AA (A child), Re

This is a tragic and extremely difficult case. On 6^th January 2011, a little boy, whom I shall refer to as J, died while in the sole care of his mother. Twelve weeks later, on 1^st April 2011, his older brother, whom I shall refer to as B, then aged four, was found in a state of acute collapse, also whilst in the sole care of his mother, and died three days later in hospital.

Police began an extensive investigation, which is still ongoing, into the causes of those deaths. The local authority started care proceedings in respect of the surviving younger sister of the boys, whom I shall refer to as A, now aged two. The local authority contends that the threshold under section 31 of the Children Act for the making of care orders is crossed in this case and seeks findings, first, that the mother neglected her children and, secondly and more seriously, that she was responsible for the deaths of the two boys by asphyxiation. The proceedings were transferred to the High Court and listed before me for a fact-finding hearing held in Portsmouth. This judgment is delivered at the conclusion of that hearing.

The mother was born in 1985. At an early age she was diagnosed with congenital hypothyroidism, for which she has been prescribed medication throughout her life although, as she accepted in oral evidence, there have been periods in her adult life when she has failed to take her medication. In particular, her medical records suggest that she was not taking her medication during 2010, before and after the birth of A, and up to and including the date of J’s death. Her GP commented to the police, via the paediatrician, Dr Trevelyan, that symptoms of missing the medication would include, inter alia, feeling tired, excessive sleepiness, depression, problems with memory and concentration, slow movements and weakness and weight gain. In her oral evidence, the mother said that she became depressed when she did not take her medication - “I don’t want to do stuff and I just go on the computer.” In addition, the mother has been diagnosed as suffering from a mild or borderline learning disability, with a full-scale IQ measured at 67 in 2000 and at 79 in May 2011 when she was seen by a psychologist at the outset of these proceedings. Psychological testing indicated that she has difficulty with some, not all, areas of cognitive function. She was able to give instructions to her legal representatives, but received extra support during the hearing, including the assistance of an intermediary when she was giving evidence, although in the event the intermediary was, so far I could see, not required to interpret any question or answer.

The mother’s parents separated when she was very young and from the age of two she was brought up by her mother, the maternal grandmother, hereinafter referred to as DA, and her stepfather. She has a younger half-brother, L, who has a degree in nursing and is working in the north of England. The mother experienced a number of problems in her childhood and her relationship with her mother, DA, was difficult. At the age of 14, she was placed in voluntary foster care and received extensive support from psychiatric and other healthcare professionals. Her medical records include a number of references to drug overdoses and other episodes of self-harm, with some suggestions of fabricated medical conditions. For the most part, however, these suggestions are not being relied on by the local authority in this case and I have expressly not been asked to consider the possibility that the deaths of the boys may be linked to any form of factitious illness syndrome.

In her teenage years, the mother had a number of sexual relationships and on 20^th September 2006 gave birth to her first child, B. B’s father has played no part in his life, nor in these proceedings. Initially the mother and B were accommodated by a local project and in June 2007 they moved into local authority accommodation. During the first year of B’s life, there were concerns about the mother’s capacity to care for him, including poor home conditions, inappropriate feeding and over-chastisement. In October 2007, the mother told social services that she felt unable to cope with the baby and took an overdose. Following a hospital admission, she was diagnosed with postnatal depression. At that point, B was placed with DA, with whom he lived for the rest of his life. It was agreed that DA would apply for a residence order and it seems that an application was duly filed, although there is no record of any such order being made. All parties, however, proceeded on the basis that DA had a residence order in respect of B. She acted as his main carer and he formed a close and loving bond with his grandmother. All the evidence suggests that he thrived in her care. For example, the manager of the nursery attended by B, told the police: “Emotionally, he was stable and happy. I had no concerns about his home environment and he loved his nan, who appeared devoted to him.” A contract of expectations was drawn up and signed, providing that the mother would not have unsupervised contact with B outside DA’s home. On occasions, however, the mother took B to nursery where the manager observed that B was comfortable in her presence and she had no cause for concern.

In 2007, the mother had started a relationship with GM, a patient at the psychiatric unit to which she had been admitted following her overdose. GM has a diagnosis of paranoid schizophrenia. Subsequently he moved into her local authority accommodation and she became pregnant by him, giving birth to her second child, J, on 27^th August 2008. A further pregnancy was terminated in March 2009. The relationship between the mother and GM was turbulent, with allegations of sexual assault against herself and J. These allegations did not lead to any proceedings. In February 2009, the mother and J moved to another flat without GM, although the relationship continued and he spent some time at her new flat. Social services were significantly involved with the family after J’s birth and he was made the subject of a child protection plan in November 2009, on the grounds of neglect. By that point the mother was pregnant again. The child protection case conference minutes, produced in the course of this hearing, recorded concerns about safety issues in the home, ongoing problems between the mother and GM, and the fact that the mother, with her learning difficulties, struggled with aspects of daily parenting. On the other hand, the minutes also spoke of “lots of positives,” including the fact that the mother had asked for help and engaged with the agencies. The care plan included provision for daily support from adult services, arranged by the learning disabilities team, and child-minding was arranged for J.

On 20^th April 2010, the mother gave birth to her third child, A. She too was made the subject of a child protection plan shortly after birth. A parenting assessment carried out after A was born concluded that the mother did not have the capacity to care for the children through to adulthood without a high input from social services, both for the children and for herself. In the first few weeks, A was admitted briefly to hospital on two occasions, once for vomiting and once following blood in her stool. Concerns continued to be voiced about a range of matters, including the condition of the home, worsening relations between the mother and some professionals, missed appointments, difficulty managing J’s behaviour, problems caring for two children and concerns that A was failing to thrive. A further contract of expectations was drawn up, setting out what was expected of the mother in order to avoid court proceedings. This document provided, inter alia, that B’s visits to the home should be limited to twice a week, with no overnight stays.

The mother continued to receive daily support provided by an organisation called SCA. Her cooperation with the support workers from that organisation was erratic. The worker with whom she had perhaps the best relationship was a woman called TW. She gave evidence at the hearing and observed that the time allotted for her to help the mother was not enough. She added that the mother should have had further support for the children to assist her with parenting skills. In cross-examination by Miss Pine-Coffin, junior counsel for the mother, however, TW said that J and A seemed happy and comfortable at home, that J was “always happy.” The children were fed and well-dressed and that the mother cuddled the children and said that she loved them.

