A County Borough Council v M

B e f o r e :

THE HON. MR JUSTICE BENNETT ____________________

____________________

From the tape recording supplied to Cater Walsh Transcription Limited 1C The Court, Newport Road, Cardiff, CF24 1RH Official Court Reporters [Copyright: No part of this document may be reproduced or transmitted in any way without prior permission]

____________________

MISS H MIFFLIN and MISS C WILLIAMS appeared on behalf of the applicant MISS R HENKE QC and MISS C HAYWORTH appeared on behalf of the 1st respondent MR J TILLYARD QC and MR C PARSLEY appeared on behalf of the 2nd respondent MR M REES appeared on behalf of the 3rd respondents MR J FURNESS QC appeared on behalf of the children's guardian ____________________

HTML VERSION OF JUDGMENT ____________________

Crown Copyright ©

These proceedings, brought on 1 August 2007, under Part IV of the Children Act 1989, are in respect of C2, born in April 2006. He is almost two years old. He is the son of M and F, who are now 36 and 35 years of age respectively. They were married in 2003. In June 2007 they separated, and divorce proceedings are in progress. In February 2005 C1 was born. He was the first child of the mother and father. On the evening of 22 April 2005, when in the sole care of the father, C1 collapsed and was taken to hospital. On 23 April 2005 C1, then being two months old, sadly died.

On 8 May 2006, at an inquest held by Her Majesty's Coroner, as a result of the evidence of Dr Steven Leadbeatter, a Senior Lecturer in Forensic Pathology in the Wales College of Medicine at the University Hospital of Wales in Cardiff, who conducted a post-mortem examination on C1 on 27 April and 10 May 2005, and Dr Paul Davis, a Consultant Community Paediatrician, based at St David's Hospital in Cardiff and at the University of Wales Hospital, found that she had heard no evidence that led her to believe that C1 suffered any trauma, and that C1 died as a result of brain swelling and subarachnoid haemorrhage, precise aetiology undetermined. The Coroner returned a verdict of "death by natural causes". It should be said that the Coroner also heard from the mother and the father and Detective Inspector Ian Roberts.

On 20 June 2006, C2 was taken by his parents to the Accident & Emergency Department at the University Hospital of Wales. He was then eleven weeks old. The parents told the hospital staff that that day there had been an accident at home, and C2 had been lying on the floor under a baby gym. The father had accidentally kicked the baby gym into C2's face, causing injuries above his right eye. The explanation was accepted.

On 22 June 2006, Dr Susan Papworth, a Consultant Neonatologist, saw C2 with his parents as a part of routine monitoring following the death of C1. She noted the bruising to C2's eye. The father indicated that he had kicked the baby gym into C2's face two days previously. Dr Papworth documented the injuries. She found bruising to the right side of the face in the periorbital area from the nose to the right ear. She also saw bruising and swelling around the eye on the upper and lower lids. She was concerned that the explanation given did not account for the injuries. She said nothing to the parents as she wanted to speak to Dr Paul Davis, who had had contact with the family both before and after the death of C1. Dr Davis felt that a full investigation was warranted. Consequently Dr Papworth contacted the Community Paediatrician, Dr Alicia Rawlinson. A referral was also made to the social services at the relevant Local Authority.

On evening of 23 June there was a joint police and social services visit to the home of the father and the mother. The purpose was to discuss a referral that had been received from Dr Papworth to seek parental consent for C2 to be examined by a paediatrician. That consent was given. C2 and his parents were transported to the Royal Gwent Hospital, and Dr Rawlinson examined him.

On taking a history, Dr Rawlinson says that she was told that C2 "had burst a blood vessel in his nose" at the age of four to five weeks, and had been taken to the University Hospital of Wales. The parents were asked to identify any marks on C2 other than to his face. The mother indicated that he had a bruise on his right leg. It was thought to have been caused by C2 kicking on his cot bars or from a changing mat which formed part of a travel cot. The parents also identified a mark on C2's left upper arm which they thought was caused by the car seat. It had never looked like a bruise. The mother described it to Dr Rawlinson as she thought it had looked like "a love bite a couple of days ago".

The examination of C2 was normal, save for the following areas of discolouration:

Because C2 had bruising to more than one part of the body, Dr Rawlinson suggested admitting him for further medical investigations. Photographs were taken of C2 by the police. C2 remained on the ward in hospital until 30 June 2006. All tests carried out at the hospital were normal, i.e. there was no medical reason for the bruising to C2. Dr Rawlinson was of the view that the explanations offered for the three areas of bruising were not consistent with the injuries. She also had concerns as to the nasal bleeding that had been reported to her by the parents. It was her view that child protection procedures needed to be invoked. A strategy meeting was held at the hospital that afternoon, and arrangements were made for C2 to be accommodated. He was initially placed with foster parents, but then moved to the care of his maternal grandparents, MGPs, with whom he has lived ever since, except for two very short periods in 2007.

The police have been conducting enquiries into C1's death and into C2's injuries. Many expert and lay witness statements have been obtained. On 31 July and 8 August 2007 the parents were arrested and interviewed. On 28 and 29 January 2008 the mother and father respectively were again interviewed by the police. The father has been charged with murdering C1 and assaulting C2. So far as it is known, no charges have been brought against the mother. The father has been remanded in custody.

My task is to decide whether the threshold criteria are met in respect of C2, it being conceded that if one of the parents is found to be deemed responsible for C1's death, then the threshold criteria is made out in respect of C2. As part of my consideration whether the threshold criteria are met, under section 31 of the Children Act 1989, I am concerned with:

The local authority's case, in a nutshell, is as follows. In respect of C1, the court must look at the overall clinical picture. There is no evidence of any natural cause of death. The pathological, neuroradiological, ophthalmological and other evidence suggest that C1 died of an inflicted head injury. He had massive brain damage, such that he would not have behaved normally after suffering such an injury. He was last seen by the father behaving normally on the evening of 22 April 2005. At the outset of the hearing the local authority asked me to find that on the evening of 22 April the father assaulted C1 by shaking him. The mother was said to have failed to protect C1, but that allegation in respect of the mother, after the evidence had been heard, was no longer pursued.

So far as C2 is concerned, the local authority's case is that he was a non-ambulant child, who had bruising on three sites, all of which were probably non-accidental injuries. The father, it is said, has been inconsistent in his explanation for C2's eye injury. At the end of the evidence and before final written submissions were given to me (for which I express my great gratitude) the local authority circulated a document headed "Outline findings sought by the local authority". The local authority's case at the end of the evidence is that if the court makes findings that the father assaulted C1, then its case is that it is improbable that C2's injuries, if inflicted, were inflicted by both parents. In those circumstances the local authority asks the court to find that the father inflicted the three bruises and that the mother failed to protect C2 in circumstances where she knew, suspected or ought to have known that C2 was at risk.

However, if the court makes no finding in respect of C1, then in so far as C2 is concerned, the local authority submit, since C2 was in the care of both parents, there is a real possibility that the bruises were caused by one or other of them, and that on the evidence there is little to point to, to exclude one or other of them. Therefore both, it is said, are within the pool of potential perpetrators. The father categorically denies inflicting any injuries whatsoever and certainly not shaking C1. He categorically, together with the mother, denies inflicting any injuries on C2.

Before embarking on any analysis of all the evidence, I should remind myself of that very important passage in the speech of Lord Nicholls of Birkenhead in Re H and Others (Minors) (Sexual Abuse: Standard of Proof) [1986] AC 563, at page 586.

Ungoed Thomas J expressed this neatly in Re Dellow's Will Trusts [1964] 1 WLR 451.

I shall now set out the witnesses and, in the case of the expert medical witnesses, their qualifications. I have been provided with a curriculum vitae of each of the expert witnesses. I can only attempt to summarise them. The Neuroradiologists are Dr Neil Stoodley and Dr Mary Gawne-Cain. Dr Stoodley is a Consultant Neuroradiologist based at Frenchay Hospital in Bristol and prior to that at the University Hospital of Wales. He is a Fellow of the Royal College of Surgeons and Royal College of Radiologists and of the Royal College of Paediatrics and Child Health. Dr Gawne-Cain completed her training at the Radcliffe Infirmary in Oxford. In 1997 she was appointed Consultant Neuroradiologist at the Wessex Neurological Centre in Southampton. Her particular interest lies in paediatric neuroradiological and non-accidental head injury.

Mr Richard Edwards is one of three Consultant Paediatric Neurosurgeons at Frenchay Hospital in Bristol. His specialist field is neurosurgery, with specific clinical and research interests in paediatric neurosurgery and head injury. He is a Fellow of the Royal College of Surgeons. He is Honorary Consultant Paediatric Neurosurgeon at Bristol Children's Hospital. He is Honorary Senior Clinical Lecturer in Neurosurgery at the University of Bristol.

The neuropathologists are Dr Colin Smith and Dr Waney Squier. Dr Smith is a Senior Lecturer in Pathology and Honorary Consultant in Neuropathy at the University of Edinburgh. He is a member of the British Neuropathic Society and of the International Neuro Trauma Society. His main area of interest and expertise is in the field of Neuro Trauma and Forensic Neuro Pathology. Dr Squier is a Consultant Neuropathologist at the Oxford Radcliffe Hospitals and an Honorary Clinical Lecturer at Oxford University. During her 24 years at Oxford she has specialised in the pathology of the developing brain in the foetus and neonate. Her expertise is based upon examination of the brain, spinal cord and dura after death, and, as such, exists in the interpretation of the mechanisms of injury and the imaging of the brain.

The Paediatric Pathologists were Dr Gordan Vujanic and Professor Risdon. Dr Vujanic is Reader and Honorary Consultant in Paediatric Pathology at Cardiff University. He is a Consultant Paediatric Pathologist. He has spent all his career in the field of paediatric pathology, and since 1991 has been involved in investigations of sudden infant deaths. The vast majority of children who have died suddenly and unexpectedly in Wales have been examined in his department. Professor Risdon is an Emeritus Professor and Consultant in Paediatric Pathology in the Department of Histopathology at Great Ormond Street Hospital for Children in London. He has been a Consultant Histopathologist since 1972. In 2004 he retired from the NHS. For the past two decades he has had a particular interest in sudden death in infants in their first year from both natural and unnatural causes. The department of which he was head does more than 200 examinations per annum, i.e. over one-third of all autopsies on sudden unexpected deaths in infancy occurring in the United Kingdom. After retirement he has continued to perform autopsies, remains up-to-date with CPD through the Royal College of Pathologists, and undergoes annual professional appraisal at Great Ormond Street Hospital.

