Nuetral Citation Number: [2008] EWHC 3320 (Fam)
IN THE HIGH COURT OF JUSTICE
In a District Registry
(Family Division)
B e f o r e:
THE HON. MR JUSTICE BENNETT
B E T W E E N
A COUNTY BOROUGH COUNCIL | Applicant |
-v- | |
M | 1st Respondent |
F | 2nd Respondent |
MGPs (MGP and PGP) | 3rd Respondents |
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
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Official Court Reporters
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JUDGMENT
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 Adam’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:
Blotchy patches of petechial bruising above and below the right eye. These were blue in colour. Bruising below the eye measured 2 centimetres by 2 centimetres by 2 centimetres and was roughly triangular. Above the eye the bruising appeared in a patch measuring 2 centimetres.
Slight soft tissue swelling under the eye.
A linear brown bruise on the anterior aspect of the right leg in the midline. This was approximately 3.6 centimetres long, with a distal linear extension of slightly lighter colouration, also brown, measuring 1.5 centimetres long.
Three petechial bruises and a cluster in the midline of the left upper arm.
A mark on the nape of his neck, which was thought to be a birth mark.
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 cause of C1’s collapse on the night of 22 April 2005, and
the cause of bruising to C2’s face and body when examined on 23rd June 2006.
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.
“The balance of probability standard means that a court is satisfied an event occurred if the court considers that, on the evidence, the occurrence of the event is more likely than not. When assessing the probabilities, the court will have in mind as a factor, to whatever degree is appropriate in a particular case, that the more serious the allegation, the less likely it is that the event occurred and, hence, the stronger should be the evidence before the court concludes that the allegation is established on the balance of probability. … Deliberate physical injury is usually less likely than accidental physical injury. … Built into the preponderance of probability standard is a generous degree of flexibility in respect of the seriousness of the allegation. Although the result is much the same, this does not mean that where a serious allegation is the issue, the standard of proof required is higher. It means only that the inherent probability or improbability of an event is itself a matter to be taken into account when weighing the probability in deciding whether on balance the event occurred. The more improbable the event, the stronger must be the evidence that it did occur before, on the balance of probability, its occurrence will be established.
Ungoed Thomas J expressed this neatly in Re Dellow’s Will Trusts [1964] 1 WLR 451.
“The more serious the allegation, the more cogent is the evidence required to overcome the unlikelihood of what is alleged and thus to prove it.”
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:
“C1 was next assessed by a doctor on the date of his immunisations (20 April 2005). He underwent a general eight week check. It is documented that his head circumference at that time was 37 cm (2nd centile). His head control and muscle tone were satisfactory. His vision was satisfactory. C1 was reported to fix and follow. His general behaviour was satisfactory. Examination of his hearing, genitalia, hips and cardiovascular system were all normal. The GP reports that C1 was given a combination vaccine against diphtheria, tetanus, pertussis (whooping cough), polio and Haemophilus influenza type B infection (Pediacel combination vaccine batched C2034AA). This vaccine contains inactivated extracts of the five different organisms that cause the aforementioned diseases. In addition C1 was given the meningitis (C) immunisation as a separate injection.”
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.
22 April 2005
On that morning the father went to work as usual but unfortunately was dismissed from his job as a customer services assistant. He told me he went into work that morning and was dismissed almost immediately because he was not up to the grade and he got the blame for the computer system crashing. He told me he felt blameless and wrongly accused. He told me that he came home and started some DIY. The garage roof had to be fixed. He told me he was not stressed on that day. However, that evidence was contrary to what he told the police on 31 July 2007 when he said, “Well, I come home at 20 past 9.00, got changed, and I just, you know… My way to deal with stress is DIY, so I just went out to the garage, or painting and decorate. That’s how I handle stress.” In the afternoon MGM came to look after C1 while the mother went to have her hair done prior to going out in the evening. MGP came with her and helped the father repair the garage roof. MGM remembers C1 as being very sleepy, but she told me that at that time she had no concerns about that.
Late afternoon and evening of 22 April
The mother went out with her girlfriends for the evening at about 7.15pm, leaving C1 in the sole care of the father. The mother describes the events of the evening in her statement of 22 February 2008 in this way:
“My mother came over to our house to baby-sit, and my father and F began fixing our garage roof, which was a job they had been planning to do for some time. The hairdressers is about a five minute walk from my home. When I got back at about 4.00 to 4.15pm, my mother had just gone home. C1 was in his bouncy chair. I fed C1 at about 5.30pm and made up bottles and placed them in the fridge. I then had something to eat and got ready to go out.
Before I went out, I again asked F if he was sure he did not mind me going out, and he was quite clear that he wanted me to go out and he seemed perfectly normal. After I had left the house, I remembered I had forgotten four cans of cider that I intended to take to my friend’s house, so I came back in to get them. Nothing was unusual in the house. C1 was in his bouncy chair in the living room and F was on the sofa watching TV.
I returned from my girls’ night out at approximately 12 o’clock, to find police coming out of my house and to be informed that C1 was poorly and had been taken to hospital. I was shocked and confused, as he was fine when I had gone out.”
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 brain is cased in three membranes. The one immediately surrounding the brain is the pia mater. The next one is the arachnoid. Between the pia mater and the arachnoid is an area known as the subarachnoid space, in which is located the cerebrospinal fluid. The third membrane, the dura, is a much tougher thicker membrane which surrounds the brain and continues down the body surrounding and protecting the spinal cord. It is commonly said that between the arachnoid and the dura membranes lies the subdural “space”. However, I was told that the “space” does not in fact exist in a healthy infant. It is a potential space. Between the arachnoid and the dura membranes are veins which are called bridging veins. The brain is divided into two halves or cerebral hemispheres which are separated by the falx, which itself is part of the dura. Below the cerebral hemispheres the brain is joined to the spinal cord at the craniocervical junction. The spinal cord extends from the brain and into the spine. Below the back of the cerebrum is the cerebellum or “little brain”. The tentorium cerebelli is a fold of the dural membrane that separates the cerebrellum from the main cerebral hemispheres.
The post-mortem examinations
Dr Leadbeatter found no fracture present in any of the bones of the skull. He did find a 3 cm wide x 2 cm high discolouration to the left of the midline of the back of the head, the upper margin some 4.5 cm below the top of the head. There was some “bloodstained fluid” below the dura at each side of the brain, but this amounted to no more than 2 ml in total. There was a minor “clot” of no significant volume and included in the 2 ml total volume in the middle part of the right side of the base of the skull and above the sheet of membrane which separates the brain from the little brain. The preliminary post-mortem findings confirmed the clinical history of subdural bleeding, albeit of a small volume, and cerebral swelling.
The brain was removed and fixed. The spinal cord was also removed. Dr Leadbeatter said in his report of 11 November 2005:
“The fixed brain weighed 780g and showed “bleeding below the middle covering” (subarachnoid haemorrhage) over each hemisphere, largely parallel with surface blood vessels and most obvious over the upper surface of the “front of the right side of the brain” (superior aspect of right frontal lobe), the “junction between the lobes at the front and the sides of the brain” (each sylvian fissure), and between the optic nerves and the midbrain. No abnormality was seen in the blood vessels of the Circle of Willis, and there was no gross abnormality of the “little brain” (cerebellum) or brain stem. Some minor subdural clot was present in association with the “membrane which separates the halves of the brain” (parafalcine subdural clot). Multimple “top-to-bottom (coronal) slices of the brain revealed no unequivocal haemorrhage within the ventricles, and no significant gross abnormality, other than apparent vascular congestion.
Examination of the fixed cervical cord confirmed the presence of “blood outside the outermost covering” (epidural blood) in the posterior cervical and posterior and anterior lumbar segments, with possible subarachnoid haemorrhage in the mid-thoracic segment and blood in the epidural fat throughout the mid-thoracic to lumbar region.”
Dr Leadbeatter then did an examination under the microscope.
“Microscopy
Examination under the microscope of multiple sections from the brain confirmed the naked eye appearances of subarachnoid haemorrhage; there was apparent haemorrhage in the left lateral ventricle and many areas of perivascular extravasation without associated inflammatory cells (no vasculitis). Several “slits” were seen within white matter but few of these were associated with significant bleeding, and they are considered to be the consequence of fixation artefact, rather than to represent true injury. There was wide variation in size, shape and staining of nerve cell bodies, with marked pericellular vacuolation, considered in keeping with the consequence of “poor supply of blood or oxygen” (ischaemic/hypoxic injury): staining with an antibody to B-amyloid precursor protein (B-APP) revealed a “geographic” distribution of staining, but only occasional scattered “bulbs” and varicosities were seen in the lenticular nucleus and internal capsule.
No iron pigment was seen and there was nothing to indicate organisation of any previous bleeding in association with the dura.
Multiple sections from the brain stem and cervical cord confirmed the presence of extradural red blood cells with focal intradural, subdural or subarachnoid bleeding in association with nerve roots. No iron pigment was seen in association with this bleeding. Staining with an antibody to B-APP revealed several varicosities or “bulbs” in cervical nerve roots; similar appearances were seen in a section from the thoracic cord.
Sections from the eyes confirmed the naked eye appearances of bleeding within, and below, the dural sheath of the optic nerves; no iron pigment was seen in association with that bleeding, but there was iron pigment within the orbital soft tissues. There was bleeding in all layers of the retina in each eye, but no bleeding was seen within the vitreous humour. Blood was present in the head of the left optic nerve and the sclera adjacent to that nerve; bleeding was present in both posterior and anterior aspects of the retina.”
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.