The social worker assigned to the family in July 2010, EA, who was not called to give oral evidence summarised the ongoing problems in a later police statement as being the mother’s poor parenting skills and unintentional neglect of the children. However, during the autumn of 2010, EA noticed some change for the better, although she queried whether the improvement was sustainable. According to the mother and DA, the restrictions on contact with B were relaxed and he was permitted to stay overnight. The local authority’s position at this hearing has been that no such relaxation was agreed, although the social workers were aware that B was in fact staying at the mother’s flat on occasions.

Just after midnight on 12^th November 2010, the mother called an ambulance, complaining that A had suffered repeated episodes of vomiting, culminating in an incident when she had become floppy and unresponsive for about 15 seconds and her lips had turned blue. Following her arrival at the emergency department, A vomited on two further occasions. In her oral evidence, Dr Trevelyan, the paediatrician at the hospital, said that the description of A in the medical notes was of a child who was not well. The doctor on duty records her impression as viral gastroenteritis and it was considered that the floppy episode may have been attributable to dehydration. A was allowed home later that day.

On another occasion in November, the mother became drunk when caring for the children, who were taken round to DA’s house. There is evidence that on occasions the mother expressed frustration about the demands for caring for the children. She was a regular user of text-messaging and the internet MSN message service and, when chatting to friends by these means, she would on occasions grumble about the children. One example, on the evening prior to J’s death, contains the statement that she could have “fucking killed” B, because he had made J cry and been disobedient, and added an additional remark: “I wish I didn’t have fucking kids.”

On 9^th December 2010, the mother rang the social worker in distress, saying that she had had an argument with DA who had told her that she was a rubbish parent. The mother said that she could not cope with the children anymore and she had packed their bags and wanted social services to take them away. Before the social worker arrived, support worker TW called at the flat. The mother told her about the argument with DA. On arrival at the home, social worker EA found that the children were ready to leave, with coats on and bags packed, but after talking to the mother it became clear that she did not really want the children removed, but rather was angry and upset by what she alleged had been said by DA. The social worker therefore left without the children. It was agreed that J’s child-minding hours would be increased. On a further visit a few days later, the social worker noted that the mother was still struggling to cope with the two children. At a meeting on 20^th December, the mother said that she was having problems dealing with J’s behaviour. It was agreed that she would attend a parenting course in the New Year. In the last few days of December, A became ill again and was seen on three occasions by the GP, who diagnosed bronchiolitis and prescribed a Ventolin inhaler.

On the evening of 1^st January 2011, the mother called an ambulance, claiming that J was having problems breathing and was having a fit. Later in the call she said that he had “turned really blue,” and further on she said: “He looks so lifeless. He’s tried to catch his breath. He can't.” When the first paramedic, SV, entered the room, his first reaction was that J had died, but on rubbing his chest, J opened his eyes and started to move. At the time of the incident SV made no note about the mother’s behaviour on the form available for such observations, but in his police statement, notably given over six months later, he said that he thought the mother’s behaviour had been odd. She did not come into the room when J was being treated and seemed to show a lack of urgency. He observed however that she appeared to have some kind of learning disability.

One matter which has featured prominently in this case is the presence and interpretation of a rash seen by some medical staff on J’s body. Cross-examined by Miss Judd QC on behalf of the mother, SV said that he would have looked for a rash and for petechiae but did not see any such signs. On arrival at hospital, however, medical staff in the emergency department did observe a petechial rash over J’s upper chest. The mother gave a consistent account of what had happened. The doctor in the emergency department recorded his impression as to diagnosis as “febrile convulsion and, question mark, meningococcal meningitis.” The senior paediatric registrar who examined J next noted that there were petechiae around his neck, increasing in number. J’s temperature was slightly raised. Her impression was “febrile convulsion, most likely secondary to upper respiratory tract infection, petechial spots noted, cannot exclude meningococcal sepsis.” On the following morning, the paediatric registrar, Dr Verling noted, “No evolution of petechial rash.” Cross-examined by Miss Judd, Dr Verling said that there were only a few petechiae and added: “we see a lot of petechial rashes, especially in the context of children with a high temperature.” He described J’s temperature on admission, 37.9 degrees Celsius, as on the cusp of a significant temperature. In the notes, Dr Verling described J as “a well baby, running around ward.” He was discharged home. The note records: “Mum happy and medical team happy for J to go home.”

Dr Trevelyan, the consultant paediatrician at the hospital, told the court in oral evidence that, although there had been some suggestion in the emergency department that the interaction between the mother and J on his admission had been minimal, staff on the paediatrics wards felt that the interaction was appropriate and had no concerns. She agreed with Miss Judd that staff on the paediatric ward were much more experienced in observing and documenting this sort of interaction, particularly taking the trouble to do so when a family was known to Social Services, so that a child protection pro forma had to be used.

On the evening of the following day, 3^rd January, the mother knocked on the door of a neighbour, GW, and asked her to come over. GW reported the mother as saying that J was making a funny noise. In her oral evidence, GW described the mother as “flustered, not crying but panicking.” Her statement continues: “We went into J’s bedroom. J was lying on his back on his bed, with his eyes wide open, fixed on the ceiling. He was making a little noise like he wanted to be sick. I put him on his side and he vomited a little bit. I was calling his name and rubbing his back. I would describe J as not responsive. On seeing J, I immediately said to phone for an ambulance.” Although GW was unable to recall who had made the call, the transcript shows that it was she who started the call and then handed the phone over to the mother. In the course of the conversation, the mother said: “this has happened twice now and I’m getting a bit scared of it, 'cause one day I may not wake, you know, I might wake up and find him not alive.”