The ophthalmologist experts are Dr Richard Bonshek and Dr John McCarthy. Dr Bonshek is Honorary Consultant Ophthalmic Pathologist at the Royal Eye Hospital in Manchester. He is a Member of the Ophthalmology Child Abuse Working Party, which published its findings in 1999 and 2004. He carries out routine coronal and hospital post-mortem examinations at the Manchester Royal Infirmary. Dr McCarthy is a very experienced Consultant Histopathologist and Ophthalmic Pathologist. He has held that post since 1979 at the Gloucestershire Hospitals NHS Trust.

The haematologists were Dr Giogrande and Dr Angela Thomas Dr Giogrande is a Consultant Haematologist at the Oxford Haemophilia and Thrombosis Centre. Dr Thomas is a Consultant Paediatric Haematologist at the Royal Hospital for Sick Children in Edinburgh, and has been since 1993.

The paediatricians were Dr Geoffrey Debelle and Dr Robert Sunderland. Dr Debelle is a Consultant Paediatrician employed by the Birmingham Children's Hospital NHS Trust since 1989. He has practised paediatric medicine exclusively since 1974. Dr Sunderland has held the post of Consultant Paediatrician to the South Birmingham Health Authority since 1984. Since 1984 he has also held the post of Consultant Paediatrician and Senior Clinical Lecturer in Paediatrics at the University of Birmingham.

Other medical witnesses who gave evidence were Dr Leadbeatter, Dr Papworth, Dr Rawlinson and Dr Paul Davis, the Consultant Paediatrician who examined C1 on 23 April 2005 before he died and who gave evidence to the Coroner. The non-medical witnesses were the mother, the father, MGPs the maternal grandparents, Helen Morgan a paediatric nurse who nursed C2, Mandy Morris a social worker, Louise Atkins a social worker, and Gail Eynon a health visitor.

I now turn to C1. In 2001 the parents met and began their relationship. The mother was separated from her first husband. She moved in with the father. Later they moved from Cardiff to one of the Welsh valleys, indeed into the same street as her parents, MGPs. As I have said, on 4 December 2003, they were married. MGPs would see their daughter and son-in-law every week, MGP more than PGP. MGP's description of the father was that he was a devoted, loving father from the day each child was born. She had never seen him lose his temper. He was patient with the children. He lost his job on the morning of 22 April. He did not appear upset. MGF did not like the father when he met him, but thereafter they appeared to get on well. He never saw the father being aggressive. The father could be confrontational if his views were not accepted. He always saw the mother and the father get on well together. He agreed with his wife that the father appeared to be a devoted and loving father. He, too, said that after losing his job on 22 April the father did not appear stressed. However, MGF did describe the father as a "Walter Mitty" character.

During the father's evidence he was asked by Mr Tillyard, his leading counsel, at the very beginning of his examination-in-chief about his involvement with MI5. The father told me that in 1993 he was in the Bahamas working on a cruise ship. He was approached and "coerced" (that being his word) into working for MI5. He had to gather information on three men, one of whom was the dining room manager. He was paid $3,000 and his involvement lasted from November 1993 to April 1994. He never contacted the man who had approached him for information. He told me that he did not work for MI5 thereafter.

When cross-examined by Mr Furness, leading counsel for the guardian, he denied being a "Walter Mitty" character. Mr Furness put to him the statement of a staff nurse, Miss Hinchman, on the ward where C2 was, following his admission on 23 June 2006. According to her, the father explained that "he was a government agent for MI5 and was therefore aware of and had access to information relating to immunisation study". Mr Furness also put to the father notes of a supervised contact session of the father with C2 on 29 June 2007. The contact supervisor made a note stating inter alia as follows: "F, during his contact, informed me that the only reason he remained in Britain was because of C2. F stated that he had spoken to his MI5 colleagues, and he had the option to go to Brazil or America and work there." The father told me in his evidence that he could not recollect saying either of those matters.

When cross-examined by Mr Tillyard, the mother said that until June 2007, when she and the father separated, their relationship was a strong one. The father was a loving and caring father. He never controlled her or the children. He was never aggressive to her or the children. He was easygoing. When cross-examined by Miss Mifflin, leading junior counsel for the local authority, the mother described the father as a strong personality. At one point he had a stressful job and became a little agitated. They did argue but no more than any normal married couple. The mother told me she felt free to disagree with the father.

As I have said, C1 was born on 20 February 2005. I believe the mother to have been in labour for some considerable time, and eventually C1 was born by emergency caesarean section. Upon delivery, C1 was in good condition, with Apgar scores of 8 and 10. There were no significant problems in the neonatal period. He was breast fed for the first week and discharged home after four days. The father told me that almost at once he assumed the role of the major carer. He told me that the mother was exhausted, and she was rather scared of handling C1. He, by contrast, was very hands-on.

Gale Eynon was the health visitor in respect of C1. She visited him on 1, 16 and 23 March, and saw C1 on 20 April in respect of his immunisations. In her opinion, the mother and father were very happy and caring parents. The father was very knowledgeable about parenting. C1 developed normally. She had no concerns about C1's environment. All necessary baby equipment was in the home, which was, in her words "always well presented".

On 20 April 2005, C1 went for his six to eight week check, and was given his first set of immunisations, which Mr Edwards has, in my judgment correctly, summarised at paragraph 3.03.3, which is to be found at G277:

The mother told me that on 20 April, C1 got home around midday and was gurgly and kicking, with no apparent ill-effects. The next day MGM and the mother, together with C1, went shopping. MGM recalls C1 sleeping all the time they were out. The mother told me that C1 did not appear to be suffering at all.

Late afternoon and evening of 22 April

In her evidence, the mother described how C1 had "whomped down his feed" at about 5.30pm. When cross-examined by Miss Mifflin, the mother told me that she took her mobile phone with her. It was switched on at all times. As she was coming home, some 20 seconds from the house, the phone was ringing. She felt there was no point in answering it until she was in her home. When she got in, the father was not there. The time was about midnight. There was a policeman there. He told her that C1 was ill and she should go to the hospital. The father than rang her. She then went to the hospital. She also told me that, contrary to what the father had told the police in his interviews, that the father did not ring her when she was in a pub in Blackwood; that is to say, earlier in the evening. If she had had a missed call, she would have rung back. The only missed call she had that evening was the one immediately before she entered her house at midnight.

The father's account of the evening is as follows. The mother left the home at about 7.15 or 7.30pm. He knew that the mother had her phone and he knew its number. He told me that if C1 had shown distress, he would have rung the mother. When the mother left, there was nothing wrong with C1. The mother had fed him at about 5.00pm and there was nothing wrong with his appetite. Between 7.30 and 8.00pm the father bathed him. C1 was cheerful and happy. At 8.00pm to 8.30pm the father put him to bed, after giving him about one and a half ounces of feed. The father then went downstairs. He had the baby monitor, which was switched on.

At about half past 10.00 that evening, he told me he heard hiccup sounds coming from C1. He did not worry about it. C1 hiccupped for about 20 to 25 minutes. He then went upstairs to look at him. When asked by Miss Mifflin why he did not go up to see C1 after about five minutes and have a quick look, the father said he had the monitor on. The hiccups began to change. They became slower and rasping. The father went into C1's bedroom. He was quite bluey and grey. The father went to pick him up. His head, legs and arms were limp. He was like a rag doll. The father told me in examination-in-chief that he put C1 on the changing mat on his back. He thought something was seriously wrong. He was in a state of panic and shock. He bolted downstairs, and returned upstairs with the hands-free telephone, and rang 999. The ambulance arrived and he and C1 were taken to hospital.

It is not in dispute that the 999 call was made at 11.05pm. The father says that he went upstairs 20 or 25 minutes after the hiccupping started at about 10.30pm. That would mean that the father went upstairs at about 10.50 or 10.55pm. Miss Henke, leading counsel for the mother, asked the father what happened between 10.50 or 10.55 and 11.05. The father said that in that period of approximately 10 minutes, he picked C1 up and tried to find out what was wrong with him. Miss Henke then put to the father the statement of Julie Jenkins, the paramedic in the ambulance. Miss Jenkins was not required to give oral evidence. Miss Jenkins remembers the father saying to her, "He didn't wake for a feed at 11 o'clock, so I came up to see if he was awake." The father in his evidence denied saying that to Miss Jenkins.

The father told me that he did ring the mother after he and C1 had arrived at the hospital at 11.36pm. He phoned her from a private room. He got a connection and could hear a lot of background noise, like general pub noise. The mother could not hear him and the line went dead.

Miss Henke further put to the father varying accounts of where he had put C1, having picked him up. In his evidence to the Coroner the father said that he had placed C1 on the changing mat. In his police interviews on 8 August 2007 he said he had placed C1 on the floor. In the 999 call, it is apparent that he kept telling the operator, "I've got the baby in the cot."

As I have said, at just 6 minutes past 11.00 the 999 call was received from the father. He said that the baby was not breathing, was blue in the face and was like a sack of potatoes. Having told the operator that C1 was in the cot, the father was told to open the front door and put the lights on for the ambulance. The sound of a child gasping for air could be heard. The father said that C1 had just taken one deep breath. The father was told to lay C1 on the floor and look into his mouth. The father told the operator that he found nothing in C1's mouth. Later the father was told to give mouth-to-mouth resuscitation and to put two fingers on C1's heart and pump the chest rapidly about five times. The father, according to the transcript of the call, did that several times. Thereafter the ambulance arrived.

The ambulance arrived at 19 minutes past 11.00 with Miss Julie Jenkins. C1 was found by the paramedic staff to be floppy, with no cardiac output and no respiratory output. At 22 minutes past 11.00 the ambulance left C1's home. Further attempts to resuscitate C1 continued en route. At 23.37pm, C1 arrived at hospital. He was still floppy, with no cardiac or respiratory output. Cardiopulmonary resuscitation was continued. C1 was intubated, and fluid resuscitation started. At 11.53pm cardiac output was recorded. At quarter to 1.00 in the morning the hospital contacted the Paediatric Intensive Care Unit at the University Hospital of Wales in Cardiff in order to discuss the transfer of C1 to that hospital. At 1.30am C1 was reviewed by Dr Robert Evans, a Consultant Paediatrician, who noted that C1 was cold and pale, with a body temperature of 33 degrees centigrade, and fundal haemorrhages in both right and left eyes. C1's pupils were mid size and un-reactive to light.