“Post-mortem examination of the head reveals bruising to the back of the head that was not present ante-mortem. I disagree with the report by Dr Leadbeatter (4.03.5) who states that there was “no bleeding through the full thickness of the scalp at either point” and “no subperiosteal bleeding”. In my opinion, the post-mortem photographs show bruising extending to the galea (a layer of the scalp) and also bleeding within the periosteum (intraperiosteal bleeding) (membrane covering the skull bones). I have undertaken surgery on hundreds of acute head injuries, and these operations involved “peeling back” the scalp in exactly the manner shown in the photographs. I have often seen similar patterns of scalp bruising, with intraperiosteal bleeding, in patients who have suffered witnessed accidental falls onto soft yielding surfaces (e.g. thickly carpeted floor). I acknowledge that these bruises were not documented ante-mortem but would comment that subtle bruising behind the hairline, particularly at the back of the head, is often missed on clinical examination; it is equally possible that the bruising was not clinically evident at the time of examination, but nevertheless involved following an injury occurring hours before. This bruising could be attributed to three causes: (i) a blow to the back of the head on a soft yielding surface such as a mattress or possibly carpet (depending on the force used), (ii) pressure on the back of the head during resuscitation, particularly in the presence of a coagulopathy, (iii) post-mortem artefact.”
The Scan
According to Dr Stoodley and Dr Gawne-Cain, the CT scan, taken at 2 o’clock on the morning of 23 April 2005, shows a number of abnormalities: (i) Extensive hypoxic-ischaemic brain injury throughout most of both cerebral hemispheres. (ii) Hypoxic-ischaemic brain injury involving the cerebellum. (iii) Acute subarachnoid blood in a peripheral distribution most consistent with trauma. (iv) Acute intraventricular blood. (v) Acute subdural blood in the posterior interhemispheric fissure and the posterior fossa. (vi) Low attenuation: frontal, subdural collections, likely to be due to an acute traumatic event.
Dr Stoodley says in his report of 10 February 2007 at G29:
“The cerebral hemispheres are of lower attenuation than normal and there is almost complete loss of grey white differentiation. Some minor relative sparing of grey-white differentiation is seen in the medial occipital regions bilaterally, i.e. these appear to be the only areas of the brain that are less involved in the hypoxic process at the time of this scan. The generalised low attenuation and loss of grey white differentiation is secondary to extensive hypoxic-ischaemic brain injury. This, somewhat unusually, involves the basal ganglia, thalami and brainstem, and the fact that these areas are involved is likely, in my view, to reflect the severity of the injury. Other than the generalised hypoxic-ischaemic injury, no other focal brain abnormality has been identified.
The cerebellum is also of abnormally low attenuation with reduced grey white differentiation. It is extremely unusual to see involvement of the cerebellum evident on scans in the majority of hypoxic-ischaemic brain injuries; the cerebellum is usually spared (in terms of scan appearances) in hypoxic insults due to events such as asphyxiation or when a patient has collapsed secondary to cardio-respiratory arrest from various causes. The ventricles are not enlarged and indeed are within normal limits for size, but the basal cisterns are partially effaced, suggesting a mild degree of brain swelling at the time of this CT scan, but see comments regarding lack of sutural splaying in this context below.
High attenuation material (representing acute blood) is seen in a patchy peripheral linear distribution, consistent with peripheral subarachnoid haemorrhage in the sulci over the surface of the brain, in the Sylvian fissures and in the posterior horns of both lateral ventricles. Whilst severe hypoxic-ischaemic brain injury (from whatever cause) can lead to oozing of blood into the subarachnoid space, the amount of subarachnoid blood and its distribution on C1’s scan is, in my view, more in keeping with traumatic aetiology for the subarachnoid haemorrhage.
In the region of the falx there is also some high attenuation material, consistent with acute blood. In some places this acute blood appears somewhat irregular in outline and this too is likely to be due to blood in the subarachnoid space. However, particularly posteriorly, the appearances are more suggestive of the presence of acute subdural blood lying adjacent to the falx, with blood extending inferiorly to layer over the upper surface of the tentorium slightly more on the left than the right. There is also a little high attenuation material seen in relation to the falx cerebelli, suggesting some posterior fossa subdural blood. It is not possible to estimate the age of any of this acute blood on the basis of the neuroimaging appearances alone, as blood can appear bright on CT scans from soon after an episode of bleeding for up to 7-19 days; very occasionally longer (but see comments regarding timing of injury below).
In addition, over both frontal regions there is evidence of subdural fluid collections of a different appearance to the acute blood. These other collections are of low attenuation (i.e. are darker than the underlying brain). The low attenuation collection on the left is slightly larger than the collection on the right. Whilst traditionally low attention subdural collections would be most likely to have been thought of as chronic subdural haematomas (i.e. evidence of older episodes of bleeding), it is increasingly recognised that low attenuation subdural collections can be seen in the context of acute injuries when the arachnoid membrane has been torn, as this can allow cerebrospinal fluid to leak into the subdural space and either collect there or dilute any acute blood present. Given the extent of the rest of the brain injury, in my view it is most likely that the lower attenuation fluid seen represents the result of an acute injury which has involved tearing of the arachnoid membrane. The scan appearances therefore are in my view explicable on the basis of being the result of a single event. The lack of any pathological evidence of older bleeding or a subdural neo-membrane would, in my view, support this conclusion.
The scan has also been photographed on bony windows. No fracture has been identified. There is no soft tissue swelling evident to suggest a recent impact injury against a hard or unyielding surface. There does not appear to be significant sutural splaying at the time of this examination. This suggests that, although some cerebral swelling is evident as the basal cisterns are effaced, this has not caused any sutural splaying and suggests that the causative event is likely to have occurred very close to the time of the CT examination, in my view, i.e. before major swelling has had the opportunity to develop. I note that the post-mortem skeletal survey (which I have not seen) was reported as showing some probable sutural splaying. Given the extent of the hypoxic-ischaemic brain injury evident on the CT scan, I am not at all surprised that there may have been some sutural splaying by the time of the post-mortem skeletal survey, as brain swelling would have continued to develop in the period between the CT scan and the time of C1’s death.
Given the extent of the brain injury, it is my view, it is extraordinarily improbable that C1 would have behaved any way normally after causative event, and is likely to have become obviously and severely unwell at the time of the causative event.”
Dr Gawne-Cain put it this way in her report of 31 January 2008:
“It is not possible to manipulate the images to view details of the bones of the skull. On the soft tissue images no obvious scalp swelling is apparent. I cannot comment on whether there is a skull fracture or whether there is spreading of the skull sutures (sutures are the gaps between the plates of bone that make up the skull). I note that Dr Stoodley, who has seen bone windows for this study, did not find evidence of skull fracture or sutural widening.
The brain is dark and featureless. The normally visible distinction between grey and white matter has been lost. Although the brain may be slightly swollen, normal fluid filled spaces are still visible around the base of the brain, and there is no herniation of the brain across intracranial compartments.
There is extensive high attenuation (looks white on the images) material seen over the surface of the brain. This represents recent haemorrhage. Much of this blood is in the subarachnoid space. That is to say, it lies in the cerebrospinal fluid that normally surrounds and bathes the brain and extends into the folds and fissures of the surface of the brain.
Some of the blood outlines the falx and the tentorium. These tough dural membranes project inwards from the superior and posterior aspects of the skull to lie between the cerebral hemispheres (falx) and between the forebrain and the hind brain (tentorium). They are covered with a more delicate layer, the arachnoid membranes. It is likely that this blood is subdural in location – lying between the layers of membranes.
There is also blood within the ventricles – the fluid filled spaces in the centre of the brain. The subarachnoid space is in free communication with the ventricles and blood can travel from one of these regions to another. The subdural space is normally separate from the subarachnoid space and blood within this compartment is less mobile.
There are collections of low attenuation (looks dark) fluid over the convexities of both cerebral hemispheres. These collections are separate from the subarachnoid space and are likely to represent subdural collections. That is to say, the fluid lies between the membranes on the inner surface of the skull. From the radiological appearances, the darker fluid could represent either (a) old subdural haemorrhage (because intracranial blood becomes darker in appearance with time), or (b) cerebrospinal fluid that has looked from the subarachnoid to the subdural space through a tear in the (delicate) arachnoid membrane. I note that at autopsy this was found to be bloodstained fluid without evidence of old haemorrhage. This supports the second possibility (leakage of fluid through a tear/tears in the arachnoid membrane).”
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:
“The pattern of acute haemorrhage (both subarachnoid and subdural) demonstrated on the scan is most likely to be due to head trauma, in my view. Any insult of sufficient severity which causes reduced blood and/or oxygen supply to the brain can lead to hypoxic-ischaemic brain damage and, as stated above, severe hypoxic-ischaemic brain injury from any cause can lead to patchy subarachnoid haemorrhage. However, in my view the pattern of subarachnoid haemorrhage seen on C1’s scans is much more likely to be due to a primary traumatic cause rather than to be due to a secondary phenomenon of hypoxic-ischaemic injury. Given that the scan was perform only a few hours after C1’s collapse, it would be very unusual, in my experience, to see this degree of subarachnoid haemorrhage in the context of a primary acute hypoxic event such as an apnoeic event.
Although there is only a small amount of acute subdural blood seen on the scan, its distribution in the posterior interhemispheric fissure and posterior fossa is unusual in conditions other than head trauma. I note that there was evidence of a blood clotting abnormality (thought to be secondary to C1’s clinical condition). I am aware that brain injury itself can lead to clotting abnormalities, but it will be important to obtain expert haematological advice regarding the nature of C1’s acute clotting dysfunction. In any case, from the point of view of the neuroradiological appearances, in cases of intracranial haemorrhage secondary to blood clotting abnormalities, the bleeding usually occurs into the substance of the brain itself rather than being subarachnoid or subdural bleeding over the surface of the brain. The pattern of subdural blood is therefore also more in keeping with a primary traumatic cause rather than being due to any secondary effect.