On arrival, the ambulance crew were told by the mother that she had found J in bed, having vomited, unresponsive, with his upper limbs shaking. The paramedic, DF, found that J’s initial Glasgow Coma Scale was only 7. In his police statement, given 15 weeks later, DF described J as “breathing but basically unconscious; his eyes were not open. He was not talking, but his limbs were moving.” DF concluded that he was post-ictalthat is to say recovering from a seizure in which there had been a lack of oxygen. Cross-examined by Miss Judd, he said that he had no concern about the mother’s behaviour on this occasion. Had he had any such concern, he would have recorded it. He did note that the mother had stayed initially outside the room. He accepted in oral evidence that the flat was small and there was not a lot of room in J’s bedroom with three or four people in it. The paramedic noted no obvious rash on his body, but on arrival at hospital the mother told medical staff that a rash had appeared on his back during the day. Further examination revealed that J was suffering from chicken pox and he was discharged home. In a note to social services, the hospital commented: “no concerns with this presentation to the emergency department.”

As J had chicken pox, he was unable to attend his nursery or go to his child-minder for the next few days. The mother subsequently told the paediatrician, Dr Trevelyan, that, in the ensuing 48 hours, he had been lively and playful and had eaten and drunk well.

In her statement in these proceedings, the mother says that on the evening of 5^th January, she gave J a bath, soothed him and put him to bed. Later that evening she went to check on him at about ten past ten. At that point he was still alive and moving. She then stayed up until the early hours before going to bed. Having checked A, she went into J’s room.

Her statement for these proceedings continues as follows: “The window was open and I closed it. I then touched J’s hand. It was cold. I nudged him but he did not move. I pulled his covers off. I got on his bed and shook him to try to wake him. I panicked when he would not. I called for an ambulance and, in my panic, screamed down the phone.”

The transcript of the emergency call is timed at 3.15 am on 6^th January. After giving her address, the mother is recorded as saying: “I was asleep and I couldn’t sleep, because I kept thinking about my son and what’s happening and, you know, New Year and whatnot. I went to check on him and, er, I shook him a bit and he’s very, very cold and he’s not moving.” The controller then instructed the mother to do mouth-to-mouth and cardio- pulmonary resuscitation until the emergency crew arrived.

First to arrive was SF, an emergency care practitioner, closely followed by an ambulance. SF described how they went into the child’s room and that the mother was with them. His statement continued, “It was very clear on seeing J that he was unconscious, not breathing and that there was no pulse. Defibrillator pads were placed on J’s chest, but there was no output and he was asystole.” The crew decided to take him to hospital immediately. The mother followed in the emergency car, having left A with the neighbour GW. In her oral evidence, GW described the mother on this occasion as obviously upset, crying, hysterical, screaming “he’s dead, he’s dead.”

On arrival at the hospital, it was confirmed that J was in asystolic cardiac arrest. Blood tests showed a severe acidosis, indicating that his heart had stopped for some time. After 20 minutes the decision was taken to stop attempts at resuscitation and he was pronounced dead at 3.59 am.

J’s body was examined shortly after death by Dr Trevelyan. She found a widespread rash consistent with chicken pox but otherwise no marks or anything remarkable. In cross-examination before me, Dr Trevelyan said that she would have looked for anything relevant on the skin, such as petechiae. She spoke to the mother and said in cross-examination that the mother had not been unwilling in any way to give details of the history and had not left her with the impression of trying to hide something. The various accounts given by the mother at different times of this incident were consistent.

The mother’s friend, SB, described in a statement to the police how the mother had stayed the night after J had died and had kept going over the events in her mind about the night before. In her oral evidence, SB said the mother had kept wondering whether she could have done anything else to resuscitate J.

A post-mortem examination was carried out by Dr Darren Fowler, consultant pathologist. The autopsy showed J was a well-nourished boy with no evidence of injury and no internal structural defects. Biological tests show the evidence of chicken pox with varicella zoster viral DNA present in J’s nose, throat, lungs, blood and cerebrospinal fluid. There was patchy but widespread active inflammation of the lungs, with neutrophils seen in all the lung lobes sampled. Dr Fowler commented that there are a few case reports of sudden death in children with varicella pneumonia, but J did not have the severe pathology seen in such cases and appeared to have recovered from the acute phase of the illness. He concluded:

“The question is whether J died as a result of complications of varicella infection or whether varicella infection contributed to his death or whether there were other factors involved. For example, I have been asked by the police to consider the possibility that J may have been smothered with some soft material such as bedding or pillow. I cannot exclude this, but there were no pathological findings to provide confirmation. Although J had chicken pox/varicella viral infection, both clinical and laboratory data confirm this, I am not able to give this as the cause of death with certainty and not to the standard of beyond reasonable doubt. I therefore give as the cause of death: unascertained.”

Subsequent further histopathological analysis at Great Ormond Street concluded that there was “unequivocally no significant pneumonia or pneumonitis. There are no viral inclusions and the majority of the lung parenchyma is completely unremarkable.” The specialist opinion was that it was very doubtful whether any lung pathology was related to the cause of death, irrespective of whether or not the child had varicella infection. Having considered this further information, Dr Fowler added that this did not change his comment or conclusion as to the cause of death, which remained unascertained.

Medical examinations of A and B conducted on the day of J’s death revealed no cause for concern. The day after J’s death, a strategy meeting was attended by, inter alia, social workers, police and Dr Trevelyan. The overwhelming view, according to Dr Trevelyan, was that there was no reason for concern that J had been harmed and a decision was taken not to initiate a section 47 investigation. In her oral evidence, Dr Trevelyan said that there were worries about neglect, but it was felt that nothing that the mother had done in looking after J had led to his death. After J’s death, the mother appeared to be in shock, according to one of the support workers.

Thereafter, the mother and A went to live with DA and did not spend another night at the flat where J had collapsed. The child protection plan for A remained in place. Fewer concerns about A’s presentation were noted after the family went to live with DA, although she continued to have some health problems, with episodes of chest infection, diarrhoea and vomiting, which required hospital admission on one occasion. Relations between the mother and DA were strained at times, with a number of arguments, in particular about the mother’s untidiness. The mother began to speak of taking over care of B again. GW said in evidence that the mother did not like the fact that B was with DA; she wanted him to be with her.