At 2.00am a CT scan was performed on C1, and he was thereafter transferred to the Intensive Care Unit. At 2.30am the Retrieval Team from the University Hospital of Wales arrived and found his pupils un-reactive to light; there was no respiratory effort, and he began his transfer to the University Hospital of Wales. At 9 minutes past 3.00 a clotting specimen was taken from C1's blood, which demonstrated a severe clotting disorder. Following this, fresh frozen plasma – that is to say, a blood product to correct the clotting abnormality – was ordered. According to Mr Edwards' research into this case, it was given to C1 at about half past 5.00 that morning when en route to the University Hospital of Wales. Mr Edwards confirmed in his evidence that no fresh plasma was given to C1 at any time before the CT scan. At 20 minutes past 4.00 that morning the results of the CT scan were available.

At the University Hospital of Wales, Dr Gajrag documented severe retinal haemorrhages in both of C1's eyes. There was no respiratory effect. Cardiac output was poor. At midday that day Dr Paul Davis examined C1 and noted the following: 2 cm x 1 cm blue bruise under the left side of his jaw; 2 cm x 1 cm blue bruise in an almost symmetrical position under the right jaw. On C1's abdomen there was extensive petechial bruising. On the lower part of his neck there was a small linear mark on the right side, which appeared to be pressure from bedding, and a 1.5 cm x 0.5 cm blue bruise on the left side. There were scattered petechial haemorrhages over all four limbs. After discussion with the mother and the father it was decided that C1 should not be further resuscitated. At 5 minutes to 4.00 that day, he died.

There is no doubt that after C1's death the father undertook a huge amount of research, principally on the internet. He was, he said, convinced that C1 had died as a result of a reaction to his immunisation on 20 April. He kept pressing the doctors to come up with an explanation for C1's death. Dr Davis told me that after C1's death, he told the parents that trauma could not be excluded as a cause of C1's death, but that, on balance, he could not exclude the possibility of sudden infant death syndrome (SIDS). The impression he intended to convey to the parents was that the cause of C1's death was unknown. The father would not accept that. He wanted the cause to be found. He challenged Dr Davis to find it.

Miss Eynon, the health visitor, confirmed to me that the father appeared desperate to find out the cause of C1's death. On 24 May 2005 she saw both parents. The father became very agitated, shaking his foot, tapping his hand on an immunisation booklet, and then waving it at Miss Eynon. He said he had 280 questions surrounding the immunisation programme, and he was being denied access to it. In the end, the father, according to Miss Eynon, became verbally aggressive.

The Anatomy

The post-mortem examinations

The brain was removed and fixed. The spinal cord was also removed. Dr Leadbeatter said in his report of 11 November 2005:

Dr Leadbeatter then did an examination under the microscope.

No microscopic evidence of significant natural disease was seen by Dr Leadbeatter in sections from various tissues in the mouth, throat and trunk. His post-mortem findings confirmed the clinical description of brain swelling, subarachnoid haemorrhage and bilateral retinal haemorrhages. There was no evidence of inflammation of the coverings, substance or blood vessels of the brain. There was none of the findings which would allow a connection to be drawn between C1's death and the preceding vaccinations. In his evidence Dr Leadbeatter told me that at post-mortem examination he would not have seen a tear in the arachnoid membrane because he does not routinely look for tears in that membrane. He saw no pathological evidence of chronic or older bleeding in the brain. There was no evidence of neo-membrane in the dura. There was no evidence of overwhelming infection.

As to any shearing of the bridging vessels he did not see it at post-mortem, but he said it was not easy to see because of the difficulty of removing an infant's brain for later examination. Although he told me that he did not see a collection of lower attenuation fluid lining in the subdural space in the frontotemporal regions, as Mr Edwards pointed out at G301 and in his evidence, in fact Dr Leadbeatter is referring to such a collection at G8, as I have set out.

So far as the bruising at the back of the head is concerned, Dr Leadbeatter agreed that Dr Edwards had given a better description in his report at paragraph 5.03.1.

The Scan

Dr Gawne-Cain put it this way in her report of 31 January 2008:

In his evidence Dr Stoodley told me that, at the time of the scan, the level of brain swelling was mild. How then do the neuroradiologists interpret that which they found at the scan? Dr Stoodley in his report said:

In his oral evidence Dr Stoodley was asked to respond to certain points made by Dr Squier in her evidence. Dr Squier had asked rhetorically why, if fluids which showed a higher attenuation in the subarachnoid space, when they had gone through a tear, if they did, in the subarachnoid membrane, then in the subdural space showed a low attenuation? She said she would expect to find the same level of attenuation and the fluid in both the subarachnoid and subdural spaces. Dr Stoodley answered that it was not blood but cerebrospinal fluid (CSF) that was passing from the subarachnoid space through the tear to the subdural space. He told me that if one sees an obvious difference in attenuation between the subdural and subarachnoid spaces, then one can be confident that there is abnormal fluid in the subdural space.

Dr Squier further questioned the hypothesis of a tear in the arachnoid membrane. She could not think why trauma could cause a tear at one point in the arachnoid membrane and not at others. Dr Stoodley said that he could not demonstrate a tear from the scan, but it was not difficult to see in this case the CSF in the subdural space. It is the CSF and not the clotted blood in the subarachnoid space which goes through the tear into the subdural space. CSF is not found in the subdural space in a healthy child. It is found only in the subarachnoid space. Thus, if CSF is seen in the subdural space on the scan, there must be a mechanism by which it gets to the subdural space, and in his opinion that is by a tear in the arachnoid membrane.

Dr Squier suggested in her evidence that the low attenuation could mean that what was seen in C1's subdural space was a chronic bleed, possibly from birth. Dr Stoodley rejected that. The CSF in the subdural space could not be birth related for the reason that it is the subarachnoid and not the subdural space that holds the CSF. In a healthy child there is no subdural space.

Dr Stoodley was asked what would be seen on the scan if C1 had suffered a simple cardiac arrest. He told me that it would give rise to hypoxic-ischaemic damage. If that was all the scan had shown, then that would be consistent with cardiac arrest. If there had been a simple cardiac arrest, then the hypoxic-ischaemic damage would take much longer to show up on a scan, possibly days, but not within hours. The unusual feature in C1's case is that if he had suffered a simple cardiac arrest, then according to Dr Stoodley it is surprising that the scan showed quite extensive hypoxic-ischaemic damage three or so hours after his collapse and also evidence of acute subarachnoid haemorrhage at that time. In his view, hypoxic-ischaemic brain injury would not give rise to scan evident, acute subdural haemorrhage. In patients that are scanned after cardiac arrest, in his experience, followed by resuscitation efforts, hypoxic-ischaemic damage is seen, but not either subdural haemorrhage or low attenuation collections.

Dr Squier told me that in a case of severe hypoxic-hypoxia, together with coagulopathy – that is to say that blood does not clot properly if it bleeds – and where resuscitation puts pressure into the veins, then blood vessels in the dura can leak into the subdural space. Dr Stoodley accepted that compression on the chest causes thoracic pressure. Nevertheless, in patients he has seen or known about, where there was simply cardiac arrest followed by resuscitation, what is not seen on the scan is subdural haemorrhage. That is his clinical experience. Dr Stoodley accepted that the extensive haemorrhage in the subarachnoid space could be secondary to either hypoxic-ischaemic injury or secondary to trauma. He agreed that the quantity of blood in the subarachnoid space was unusual in C1, but the large amount of blood in the subarachnoid space was not unique, in his experience. To him, the amount of blood reflected the degree of severity of the trauma.

Dr Squier raised another matter, namely that it was difficult to know and/or see whether the blood seen on the scan was within the falx, where there are many blood vessels, or whether it was adjacent to the falx. Dr Stoodley rejected that. From the scan he said it was not difficult to see. There was no intradural blood. He did not see on the scan any leakage of intradural blood into the subdural space.

Finally, as to overwhelming infection, he accepted that ischaemic injury can occur after, for example, meningitis, but ischaemic change in such a case is focal and not general. It is also very unusual in such a case to see haemorrhage into the subdural space unless there was a severe clotting disorder, or the venous sinuses (that is the veins that carry the blood back to the heart) were clotted with blood, and there was no evidence of that.

Dr Gawne-Cain in her report said as follows under paragraph headed: "Opinion":

In her evidence, Dr Gawne-Cain adhered to her conclusions. She told me that the radiological pattern in C1 is not at all typical of intracranial infection. There was no patchy change. Within infection one will not find extensive subarachnoid haemorrhage or dense subdural haemorrhage. When cross-examined by Mr Tillyard, she told me she would not expect to see the amount of subarachnoid haemorrhage with hypoxic-ischaemic damage. She would be surprised if the hypoxic-ischaemic damage had caused the amount of subarachnoid damage, but if it did, then the cause could be coagulopathy. So far as the falx was concerned, some of the blood she saw on the scan was adjacent to the falx. So far as the subdural blood found at post-mortem was concerned, Dr Gawne-Cain told me that she could not exclude the possibility that it had been caused by oozing of the blood vessels together with coagulopathy, but she was confident that CSF in the subdural space shows up on the scan as low attenuation. She told me that she thought it pretty unlikely, but possible, that the fluid seen in the subdural space was from leaky blood vessels because the scan was performed two or three hours after the event causing C1's collapse, which is a very short time. She is used to seeing effusion occurring over days and not hours. In her neuroradiological experience, she had never seen subdural haemorrhage come after hypoxic-ischaemic damage.

As to how the CSF got from the subarachnoid space into the subdural space, she told me that a tear in C1's subarachnoid membrane is the best explanation there is because not enough time had elapsed between the event causing the collapse and the scan for effusion to occur. There was no evidence of old blood in the subdural space and there was no inflammation. Mr Tillyard suggested to her that in C1's case there may have been asymptomatic bleeding at birth. Dr Gawne-Cain said that if that was so, then there would be hemosiderin staining, which there was not.