The degree of hypoxic-ischaemic brain injury evident on the scan performed at around 0200 hrs (i.e. within a very few hours of C1’s clinical collapse) is very extensive and involves almost all of both cerebral hemispheres, the deep grey structures, brain stem and cerebellum. In view of the extent of this injury, it is virtually inconceivable that C1 could have behaved in any way normally after the event which caused this degree of brain injury, and he is, in my view, likely to have become obviously and severely unwell at the time of the causative event. Very occasionally in clinical practice, a child who has stopped breathing for some reason at home or elsewhere is brought into hospital having been resuscitated by carers and/or paramedics. It is very unusual, in my experience, to see any degree of hypoxic-ischaemic brain injury in any of these cases on such early scans, and I cannot recall ever having seen such a degree of hypoxic-ischaemic brain injury as is seen on C1’s scan in such a clinical situation. Infants and children who stop breathing for various reasons or who, for example, suffer seizures are not infrequently resuscitated by carers and professionals with various degrees of training and experience. Those infants and children who have head scans following such events do not, in my experience, show the features demonstrated on C1’s scan. In addition, in such circumstances it would be extremely unusual to see this degree of change in the cerebellar hemispheres secondary to such a primary hypoxic insult. Evidence of hypoxic-ischaemic change in the cerebellum on scans is occasionally seen in cases of non-accidental head injury, especially in injuries toward the more severe end of the spectrum of severity. In my view, therefore, the head injury is likely to have been the cause of C1’s collapse and the reason he required resuscitation, rather than resuscitation being the cause of these appearances.
Looking at all of the neuroimaging appearances and interpreting those in the context of a very acute sever clinical deterioration, the only reasonable explanation that I can put forward which explains all of these features is that C1 suffered an episode of head trauma. The types of head trauma that infants of C1’s age can be subject to are:
(i) birth related;
(ii) accidental head injury, and
(iii) non-accidental head injury.
The acute blood event is unequivocally recent and could not date back to the time of delivery, and I am unaware of any condition that could have occurred at the time of delivery which would lead to such a devastating and sudden clinical deterioration as occurred to C1 on April 22nd 2005.
There is no history of accidental head trauma of sufficient severity to account for the neuroimaging appearances, and C1 was not of an age where he could have manoeuvred himself into position to have caused himself such harm.
The neuroimaging appearances seen are, however, entirely consistent with being due to an episode of non-accidental head injury. This is likely to have involved a shaking or shaking/impact mechanism, although it would not, in my view, have been necessary for any impact to have occurred with an external surface. Majority medical opinion is of the view that what is required to produce such injuries is likely to be the repetitive backwards and forwards movement of the unsupported infant head which pivots on the neck.”
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”:
“The combination of radiological findings – cerebral oedema with subarachnoid and multifocal subdural haemorrhage – is very suggestive of a traumatic cause. The additional finding of retinal haemorrhages is also in keeping with trauma, and completes the ‘triad’. This pattern of brain injury and haemorrhage is one that we associate with a rotational acceleration/deceleration injury such as might be caused by shaking. It is believed that rotational acceleration/deceleration of the head results in (a) stretching and tearing of bridging veins passing from the brain to the skull causing small volume subdural and subarachnoid haemorrhages; (b) stretching and damage to nerve fibres in the brain stem causing apnoea of variable duration (cessation of breathing) resulting in hypoxic insult to the brain; (c) in severe cases, tearing of fibres within the brain substance, or shear injuries. That rotational trauma can cause such injuries is generally accepted. However, the strength and nature of the forces required to cause the injuries is more in dispute. Confession evidence exists that suggests that shaking alone is capable of causing brain injury [1] but confessions are not always reliable. It has been suggested that the rotational forces generated by shaking are insufficient to cause brain injury, but are greatly increased if there is impact at the end of the rotational movement [2]. Arguments revolve around whether the biomechanical models used in experiments are sufficiently true to real babies, and whether the impact needs to be with an external object or could be with the infant’s own back/chest [3]. Certainly in cases of this kind, evidence of impact is not always found [4], and this is one of the reasons prompting workers in the field to search for alternative explanations for the constellation of findings. Even if it is accepted that the ‘triad’ may be caused by shaking a baby, the presence of the ‘triad’ does not automatically prove that shaking has occurred, and other possibilities should always be considered.
I retain rotational acceleration/deceleration injury as a reasonable explanation of the radiological appearances.
In this case, no history of shaking has been given, and it is necessary to explore other possible explanations for C1’s collapse.
Birth may cause intracranial haemorrhages. However, the bleeding and brain injury are too recent and could not be explained by a traumatic birth. This possibility is rejected.
Accidental Trauma: An accidental fall resulting in impact to the head, with a significant rotational element, might result in intracranial haemorrhage and cerebral oedema. The generalised pattern of haemorrhage and the lack of evidence of impact in this case would be atypical for an accident. No accidental injury has been described. This possibility is rejected.
Cardiac Arrest: We know from the medical notes and statements that there was a significant episode of cardiac arrest. Could a cardiac arrest on its own, from whatever cause, be responsible for all of the intracranial findings in this case? It could account for the extensive ischaemic damage to the brain. It might result in a small amount of oozing of blood into the subarachnoid space from damaged capillaries. It has been suggested that it might also account for subdural haemorrhages. This controversial hypothesis (or theoretical possibility) was advanced by Geddes et al [5]. It does not fit with our clinical or radiological experience of babies with hypoxic brain damage of any known non-traumatic cause. The hypothesis was considered and rejected in the Court of Appeal in 2005.
C1 had a documented clotting abnormality, believed to be secondary to the hypoxia/cardiac arrest. Could this, added to the brain ischaemia, account for the intracranial haemorrhage? It might explain why the subarachnoid haemorrhage was extensive (rather than a tiny amount of oozing). However, if there were a significant amount of haemorrhage from reperfusion of damaged capillaries, it is surprising that there was no evidence of haemorrhage into the brain substance. Even with clotting abnormality, it is difficult to explain the subdural haemorrhages without some element of trauma.
In this respect, the dark subdural collections over the cerebral convexities are very important. They do not represent recent haemorrhage alone, and thus cannot be the straightforward result of oozing from blood vessels, even if it is accepted that this could be caused by hypoxia and/or a blood clotting abnormality. In my opinion, the ‘bloodstained fluid’ is most likely to represent bloodstained cerebrospinal fluid that has leaked into the subdural space through a tear/tears in the arachnoid membrane and such a tear/tears would be caused by trauma.
Thus I reject primary cardiac arrest, from whatever cause, with or without a blood clotting abnormality, as a cause of the intracranial appearances in this case.
Traumatic Resuscitation: It was suggested in the Coroner’s Court that the constellation of findings could result from a combination of cardiac arrest, clotting abnormality and a traumatic attempt at resuscitation by a non-professional. As discussed above, it is my opinion that some trauma occurred to account for the subdural collections, in particular the dark subdural collections. Cardiopulmonary resuscitation might cause certain rib fractures, but would not normally cause head trauma. I cannot see that resuscitation, even if inexpertly performed by an amateur following instructions over the phone, could cause traumatic head injury. However, if there was shaking in an attempt to revive, then it is plausible that intracranial haemorrhage might be caused. In the documents available to me, including transcripts of the extensive police interviews, no history is given of shaking to revive.
This explanation is plausible but very unlikely.
Intracranial infection may be associated with brain ischaemia, subdural collections and small amounts of intracranial and subdural haemorrhage. The radiological pattern in this case is not at all typical of intracranial infection. It is my understanding that there is no clinical or post-mortem evidence for intracranial infection. This explanation is rejected as a possible cause of the injuries.
Choking or Aspiration: This has been advanced by some workers as a possible cause of the triad of encephalopathy, subdural haemorrhage and retinal haemorrhages. The hypothesis is not, at present, backed by clinical evidence or experience, and is not generally accepted. The details of the arguments for and against this hypothesis are best discussed by other experts, including clinicians. From the radiological perspective, even if it is accepted that choking could cause subdural haemorrhage, it would not cause leakage of cerebrospinal fluid into the subdural space and would not explain the dark subdural collections. This explanation is rejected as a possible cause of C1’s injuries.
Immunisation: That immunisation might cause encephalopathy and intracranial haemorrhage is a minority view, and is not generally accepted. I leave it to other experts to discuss to what extent this is plausible. From my radiological perspective, even if a reaction to immunisation could cause cardiac arrest, hypoxic brain damage and intracranial haemorrhage, it would not explain the dark subdural collections. This explanation is rejected as a possible cause of the injuries.”
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
He told me that he frequently looks at scans to make clinical and operative decisions. If he is to operate, he has to interpret from the scan the size of haematoma which he may have to remove. At paragraph 3.9 he reviewed the scan. His findings are similar to those of Dr Stoodley and Dr Gawne-Cain. He told me that any fluid seen in the subdural space is pathological and not a naturally occurring fluid. C1 did not show symptoms of cardiac arrest because there was subdural haemorrhages and because of the low attenuation. For there to have been oozing of vessels into the subdural and subarachnoid spaces, then the haematoma would have been increased in size. The amount of swelling of the brain was modest at the time of the scan.
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:
“I am not aware of any clinical cases in which subdural haemorrhage of this appearance was seen in the context of a non-traumatic hypoxic-ischaemic encephalopathy. This is supported by the medical literature: a paper by Byard et al (2007) reviewed 82 infants and children who underwent autopsy for proven non-traumatic hypoxic ischaemic encephalopathy. None were found to have a subdural haematoma at autopsy. I am aware of the more recent abstract presented at a recent neuroradiology conference. The authors undertook a retrospective case note and imaging review of all infants under the age of three years, dying in the emergency department or admitted to the paediatric intensive care unit after a cardiorespiratory arrest, over a six year period. Of the 60 children evaluated, 45 had a combination of post-mortem examination, CT brain imaging or both. None of these infants had a subdural haematoma. It should be noted that the abstract would have been subject to peer review, but the full details of the study have not been published. In my opinion it is unlikely that the subdural haematomas seen in this case have arisen from a non-traumatic cause.”
The Haematologists
In her report of 14 January 2008, Dr Thomas speaks about C1’s coagulation tests at G261:
“Coagulation tests were also checked and in Dr Collins’s report [E379] it is stated that they were received in the laboratory at 11.11 on 23.4.05, which is some time after the initial collapse, hypoxic and hypothermic episodes and a period of acidosis and hypotension (F17). The results are reported as follows: prothrombin time 15 seconds (prolonged), activated partial thromboplastin time 32.8 seconds (within the normal range) and fibrinogen 0.8 g/L (NR 2-4 g/L). A thrombin time, a measure of functional fibrinogen, was correspondingly prolonged at 19.6 seconds. These are also recorded in a laboratory report (F100). Dr Collins has concluded that these results are compatible with the clinical picture of collapse and hypoxia, reflecting an early form of disseminated coagulation which is a condition in which a trigger (such as hypoxia, infection or inflammation) activates the coagulation cascade systemically and causes consumption of clotting factors and platelets resulting in prolonged clotting tests and decreased platelets. This seems the most likely explanation of the abnormal coagulation tests in this child.”