On the morning of 1^st April, B went to nursery where, according to the manager, he played happily all morning and seemed his usual, normal self. Support worker TW saw B in the nursery playground and thought he looked fit and healthy. During the morning, the mother took A round to her friend, SB, and they all went into town. TW had a meeting scheduled later that day, but around noon she received the text from the mother, saying that she and DA had fallen out and she doubted whether she would be at the meeting. After further texting, TW went round to SB’s house and collected the mother and A at about 15.30. On the way the mother told her more about the argument. DA had complained again about the state of the mother’s bedroom. According to TW, the mother said that she hated living there and could not wait to get out of there. They stopped at B & Q, where the mother picked up some wallpaper samples and paint charts. TW told the police that the mother was in a good mood and was talking about decorating a room for A, like a princess’ room, if she was rehoused. They then returned to DA’s house. On arrival, DA said to the mother, “You’d better get up to that room and tidy it now.” An argument ensued in the course of which, according to TW, the mother said to DA, “I hate you, I wish you were dead.” TW had not heard the mother say this to DA before, but she told Miss Pine-Coffin in cross-examination that it did not concern her. It was like her arguments with her own mother. TW stated that B came downstairs during the argument. According to DA, the argument continued after TW left. The mother shouted: “I’m going back to my flat.” DA replied: “Don’t be stupid.” DA said they both then calmed down and she asked the mother: “isit because Mother’s Day is coming up?” The mother replied: “yes.” After that, the mother went upstairs to tidy the room.

B had a bath and was put to bed. At some point after 18.30, DA left the house. In her statement she said that she left about 19.15, but it must have been earlier, as she was seen on CCTV entering the local supermarket at 18.53. She left that shop at just after 7 o'clock and went to the mother’s flat. The mother and B remained at DA’s home. Subsequent analysis of the mother’s computer showed that she started to use the internet at 18.59. She logged onto a gambling site at 19.05 and purchased four online bingo tickets, at 19.07, 19.15, 19.22 and 19.28. At 19.26 the mother texted SB and asked: “Are you coming on the comp?” By this she was enquiring whether SB was going to chat over the internet via the MSN site. SB replied by text “later maybe, why hon?” At 19.28 the mother replied: “just asking.” At 19.33, DA’s sister telephoned the landline at DA’s home but the call is timed as having lasted only one second. At the same time, the mother logged out of the online website.

According another friend of the mother’s, NF, at some time before 19.45 she had a brief conversation with the mother via MSN, in which the mother had said that B was not going to sleep, to which NF replied “bless.” No records are available to confirm this conversation. Analysis of the mother’s computer indicated that at 19.45 internet usage ceased for 17 minutes.

At some point (the precise time is unclear) the mother states that she found B sitting outside the front door waiting for his nan. She says that she took him inside and put him back to bed. She put a DVD on in his bedroom and sat with him for a few minutes until he was nearly asleep. A group of local boys told the police that they saw B on the front doorstep and the mother putting him indoors and shouting and telling him off. There is some inconsistency between the boys’ accounts to the police as to the timing of this incident. None of the boys was called to give evidence before me.

At 20.02, the mother started using the internet again and connected briefly with the MSN site before ceasing internet use again at 20.05.

At 20.16, according to DA’s phone records, the mother telephoned the home of SB from a landline in DA’s house. The phone was answered by SB’s mother’s partner, MP. There is some disagreement about the timing of this call. MP put it at 19.30, because he recalls “Emmerdale” finishing and “Coronation Street” starting. His partner, EH, SB’s mother, stated that the call came while she was on the balcony smoking a cigarette after the conclusion of “Coronation Street” and before the start of “East Enders” at 20.00 hours, and lasted about 20 minutes. According to the phone records, however, the call lasted about five minutes and started at 20.16. I conclude that both MP and EH are simply wrong about the time of the call. MP states that after some friendly banter, the mother said she thought B “has shit,” to which he replied that she had better check it was not running down his leg. The mother’s account is that she “smelt poo,” went upstairs whilst still on the phone to MP, checked A first and then went into B’s room where she found him in a collapsed state.

According to MP’s police statement, taken four days later, the mother said: “Oh, B is dead,” and started gasping, as if about to cry. Not knowing what to make of this, MP went and fetched SB and handed the phone to her. The mother said, “S, I’ve got something to tell you, I think B is dead.” She said that she had smelt poo and had gone to check him while on the phone; he was not breathing. SB screamed and passed the phone to her own mother, EH, who told the mother to fetch a neighbour.

At some point around or after 20.15 the mother knocked on the door of other neighbours, TR and her partner MM. When TR answered the door, the mother told her that B was not moving. TR described the mother as hysterical and frightened. She grabbed the mother’s hand and they ran back to DA’s house, closely followed by MM. When TR entered B’s bedroom, she saw B on the bed with the quilt pulled back and his head on the pillow. The wooden frame of the bed is constructed to resemble a car. The mattress is a few inches below the top of the frame. TR described B as lying on his back with his head back and his eyes and mouth half-open. He was blue in colour. Both TR and MM rang 999 and transcripts of their respective calls, each timed at 20.23, were produced in these proceedings. In both calls, TR is heard telling the mother, “Get away, get away.” MM entered the bedroom and started resuscitation, under instruction from the ambulance controller, lifting B from the bed and putting him on the floor. He carried out both mouth to mouth and cardiac pulmonary resuscitation. In oral evidence he described B as cold when he touched him.

While MM was trying to resuscitate B and before the arrival of the ambulance, the mother went into her bedroom and had a conversation via MSN with her friend, NF. The conversation was started at 20.24 by NF who asked: “you okay?” to which the mother replied: “no, B not breathing.” NF asked: “what you mean?” The mother replied: “he’s dead.” The conversation continued for three minutes, the mother’s last remark being timed at 20.27. In her oral evidence, TR said that she recalled the computer being on, but was with the mother throughout and did not see her touch it.

At 20.25 the paramedic first responder, AT, arrived at the house. He found two women in one bedroom, evidently the mother and TR. The mother was screaming hysterically. AT entered the other bedroom and found MM doing chest compressions on B. It was obvious to AT that the boy was not breathing. He attempted to get B’s heart started with a defibrillator and attached a breathing mask to B’s face, all without success. In a statement signed two days later, AT referred to the photographs taken of B some hours later, showing a petechial rash and said that he had no recollection of seeing this rash when he was treating B. In cross-examination by Miss Judd, he said: “we would be observant for marks but I didn’t see any.” In his police statement he said that a mark on B’s chest in the same set of photographs was consistent with where the defibrillator pads had been placed, although he could not say for certain that the pad caused this mark.