Mr Edwards

As to the arachnoid membrane, he told me it is very delicate. One can actually see through it. The most likely point of tearing would be at a point where the blood vessels traverse the subdural space. A tear would allow the CSF to pass through from the subarachnoid space to the subdural space. There was no other explanation for the presence of CSF being in the subdural space than that it got there through a tear in the arachnoid membrane. He told me that, in his opinion, subarachnoid bleeding can occur in the presence of both brain swelling and coagulopathy. He has seen a similar amount of blood in other cases of trauma. Furthermore, in C1's case the degree of subarachnoid haemorrhage was no worse at the time of the post-mortem examination than it was in the scan. Thus, as the clotting anomaly was not corrected for at least three and a half hours after the scan (that is to say, by the administration of fresh frozen plasma) were the subarachnoid haemorrhage to be a direct result of oozing from the encephalopathic brain, he would have expected to see an increased amount of subarachnoid haemorrhage present.

So far as intradural bleeding was concerned, he saw from the scan that the blood was adjacent to the falx. Furthermore, the post-mortem photographs showed the same. He did not accept that the subdural blood was a result of hypoxia together with coagulopathy and/or that attempts at resuscitation would lead to the presence of haemorrhage in the subdural space. He told me he had never seen oozing from the dura. In his report at paragraph 5.03.16, he said this:

The Haematologists

In her report of 14 January 2008, Dr Thomas speaks about C1's coagulation tests at G261:

At G263 Dr Thomas said this:

At G265 she concluded that there is no evidence, either clinical or laboratory, that C1 had a bleeding diathesis that would predispose him to subdural and retinal haemorrhages. In her evidence she agreed with Mr Edwards that the platelet count of C1 was not low enough to cause spontaneous haemorrhage. She agreed that coagulation would be brought about by hypoxia, and a simple cardiac arrest might have triggered a clotting disorder. Septicaemia would have to be severe and overwhelming to cause coagulopathy. The antibiotics administered at about midnight to C1 would not have reversed an infection. She said that there was no evidence of any overwhelming infection. The post-mortem examination showed to her no evidence of infection.

Dr Giogrande agreed with Dr Thomas's report. He told me that in respect of Mr Edwards' seeking clarification at paragraph 5.04 of his report as to the severity of C1's coagulopathy, he would say that the blood sample indicated a mild coagulopathy. Both haematologists agreed that C1 had abnormal clotting results, which showed evidence of coagulopathy which was secondary to the clinical state of C1 and not the cause of it. Dr Thomas further explained that the effect of coagulopathy is to make the sufferer more susceptible to bleeding and to bleed for longer but not any faster.

The Neuropathologists

As I understand it, the only disagreement between Dr Smith and Dr Squier is as to the causation of the axonal swellings and the spinal nerve roots, to which I will come in due course. Both are agreed that the swelling of the brain, as at the time of the scan, was mild and that the brain swelled after the scan, so that at death the brain was seen to be swollen with a tight dura and brain herniating through cuts in the dura. Both agreed that there was more subarachnoid haemorrhage than usual. Dr Smith said it was far in excess of what he had seen in his experience. Dr Squier described it in her evidence as "very extensive, particularly over the cerebellum". Neither Dr Smith nor Dr Squier found any evidence of infection.

I shall now describe the divergent views of the neuropathologists as to the axonal swellings. 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 BAPP, 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. The neuropathologists have identified that the axonal swellings in the spinal nerve roots are at a point where the nerves crossed the dura.

At G238, Dr Smith put it in this way:

In his oral evidence, Dr Smith said that axonal swellings in the spinal nerve roots can be associated with trauma. They can also be associated with a swollen brain, but in such a case one does not see bleeding into that area. In trauma nerve damage and bleeding is seen. In cases of a swollen brain with no trauma, the swelling is a slow process and, importantly, haemorrhages have never been described.

Dr Squier told me that the removal of the spinal cord at post-mortem examination is often a traumatic procedure and that the bleeding may be a post-mortem artefact. As to that latter matter, she accepted, when cross-examined, that any bleeding could not have been a post-mortem artefact because, as per Dr Smith at GQ24 and 25, the BAPP accumulation is an active process which requires cellular energy, i.e. it will not occur after death. Dr Squier told me that pulling out the spinal cord at post-mortem examination could cause the axonal damage. Dr Smith told me that the removal of the spinal cord would not necessarily cause axonal damage but, in his experience, the technique of removing the spinal cord is not an explanation for the bleeding around the damaged nerve roots in the spinal cord. Dr Smith told me that the presence of damage to the nerve roots has no relevance to coagulopathy. He believes that it is a coincidence that there was damage to the nerve roots and there is also localised bleeding. Furthermore, it was a remarkable coincidence that blood had gathered at the site of the damaged nerve roots and nowhere else in the spinal cord. If, as was suggested by Dr Squier, there was leakage of blood as a result of the coagulopathy, he was careful to say that the localised area of bleeding around the nerve roots must be cautiously interpreted.

Dr Squier was struck by the position of the axonal swellings, i.e. they occurred at the point where they crossed the dura and where fresh bleeding occurred. Into this she factored C1's coagulopathy. But, as she said at GQ120/121, she could provide no explanation for these swellings, and that it would be unsafe to make a diagnosis of trauma. "I simply do not know how to interpret this finding". In her evidence she told me that Dr Smith was saying that it was suggestive of trauma, but she was saying it was equivocal. Neither she nor Dr Smith was saying that their findings were diagnostic.

The Ophthalmologists

Dr Bonshek undertook microscopic examination (G75):

As I read Dr McCarthy's report at G54, he is in agreement with those findings. As I understand their evidence, there is no disagreement between them as to the nature of the injury in C1's eyes. Dr Bonshek put it this way, at G77:

The ophthalmologists are also agreed as to the likely cause of these injuries. Looked at in isolation, they told me, the causes of retinal haemorrhage are numerous. But there is no history of accidental trauma. No natural cause of the retinal haemorrhages has been identified. Coagulopathy and CPR may be associated with retinal haemorrhages, but in these situations the bleeding is typically in the posterior retina and is limited in extent. Although there was a blood clot within two orbital veins of the right orbit and within the central retinal vein within the right eye, Dr Bonshek understood that C1 suffered from secondary coagulopathy. He found no clotting elsewhere. The post-mortem and histology report give no description of excessive/intravascular clotting elsewhere in the body. C1 was given fresh frozen plasma. Dr Bonshek thus interprets the blood clots to be due to coagulopathy. Meningeal coccal meningitis and septicaemia have been described as associated with retinal haemorrhages, but in his opinion there was no evidence of any infection. Birth is a recognised cause of retinal intracranial bleeding, but with C1, he said, the retinal bleeding was recent.

Dr Bonshek said in his report that the injuries were not caused by resuscitation. The view of the working party of The Royal College of Ophthalmologists was that CPR alone was very unlikely to cause retinal haemorrhage, even if carried out by unskilled people. Dr Bonshek also excludes the injuries being caused by C1's immunisation. [See G80]. Most experts, Dr Bonshek said in his report of 30 July 2007, agree that the combination of retinal haemorrhage, subdural haemorrhage and acute encephalopathy, is very suggestive of NAI, if other causes cannot be identified. Taking all the findings, both ocular and non-ocular, Dr Bonshek is left with NAI as the most likely cause of the irregular findings. Findings within the eyes and the orbital tissues are at the severe end of the spectrum in cases which he has examined. In his opinion, the likely mechanism for the injuries was shaking. Dr Bonshek was careful in his report to state that the "triad" of injuries cannot be taken in isolation as conclusive of C1's death, but it is a strong indicator. He told me that he was at a loss to find a credible alternative explanation for the findings within the eyes and associated structures of C1.

Dr Bonshek explained to me how, in both eyes, the epithelium structure was lifted and haemorrhages were beneath it. The epithelium is a single layer of cells between the retina and the choroid. In C1's left eye the choroid itself has had haemorrhages, but there were also haemorrhages in the fat, muscles and nerves outside each eye. The retinal haemorrhages were seen two hours after his collapse, which was very quick. In his opinion, the retinal haemorrhages had occurred at or before C1's arrival in hospital. His coagulopathy occurred after his brain was damaged. He told me that the combination of retinal haemorrhage, optic nerve haemorrhage and subdural haemorrhage is quite closely associated with trauma, however that trauma may have been caused. He also told me that the presence of perimacular folds in both eyes is an indicator of the severity of the injury but it was not an indicator whether the injury was accidental or not. There was no evidence of infection over the surface of the brain in C1. As I have said, he told me that the findings in C1's eyes were very suggestive of trauma. If no history of accidental trauma was given, then non-accidental injury was left as the only possibility.

Dr McCarthy in his report, on 3 January 2008, posed three questions: (1) Is this non-accidental injury of a shaking/impact aetiology; or (2) is this accidental injury with impact aetiology; or (3) are the brain swelling subdural haemorrhages, ocular and optic nerve haemorrhages secondary to an event in which there was a spontaneous cardiac arrest, of undetermined cause, and there was subsequent coagulopathy and resuscitation? At G255 Dr McCarthy sought to answer his questions:

In his oral evidence, Dr McCarthy reiterated, so far as infection was concerned, that he had no personal experience of having seen retinal haemorrhage and haemorrhage around the optic nerve with extensive subdural haemorrhage as a result of meningitis and/or septicaemia. In C1's case he saw no evidence of infection or septicaemia. He accepted that, if there was infection, it could cause brain swelling which, together with cranial and resuscitation pressure of a secondary coagulopathy, could give rise to retinal haemorrhage. As to the possibility of blood vessels leaking as a result of raised venous pressure from resuscitation together with coagulopathy giving rise to retinal haemorrhage, he told me he had never seen it. He would not exclude it, but in other situations, in his experience, where he knew of raised pressure, he had not seen retinal haemorrhages.

As to retinal folds, they are frequently seen at post-mortem, and thus one must be careful not to confuse retinal folds (which are a post-mortem artefact) with retinal splits (which are a pre-mortem event). But where retinal folds are seen and they are, as in C1's case, associated with retinal haemorrhage or retinal damage, then the retinal folds are a pre-mortem event. In his opinion, the findings in both of C1's eyes are not explicable by any cause other than trauma. The retinal haemorrhage in C1's eyes are of the type seen in baby shaking cases. That is known because they are seen in cases where the perpetrator has admitted shaking an infant. For Dr McCarthy, the degree of haemorrhage in both eyes was most striking. The haemorrhage went all the way round the retinas in both eyes, from the front of each eye to the back, and of the optic disc. Further, the haemorrhages were through the full thickness of the retinas. The retinal detachment was at the outside where the retina joins the eyeball. He told me that what was so striking to him was the confluence of haemorrhage from the front to the back of both eyes, or haemorrhages through the full thickness of the retinas, with equal magnitude of haemorrhage on both sides of each eye.