At G263 Dr Thomas said this:
“C10 There are two coagulation test results for C1: one which shows a normal fibrinogen and one taken later which shows a significantly low fibrinogen in association with a prolonged prothrombin time and normal activated partial thromboplastin time. Given the clinical picture of collapse, hypoxia, hypothermia, hypotension and acidosis, these tests are compatible with a progressive consumption coagulopathy, secondary to the clinical state and not the cause of it.”
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
Dr Smith and Dr Squier examined microscopically a number of brain and spinal cord sections taken at the post-mortem examinations. They also examined macroscopically the brain by way of digital images taken at the time of the post-mortem examination. Dr Squier, in her report of 31 January 2008, summarises the pathological findings acute brain swelling, acute subarachnoid haemorrhage, axonal APP expression consistent with impaired blood and/or oxygen supply, axonal swellings in spinal nerve roots, subcortical splits, acute intra and subdural bleeding, fresh spinal extradural bleeding, and haemorrhage into the base of the pons.
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:
“The pattern of spinal cord nerve root axonal injury, however, does not appear to be ischaemic in origin. I am aware of focal nerve root injury being described in the setting of brain swelling (unpublished observation) and the brain was swollen in this case. Equally, focal nerve root injury has been described in the setting of trauma.
I will attempt to interpret the neuropathological findings in relation to the specific question of whether or not there has been trauma in this case. It is important to note that there is no external evidence of trauma in this case. Much of the neuropathology is non-specific and can be attributed to the coagulopathy demonstrated by haematological investigations. I am, however, concerned by the focal subdural spinal cord bleeding associated with axonal damage within nerve roots. In my experience, this is frequently seen in alleged cases of non-accidental injury, and the cases of focal nerve root injury associated with cerebral swelling do not have surrounding haemorrhage present.
I can find no evidence of any non-traumatic disease process within the brain or spinal cord which would account for the sudden collapse of this infant. It is, however, possible that a vast majority of the neuropathological changes seen may have developed secondary to a non-neurological collapse in this infant. As noted above, however, I do have concerns regarding the focal subdural bleeding in relation to nerve roots which at one level is associated with focal axonal injury.
In summary, there is nothing from neuropathological examination of this case which would allow a definitive diagnosis of non-accidental injury to be made. Equally, there is no evidence of any neurological disease to account for the sudden demise of this infant.
In summary (in response to specific questions stated in correspondence 12.10.07):
“C1 has developed global cerebral ischaemia (lack of blood to the brain) resulting in irreversible brain injury and brain swelling. The cause of the sudden collapse cannot be definitively ascertained by neuropathological examination.
C1 has died as a result of lack of blood flow to the brain and subsequent brain swelling. This does not, however, account for his sudden collapse.
The potential causes of sudden collapse at this age are numerous. For example, there has been an undiagnosed cardiac cause for collapse which would produce much of the subsequent neuropathological features. However, I am concerned by the focal spinal cord pathology which, in my opinion, is suggestive of an episode of trauma. I cannot give an alternative explanation for such a lesion in the absence of trauma.
In my opinion, trauma is the most likely cause of sudden collapse and subsequent brain injuries, but I cannot exclude the possibility of non-neurological causes for sudden collapse (such as cardiac).
As above”.
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 and Dr McCarthy examined the embedded tissue blocks and glass histology slides from C1’s eyes, together with digitised photographic images of the eye specimens when dissected by Dr Leadbeatter prior to the preparation of the slides. Dr Bonshek undertook macroscopic examination. In his report at G74, under “Macroscopic Examination”, he said:
“There is no key provided to identify exactly which images were made of which eye, but examination of the digital images on the CD provided by Dr Leadbeatter shows that there is extensive optic nerve sheath haemorrhage involving both optic nerve sheaths. This appears more severe at the proximal ends of the optic nerve (i.e. in the region immediately behind each eye). Here is macroscopically visible blood within the orbital soft tissue adjacent to each optic nerve and further back within the orbital fat. No views of the anterior surface of the eyes are provided, so I am not able to comment on the front of the eyes, conjunctivae and corneas. The eyes have been opened in the coronal plane, and a diagram provided on the copy of the neuropathology request form confirms that this is approximately at the equator of each eye (the mid-point from front to back). There is extensive bleeding over the surface of the retina of each eye in all retinal areas. There is widespread retinal thickening due to oedema and, in addition to post-mortem retinal folding, there also appear to be broad perimacular folds present in both eyes. Widespread intraretinal bleeding amounting to retinoschisis (splitting of the retina) is evident along the cut margins of the retina of each eye. Haemorrhage in the posterior portions of the eyes, associated with the perimacular folds, obscured the optic nerve heads in both eyes so that these structures are not visible. In one of the eyes – it is not indicated whether this is the left or the right in the information provided to me – there is quite marked detachment of the anterior vitreous gel which can be seen appearing to ‘billow out’ behind the lens. Some blood can also be seen trapped within the interstices of the various vitreous compartments. Given the way in which the eyes have been opened (in the coronal plane) there is no opportunity to examine the anterior chamber structures macroscopically. The lenses appear to be macroscopically normal.”
Dr Bonshek undertook microscopic examination (G75):
“Examination of the sections prepared in the Cardiff laboratory reveal that there is very extensive retinal haemorrhage affecting all retinal layers and all retinal areas in both eyes. There is some degree of autolysis, which may be a reflection, in part, of the considerable damage to these retinas. There is extensive pre-retinal blood, as well as subhyaloid (beneath the vitreous) bleeding and focal bleeding into the vitreous. Many areas of retinal detachment, with subretinal blood, are present and, in some areas, there are small foci where there has been retinal pigment epithelium (RPE) detachment with sub-RPE bleeding. However, much of the RPE in both of the eyes is detached by artefact. There is extensive vitreous detachment. Whilst vitreous detachment may occur due to post-mortem artefact, in both of these eyes it is associated with, in the area of the vitreous base, detachment of peripheral anterior retina and ciliary body. Here some areas of haemorrhage beneath the detached ciliary body epithelium are evident, indicating that this is an ante-mortem phenomenon. Somewhat oblique cuts have been prepared through the histology blocks which include anterior segment. Here the anterior chamber of each eye can be seen to contain proteinaceous exudates, but no blood. There is some artefactual detachment of the corneal endothelium and some artefactual lifting and detachment of corneal epithelial cells. There is no evidence of conjunctival, subconjunctival or episcleral haemorrhage. The cornea, iris and lens do not appear to have been disrupted, but the histological view is quite restricted because of the orientation of the tissue blocks. In both eyes there is extensive bleeding within the sclera in the area of the vascular circle of Zinn adjacent to the optic nerve insertion into the eye. In the left eye this bleeding is linked to a focus of choroidal haemorrhage. In the central retinal vein of the right eye, at the optic nerve head, there is a collection of blood clot adherent to the vessel wall. In two veins within the orbital tissue adjacent to the right eye there is also more blood clot. In further sections prepared in the Manchester laboratory, this clot is seen to extend to the branching point of a large vein. Many of the peripheral nerves within the orbital tissue adjacent to both eyes contain blood beneath their external sheaths. Bleeding has also occurred free within the orbital fat and within the eye muscles. There is very severe optic nerve sheath bleeding (most marked in the anterior parts of the nerves) with intrasheath blood, subdural and subarachnoid bleeding, and bleeding external to the optic nerves.”
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:
“In the case of C1, whilst extensive and severe retinal haemorrhages are a major feature, other significant findings present are: perimacular folds, retinal detachment, retinal oedema, vitreous detachment, RPE detachment and haemorrhage, choroidal haemorrhage, scleral haemorrhage, haemorrhage beneath the ciliary body epithelium, anterior chamber exudates, optic nerve, sheath haemorrhage and orbital haemorrhage, and acute inflammatory cells within the conjunctive eye.”
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:
“The reports provided by Dr Steven Leadbeatter and Dr Richard Bonshek are both extensive and detailed, and refer to various descriptions of causation contained in Medical Literature. There is an abundance of Medical Literature on this subject. However, in my opinion, there has been little true scientific progress in the last five or so years regarding the pathophysiological causation of the features seen in this so-called triad.
In this case the minor injuries that have been noted, and in particular I refer to the small bruising to the left side of the back of the scalp and the small areas of bruising below the jaw, have been attributed to the acts of resuscitation and the subsequent coagulopathy. In this respect, if this is the case, then there is no unequivocal evidence of any impact injury to his child.
The possibility of a soft impact is also considered wherein no actual bruising has been caused. This can neither be included nor excluded.
Thus, in the absence of any definite impact injury to the head of this child, one has to consider the possibility that the subarachnoid haemorrhage, the cerebral encephalopathy and the haemorrhages into the eyes have been caused during an act of shaking injury. This child was eight weeks of age and prior to Wednesday 20th April 2005, was in apparent good health and thriving. This child received multi-agent vaccination on the 20th April 2005 from which time the child was said to be more sleepy than usual. This is clearly subjective and is not amenable to verification. However, in terms of causation of the type of haemorrhage, brain swelling and lesions identified in this child at the time of admission to hospital, I believe that the temporal association with vaccination is merely coincidental. I know of no peer reviewed literature which would suggest that this triad of features can be caused by vaccination.