An ambulance then arrived and a crew, including paramedic PC, removed B immediately to hospital. Attempts at resuscitation continued in the ambulance, again without success. The defibrillator pads remained on B’s chest throughout the journey while the team continued chest compressions. PC completed the ambulance form in respect of this incident. He recorded: “patient checked by mother ten minutes previous to calling 999.” In his statement he added: “there was the smell of bowels being emptied coming from the child; there was no obvious sign of any injuries to the boy.” Cross-examined by Miss Judd, PC said that he did not see a rash and added that it was common to leave a mark or two on a child when attempting to resuscitate in these circumstances.

At 20.29, SB telephoned the mother on DA’s landline. TR then, in her words, grabbed the mother and drove her down to the hospital in her car. On the way the mother told her about how she had smelt poo and, having checked on A, she then entered B’s bedroom and found him blue and not breathing. In her statement to the police given on the same day, TR added: “she told me that she had checked on him two minutes before this and said that he was okay and was sleeping normally, but I think she must have been confused about this time, as B looked as if he had been in the condition he was longer than just two minutes.” MM also recorded his statement taken the same day that at some point the mother had said that she had checked on B two or three minutes earlier.

DA, who had been telephoned by TR, was driven back from the mother’s flat to her house by GW, the mother’s neighbour. Another local resident, VJ, claimed in a statement to the police, signed on 17^th August 2011, some four and a half months later, that she heard DA say as she arrived back at the house: “she’s fucking done it again.” DA denies saying those words or anything to suggest that she suspected the mother of injuring the boys. Having heard VJ’s evidence, I do not consider her to be a reliable witness and I attach no weight to her evidence on that point.

On arrival at the hospital at 20.45, B was taken into the resuscitation room and advanced life support treatment undertaken. His mother, grandmother and a number of friends and neighbours gathered at the hospital. The consultant in emergency care, Dr Beardsall who did not give oral evidence, told the police that B was noted as a well-looking boy, who looked like he was sleeping rather than suffering a life-threatening event. Dr Beardsall added that a brief inspection of B’s body whilst resuscitation was going on did not reveal any signs of trauma to explain his condition. He told the police that in his experience, which included over ten years in emergency medicine, he had never seen a child in cardiac arrest where the precipitant was not obvious, be it trauma or illness.

Two other consultants were also involved in the efforts to save B’s life, Dr  Erlewyn-Lajeunesse, a paediatrician, and Dr Macintosh, specialist in paediatric intensive care. Both gave oral evidence and described the treatment given to B that evening. After intubation, B’s heart resumed beating after about 20 minutes in hospital, but it fluctuated for a further 15 minutes before it subsided and resuscitation was stopped. Thus, B received a total of resuscitation from MM, the paramedics and the hospital staff in excess of 30 minutes before any heartbeat was restored and at least 45 minutes in total. I was told that this is at the outer limit of attempts one would have made to resuscitate a patient. Dr Erlewyn-Lajeunesse made a note retrospectively at 20.30 in which he said, inter alia: “no abnormal bruises or injuries (back not yet inspected.)” Cross-examined by Miss Judd, he initially said that had there been any petechiae he would have noticed them. He added that he was not clear about how much access he had had to B’s face; the focus had been on saving B’s life and he could not say that petechiae were not there. However, in answer to further questions from Miss Judd, he described as examination as “more than a once-over,” that he was suspicious and therefore looking for marks and that one of the things he would have been looking for was petechiae. He also said from his experience that after a prolonged period of resuscitation, these sorts of petechiae would not have been unusual.

Subsequently Dr Macintosh completed the Safeguarding Children pro forma document, which included a body-map on which were drawn petechiae on the left side of B’s face and on the left side of his chest, above the nipple. The timing of this drawing is unclear from the documents but in oral evidence it became apparent that Dr Macintosh had completed it around midnight. Apart from the body-map, there was no note taken of Dr Macintosh’s examination. The document also contained a history, described as being from the mother and DA and friends. In oral evidence, Dr Macintosh described how a crowd of about nine or ten people had participated in this discussion. Several people took part in giving the history and it had been difficult to pin things down. The mother did not say a lot and seemed quite withdrawn, and Dr Macintosh had to put questions to her several times to get an answer. When he asked questions, other people would chip in. DA, who was understandably devastated, was the most vocal. Often there would be a discussion between more and more people, as they tried to establish what had happened, and then Dr Macintosh would ask the mother to confirm the account. The note records that the mother had put B back to bed sometime between 19.30 and 20.30 and went in to check him about ten minutes after he had been put to bed and found him blue, his eyes open and there was no response. Dr Macintosh was unable to recall, in answer to Miss Davis, senior counsel for the local authority, whether the comment that she had gone in after ten minutes had come from the mother or from others. The order of events had been clear, but not the timing.

In the course of the evening, DA asked the mother whether she had done anything to B. The mother denied doing anything. EH also said that she had looked at the mother straight in the face and asked her if she had hurt B. The mother had said no, without hesitation. In cross-examination, EH said that she believed the mother.

B made no further progress and it became apparent that he had no prospect of recovery. During his stay in the intensive care unit, ECG examination showed a prolonged QT interval. I shall consider the significance of this below. On subsequent days, other petechiae were noted on his right arm and lower back.

The doctors discussed the situation with the family, who acknowledged that life support should be withdrawn and B died on the afternoon of 4^th April.

A post-mortem examination of B was carried out on 5^th April by Dr White, consultant pathologist. On his external examination of B, Dr White noticed a small red mark, 0.5 centimetres in diameter, on the right side of the top of the head, and a bruise one centimetre in diameter in approximately the same position on the left side of the head. He noticed some scattered petechiae around the left side of the face, but in his post-mortem report stated that there was “none on the right side or in either eye.” In his external examination, Dr White found a focus of bruising, one centimetre in diameter, noting the scalp tissues beneath each of the external bruises. So far as the respiratory system was concerned, there was some brownish mucus at the junction of the lower end of the trachea and the right main bronchus, but the larger airways otherwise appeared normal. A section through each lung revealed a heavily congested parenchyma. Histological examination of the lungs found that they were congested with focal areas of intra-alveolar haemorrhage with very occasional haemosiderin deposits noted in one section. The lungs showed patchy, acute bronchopneumonia, but not at the level suggested that would account for death. In addition, there were two small fibrin thrombi. Dr White concluded that these signs were consistent with the ventilation that had taken place over a number of days. The microscopic presence of a virus observed in a section of one of them was thought to be indicative of past infection.