Paediatric Pathologists

(That is a reference to the bruising on the exterior of C1)

Having then referred to Dr Smith's views and Dr Bonshek's findings, he wrote at G409:

In his oral evidence, he confirmed that nothing he had seen or read altered his opinion. In relation to the bruises on the back of C1's skull, they could be attributed to the three causes as set out in Mr Edwards' report at paragraph 5.03.1, namely a blow to the back of the head on a mattress or carpet; pressure on the back of the head due to resuscitation; and post-mortem artefact. Dr Vujanic was taken to task by Mr Tillyard for not mentioning this opinion in his report. Dr Vujanic told me that post-mortem artefact could be excluded. Contact with a soft surface was more likely than bruising following resuscitation attempts, but he did not rule out the latter. He agreed with Dr Smith that the hypoxic-ischaemic injury was second to the cardiac arrest, but that the whole picture had to be looked at.

So far as Prolonged QT Syndrome was concerned, it was a theory, with no firm, confirmed evidence. He agreed that there may be a connection between cardiac arrest and Prolonged QT Syndrome, but that in babies who die after cardiac arrest from Prolonged QT Syndrome there are no retinal haemorrhages seen, and certainly not the degree of retinal haemorrhages suffered by C1. He concluded his evidence by saying that the retinal haemorrhages in C1 were seen within two hours of his admission. One hour of resuscitation, even with coagulopathy, was very unlikely to cause the retinal haemorrhages.

Professor Risdon in his report at G95 sets out the history. He sets out the reports of Dr Stoodley and Dr Bonshek, and at G101 his comments were as follows:

Professor Risdon told me in evidence that he had seen all the experts' reports and the questions and answers at section GQ. He had seen nothing to change his mind. Mr Tillyard cross-examined him shortly. He confirmed that in his police statement at G95 he had been asked to address two questions in particular, i.e. the relevance of C1's immunisation and his resuscitation to his death. He told me that, in his opinion, immunisation and/or resuscitation had played no part in C1's collapse or death. He told me he had no argument with either the findings or the opinions of Dr Stoodley and Dr Bonshek. He agreed that in looking at the "triad", one does not just tick boxes. One must look at each case on its own and look at each component of the "triad". He rejected simple cardiac arrest as a possible cause of C1's collapse. It did not explain the intracranial haemorrhage nor the retinal haemorrhages. With SIDS babies, one does not have significant findings at post-mortem examination. SIDS is not associated with subdural, subarachnoid or in particular retinal haemorrhages. In his view, C1's case was not unusual.

Professor Risdon further told me that any serious head injury case will affect the clotting. It is likely to involve a clotting disorder. Further, a cardiac arrest for about one hour, together with coagulopathy, would not produce what was seen on the scan. He told me that in infants that suffered cardiac arrest and then resuscitation, together with coagulopathy, he had never seen subdural haemorrhage. He agreed that hypoxic-ischaemic damage alone did not relate to trauma. On the other hand where there was trauma, it was usually to see not only subdural and retinal haemorrhages, but also hypoxic-ischaemic injury. Dr Smith, he told me, was looking at the matter from a neuropathological view. He, Professor Risdon, had to provide an overview.

Paediatricians

In his evidence, Dr Debelle told me that C1 suffered a single event, causing almost immediate collapse. He agreed that hypoxic-ischaemic damage could arise from cardiac arrest, but you cannot just block out all the other factors, i.e. intracranial and ocular findings. Mr Tillyard put to him the hypothesis of cardiac arrest, hypoxic-ischaemic damage, coagulopathy and resuscitation leading to oozing of vessels into the subdural and subarachnoid spaces. Dr Debelle was not dismissive, but in his opinion the subdural haemorrhage and subarachnoid haemorrhage were present (that is to say, looking at the scan) before there was evidence of hypoxic-ischaemic damage. He agreed that the degree of blood in the subarachnoid space was unusual in a setting of NAI. He agreed that the idea of a tear in the arachnoid membrane was a fairly recent one, within the last two years. If septicaemia was present in C1, he would not expect C1 to behave normally and then suddenly collapse. He could find no evidence of overwhelming infection. There was no evidence of suffocation. He accepted that Prolonged QT Syndrome can be the cause of cardiac arrest, but that in C1's case it is inconsistent with the presence of subdural and subarachnoid haemorrhage. Babies with Prolonged QT Syndrome do not have subdural, subarachnoid and retinal haemorrhage. It was extremely unlikely that C1 was suffering from that syndrome.

Dr Robert Sunderland made it clear in his evidence that he did not believe that shaking, as opposed to shaking followed by the head impacting on a surface, could cause the injuries seen in C1. He plainly believes that the "shaking hypothesis" is wrong. He referred to research papers at H1 and again at H16, which involve neck injuries in children involved in frontal collisions in road accidents. He referred to an email at H29, which he says sets out the biomechanical case that shaking does not cause trauma in infants. In his report he said that he could not exclude trauma, but he had cited mechanical research that questions the shaking theory. He could not exclude suffocation. But this he subsequently retracted in cross-examination. He could not exclude infection, by which he said in his evidence he meant septicaemia. What led him to septicaemia was C1's raised white cell count and seeing the presence of petechiae on C1's tummy. As I understand his evidence, he did not suggest that C1 was a SIDS baby. In his evidence-in-chief he explained that a SIDS baby was a dead baby who was, in life, completely normal and where at post-mortem examination no abnormality was found. Thus C1 could not be a SIDS baby. I shall refer later in this judgment to further aspects of the evidence of Dr Sunderland.

The Triad

The Court of Appeal, Criminal Division, then went on to consider the unified hypothesis, i.e. Geddes III. At paragraphs 66 to 67, the Court of Appeal said:

How then do the local authority, the guardian and the father put their cases about C1, now that all the evidence, both written and oral, has been given? I shall attempt to summarise them.

Mr Furness, having analysed the medical evidence between paragraphs 12 and 19 and the lay evidence at paragraphs 20 to 25 of his written submissions, submits that the various causes of collapse, which he sets out in extenso at paragraph 26, have been excluded, leaving only inflicted head injury, and that injury was caused by the father shaking C1 at or about 10.30pm on 22 April 2005.

The fundamental points made by Mr Tillyard and Mr Parsley are to be found between paragraphs 12 and 20 of their written submissions. Thereafter they too carefully analyse the medical evidence. They rightly draw attention to what they describe as "the wider canvas", namely the evidence of the father's devotion and care of C1 and C2, his love for the mother and the good home conditions. (See Re B, Children [2006] EWCA Civ 1186 ). I have set out the evidence upon which they rightly rely. They go on to make the point that in the light of the doctor's beliefs in 2005 about C1's death, had the father shaken C1, surely he would have let sleeping dogs lie and not challenged them to come up with a cause for C1's death. The father's obsession with immunisation was not the action of someone who knew full well why C1 had died. Mr Tillyard and Mr Parsley submit that the improbability of the father inflicting injury on C1 is "very high indeed", and why on this particular night when (I paraphrase) there was nothing untoward in himself or about C1?

They then submit that there are alternative explanations to the supposed triad of signs. They invite the court to start with what happened in 2005 and 2006. Dr Leadbeatter and Dr Davis both came to the conclusion that they could not exclude Sudden Infant Death Syndrome as being the cause of death, and that the bleeding that was found at post-mortem and on the scan was attributable to the abnormal coagulation, the prolonged period of hypoxia, together with attempts to resuscitate over a period of about an hour. They submit that this cannot lightly be dismissed as being plainly wrong. Dr Leadbeatter and Dr Davis are both very experienced experts in their field, and had in mind the possibility that this may have been an inflicted non-accidental head injury. SIDS does occur, and when it does, the baby's heart stops and there follows an hypoxic-ischaemic insult to the brain. What is unusual in this case is that after such a long period of time, the child is resuscitated and is then kept alive for another 15 hours. When C1 arrived at hospital, he was clinically dead, and it was Dr Vujanic who said that it was a miracle that they revived him at all. This is very unusual, notwithstanding the evidence of Dr Risdon that it was likely to give rise to very unusual intracranial findings. Mr Tillyard and Mr Parsley went on to submit that:

So having carefully analysed all the matters, Mr Tillyard and Mr Parsley conclude in this way:

The Cause of C1's Collapse

Suffocation

Infection

As to the petechiae, the furthest that Dr Sunderland went was to say that they would alert him to possible blood poisoning. However, when cross-examined by Miss Mifflin, he clearly and categorically accepted that septicaemia could not account for the subdural haemorrhage or the low attenuation seen in the frontal subdural collections on the scan. Further, he deferred to the ophthalmologist. At paragraph 3.9 of his report, Dr Sunderland raised a case within his experience of fatal meningitis septicaemia involving subdural and retinal haemorrhage, but he accepted Dr Bonshek's comments at GA70:

Accordingly, since C1 did not suffer from meningitis, this one case provides no support whatever for Dr Sunderland's supposition. Furthermore, when cross-examined by Mr Furness, he agreed that the presence of petechiae as on C1 frequently happened with children suffering from disseminated intravascular coagulopathy. I agree with Mr Furness's submission at paragraph 17.6 that the presence of petechiae on C1 is a non-specific sign.

Finally, the overall effect of the evidence of the father and the mother and MGPs is that up to the time of C1's collapse in the late evening of 22 April, C1 was a well and thriving baby. In my judgment, the evidence on this issue is all one way. I find that C1 did not collapse as a result of and/or die from any infection, for the simple reason that the evidence drives me to the conclusion that there was no infection.

Reaction to Immunisation

QT Syndrome

Very late in this case there was a flurry of emails just before the start of the hearing before me about Prolonged QT Syndrome. All the medical experts said that it was outside their field of expertise, but that certain findings were not consistent with cardiac arrest following QT Syndrome. What is QT Syndrome? It is a genetic complaint. It has been explained by Professor Fleming in that passage of the letter that I have just read out. Furthermore, an article by Dr Skinner, a Paediatric Cardiologist in Auckland, New Zealand, which is to be found at GQT20, describes the syndrome. The presence of the syndrome can lead to cardiac arrest.