Turning now to the suggestion that the encephalopathy, the subarachnoid haemorrhage and the retinal haemorrhages were a consequence of a cardiac arrest of unknown cause with subsequent coagulopathy, this similarly falls into a category wherein there is no verified peer reviewed literature to indicate that this is an event that occurs or can occur with any frequency. I know of no verified accounts of cardiac arrest resulting in the triad of features as seen in this child. This suggestion appears to be based on a hypothetical situation and perhaps has been reinforced by fairly recent medical literature, which hypothetically regards the features of the triad as being secondary events subsequent upon some other causative event. These have variously been suggested as Pertussis infection, bouts of continuous coughing, retching and vomiting, and other non-specific events that result in raised venous pressure within the brain and within the eyes. Apnoeic events and trivial injury have also put forward as suggestions, as have other events. …
Regarding the wellbeing of this child and the history given, it is highly unlikely that this child would have been able to function to any normal extent following the development of the brain swelling, subarachnoid haemorrhage and retinal haemorrhages. Therefore, it is entirely likely that these findings developed at or very close to the time that the haemorrhage occurred, i.e. the history given that this child was sleeping in the bath at 20.00 hours and then took a small feed at 21.00 hours, indicates that the child could not have been suffering these devastating injuries at that time. The paramedics attended at 23.20 hours and it is entirely likely that these injuries occurred shortly before that time.
In final conclusion, therefore, I would agree with the report that has been issued by Dr Richard Bonshek, and in particular the statement that Dr Bonshek has made on page E437 where he says: ‘I am at a loss to find a credible alternative explanation for the findings within the eyes and associated structures of C1”. As such, Dr Bonshek is indicating that this child has sustained these features and lesions as a result of shaking with or without a component of impact.
I am unaware of any peer reviewed medical literature relating to the development of the features seen in this child as a result of a spontaneous inexplicable cardiac arrest episode. I agree with the suggested causation as given by Dr Bonshek that shaking has been the most likely cause of this child’s cerebral swelling, encephalopathy and ocular haemorrhages. I am unable to specifically support the suggestion of an impact injury, although I cannot exclude impact onto a yielding soft surface. There is no witness evidence to suggest accidental injury. I do not believe that this is a natural disease process.”
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
Dr Vujanic, as with other experts, has read a mass of documentation in this case, which is set out in his report of 31 January 2008. In addition to examining the slides in respect of the brain and the eyes, Dr Vujanic examined no less than 62 histological slides of many parts of C1’s body. He sets out in extenso Dr Leadbeatter’s post-mortem findings. He refers to Dr Smith’s neuropathological examination, to Dr Bonshek’s examination, and to Dr Stoodley’s report and findings. At G408 he said:
“I agree that the numerous marks found on post-mortem examination…”
(That is a reference to the bruising on the exterior of C1)
“…could be attributed to attempted resuscitation. Also the finding of two bruises on the underside of the chin and bruises on the anterior abdominal wall could be secondary to consumptive coagulopathy rather than representing genuine non-accidental bruises. Finally, the microscopic rib fracture not seen on any other examination but found on post-mortem histological examination also could be attributed to attempted resuscitation.”
Having then referred to Dr Smith’s views and Dr Bonshek’s findings, he wrote at G409:
“I agree that many of the findings could be related to a prolonged period of circulatory arrest and resuscitation with consequent consumptive coagulopathy. Many of the mentioned pathological findings may explain the mode of death but they do not account for how the original collapse that precipitated hospital admission occurred. Possibilities that might explain such a collapse include:
(a) A specific natural cause.
(b) So-called ‘near miss’ Sudden Infant Death Syndrome (now called apparent life-threatening event – ALTE).
(c) Shaken Baby Syndrome.
A) A specific natural cause
A very through post-mortem examination and subsequent second neuropathological and eye examinations failed to identify any natural cause or non-traumatic disease process within the brain or spinal cord which would account for the sudden collapse of the child. Therefore, I think that a specific natural cause was not the cause of the sudden collapse.
B) ‘Near Miss’ Sudden Infant Death Syndrome
C1 was in an age group where natural deaths of obscure causation are known to occur. In some cases the infant is discovered after the initiation of whatever process it is that leads to death but before death has actually occurred (‘near miss’ SIDS). Although resuscitation might be successful, there may be serious consequences if the heart has stopped beating for a significant period of time. However, in such cases extensive retinal haemorrhages and other brain damage seen in this child are not found, and I think that this was not the cause of C1’s sudden collapse.
C) Shaken Baby Syndrome
Shaken Baby Syndrome (SBS) is a widely recognised diagnosis in the medical literature. The medical components of SBS include retinal haemorrhage, subdural or subarachnoid haemorrhage and associated fractures with a paucity of external physical findings (Caffey J. The whiplash shaken infant syndrome: Manual shaking by the extremities with whiplash-induced intracranial and intraocular bleeding, linked with residual permanent brain damage and mental retardation. Paediatrics 1974; 54: 369 -403). The presentation of SBS originates from a mechanical injury, which results in angular rotation of the infant’s head sufficient to crate acceleration and deceleration forces of the type frequently encountered in major automobile collisions. The clinical presentations vary from a pure shaking incident, where the child is violently shaken; blunt force injury, where the child is thrown or receives a blunt impact injury to the head; and, finally, as a component of other injury in the battered child syndrome.
Many reports have offered evidence that shaking alone can produce life-threatening injuries in infants (Alexander R, et al: The incidence of impact trauma with cranial injuries ascribed to shaking. Am J Dis Child 1990; 144: 724 – 726; 3. Gilliland MGF, et al: Shaken babies: some have no impact injuries. J Foren Sci 1996; 41: 114 – 116; 4. Lazoritz S, et al: The whiplash shaken infant syndrome: has Caffey’s syndrome changed or have we changed his syndrome? Child Abuse Neglect 1997; 21: 1009 – 1014). Further support for the latter claim comes from the statements of perpetrators and other witnesses and the lack of evidence of impact. The relative incidence of brain injury due to the shaking or the impact injury remains unknown; in many cases both forms of injury may be present. However, despite the debate over the exact mechanism of injury, the classical findings of retinal haemorrhages, subdural haematoma, and brain damage cannot be fully explained by any other medical entity.
The SBS apparently results when a young child is shaken by holding the thorax, shoulders, or abdomen. This shaking must be done by an individual much larger than the child, usually an adult, in order to achieve sufficient acceleration of the body of the child. During the shaking it is assumed that the head can be whipped back and forth because of the relative inability of the infant to control its neck muscles and because of the relatively large mass of the head in relation to body. This mechanical instability perhaps explains why whiplash-shaking deaths are uncommon in children older than one year. In addition, the infant skull has the flat base and still not developed fossae (that typically hold the adult brain in place) permitting more rotation to the brain than in adults during acceleration-deceleration. Finally, the underdeveloped myelinisation of the neuronal axons of the child’s brain predisposes to laceration of long neurons which is a typical injury/finding in SBS.
The victim of the SBS may have bruising over the upper extremities, neck or the chest where the child was held and shaken. However, bruising is more the exception than the rule. Old or new fractures of the long bones and/or ribs may be present in the shaken baby syndrome but they represent associated secondary injuries which indicate that the child has been abused during his/her life and not primary injuries due to the primary effect of shaking forces.
Retinal haemorrhages have been rarely documented after resuscitation. (Wissow LS. Child abuse and neglect. N Engl J Med 1995; 332: 1525-31; Odom et al. Prevalence of retinal haemorrhages in paediatric patients after in-hospital cardiopulmonary resuscitation; a prospective study. Paediatrics 1997; 99: E3). Studies addressing this issue have not shown as association between retinal haemorrhages and cardiopulmonary resuscitation in the absence of pre-existing brain trauma, seizures, tumours, sepsis, severe dehydration or coagulation defects. (Gilliland MG et al. Are retinal haemorrhages found after resuscitation attempts? A study of the eyes of 169 children. Am J Forensic Med Pathol 1003; 14: 187-92; Kantor R. Retinal haemorrhage after cardiopulmonary resuscitation or child abuse? J Pediatr 1986; 108: 117-32). An experimental study using piglets could not induce retinal haemorrhages through resuscitation (Fackler J et al. Retinal haemorrhages in newborn piglets following cardiovascular resuscitation. Am J Dis Child 1992; 146: 1294-6). The severity and type of retinal haemorrhages and other pathological findings in this case, as Dr Bonshek concluded, indicated severe trauma due to non-accidental injury.
As for the impact of the vaccination of C1 and whether this could, in whole or in part, explain the injuries that C1 subsequently displayed, I confirm that I am not aware of any literature linking routine immunisation with pathological changes found in the brain and retina of C1, but this is not my area of expertise and I defer to Dr G Debelle’s comments in his paediatric overview.
Taking into account all clinical, imaging and pathological findings and opinions, I think that C1 had collapsed and later died due to a non-accidental head injury. He showed a combination of findings which indicate inflicted injury by shaking.”
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:
“Both Drs Stoodley and Bonshek are of the opinion that baby C1 had suffered brain injury resulting in his collapse and unconscious state on admission to hospital, and that the injury had been sustained shortly before his admission. Both rejected the concept that the child’s death was in any way related to the routine inoculations he had received shortly before his death.
I would agree with this conclusion. I know of no concrete evidence linking routine immunisations with intracranial pathology of the type seen in this case. Head injuries and sudden unexpected death from other causes often affects children of this age, and this is also the time at which immunisation is given. The two events may well be temporally related, but not in a causal sense.
Dr Bonshek did not think that the retinal haemorrhages were related to resuscitation.
I entirely agree with both Drs Stoodley and Bonshek that this child had died as a result of a head injury, the characteristics of which indicate an inflicted nature.
The triad of findings that most authorities involved in child protection would regard as indicative of a shaking or shaking impact injury, namely intracranial haemorrhage (subdural and subarachnoid haemorrhage), retinal haemorrhage and encephalopathy, were present in this case.
Dr Stoodley refers to a minority medical opinion that this triad of findings can occur in situations other than non-accidental head injury. They have suggested factors such as aspiration of milk during feeds, choking, vomiting, paroxysmal coughing or gastro-oesophageal reflux. Dr Stoodley remarks that these opinions are in the main expressed by those who do not have day-to-day involvement in a clinical or radiological management of infants or children who suffer from these conditions and that the opinions expressed by these practitioners is not supported by everyday clinical experience.
I would wholly endorse this opinion and would note that the characteristics of the individual components of the triad are of great importance in distinguishing those cases due to non-accidental injury.