Dr White’s post-mortem report noted the observations of a consultant paediatric cardiologist. During B’s stay in the Intensive Care Unit, ECG examinations showed prolonged QT intervals. The cardiologist advised that it was strongly believed that prolongation of the QT interval was secondary to neurological status post cardiac injury. Molecular genetic analysis had failed to detect any pathogenic variant of Long QT Syndrome in B, which significantly reduced the chance that the symptoms were attributable to mutation in those genes. That comment has to be considered in the light of subsequent genetic analysis, to which I shall return below. Cardiac post-mortem examination by Dr Ashworth, consultant paediatric pathologist, confirmed that B’s heart was structurally normal. There was some haemorrhagic necrosis of the apex intra-ventricular septum and the papillary muscles of the mitral valve. These changes were considered to be secondary to the collapse. There was no histological evidence of myocarditis.

Extensive further pathological examination revealed no other factors which might be linked to his death. Dr White was expressly asked by the police to consider the possibility that B may have been smothered by some soft material. He was unable to exclude the possibility, but added that there were no pathological findings to provide confirmation. Dr White therefore gave the cause of death as “unascertained.”

The police and Social Services had been involved at an early stage after B’s admission on 1^st April. The police started a very extensive investigation. The mother was interviewed on 5^th April in the presence of her solicitor and an appropriate adult. On the advice of her solicitor, which is recorded on the transcript, she replied, “No comment,” to most of the questions asked.

On the same day, the local authority applied for and were granted an emergency protection order in respect of A, and on 7^th April, they started these care proceedings. A was placed under an interim care order in foster care where she remains to this day.

The fact that two children had died attracted considerable publicity and an application was made for a reporting restriction order. That application was the subject of a series of hearings, culminating in the hearing before me in which I made an order for the reasons set out in a judgment, now reported as Re A, Reporting Restriction Order [2011] EWHC 1764 (Fam). It is unnecessary to refer to the issues arising on that application in this judgment.

Prior to that injunction application, it had been determined in any event that the case should be transferred to the High Court and it was listed before me for a fact-finding hearing, initially in February 2012, but then adjourned to facilitate the obtaining of further expert evidence. Ultimately the hearing took place over 13 days between 28^th May and 22^nd June 2012.

The issues for the court to determine can be summarised very simply. (1) To what extent did the mother neglect the children? (2) Have the local authority proved, on the balance of probabilities, that the mother was responsible for the deaths of J and B? The latter issue is manifestly the more serious, but it is appropriate to consider the question of neglect first, to provide a context for considering the deaths of the boys.

A very substantial volume of paper was filed in these proceedings. The bulk of it was produced by the police, whose investigation into the deaths of the boys is ongoing. I am grateful to the police for their help and cooperation with these proceedings. At the outset of the hearing, I was asked by the police to permit an officer to sit through the expert evidence. I concluded that it would not be appropriate. These are private proceedings and it is generally inappropriate for persons who are not parties to sit in, save where permitted by statute. I have directed, however, that the police should be supplied with the full notes of the expert evidence taken by junior counsel for the local authority and for the mother, and I shall permit disclosure of the transcript of this judgment. I will consider further requests for disclosure made hereafter. Indeed, I have received an application in the last few days for disclosure of the record of the experts’ telephone conference and any schedule of agreement or disagreement drawn up by the experts. I do not anticipate any opposition to that application, but I shall consider it at the conclusion of this hearing.

In addition to the police disclosure, the documents put before me included statements by the parties and other witnesses taken for the purposes of these proceedings, medical records of the three children and the mother, including hospital records, local authority material and experts’ reports. The issues arising concerning the boys’ deaths raised a series of complex points of medical science, and a number of experts were therefore instructed, as I shall describe below.

Finally, I received detailed preparatory written material from counsel. I would like to thank counsel for their assistance in this very difficult case and in particular, if I may, to the two teams for the principal protagonists, Miss Lucinda Davis and Miss Eleanor Dewhurst on behalf of the local authority and Miss Frances Judd QC and Miss Margaret Pine-Coffin on behalf of the mother. Those two parties played the principal roles in these proceedings and I am exceedingly grateful to all counsel acting for the mother and the local authority. The father, DA and the guardian were also represented by counsel, who took a lesser role in these proceedings, but I am nonetheless grateful to them for their assistance. I record that DA attended for most of the hearing, save when overcome by understandable distress. The father, on the other hand, took no part in the case. I would also like to acknowledge, if I may, the professionalism with which solicitors carried out their duties and if I may in particular single out Mr Barker on behalf of the local authority, who has shouldered a very considerable burden for managing the documentation in this case.

Over the course of the hearing, no fewer than 32 witnesses gave oral evidence. At the conclusion, the mother and the local authority and the guardian delivered their final submissions. In the following analysis, I shall summarise parts of the evidence, but inevitably, after a hearing of that length, it will not be possible or appropriate to refer to all matters. I have, however, considered all the evidence carefully, together with all the written submissions put forward on behalf of the parties.

The law to be applied in care proceedings concerning allegations of child abuse is well-established, but, as Miss Judd observed on behalf of the mother, a number of the relevant principles are particularly important in this case. I therefore propose to set them out in rather more detail than is customary.

Under section 31(2) of the Children Act 1989

“A court may only make a care order or a supervision if it is satisfied, (a) that the child concerned is suffering or is likely to suffer significant harm, and (b) that the harm or likelihood of harm is attributable to, (1) the care given to the child or likely to be given to him if the order were not made, not being what it would be reasonable to expect a parent to give to him or (2) the child has been beyond parental control.”

In these proceedings, the local authority asserts that A has suffered and is likely to suffer significant harm. How is the court to be satisfied of this? As Baroness Hale of Richmond observed in Re B [2008] UKHL 35,

“The likelihood of harm is a prediction from existing facts or from a multitude of such facts about what had happened in the past, about the characters and personalities of the people involved and things which they have said and done.”