Mr Tillyard and Mr Parsley at paragraph 46 of their written submissions submit that Prolonged QT Syndrome is raised as part of the father's case not to prove that this was the cause of collapse, but to show that there are conditions which can lead to cardiac arrest, and this particular cause has not been excluded in C1's case.

I accept the submissions of Miss Mifflin at paragraph 58 to 63 and of Mr Furness at paragraph 19 of their written submissions. There is no evidence that C1 suffered from Prolonged QT Syndrome. Professor Fleming thought that C1 having QT Syndrome was "extremely unlikely". Both C2 and his parents have undergone ECGs and do not suffer from this condition. Since this condition is a genetic complaint, the fact that neither his parents nor his siblings have it must give added weight to Professor Fleming's view about the unlikelihood of C1 suffering from it. Dr Stoodley and Dr Gawne-Cain stated that cardiac arrest could give rise to hypoxic-ischaemic damage, but it would not lead to a pattern of acute subdural haemorrhage, acute subarachnoid haemorrhage and intraventricular haemorrhage in the interval of time between C1's collapse and the CT scan, nor could it account for the low attenuation fluid collections. Dr Bonshek stated that he was not aware of any published literature regarding any association between the syndrome and retinal and optic nerve sheath bleeding. Dr Debelle agreed, and said that Prolonged QT Syndrome would not cause subdural haemorrhage. He describes the syndrome as "extraordinarily rare". Dr Vujanic told me that children with Prolonged QT Syndrome do not have retinal haemorrhages.

I am aware and have read Dr Skinner's article. He believes that Prolonged QT Syndrome can cause sudden unexpected death through rapid ventricular tachycardia leading to ventricular fibrillation. I am prepared to accept that there may be a connection between Prolonged QT Syndrome and cardiac arrest. However, for the reasons I have given, there cannot be such a connection in C1's case because there is no evidence that he suffered from it. However, my finding that there is no evidence that C1 suffered from Prolonged QT Syndrome does not lead me ipso facto to the conclusion that C1 did not suffer a cardiac arrest simpliciter. I must bear in mind that despite the advances in medicine and medical science, infants still die of unexplained causes which may have nothing whatever to do with trauma. I bear that well in mind, particularly as I now turn to deal with the cause, propounded by both the local authority and the guardian, of C1's collapse and subsequent death, namely non-accidental injury by shaking or shaking impact. I must also bear in mind that, in the future, medical science, after further research, may demonstrate that the "shaking hypothesis" is or may be unsound.

Miss Mifflin and Miss Williams at paragraph 22 make the point that Dr Leadbeatter and Dr Davis were experts as to fact, i.e. what they found at post-mortem examination and shortly before C1's death respectfully. Neither is in a position to give an overview, and both acknowledged that the evidence before the court is much more extensive than in 2005.

I have set out the evidence of the neuroradiologists. Their evidence was of the united view that the neuroradiological picture could only be explained by C1 having been subjected to a traumatic injury, most likely to have been shaking or shaking impact injury, in the absence of any evidence of accidental trauma. Each restricted themselves to their expertise. Each, in my judgment, was very careful in the manner in which they gave their evidence. In my judgment, Miss Mifflin and Mr Furness have accurately analysed the evidence of Dr Stoodley and Dr Gawne-Cain. Dr Stoodley was careful to look at all the neuroradiological evidence, as was Dr Gawne-Cain. As to the hypoxic-ischaemic injury, both agreed that this could occur after cardiac arrest as well as trauma, and so by itself it was non-specific. As to the subarachnoid haemorrhage, both they and Mr Edwards agreed that if the subarachnoid haemorrhage was due solely to hypoxic-ischaemic injury, it would take much longer to develop. Subdural haemorrhage would not be present if the hypoxic-ischaemic injury was due to infection or cardiac arrest but are common in inflicted head injuries. The low attenuation collection was as a result of a tear in the arachnoid membrane. Neither the neuroradiologists nor Mr Edwards accepted Dr Squier's assertion that these collections were naturally occurring childhood collections. It is also to be noted that on post-mortem examination Dr Leadbeatter found no pathological evidence of chronic or older bleeding, and no evidence of neomembrane in the dura.

Mr Edwards provided the only neurological evidence. He provided a very long and very detailed report of 31 January 2008. It runs, with appendices, to 104 pages. Despite its length, I have to say, it is a thorough, detailed and impressive report from a neurosurgical standpoint. Having gone through all the relevant records and reports, his opinion comes at pages 38 and continues through to page 73. Again he goes through the matters in quite meticulous detail. I can at best only summarise what he says, particularly from paragraphs 5.03 to 5.09. I only set out that which I have not already recorded as his evidence. I have already dealt with his opinion about the bruising found to C1's skull, paragraph 5.03.1. He records there was no skull fracture but that the separation of the suture seen at post-mortem was not present on the CT scan, i.e. the brain swelling and the intracranial pressure was not as severe at the time of the scan as it was at the time of death. Mr Edwards said this in his report at paragraph 5.03.9:

At paragraph 5.05.27, Mr Edwards tells me that in his clinical practice he regularly examines the fundi of infants and children with both head trauma and non-traumatic cases of raised intracranial pressure, and in his clinical experience he has only ever seen retinal haemorrhages that affect all areas of the retina in the context of inflicted head injury. At paragraph 5.05.2 he states that there are three possible explanations for the pathological sequence of events, namely:

Mr Edwards further relies upon the triad, CG227. It is unnecessary for me to set all that out.

The Neuropathologists

I have been asked to, and indeed in my judgment must, decide whether the evidence about the axonal swellings and the associated bleedings given by Dr Smith is to be preferred to that of Dr Squier. It is a very unhappy experience for a judge to have to choose between two experts, particularly as distinguished as Dr Smith and Dr Squier. But I am driven to the conclusion that Dr Smith's evidence is the more reliable. In my judgment, Mr Furness puts it succinctly and accurately in paragraph 13.4 of his submissions where he says that Dr Smith does not accept the hypothesis put forward by Dr Squier that the bleeding may be unconnected to the nerve root damage because, he says, the coincidence of location is too strong. He cannot understand why the blood would accumulate just in that position rather than run down the spinal cord. If Dr Squier's hypothesis was correct, then there should be blood all down the spinal cord, but there was not. He rejected the suggestion that the brain swelling may cause traction on the spinal cord, causing haemorrhages. The significant difference between that case and trauma is the repetitive process. With trauma it is very rapid, whereas brain swelling would be a slow process. "In a swollen brain, with no trauma, haemorrhages have never been described." He said that Mr Edwards made similar points with regard to this finding, as did Dr Bonshek in relation to retinal haemorrhaging.

Mr Tillyard spent the better part of two hours – and I certainly do not criticise him at all – examining Dr Squier in evidence-in-chief on many, many areas other than on her one disagreement with the evidence of Dr Smith. But the reality, as she had to accept when cross-examined by Miss Mifflin, is that in the interpretation of the CT scan, she had to defer to the neuroradiologists and, as to the eyes, to the ophthalmologists, and to the haematologists in respect of bleeding issues. Nevertheless, her evidence-in-chief showed little, indeed scant, deference to the experts in fields in which she is not an expert. Mr Furness accurately summarises the point at paragraph 13.6 of his submissions. First, Dr Squier had difficulty seeing the low attenuation collections in the subdural space which the neuroradiologists and Mr Edwards did not. Second, she did not understand how the material could be of low attenuation, whereas this was convincingly, in my judgment, explained by Dr Stoodley, Dr Gawne-Cain and Mr Edwards as being CSF which has got into the subdural space through a tear in the arachnoid membrane. Third, that the fluid could be explained as a natural collection often seen in babies, whereas the neuroradiologists and Mr Edwards said that the choice was between a tear in the arachnoid membrane and an old subdural haematoma. Fourth, she went on to suggest that the fluid could be a birth injury, but in my judgment this was pure speculation and went wholly contrary to the other medical evidence. Fifth, she said she deferred to the ophthalmologists' evidence, but nevertheless disagreed with them.

In my judgment, if Dr Squier did defer, which she said she did, to the other experts, then her evidence where she seeks to challenge those experts on their own ground must be open to criticism, if not outright rejection. Furthermore, the hypothesis which she puts forward and which Mr Tillyard puts forward as a credible hypothesis in his written submissions, which I have already summarised, is really in reality based on Gettes III. In her evidence Dr Squier had to retreat into saying that the cause of C1's death was "multifactorial". She said: "The factors were severe hypoxic-ischaemic brain injury, coagulopathy and pressure caused by brain swelling".

The Ophthalmologists

Paediatric Pathologists

The Paediatricians

I am afraid that I have to say, when I stand back and look at the medical evidence as a whole, it is apparent to me that where the medical evidence of Dr Squier and Dr Sunderland conflict with the evidence of the other experts, I have to reject it, for the reasons I have given. Thus, in my judgment, the medical evidence, standing alone, does point strongly, at the very least, to inflicted head injury and to non-accidental inflicted head injury.

So that nobody can say that I have lost sight of or undervalued the "wider canvas", all of which I put into the balance very much indeed, I have some comments to make on it and upon the lay evidence:

Dr Stoodley told me at G35 as follows:

The hiccupping of C1, on the father's own evidence, continued for 20 to 25 minutes without the father doing anything to see if C1 was all right. The mother told me that the father was not the sort of person to wait that long. To my mind, the father's behaviour in leaving C1 for that long before doing anything is simply not believable.

There is no explanation for the father waiting for about 10 minutes before ringing 999. His explanation that he was trying to find out what was the matter with C1 is not believable. Either the father would have instantly rung 999, or the mother, or both.

He did not ring the mother until nearer midnight, as she said. His delay does not lend credence to his evidence.

As Miss Henke demonstrated in her cross-examination of the father, the father was at least inconsistent as to how he handled C1, i.e. where he put him when he discovered that C1 was like a rag doll.

The father's evidence about being employed by MI5 is bizarre, particularly when he told C2's nurse in the hospital and the contact supervisor that he was a member of MI5. At the very least, his comments to the nurse and to the contact supervisor were make-belief.