Shaking or shaking/impact involves severe rotational acceleration/ deceleration forces that have the effect of causing the brain to rotate within the skull. This ruptures small communicating veins on the surface of the brain that are the source of the subdural haemorrhage. These haemorrhages are important only as an indicator of the mechanism of injury. They do not form significant space occupying lesions, as do the more extensive collections of blood (subdural haematomas) mostly seen in older patients. The subdural and subarachnoid haemorrhages in this case clearly form only thin films as indicated by the post-mortem photographs.
The retinal haemorrhages associated with rotational acceleration/ deceleration injuries are typically extensive, involve all layers of the retina and are usually associated with haemorrhage around the optic nerves, all features that were present in this case. Retinoschisis and perimacular folds are also features characteristic of this type of injury.
Detailed neuropathological examination can indicate evidence of trauma to nerve cells and their extensions within the brain. These may be in addition to changes caused by hypoxia and ischaemia that are almost invariably present in babies who survive on life support. There may also be evidence of previous head injury, and for both these reasons I await the expert neuropathological report by Dr C Smith with interest.
Because non-accidental injury is often a repeated phenomenon by abusing carers, the presence of more than one head injury or evidence of non-accidental injury in other systems of the body are often regarded as useful additional factors in distinguishing between accidental and non-accidental injury.
Dr Bonshek mentioned the presence of haemosiderin in the optic nerve haemorrhages as a possible indicator of previous injury in this child and, like me, looked for possible further confirmation of previous head injury from the report by Dr Smith.
The fact that apparently non-accidental injury has occurred to the sibling of this child could be taken as evidence of further abusive behaviour by a carer.
I can see no reason to link this child’s death with resuscitation. The child was only resuscitated after he had collapsed. Resuscitation would not cause subdural or subarachnoid haemorrhage.”
He also has given a further witness statement, which is at G102A and B, which I have read and was part of his evidence.
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
Dr Geoffrey Debelle’s report is dated 22 February 2008 and is at G432. Dr Debelle, having anxiously and carefully considered all the various matters and the opinion of the other expert, concluded at paragraph 78 as follows:
“In my opinion, C1 suffered a single episode of inflicted traumatic head injury, with sudden collapse with hypoxic encephalopathy, hypothermia, retinal haemorrhage and subdural haemorrhage on the surface of the brain and in the cervical and lumbar area, the latter being possibly due to post-mortem artefact. The absence of any scalp swelling fracture does not lessen this possibility as the proposed mechanisms of injury do not involve linear impact onto a hard surface, nor does the apparent difference of opinion about the spinal nerve root damage. No other cause for his collapse and death, such as infection, vaccine-induced encephalopathy, near-miss Sudden Infant Death Syndrome, neurovascular anomaly, inherited metabolic disease or primary coagulation defects could be identified. I accept that the external bruising and the microscopic rib fracture may well be secondary to coagulopathy and efforts at resuscitation. However, the extent and distribution of the retinal haemorrhages and distribution of the subdural blood is consistent with inflicted traumatic head injury. In addition, the suddenness of the collapse is consistent with inflicted traumatic head injury.”
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
I adopt, with respect, the descriptions given by the Court of Appeal, Criminal Division, in its judgment on 21 July 2005 in R v Harris, Rock, Cherry and Faulder [2005] EWCA Crim. 1980, at para 63-65:
“As already stated, when the three elements of the triad coincide for some years conventional medical opinion has been that this is diagnostic of NAHI. Typically the brain is found to be encephalopathic; blood is found in the subdural space between the dura and the arachnoid subdural haemorrhages; and there are retinal haemorrhages. There may also be other pathological signs such as subarachnoid bleeding and injuries at the cranio-cervical junction. Further, there may be injuries to nerve tissue (axonal injuries) and external signs of broken bones, bruising and other obvious injuries such as extradural oedema (bruising). Determining these findings requires medical experts from a number of different disciplines interpreting often very small signs within the complex structures of an infant’s brain and surrounding tissue.
The mechanism for these injuries is said to be the shaking of the infant, with or without impact on a solid surface, which moves the brain within the skull, damaging the brain and shearing the bridging veins between the dura and the arachnoid. The shaking may also cause retinal haemorrhages. In the sense that the explanation for the triad is said to be caused by shaking and/or impact it also is a unified hypothesis, albeit that each element is said to be caused individually by trauma.
The triad of injuries becomes central to a diagnosis of NAHI when there are no other signs or symptoms of trauma such as bruises or fractures.”
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:
“Dr Geddes and her colleagues, following research into almost 50 paediatric cases without head injury, proposed that the same triad of injuries could be caused by severe hypoxia (lack of oxygen in the tissues) which in turn led to brain swelling. The hypothesis was that brain swelling combined with raised intracranial pressure (ICP) could cause both subdural haemorrhages and retinal haemorrhages. Thus, is was argued that any incidents of apnoea (cessation of breathing) could set in motion a cascade of events which could cause the same injuries as seen in the triad. It will be appreciated that there are many events which could accidentally cause an episode of apnoea.
In Geddes III the unified hypothesis was summarised as follows:
‘Our observations in the present series indicate that, in the immature brain, hypoxia both alone and in combination with infection is sufficient to activate the pathophysiological cascade which culminates in altered vascular permeability and extravasation of blood within and under the dura. In the presence of brain swelling and raised intracranial pressure, vascular fragility and bleeding would be exacerbated by additional homodynamic forces such as venous hypertension, and the effects of both sustained systemic arterial hypertension and episodic surges in blood pressure.’
Thus, it was suggested that all the injuries constituting the triad could be attributed to a cause other than NAHI. We understand that this paper has been much cited in both criminal and civil trials since its publication.”
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.
The Local Authority
The overwhelming medical evidence is that the abnormalities found in the brain and eyes of C1 can only be fully explained by him suffering an episode of trauma, probably shaking. Between paragraphs 22 and 63 of their written submissions, Miss Mifflin and Miss Williams analyse the medical evidence. In paragraph 64 they submit that the court needs to be able to find an explanation that fits all the abnormalities found in C1. The only cause that fits all is trauma, and, in the absence of accidental trauma, that leaves only inflicted head trauma. Taking into account all the circumstances both medical and non-medical, they submit that the court is drawn to the inevitable finding that C1 was assaulted by the father on the night of 22 April 2005 by shaking and/or shaking impact.
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:
“Both doctors explained to the court in some detail their conclusions and the basis upon which they were reached. We would submit that they were well thought out and are supported in many respects by the other experts in the case.
(a) The widespread hypoxic-ischaemic brain injury was secondary to cardio-respiratory arrest, with a prolonged period of no cerebral blood flow. It is a non-specific finding and in itself does not indicate trauma.
(b) C1 had a coagulation abnormality, together with a prolonged period of hypoxia, together with resuscitation. Under such circumstances the blood vessels in the brain may become leaky and the blood flow through them is re-established reperfusion injury. This becomes the more likely the longer there has been a failure of blood and oxygen supply because it damages the linings of the small blood vessels.
(c) Most of the bleeding seen on post-mortem is around the blood vessels. There are small areas of bleeding with few cells getting out. There are not large collections of blood that you might have expected had any of the blood vessels ruptured. In our submission, this supported the idea that the abnormal coagulation was causing blood to seep from the blood vessels into the subdural and subarachnoid spaces, and that it was causing the retinal haemorrhages.”
They submit that the Coroner was impressed by their evidence at the inquest and found death by natural causes. In paragraph 20 they say:
“What has changed? There are no new facts. The only difference is the evidence from the neuroradiologists and the ophthalmologists. If there is an alternative explanation for their findings or there may be, the verdict of the Coroner should carry some considerable weight.”
So having carefully analysed all the matters, Mr Tillyard and Mr Parsley conclude in this way:
“We accept that the court cannot look at individual components of the trial in isolation, and that the court has to take an overall view of the evidence. However in doing that, a thorough investigation of each individual component of the triad needs to be carried out, and it is only when all other causes have been realistically excluded and the only remaining explanation is trauma that the court should find the case proved.
There are other non-traumatic explanations for all the findings in this case. There is a wide diversion of medical opinion as to how valid each of the explanations is. When the wider canvas is put in the balance as it should be, we submit that the court cannot be satisfied that those explanations, taken together and individually, are so improbably the cause or the findings as to leave shaking the only acceptable explanation. The evidence cannot be regarded as sufficiently cogent as to overcome the improbability of this father killing his son.”
The Cause of C1’s Collapse
The following causes for C1’s death have been explored in the evidence. They are trauma to the head, overwhelming infection, suffocation, cardiac arrest, whether or not following from Prolonged QT Syndrome, and reaction to immunisation.
Suffocation
In my judgment, suffocation of C1 is not even a possibility on the evidence. The only medical expert to put it forward was Dr Sunderland. He told me that he had raised it for completeness’ sake. There was, he said, very marked hypoxic-ischaemic damage. C1 was heard and seen by the father to be hiccupping. It was that which could support suffocation. However, when cross-examined by Mr Furness, he told me categorically that suffocation was not the cause of C1’s death and that his report at paragraphs 3.17 and 3.10 should now be amended to read that suffocation could be excluded.
Infection
Dr Leadbeatter, at post-mortem examination, found no evidence of infection. The neuro-pathologist found no evidence of infection. Both were agreed about that. The haematologists agreed there was no evidence of infection. The paediatric pathologists could find no evidence of infection, nor could the ophthalmologists. Dr Debelle saw no evidence for infection and he repeated that opinion several times in his evidence. The only medical expert who did support infection as the cause of C1’s collapse was Dr Sunderland. He told me that he was suggesting septicaemia as a cause of C1’s death. He seemed to me to base that suggestion on two matters. First, C1’s white blood cell count was raised. Indeed, he said it was very high. Second, when C1 was admitted to hospital, he was found to have petechiae on his tummy which, in Dr Sunderland’s hospital in Birmingham, would be treated immediately as a sign of blood poisoning. As to the white blood cell count, the passage at 5.02.2 of Mr Edwards’ report, which is to be found at G311 and G312, was put to Dr Sunderland by Mr Rees for the grandparents and then by Mr Furness, namely.