The burden of proof lies with the local authority. It is the local authority that brings these proceedings and identifies the findings that they invite the court to make. Therefore, the burden of proving the allegations rests with them and to that extent the fact-finding component of care proceedings remains essentially adversarial. Although the court has an important discretion as to the ambit of the enquiry and, in the era of greater judicial case management, is under a greater obligation to ensure that only the relevant issues are litigated, that does not alter the basic principle that the burden of proof rests with the local authority.

Secondly, as conclusively established by the House of Lords in Re B, the standard of proof is the balance of probabilities. If the local authority proves on the balance of probabilities that the mother killed J and/or B, this court will treat that fact as established and all future decisions concerning A’s future will be based on that finding. Equally, if the local authority fails to prove that J and/or B were killed by their mother, this court will disregard the allegation completely. As Lord Hoffman observed in Re B,

“If a legal rule requires the facts to be proved … a judge must decide whether or not it happened. There is no room for a finding that it might have happened; the law operates a binary system in which the only values are nought and one.”

Baroness Hale of Richmond expressed the principle thus, at paragraph 32 :

“In our legal system, if a judge finds it more likely than not that something did take place, then it is treated as having taken place. If he finds it more likely than not that it did not take place, then it is treated as not having taken place. He is not allowed to sit on the fence. He has to find for one side or the other. Sometimes the burden of proof will come to his rescue. The party with the burden of showing that something took place will not have satisfied him that it did, but generally speaking, a judge is able to make up his mind where the truth lies without needing to rely on the burden of proof.”

The rationale for requiring assessments of the likelihood of harm and consequent decisions about the future of a child to be based on facts proved to the requisite standard was explained by Baroness Hale at paragraph 59.

“To allow the courts to make decisions about the allocation of parental responsibility for children on the basis of unproven allegations and unsubstantiated suspicions would be to deny them their essential role in protecting both children and their families from the intervention of the State, however well-intentioned that intervention may be. It is to confuse the role of a local authority in assessing and managing risk, in planning for the child and in deciding what action to initiate with the role of the court in deciding where the truth lies and what the legal consequences should be. I do not underestimate the difficulty in deciding where the truth lies, but that is what courts are for.”

Thirdly, in assessing whether or not a fact is proved to have been more probable than not,

“Common-sense, not law, requires that in deciding this question, regard should be had to whatever extent is appropriate to inherent probabilities,” (per Lord Hoffman in Re B at paragraph 15).

Finally, findings of fact in these cases must be based on evidence. The court must be careful to avoid speculation, particularly in situations where there is a gap in the evidence. As Lord Justice Munby observed in Re A (A Child) (Fact-finding Hearing: Speculation) [2011] EWCA Civ. 12,

“It is an elementary proposition that findings of fact must be based on evidence, including inferences that can be properly drawn from the evidence and not on suspicion or speculation.”

When considering cases of suspected child abuse, the court “invariably surveys a wide canvas,” per Dame Elizabeth Butler-Sloss, P, in Re U, Re B (Serious Injury: Standard of Proof) [2004] EWCA Civ. 567, and must take into account all the evidence and furthermore consider each piece of evidence in the context of all the other evidence. As Dame Elizabeth observed in Re T [2004] EWCA Civ.558,

“Evidence cannot be evaluated and assessed in separate compartments. A judge in these difficult cases must have regard to the relevance of each piece of evidence to other evidence and exercise an overview of the totality of the evidence in order to come to the conclusion of whether the case put forward by the local authority has been made out to the appropriate standard of proof.”

It is particularly important to bear in mind the point just made above where, as is invariably the case in cases of suspected physical abuse, the evidence adduced includes the opinion of the medical experts. As Ryder J observed in A County Council v A Mother and others [2005] EWHC Fam. 31,

“A factual decision must be based on all available materials, i.e. be judged in context and not just upon medical or scientific materials, no matter how cogent they may in isolation seem to be.”

Whilst appropriate attention must be paid to the opinion of the medical experts, their opinions need to be considered in the context of all the circumstances. In A County Council v K D & L [2005] EWHC 144 (Fam) at paragraphs 39 and 44, Charles J observed,

“It is important to remember (1) that the roles of the court and the expert are distinct and (2) it is the court that is in the position to weigh up the expert evidence against its findings on the other evidence. The judge must always remember that he or she is the person who makes the final decision.”

Later in the same judgment, Charles J added at paragraph 49,

“In a case where the medical evidence is to the effect that the likely cause is non-accidental and thus  human agency, a court can reach a finding on the totality of the evidence either (a) that on the balance of probability an injury has a natural cause, or is not a non-accidental injury, or (b) that a local authority has not established the existence of the threshold to the civil standard of proof … The other side of the coin is that in a case where the medical evidence is that there is nothing diagnostic of a non-accidental injury or human agency and the clinical observations of the child, although consistent with non-accidental injury or human agency, are the type asserted is more usually associated with accidental injury or infection, a court can reach a finding on the totality of the evidence that, on the balance of probability there has been a non-accidental injury or human agency as asserted and the threshold is established.”

In assessing the expert evidence, I bear in mind that cases involving an allegation of smothering involve a multi-disciplinary analysis of the medical information conducted by a group of specialists, each bringing their own expertise to bear on the problem. The court must be careful to ensure that each expert keeps within the bounds of their own expertise and defers where appropriate to the expertise of others (see the observations of Mrs Justice Eleanor King in Re S [2009] EWHC 2115 (Fam).

On behalf of the mother, Miss Judd and Miss Pine-Coffin invite me to bear in mind the decision of the Court of Appeal in the criminal case of R v Cannings [2004] EWCA 1 Crim. In that case a mother had been convicted of the murder of her two children who had simply stopped breathing. The mother’s two other children had experienced apparent life-threatening events taking a similar form. The Court of Appeal Criminal Division quashed the convictions. There was no evidence other than repeated incidents of breathing having ceased. There was serious disagreement between experts as to the cause of death. There was fresh evidence as to hereditary factors pointing to a possible genetic cause. In those circumstances, the Court of Appeal held that it could not be said that a natural cause could be excluded as a reasonable possible explanation.