I consider that the father was on 22 April 2005 under some degree of stress at losing his job. As he told the police, on 22 April he did DIY to relieve stress.

What he told Miss Jenkins, the paramedic, is very much at variance with what he told me.

I reject his evidence about telephoning the mother. I accept her account.

The father's obsession with trying to find out whether immunisation could have caused C1's death is not as unequivocal as Mr Tillyard makes out. I agree that it is consistent with a person who has nothing to hide, but it is not inconsistent with a parent who has shaken the baby and is trying desperately to find a smokescreen behind which to hide. After all, there is no dispute that the event which caused C1's collapse happened at about 10.30pm when he alone was caring for C1. The medical experts were unanimous on that point, including Dr Squier and Dr Sunderland. Thus, it is he alone who knows what really happened.

In my judgment, the father's evidence on what happened that evening, I regret to have to say, cannot be relied upon. His evidence lacks the important elements of consistency and integrity. Some parts of his behaviour are, on his own evidence, inexplicable; indeed unbelievable. His evidence that nothing of a traumatic nature happened to C1 is, in the absence of any evidence from him about the accident, quite inconsistent with the medical evidence.

I am therefore driven to these conclusions. At about 10.30pm the father shook C1 with sufficient force that not only caused his collapse and subsequent death, but also, which he would have instantly realised, was quite inappropriate. Having shaken C1, he put him back in his cot and went back downstairs. He heard the hiccupping, which was the beginning of C1's collapse. I suspect he was very worried indeed, having shaken C1 and hearing him hiccupping and hiccupping for so long, that he might have done something to C1 which he hoped would not materialise. After much too long a period, he went upstairs and saw C1 blue and grey and, on picking him up, he was limp like a rag doll. I am sure that he must then have felt dreadful and very apprehensive for C1 and indeed what he was going to tell the mother. That must be the only credible explanation for why he did not ring the mother at any time whilst C1 was hiccupping or for just about one hour after he says he discovered C1 in such a parlous condition at 10.50 or 10.55pm.

So far as the mother is concerned, the local authority concede that, given my finding of C1 being shaken by the father at 10.30pm that evening, there is insufficient evidence to make any finding against the mother. The guardian accepts (see paragraph 46 of Mr Furness's submissions) that the mother played no role in C1's collapse and death. She left a well baby in the care of the father, who, although stressed, had shown no previous inclination of violence towards C1. Once all the medical evidence was in, she accepted, and I believe genuinely, that the father must have shaken C1. It is to her credit that she did so. I accept that submission.

I should say, for completeness' sake, I have come to this conclusion having decided that all the bruising on C1, including at the back of the skull, was likely to be due to the resuscitation efforts.

I now turn to C2 . Dr Papworth is a Consultant Neonatologist. Towards the end of March 2006 she received a referral in respect of the mother and the father. The referral was, because C1 had died, they wanted counselling on how to prevent things happening to C2, who was about to be born. Dr Papworth told me that they wanted to be reassured that a sudden death would not happen again. The father had done much research, as I have said, and was convicted that C1 had died as a result of the immunisation on 20 April 2005. The parents were anxious to make sure that things were all right for their new child. The next contact with the parents was on 11 May 2006 when they brought C2 to the clinic. He was well and developing appropriately.

On 20 June 2006 the parents took C2 to the University Hospital of Wales in respect of injuries to his right eye and cheek. C2 arrived at the hospital at 22:26 hours. The triage notes record the fact that: "The child was playing on an activity gym and dad kicked (accidentally) the side of the gym, and a plastic tube from the gym hit the child on the side of the face." The medical note by a locum doctor was that C2 "was in a chair of a mobile. His dad was walking past the chair and kicked a mobile swing. The plastic uncovered bit hit the child on the right side of the face. The child cried immediately for five to seven minutes and was sleepy." The doctors felt the story was plausible.

On 22 June 2006 Dr Papworth saw C2 and the parents. Dr Papworth's statement, of 17 July 2007, reads as follows:

The next day, 23 June, she spoke to Dr Paul Davis. He told her that C1 had presented in a collapsed state, with retinal haemorrhage, subdural haemorrhage and coagulopathy. Dr Papworth told him how C2 had presented on 22 June. Dr Davis felt that the incident merited a full investigation. She then contacted Dr Rawlinson.

Dr Rawlinson

The parents then told Dr Rawlinson about C1, and that the father attributed his death to immunisation. Dr Rawlinson then examined C2, whom she found to be a lovely responsive smiling baby, who handled normally. She found three areas of bruising, which she sets out at G62, which were as follows:

The father then produced the baby gym. He showed Dr Rawlinson how he had positioned the baby in the middle of the mat, but he had moved nearer to the right side of the gym. Dr Rawlinson noted that the baby gym had a hollow, lightweight, plastic, tubular frame, with material cover at the base and the legs, but no padding. The car seat was also produced. Dr Rawlinson explained to the parents that C2 appeared to be well developed mentally, but bruising in a young non-mobile baby raised significant child protection concerns and was not consistent with the explanations given, and that she was concerned that C2 had bruising on more than one area of the body. She told him that C2 would be admitted to hospital for further investigations. Towards the end of the consultation, the father became agitated. He wanted to know precisely when the investigation would be carried out. Dr Rawlinson said that C2 was likely to be on the ward for a week. C2 was admitted. Dr Rawlinson went on leave.

In her evidence, Dr Rawlinson told me that the police photographs of C2, taken on 23 June, were of poor quality from a clinical perspective. The pattern of bruising over C2's right eye as she saw it upon her examination of C2 was over a large area. It was dark blue. Indeed, that is how the mother describes it. The bruise Dr Papworth saw was within the three linear lines below C2's right eye. The bruise Dr Rawlinson saw to the right leg was readily noticeable. In respect of the arm and leg bruising, Dr Rawlinson was not given an explanation of a particular incident referable to the cause of the bruises. She was only given explanations of how they might have happened.

During her evidence, Dr Rawlinson was asked to explain how the father had demonstrated to her, with the baby gym, that the injury to C2's face had occurred. She told me that this was all nearly two years ago. Nevertheless, she came out of the witness box and demonstrated with the baby gym. The father had placed the baby gym on the floor. He had stood at the front of the frame with the baby's feet nearest to him, with C2's head furthest from him. C2 had been lying on his back. The father had then walked forward and walked into the baby gym. Mr Tillyard put to her that the father told her that C2's head, not his feet, was nearest to the father. Dr Rawlinson emphatically rejected that. She told me that from what the father had told her on 23 June and what she saw being demonstrated on that day, she could not understand how the injury had occurred. Dr Rawlinson told me that she had asked the father more than once during the examination whether his foot had hit C2's face. The father was clear, she said, that his foot had not hit C2; it was the frame of the baby gym. Mr Tillyard pointed out to Dr Rawlinson in his cross-examination that she had made no note of asking the father whether his foot had hit C2. Dr Rawlinson could not explain why there was no such note. However, she did tell me that had the father told her that his foot had hit C2, she would have made a note of that. Further, in response to a letter from Rhiannon Jones, a social worker, she had written on 9 August 2006:

On 29 June, Dr Rawlinson met the parents again. She explained to them that the investigations had been normal, i.e. there was no medical reason for C2 to bruise more easily, but that unexplained bruising in a non-mobile infant raises significant paediatric and child protection concerns. In her statement at G65 she said:

Further down Dr Rawlinson says:

As with C1, MGPs described both parents as loving and devoted. In 2005 the parents had taken part in three SUDI (sudden unexplained death in infancy) strategy discussions. Both parents told me they were overjoyed with the mother's pregnancy and C2's birth. The father, who the mother agreed was C2's day-to-day carer as she had returned to work, told me that he had never had any difficulty with C2. When the health visitor visited C2, he was found to be a happy and thriving baby.

On 4 May 2006 the father told me that when changing C2, he vomited and saw bloodstained vomit in the baby-grow. He told me that he saw no blood on C2's nose. He called to the mother, who was upstairs at the time. She saw a streak of blood in C2's vomit. She could not see any blood from his nose. The health visitor, who was due that day, came earlier, at the parents' request. Both parents told me that Sue Field, the health visitor, suggested to them that the blood might have come from the nose. The father told me that the health visitor had said that many cases of baby's vomiting involved vomiting through the mouth and nose. The records state that the cause of C2's vomiting might have been overfeeding. As I have already recorded, on 11 May C2 was reviewed by Dr Papworth and all seemed to be well. On 20 June he was taken to the University Hospital of Wales. I have dealt with that and how the parents' explanation was accepted.

On 22 June the parents brought C2 to see Dr Papworth as part of the CONY programme. During the mother's cross-examination by Miss Mifflin she put to the mother a passage in the father's police interviews where he said he did not want to take C2 to see Dr Papworth. The mother agreed that the father was reluctant to go. The father told me that he was not reluctant. He had been joking with the mother that if they took C2 to Dr Papworth, then in the light of the injury to C2's right eye, they might be accused of assaulting C2. When he was cross-examined by Miss Mifflin, the same passage was put to him in his police interview. He agreed that when answering questions from the police, he had not been joking.

Both parents told me that the bruise to C2's leg had occurred before the baby gym incident on 20 June. The father told me that he first saw the bruise on the previous weekend. The mother told me that she had asked the father how it had happened. The father told her that C2 must have rolled against the bar of his cot or against the side of his changing equipment. Both parents agreed in evidence that neither told Dr Papworth of the bruise on C2's leg. The mother had no explanation why they did not. The father, when asked about that, sought to say that it was Dr Papworth's responsibility to notice it. The mother told me that she was present when the history was given to Dr Papworth. She agreed that Dr Papworth's note that the baby gym "fell" on C2 was not saying that the gym was kicked into C2. The father told me that he believed he had told Dr Papworth that his foot and the baby gym had come into contact with C2's right eye.

I now turn to recount the parents' evidence of the baby gym incident. At about 7.30pm on 20 June the mother told me that she went out to her aqua aerobics, leaving C2 in the care of the father. There was no mark on C2's face. At about 9.00 or 9.15pm she came home and came into the sitting room. She saw C2 lying under the baby gym, which was placed between the two settees. She saw the father come out of the kitchen door. She walked over to the table, shown on the plan with her marking – See E2238a. The small matchstick person represents C2 lying under the baby gym with his feet nearest the V, formed by the two settees, and his head closest to the kitchen door. The mother was unpacking her bag on the table with her back to C2 and the father. She heard a noise of the bells hanging down from the baby gym. C2 started crying. She rushed over to C2, who had been picked up by the father. C2 was upset and crying. The father was consoling him. Once C2 was quiet and asleep in the father's arms, the mother noticed a redness on C2's right cheek. The father told her that he had kicked the baby gym into C2. By the time they had taken C2 to the hospital, the mark was puffy and swollen. The mother told me she did not know which leg of the baby gym the father had kicked.

