rate was slow and the QT short. W hen the heart rate returned to normal there were short QT intervals, but only just outside normal and post-resuscitation they were “even more normal and not so short”.

Dr. Till described how the reliable interpretation of these ECG’s was extremely difficult and made more difficult by a number of confounding features:

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:

“The evidence is that there is no recognised association. There is a very small chance that it is Short QT syndrome. I was extremely sceptical anyway on the cardiac evidence and you cannot explain retinal haemorrhage in connection with Short QT, so that makes me even more doubtful...I cannot rule it out, it is very rare and with the other findings at post-mortem, which I cannot explain with it, it would make me doubt very much the presence of this condition.”

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:

“The baby was given a feed of powdered milk at about 1700hrs and placed in a bouncer in the living room where he slept. At about 2030hrs the father came home on a break and checked on the baby who was okay. The baby then started to choke whilst asleep in the bouncer. The mother, who does not speak any English, had to call her husband to telephone for an ambulance.”

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,

“Was well until now.

He may have had a temperature 2/7 ago Calpol.

Today had been okay.

Was in cot – mother in the room.

Heard him making a noise as if to vomit, but nothing came out.

Started to have difficulty breathing sounds like gasping reflexes.

Mother called dad – working nightshift - to say there’s a problem, he called brother to call ambulance.

Mother said he gasped for 5-6 minutes.

Changed colour and pale.

Then stopped breathing.”

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 mother’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:

“I have made a lot of statements to a variety of people relating to Z’s collapse on 29^th October ... I don’t think it would help to go through each one in this statement, but I know my account of Z collapsing at home is not accepted so it is important that I am clear about what I say happened and what I reported as happening.”

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:

“I am clear that Z seemed generally okay during the day and things went wrong from when he woke up after his nap at 8.15/8.30pm. He had his last feed at 6.30pm and he had gone to sleep in his baby bouncer in the front room with no problems after being winded... Z cried when he awoke, but that was not unusual. However, it was not normal for him to continue crying, as he then did, after being picked up and comforted. His cries got more persistent. I tried the usual things to sooth him. I winded him over my shoulder. I walked around the room with him. I tried to give him milk, but he resisted by moving his mouth from the teat and pushing it out of his mouth. He would not stop crying – not little ones, but big ones with tears in his eyes. He made noises as if he was trying to vomit or bring something up, but nothing did. He was crying and was clearly having difficulty in breathing. His colour changed, it became paler.”

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:

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:

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 Reflux 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.

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:

“In the presence of chronic subdural membrane, small vessels are damaged by hypoxia and they may bleed, particularly following resuscitation which leads to reperfusion injury. I assume that the vessels of the retina, being similar to the vessels in the brain, should be subject to similar damage by hypoxia and would bleed on reperfusion”.

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:

Dr. Peters told the court:

“What has been seen overall is very occasional and unilateral haemorrhages with a pattern of bilateral haemorrhages in multi-levels only being seen within the cohort which represents unequivocal trauma. So far as CPR is concerned there has been one observation of retinal haemorrhages after CPR, but that was a single isolated unilateral haemorrhage. Similarly cases of hypoxia, following respiratory failure, following infection has only exhibited isolated unilateral retinal haemorrhages.”

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:

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:

“I think it is generally agreed that from the overall body of published literature (subject to selection bias) is that trauma outside of the birth related haemorrhage period is the most commonly seen cause of extensive retinal haemorrhages and combined optic nerve haemorrhages...In my experience, in most instances where there is retinal haemorrhages, I see optic nerve haemorrhage so I think the two are closely linked together in this syndrome with swollen brain, subdural haemorrhage within the intracranial cavity and retinal haemorrhages.”

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:

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:

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:

“The history is the most important information from which to form a diagnosis and mother’s description of Z trying to vomit was a very reasonable description of what could happen in a choke. Baby becomes hypoxic, starts to bleed, becomes coagulopathic and the bleeding gets worse.”

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:

“To examine the brain and spinal cord is very complex and you have to look at all areas and correlate very carefully. So an out of focus photograph of an area I cannot properly identify is wholly unacceptable. I would need to see the brain, the cord and the cranial nerves.”

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:

“However, the pathology of the triad is identical in cases where you do see grip-like bruising and the cases in which you don’t”.

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:

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:

“They come in all the defence cases, so you do not realise that they are in such a minority.”

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:

“The triad of injuries becomes central to a diagnosis of non-accidental injury where there are no other signs or symptoms of trauma, such as bruises or fractures.”

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:

“Throw light into corners that were then dark and that the hypothesis of Dr. Geddes may yet be proven to be in all, or in part, correct.”

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:

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:

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:

Discussions with fellow experts:

“We talk”, he said, “to paediatric pathologists and the neuro-radiologists and in real life we simply just do not see subdural haemorrhages in hypoxic ischemic injuries”.

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:

Dr. Squier also relied heavily upon research material in support of her contention that babies have choked, become hypoxic and then presented with subdural haemorrhages and retinal haemorrhages in the absence of trauma. In Dr. Squier’s report, she said:

“It is my opinion that the presence of the chronic subdural haemorrhage is also very significant. It is possible that this caused a seizure and collapse, or caused this baby to choke and impaired the baby’s normal protective reflexes. There are well described cases in the literature of babies who have choked and presented with subdural and retinal haemorrhages (Hilton 2004, Martinez-Lage 2006).”

It has to be said that, within the decorous confines of maintaining professional courtesy and respect, the proposition put by Dr. Squier that these two papers provided evidence that choking can lead to subdural haemorrhage and retinal haemorrhage caused considerable professional disquiet amongst her colleagues. Dr. Bonshek said that in referring to these two articles, Dr. Squier was being “disingenuous”. When this was put to Dr. Squier she said she was rather upset by such a comment and, indeed, she looked distressed.

Mr Richards concluded by saying that “nothing is impossible”. But here, he said, all the features “scream trauma”. Things happen, he said. “Odd cases that do not follow the rules”, but there is nothing he had seen in Z’s case to suggest his case would be one such.

Any Court dealing with these cases on a regular basis will be aware that Dr. Squier is a strong believer that many cases hitherto regarded as SBS have in fact been precipitated by a choke and that there has thereafter been a cascade of events, including hypoxia, which has been responsible for the subdural haemorrhages and retinal haemorrhages.

I had the privilege of hearing evidence from a number of eminent clinicians,

Ms Delahunty was meticulous in examining each and every possibility and was supported Lord Brennan QC, on behalf of the father. She dealt with CPR, reperfusion and coagulopathy, as well as the possible causes of the ”primary event”. The Local Authority’s case was rigorously tested at every stage and in every respect.

Dr. Cary in his evidence was cautious about the approach to a diagnosis. He told the Court:

“You need to be very careful. The triad is only diagnostic when it is properly worked up. The finding of subdural and retinal haemorrhages and encephalopathy are not diagnostic. When I express my view at the experts’ meeting, I am making my assumption that, by the time of the meeting, each element has been worked through. I hope what I have done is tested against the science.”