“As part of his resuscitation, intraosseous needles were placed and the Prince Charles Hospital medical records state that the initial blood and haematological investigations sent showed evidence of a grossly elevated white cell count of 53.6 x 10 9/1. I have been in many situations where infants have been resuscitated using intraosseous needles. Intraosseous needles access the central part of the tibia bone which contains the ‘bone marrow’. This part of the bone has a rich blood supply and in an emergency setting can be used for the administration of drugs and fluid when blood vessels access cannot be obtained. It is my opinion that the elevated white count on the first specimen sent from the intraosseous needle is entirely consistent with a ‘normal’ intraosseous specimen. The bone marrow is responsible for white cell production and therefore normally contains more white blood cells than venous blood. Therefore, I am not surprised that the white cell count is elevated and do not think this is of any significance. I do not believe that it reflects either a severe reactive response to the trauma or supports any evidence of acute infection.”
Dr Sunderland, having had that passage put to him, agreed that in the light of those observations, he could not rely upon the elevated white blood cell count as any evidence of infection. The elevation, he said, could be related to stress.
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:
“I have provided some related comment in my answer before question 32 (Re Dr Sunderland’s 3.14). I believe that I may have seen microscope slides from the case to which Dr Sunderland refers. The case I have seen has been presented by Prof Luthert to eye pathology meetings and I have been given the opportunity to review them. This is a case of bacterial meningitis and bacterial meningitis is a rare but recognised cause of retinal bleeding. The cases which have been reported in the literature, however, have not shown such extensive retinal bleeding as found in the case shown by Prof Luthert. It remains the case that the case mentioned by Dr Sunderland (and shown by Prof Lutert) did have meningitis. I am not aware that C1 had meningitis.”
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.
There is a further factor which points away from infection. Dr Thomas told me that antibiotics were administered to C1 at about midnight. At just after 11.00 am on 23 April the blood was analysed. There was no sign of infection. If infection had been present, one dose of antibiotics would not have reversed it. The blood culture was negative for infection.
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
I wish to say that it is a very natural and understandable reaction that when a child suddenly dies within a short span after he has been immunised, a parent or parents might conclude that the only explanation for the child’s death was an adverse and fatal reaction to that immunisation. But, I must emphasise, no medical expert has given any credence whatsoever to such a belief. Therefore I have to say, on the evidence, that I am driven to rule it out as a cause of C1’s collapse and/or death.
QT Syndrome
The parents went to see Professor Peter Fleming, Professor of Infant Health and Development Physiology in the Department of Neonatral Medicine at St Michael’s Hospital in Bristol. It is apparent from his letter of 24 October 2005 to the parents that he spent a lot of time explaining to them that it was unlikely that C1 had died as a result of his immunisation. At the end of his letter he wrote the following passage:
“There are some very rare conditions which can contribute to sudden and unexpected deaths in infancy and which can be precipitated by minor stresses; for example, infections or immunisation and which are not detectable post-mortem. The most important of these is a group of conditions called the Prolonged QT Syndrome in which there is an abnormality of the electrical conduction system in the heart, which may cause sudden death, particularly under such circumstances.
Although from your description it sounds extremely unlikely that C1 suffered from this condition, my recommendation would be that your new baby should be checked for this condition by having an ECG, an electrical recording of heart activity. In order to be certain that this will identify Prolonged QT Syndrome, the ECG must be done when the baby is at least two weeks of age.”
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:
“Extensive hypoxic-ischaemic change, involving the thalami and cerebellum are occasionally seen in the context of trauma, including more severe cases of suspected inflicted head trauma. I am occasionally asked to give opinions regarding intracranial pressure monitoring in children who have suffered a hypoxic-ischaemic insult following non-traumatic cardiorespiratory arrest from which they have been resuscitated, but have never seen such extensive changes manifesting on a scan taken within three hours in this patient group.
There is extensive subarachnoid haemorrhage present particularly over the cerebral convexities (3.0/04). In the absence of any identified vascular pathology or evidence of cerebral vasculitis, in my opinion the most likely cause of the subarachnoid haemorrhage in this case is trauma. Although in hypoxic-ischaemic encephalopathy, particularly in the presence of a severe coagulopathy bleeding can occur, it would be unusual to see a subarachnoid haemorrhage of this extent. I am also of the opinion that the degree of subarachnoid haemorrhage is no worse at the time of post-mortem than it was on the scan performed at 2.00 am on the 23rd April 2005. As the clotting anomaly was not corrected for at least three and a half hours after the CT scan, were the subarachnoid haemorrhage to be a direct result of oozing from an ‘encephalopathic’ brain, I would have expected to see an increased amount of subarachnoid haemorrhage present.”
The pattern of subdural haemorrhage seen in C1 is typical of those seen in suspected head injury, was Mr Edward’s view. Further in his report at paragraph 5.03.20, he said this:
“The only other possible cause of a low attenuation collection in the subdural space is a ‘chronic’ (old) subdural haematoma. These would typically be at least two weeks of age. Chronic subdural haematomas of this age are invariably associated with a subdural neomembrane. Such a neomembrane was not found on post-mortem examination. Furthermore there was no evidence of old haemorrhage on the post-mortem examination. In addition to this the low attenuation collections had significantly reduced in size at the time of the post-mortem examination. This would be consistent with the fact that the low attenuation collections are of bloodstained cerebral spinal fluid, rather than clot, as the blood stained spinal fluid would have been dispersed by the progressive brain swelling that occurred in the hours after the CT scan. In my opinion, in this case the only possible explanation for this finding is an acute traumatic event.”
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:
“A single event which caused hypoxic-ischaemic encephalopathy and the intracranial spinal and retinal haemorrhages;
an event which causes HIE followed by a secondary event resulting in bleeding; that is to say, a pre-existing or secondary acquired encephalopathy; and
a primary bleeding disorder leading to HIE.”
I spend no time on (iii) because the haematologists ruled that out. Thus, that leaves (i) and (ii). Mr Edwards then set out in report at paragraphs 5.05.18 through to 5.05.22 as follows:
“It is my opinion that a traumatic event is the only single event that could lead to both hypoxic-ischaemic encephalopathy and the bleeding seen.
There are three possible causes of trauma in this age group.
Firstly that it was related to birth injury: this can be discounted as there is no suggestion either from the clinical history (C1 was completely well up until the day of his collapse), the radiological findings (none of which was an ‘old’ injury) and the post-mortem findings which showed no evidence of ‘old’ bleeding that could date back to the time of birth.
The second possibility is that the trauma was accidental. However, no accidental trauma was reported by either parent or the maternal grandmother who were the only people in sole charge of C1 prior to his death. Furthermore, C1 was non-ambulant; therefore, even the ‘trivial’ falls occasionally put forward as explanations for findings such as these can be excluded.
By deduction, the only possible traumatic cause of C1’s injuries that remain is therefore inflicted head injury.”
Mr Edwards further relies upon the triad, CG227. It is unnecessary for me to set all that out.
The Neuropathologists
Dr Squier, instructed on behalf of the father, agreed in cross-examination by Mr Furness that there was very little dispute between her and the jointly instructed expert, Dr Smith. The only difference related to the axonal swellings and associated blood, as I have set out in this judgment above. However, before I come to that, there is one piece of evidence given by Dr Squier which I have touched upon and which, in my judgment, was a mistake by her and a significant one at that. In her report at G419 she said:
“Removal of the spinal cord is often a very traumatic procedure, and I believe that the bleeding may be an artefact induced by removal of the cord.”
She is there referring to removal of the spinal cord at post-mortem examination. Dr Smith, having seen Dr Squier’s report, responded at GA46 that it could not be a post-mortem artefact for the reasons he gave and which I have set out earlier in this judgment. It was not until she came to give evidence did she concede that it could not be a post-mortem artefact. Her revised position became that the damage was due to coagulopathy, which Dr Smith had not factored in. I have already recounted Dr Smith’s response to that. I accept the criticism made of Dr Squier’s evidence in paragraph 58 of Miss Mifflin’s and in paragraph 13.3 of Mr Furness’s submissions. Dr Squier, in my judgment, made a mistake which, if she had thought about it, she ought not to have made. The shifting of her ground on this basic point makes me look at the remainder of her evidence with especial scrutiny.
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
Both Dr Boshek and Dr McCarthy were in agreement, so I will not repeat their evidence. They found not only extensive and severe retinal haemorrhage, but also other significant findings which I have set out above. The effect of their evidence is, in my judgment, that their findings in relation to C1’s eyes can only be explicable as a result of trauma. Both doctors recognise the need for caution and considered all the alternative postulated causes, and none of those alternative causes could result in the ocular findings in C1’s eyes, in their opinion.
Paediatric Pathologists
Both Dr Vujanic and Professor Risdon are in agreement that the cause of C1’s collapse was a non-accidental inflicted injury for the reasons each gave in their evidence, and which I will not repeat.
The Paediatricians
Dr Sunderland accepted in his evidence that his view that shaking could not cause the injuries seen in C1 is a minority view. He accepted he relied upon biomechanical research evidence, specifically crash dummies. He conceded that this area was outside his expertise. I agree with the submissions of Miss Mifflin and Mr Furness that the opinions of Dr Sunderland are of much less value than they might otherwise have been because he is not really prepared to accept that the shaking hypothesis has any validity at all. He relied on biomechanical research, but no biomechanical consultant was called before me. Furthermore, as I have demonstrated, he was compelled to abandon suffocation as a cause, and his evidence relating to infection as a possible cause was shown to be, in my judgment, completely flawed. The fact of the matter is that Dr Sunderland’s evidence was not objective, but started from a preconceived position that shaking cannot cause the injuries seen in C1.
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:
“Despite the force required being obviously inappropriate and having been involved in many cases of alleged non-accidental head injury, I am of the view that the majority of these injuries occur when an otherwise reasonable carer suffers a momentary loss of control, usually out of frustration at a situation such as being unable to settle an inconsolable child, without there being any intent to cause the child harm.”
That observation was not gainsaid by any other expert. Thus, what he is telling me is, from his experience, this sort of trauma can be caused to the child by reasonable as well as unreasonable carers.