The father's evidence was as follows. As the mother came into the sitting room, he went into the kitchen and came out again. The mother was unpacking her bag on the table. As he walked past the settee nearest the wall of the sitting room and kitchen, his left foot, more particularly that part nearest his little toe, connected with the bar of the baby gym on C2's right hand side and nearest to C2's hip. He actually gave it a forceful kick, and the baby gym and the foot hit C2's face. C2 was on his back and slightly rolling to his right. The father believes that his foot did hit C2 because his left little toe was injured.

The father then came out of the witness box and stood in front of it to demonstrate to me what had happened. The baby gym was placed on the floor. C2, he told me, was lying with his head nearest to the father, slightly nearer the relevant strut. The father then walked forward "kicking" the strut. But what was immediately obvious to me and indeed to counsel watching the demonstration was that the baby gym, upon being kicked, was turned in an anticlockwise direction, and the strut, instead of moving in to where C2's face would have been, moved in the very opposite direction; that is to say, out and away from C2's face. The father did the demonstration again. This time it could be said that the strut might just have moved into C2's face. Nevertheless, during his cross-examination by Miss Mifflin, the father again demonstrated twice what had happened. On each occasion the relevant strut of the baby gym moved out and away from where C2's face would have been.

Causation of the Bruises

Leg

The Arm

The Face and Eye

The father's demonstration of kicking the baby gym established that not only is it very likely that the baby gym rotated away from C2's face, but also that the strut of the gym, which is said to have hit C2, was pushed along the floor and did not rise up from it. Dr Sunderland, in his evidence, postulated and demonstrated to me that the leg would have had to have been lifted up off the ground and the bottom of the strut would then have had to have impacted into the eye orbit. After the kicking, he said the gym would have travelled over the baby's face. He did not think that the father's trainers would cause such bruising. It would have had to have been the force of a kick on a football field.

What was so striking to me is that Dr Sunderland's suggestion as to how the bottom of the strut struck C2's right eye was nothing like the mechanism described and demonstrated to me by the father in his evidence. Again what was so noticeable to me, from the father's demonstration, was that the movement of his left foot into the baby gym could scarcely be described as a kick. It was more of a stumble. The baby gym, from his demonstration, never left the floor, and thus the very foot of the strut could not have struck C2 on the face or in the eye. The demonstration also showed that the baby gym did not travel over C2's face, as postulated by Dr Sunderland. Dr Debelle told me that if the strut had struck C2, it would have affected the bony prominence around the eye, but the bruising on C2 was above, below and in the recess of the eye. The distribution and pattern of the bruising was unusual, given the explanation put forward. He found it difficult to say what had caused the injury, but as he graphically put it, "it should not be there". A foot in contact with the eye made no difference. The pattern was still not explained. Dr Rawlinson told me that the impact of a wholly lightweight, tubular, plastic structure and/or a foot could not produce such an extensive distribution of bruising.

Furthermore, in my judgment, the father has put forward inconsistent explanations. I believe Dr Rawlinson to be accurate in her description of what the father demonstrated to her on 23 June, which is quite different from what the father demonstrated to me. He did not tell Dr Rawlinson that his foot had struck C2's face. If he had, I am satisfied that Dr Rawlinson would have made a note of it. The father told Dr Papworth that he had kicked the baby gym which "fell" against C2's face. She was sure that the father had not said anything about his foot coming into contact with C2's face. Mandy Morris, a social worker, noted (see D82) when going to the parents' home on 23 June, that the father told her that he had "walked past and accidentally kicked the gym into C2's face". She told me that had the father told her that his foot had hit C2's face, she would have recorded it. Louise Atkins told me that on 19 July 2006 at the case conference, the parents said that when the father accidentally kicked the frame, the force of his foot was still behind when the frame made contact with C2's face. A year later, on 8 August 2007, the father told the police that his foot had hit the baby's face and the bar together. It was quite a forceful kick, and he felt the impact. The gym moved quite a bit from its position.

I agree with Mr Furness at paragraph 32 of his written submissions that the father has developed his explanations. First, the baby gym was knocked into C2's face. Next, the baby gym hit C2's face and his foot was behind it. Finally, the baby gym and his foot hit C2's face together, and his foot was hurt.

Mr Tillyard and Mr Parsley submit (see paragraph 62) "Where is the cogent evidence that it did not happen in the way described by the father?" There is not enough evidence to overcome the probability of this having occurred in any way other than as described by the father and supported by the mother. The answer to the rhetorical question is the evidence which I have recounted. The father has at no time suggested the mother caused this injury. The explanation advanced is that of the father. I regret to have to say that the father's explanation is untrue. His lies are designed to cover up an incident which happened when he was alone with C2, either deliberately or accidentally. He did come into contact with the baby gym moments after the mother had come home. The baby gym did not strike C2, but the father saw that incident, particularly when C2 cried no doubt from the shock of the baby gym unexpectedly moving, as a way of explaining away what he had done to C2 sometime earlier that evening. In my judgment, it was a nasty piece of deceit practised on the mother. He tried it on with the doctors and it did not work. So he tried to add to his story by saying that his foot had hit C2's face. The doctors did not buy that either, and neither do I. I regret to have to say that the father has persisted in these lies right the way through his evidence before me.

The bruising on the leg was visible on the weekend before the baby gym incident. There was no viable explanation. There was no viable explanation for the bruising to the arm. In my judgment, it is much more likely that the father is the perpetrator of the bruises to C2's arm and leg than the mother. I say that because first I have found that the father shook C1, and second he caused the injury to C2's face and eye, about which he has not told the truth.

What then is the mother's position so far as C2 is concerned? She told me that she knew that the bruise was on C2's arm before they visited Dr Papworth on 22 June. She told Dr Papworth, but she did not tell Dr Papworth about the bruise on the leg, even though she knew it was there. She knew that neither she nor the father had any viable explanation as to the bruising on the leg and the arm. She herself had never witnessed any incident which could remotely account for the bruising on either the arm or the leg. In my judgment, she must have known that the father was giving vague explanations. Further, the mother knew that the father knew that the bruise to the leg had been caused prior to the visit to Dr Papworth and yet he said nothing to Dr Papworth about it.

At the time of the baby gym incident the mother appears to have readily accepted the father's explanation, although with her back turned she did not actually see it happen. Furthermore, if the father's account to the mother of him kicking the gym into C2's face was true, why then did she go along with the father saying to Dr Papworth that the gym had fallen on C2? The mother did not tell her parents about any of C2's bruises until C2 was in hospital. According to the mother, by 21 June C2's eye injury looked worse, and it was black and bruised by the time C2 was taken to Dr Papworth on 22 June. The mother admitted in cross-examination that she did not tell her parents about C2's eye injury until after his admission to hospital.

MGPs lived, as I have said, just across the same street and were in the habit of seeing C2 frequently. MGM was then in plaster with a broken ankle and so was housebound, and yet C2 was not brought over to see her. MGP has had paramedic training in the past, yet the mother sought no advice or reassurance from him about C2. Both Miss Mifflin and Mr Furness submit that the only inference is that the parents did not want C2's grandparents to see any of his injuries.

Miss Henke and Miss Hayworth submit that the mother took C2 to see Dr Papworth despite the father's reluctance. That is so, but she did not point out the bruising to the leg. It is also submitted that Dr Papworth did not tell the parents of her suspicions, which is correct, and that there was nothing at that time to put the mother on enquiry. I respectfully disagree. Here was a non-ambulant child who had suffered three injuries, two of which the mother must have known at the time were completely unexplained and un-witnessed. The father had told her that he was reluctant to take C2 to Dr Papworth because they might be accused of assaulting C2. That must have struck the mother at the time as being a very strange remark, coming as it was from C2's principal carer. Miss Henke and Miss Hayworth try in paragraph 44 of their written submissions to persuade me that if as far as the mother was concerned everything was as it should be, why would she then alert her parents about marks she thought to be innocent? I am not so persuaded. I do not believe the mother thought that "everything was as it should be".

Furthermore, I accept the submissions of Mr Furness that the mother had noticed indeed before the time of C2's injuries that the doctors were concerned that C1 did not die from natural causes. Dr Davis had told them that trauma was one of the postulated causes for C1's death, which was never excluded. The possibility of C1's death being as a result of an unnatural act was specifically referred to at the inquest, although Miss Henke and Miss Hayworth are absolutely right to point out at paragraph 15 that the Coroner said she did not see "any likelihood of unnatural causes". I accept Mr Furness's submission that the mother appears to have readily accepted the father's "explanation" for the bruising to the leg, but it was not until she was cross-examined did she accept there was no explanation for that bruise. As to the eye and facial bruising, the mother seems to have accepted the father's explanation. She seems never to have questioned it, nor its changing detail.

My analysis is that the mother suspected that injuries had been inflicted on C2, and as they had not been caused by her, then realistically it could only be the father. In my judgment, she shut her eyes to what was happening to C2 out of misplaced loyalty to and love for the father, no doubt hoping that indeed there might be "innocent" explanations which would be accepted by the doctors. Although in her statement she said that she accepted in the light of all the medical evidence that the father must have shaken C1, she has not and did not accept that he had caused the injuries to C2. I regret to have to say that in my judgment the mother has failed to protect C2 in the ways I have described.

Thus I conclude that the threshold conditions under section 31 of the Children Act 1989 are established. C1's collapse was caused by the father shaking him. C1 therefore suffered harm as a result of a lack of care by the father. The mother I find to be completely blameless. C2's bruises were caused by the father, and C2 therefore suffered harm. The mother failed to protect C2 in the way that I have indicated.

The father, I am quite certain, will be devastated by my conclusions. I am afraid I can offer him little comfort, except to say that in respect of C1, although what he did had catastrophic results, his shaking of C1 was done in a moment of loss of temper or frustration, without there being a specific intent to cause C1 serious harm.