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:
“I next saw C2 and his parents on the 22nd June 2006 (22/06/2006) when C2 was 11 weeks and one day old. At this consultation C2 was in a baby seat and when I asked how things were going, F replied something like ‘All right until two days ago.’ This then opened our conversation regarding an incident two days earlier when F had C2 lying on the floor under a plastic baby gym, with tubing and some fabric covering and toys hanging down. F had walked past to the kitchen to make a drink.
On return he had been going to pick C2 up and, while walking past, he accidentally kicked the baby gym which fell against C2’s face. I clearly recall that F was sure that his foot had not made contact with C2’s face and that it was in fact the baby gym.
They informed myself that they had taken C2 directly to the A and E Department at the Heath Hospital on Tuesday evening, but that he had been discharged. I then documented the injuries as I saw them. He had bruising to the right side of the face from the peri-orbital area, from the nose area to the right ear. There was also bruising and swelling around the eye on the upper and lower lids. I did not inform the parents at this stage, but I had concerns whether a plastic toy could cause such injuries, as I was now seeing C2 with these injuries some two days after the event.”
Dr Papworth’s notes are at F360. She told me in evidence that she made a note of exactly what the father had told her. Nothing was said about the father’s foot coming into contact with C2’s face.
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
She is a Consultant Community Paediatrician. At the request of the local authority, she saw C2 on 23 June at 3.00pm at the Royal Gwent Hospital. Prior thereto she had understood from Detective Constable Chard and Mandy Vernon, a social worker, that they understood that C2 had been lying on the floor under the baby gym and the father had caught his foot on the frame, which had hit C2’s face. In her statement of 25 July 2007, Dr Rawlinson says at G60:
“I next saw C2 who was accompanied by both parents. Also present was my registrar Dr Jo Saunders. Informed consent was obtained for an examination under child protection procedures from the baby’s father, F. They told me that he is a healthy baby who had been born at the University Hospital of Wales weighing 8lbs 8ox by an elective caesarean section. He had not required any special care. He had been breastfed for around seven days and subsequently commenced in bottle feeding. He is feeding well on SMA white cap and is now eleven weeks of age. I was told that at four to five weeks of age C2 had had bleeding from his nose and had also been taken to the University Hospital of Wales where he was seen on the Paediatric Unit and discharged. I was told ‘he had burst a blood vessel in his nose’. They went on to tell me that he has been developing well and now smiles and laughs. I was told that he has rolled from his back to his front last week, is holding his head up well and can move around on the floor. He will grab onto clothing when he is picked up.
The family told me that on the evening of Tuesday 20th June his mother had been out for the evening and C2 had been in the care of his father. After his mother had returned at around 9.40pm, C2 was on the floor under his baby gym. His father told me that he had gone out of the room, and when he came back in he had caught his foot on the baby gym frame and had kicked the frame accidentally into C2’s face. Both parents had been present. They had noted swelling around C2’s right eye and had gone to A and E at the University Hospital of Wales at approximately 10.20pm where he had been checked over and sent home.
Mum told me that the bruising had come out more yesterday and was actually a little less evident today. C2 had been fine since and had been feeding well. I specifically asked if C2 had any marks anywhere else before I commenced the medical. His mother told me before I examined him that he had a bruise on his right leg. The family thought that this was from his cot sometime last week, and told me that he kicks against the wooden cot bars. They also felt this could have occurred from a changing mat with metal framework which is clipped to the travel cot and is a piece of equipment with which I am not familiar. They also told me that he had a little mark on his left upper arm which they thought was from the car seat which is apparently difficult to use and was shown to me. Mum told me that this never looked like a bruise, but went on to tell me that, in her words, ‘it had initially looked like a love bite a couple of days ago’.”
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:
“Head and Neck
There were blotchy patches of petechial bruising present over an area above and below the right eye and extending onto the eyelid and cheek. These patches of bruising were blue in colouration. There was slight soft tissue swelling present under the eye; there was a full range of eye movements, and no subconjunctival haemorrhages visible, although the sclera (white of the eye) looked slightly injected laterally. The bruising below the eye was in a roughly triangular distribution over an area approximately 2cm by 2cm by 2cm. Petechial bruising extended in a patch about 2cm above the right eye. There was therefore evidence of quite extensive petechial bruising to this area of the baby’s face some three days later.
Right Leg
There was a linear brown bruise present on the anterior aspect of the right leg in the midline. This was approximately 3.6cm long with a distal linear extension of slightly lighter colouration. This was also brown in colouration and approximately 1.5cm long. Both parents told me that they thought this could be from his wooden cot bars or the metal frame of his changing mat in his travel cot.
Left Upper Arm
In the midline of the left upper arm there were three small petechial bruises in a cluster. These appeared to be small linear petechial bruises. Whilst I was examining C2, his mother commented that they resembled a pinch mark and earlier had looked ‘like a love bite’. His father told me that this was from his car seat, which he then showed to me.
Neck
There was a small red mark just below the nape of the neck posteriorly in the midline, which his mother told me had been present since birth and seems likely to represent a birth mark.
I note that in Dr Papworth’s clinic notes of the previous day, she had also documented petechial bruising to the right face and the marks on the left upper arm, but there was no documentation of any bruising to the right lower leg.”
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:
“The history as given is as documented in my original report. Whether or not dad’s foot was ‘in contact’ with the baby gym (and the fact that I specifically asked whether his foot itself had hit C2), it is my opinion that the extent and distribution of the bruising to the face cannot be adequately explained. This does need to be seen in the context of the whole child, i.e. a non-mobile baby with evidence of bruising to three areas of the body.”
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:
“In summary therefore C2 is an 11 week old non-mobile baby who appears healthy and is developing normally. He shows evidence of bruising to three sites of the body, some of which is petechial (tiny blood vessels). Further investigations have shown a normal coagulation screen and a normal CT scan of the brain, with no evidence of retinal haemorrhages on fundoscopy. The coagulation screen is normal, i.e. no medical reason for him to bruise more easily, had been detected at this time on baseline investigation. Such medical conditions are rare, and in any case both inflicted injury and bleeding disorder may coexist and the diagnoses are not mutually exclusive. I do, however, understand that his sibling C1, who died at eight weeks of age with a sudden unexplained death in infancy, was said to have abnormal coagulation following his collapse, but that this returned to normal before he died. I understand that Dr Collins, Consultant Haematologist at University Hospital of Wales, was involved in his management, and I will therefore write to him to ask if he feels any further haematological investigations in C2 are warranted.
In my opinion, however, the pattern and distribution and extent of bruising around the right eye in C2 is not consistent with the explanation being offered of the incident with the baby gym, and although this may well have occurred, I do not think that this is the mechanism by which he sustained the bruising as seen. The fact that this baby has had three areas of documented bruising, including his face, is of concern. (Ref: Maguire, Archives of Disease in Childhood, 90(2) 196 – ‘Those who don’t cruise, rarely bruise”). It is generally accepted that a young non-mobile baby would not be able to bruise themselves by kicking against cot bars or changing equipment. The petechial bruising on the left upper arm was suggestive of a possible pinch mark. Overall therefore this presentation of unexplained bruising in a young non-mobile baby raises concerns regarding non-accidental injury.”
Further down Dr Rawlinson says:
“I am also concerned at the history as given of C2 presenting at a few weeks of age to University Hospital of Wales with reported bleeding from the nose. This in itself is an extremely unusual finding in a young child and is in fact one of the ways in which imposed upper airway obstruction can present. (Ref: Child Protection Companion, Royal College Paediatrics and Child Health, April 2006). The hospital records of this presentation do need to be obtained as well as copies of the A and E attendance to the University Hospital of Wales with bruising around the eye in June 2006.”
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
All the experts relevant to these bruises told me that bruising to a non-ambulant child of C2’s age, i.e. two months as at 23 June 2006, was very rare. Dr Debelle told me that in his experience bruising was not a common experience and that studies had shown that bruising on a non-ambulant child was a rare event. Dr Sunderland agreed. Both accepted that one had to look not only at each bruise, but also at all the bruises together. Both told me that generally speaking they would expect the carers of a non-ambulant child to have seen how the bruising was caused.
Leg
It is crucial to note that the bruising to C2’s leg was a linear mark which runs vertically up and down the front of his shin. Dr Sunderland told me that the rolling of C2 into the cot bars would not create enough momentum to cause such bruising. It was unlikely that a baby kicking out and his leg hitting the cot would cause such a bruise. Furthermore, it is an important point that the cot bars, as seen in the photographs, would have been at right angles to C2’s legs if he had rolled into them. The cot bar at right angles to the linear bruise would be most unlikely to cause such a bruise. Furthermore, Dr Sunderland told me that, to him, it was some sort of pinch mark. Dr Rawlinson did not consider the parents’ explanation to be satisfactory. She told me that cot-bound babies do not injure themselves. Mr Debelle said that the parents’ explanation was plausible, but bruising in infants was rare and it should have been witnessed. Both parents in their evidence were completely unable to relate the bruise on C2’s leg to any incident at all. The mother agreed in cross-examination by Miss Mifflin that C2 rolling into the cot bars was not an explanation of the bruising.
The Arm
The mother described the marks on C2’s left upper arm as looking puckered and like a “love bite”. Dr Rawlinson agreed that is what it did look like. It looked like a pinch petechial bruising. The father suggested that the seatbelt straps of C2’s seat could have caused that bruise. Dr Sunderland pointed out that the bruise was in the wrong place of the arm for any trapping by the seat strap. Dr Rawlinson told me that there was nothing to suggest any chafing because the mark on the arm had not been abraded or rubbed. Dr Debelle told me that if the seatbelt had in some way caused the bruising, a carer would have witnessed C2 being in pain at the time, but there is and was no clear and consistent explanation. Neither parent told me in their evidence of any incident in which C2 had been caused pain when in his car seat.
The Face and Eye
In my judgment, C2’s injuries were not caused by either the strut of the baby gym and/or the father’s foot. I am satisfied that the strut of the baby gym never came into contact with C2’s right eye and/or right cheek. There is no incident other than the baby gym which is put forward by the parents to account for his injuries. The short point is, in my judgment, that the father has not told me the truth. Whilst I am prepared to accept that the father on the evening of 20 June did accidentally walk into the baby gym, I specifically find that it did not hit C2’s face.
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.
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