The impact of the Cannings decision on care proceedings was considered by the Court of Appeal in Re U, Re B, supra. Dame Elizabeth Butler-Sloss P identified the following considerations arising from the Cannings decision as being of direct application in care proceedings:

“(1)

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

Usually, it is unnecessary for the Family Court to go further into the analysis by the Court of Appeal in Cannings, but in this case Miss Judd invites the court to have regard to the whole of that decision. I remind myself that it was a criminal case involving the deaths of infants under the age of six months, whereas these are family proceedings involving the deaths of two children aged two and four. Nevertheless, I find the analysis by the Court of Appeal of what Judge LJ, as he then was, described as two critical problems, as relevant to the current case.

First, I note the paragraphs specifically cited by Miss Judd, in particular paragraphs 10 to 13 of the judgment in Cannings, which amplify point 2 in Butler-Sloss P’s summary in Re U, Re Bcited above.

“(10)

It would probably be helpful at the outset to encapsulate different possible approaches to cases where three infant deaths have occurred in the same family, each apparently unexplained and for each of which there is no evidence extraneous to the expert evidence that harm was or must have been inflicted, for example, indications of or admissions of violence or a pattern of ill-treatment. Nowadays such events in the same family are rare, very rare. One approach is to examine each death to see whether it is possible to identify one or other of the known natural causes of infant death. If this cannot be done, the rarity of such incidents in the same family is thought to raise a very powerful inference that the deaths must have resulted from deliberate harm. The alternative approach is to start with the same fact, that three unexplained deaths in the same family are indeed rare, but thereafter to proceed on the basis that if there is nothing to explain them, in our current state of knowledge at any rate, they remain unexplained and still, despite the known fact that some parents do smother their infant children, possible natural deaths.

(11)

It would immediately be apparent that much depends on the starting point which is adopted. The first approach is, putting it colloquially, that lightning does not strike three times in the same place. If so, the route to a finding of guilt is wide open. Almost any other piece of evidence can reasonably be interpreted to fit this conclusion. For example, if a mother who has lost three babies behaved or responded oddly or strangely or not in accordance with some theoretically “normal” way of behaving when faced with such a disaster, her behaviour might be thought to confirm the conclusion that lightning could not indeed have struck three times. If, however, the deaths were natural, virtually everything done by the mother on discovering such shattering and repeated disasters would be readily understandable as personal manifestations of profound natural shock and grief.”

Later at (13):

“Reverting to the two possible approaches to the problems posed in a case like this, in a criminal prosecution we have no doubt that what we have described as the second approach is correct. Whether there are one, two or even three deaths, the exclusion of currently known natural causes of infant death does not establish that the death or deaths resulted from the deliberate infliction of harm. That represents not only the legal principle, which must be applied in any event, but, in addition, as we shall see, at the very least, it appears to us to coincide with the views of a reputable body of expert medical opinion.”

Secondly, in considering the Cannings judgment, I note the observations of Judge LJ at paragraph 22, which amplifies point 5 in Butler-Sloss P’s summary in Re U, Re B cited above.

“We have read bundles of reports from numerous experts of great distinction in this field, together with transcripts of their evidence. If we have derived an overwhelming and abiding impression from studying this material, it is that a great deal about death in infancy, and its causes, remains as yet unknown and undiscovered. That impression is confirmed by counsel on both sides. Much work by dedicated men and women is devoted to this problem. No doubt one urgent objective is to reduce to an irreducible minimum the tragic waste of life and consequent life-scarring grief suffered by parents. In the process however much will also be learned about those deaths which are not natural, and are indeed the consequence of harmful parental activity. We cannot avoid the thought that some of the honest views expressed with reasonable confidence in the present case (on both sides of the argument) will have to be revised in years to come, when the fruits of continuing medical research, both here and internationally, become available. What may be unexplained today may be perfectly well understood tomorrow. Until then, any tendency to dogmatise should be met with an answering challenge.”

With regard to this latter point, recent case law has emphasised the importance of taking into account, to the extent that it is appropriate in any case, the possibility of the unknown cause. The possibility was articulated by Moses LJ in R v Henderson-Butler and Oyediran [2010] EWCA Crim. 126 at paragraph 1:

“Where the prosecution is able, by advancing an array of experts, to identify a non-accidental injury and the defence can identify no alternative cause, it is tempting to conclude that the prosecution has proved its case. Such a temptation must be resisted. In this, as in so many fields of medicine, the evidence may be insufficient to exclude, beyond reasonable doubt, an unknown cause. As Canningsteaches, even where, on examination of all the evidence, every possible known cause has been excluded, the cause may still remain unknown.”

In Re R, Care Proceedings Causation [2011] EWHC 1715 (Fam), Hedley J, who had been part of the constitution of the Court of Appeal in the Henderson case, developed this point further. At paragraph 10, he observed,

“A temptation there described is ever present in Family proceedings too and, in my judgment, should be as firmly resisted there as the courts are required to resist it in criminal law. In other words, there has to be factored into every case which concerns a discrete aetiology giving rise to significant harm, a consideration as to whether the cause is unknown. That affects neither the burden nor the standard of proof. It is simply a factor to be taken into account in deciding whether the causation advanced by the one shouldering the burden

of proof is established on the balance of probabilities.”

Later in the judgment, at paragraph 19, Hedley J added this observation:

“In my judgment a conclusion of unknown aetiology in respect of an infant represents neither professional nor forensic failure. It simply recognises that we still have much to learn and it also recognises that it is dangerous and wrong to infer non-accidental injury, merely from the absence of any other understood mechanism. Maybe it simply represents a general acknowledgment that we are fearfully and wonderfully made.”

The local authority alleges that the mother is culpable of serious and repeated acts of neglect of her children and has set out this allegation in the schedule of findings filed in these proceedings. In their response on behalf of their client, the mother’s representatives have very substantially accepted the allegations. Some issues, however, remained and they have formed part of the hearing before me.

Having considered the evidence, written and oral, I make the following findings on this aspect of the case:

There is a further allegation which concerns the father of the two younger children, GM. The mother reported that she had seen him poke J’s genitals with his finger. Despite her concern about this alleged behaviour, the mother continued to allow GM contact with the children. She states that she found it difficult to say no to him and still had feelings for him. The father has played no part in these proceedings. There has been no oral evidence about this matter and I am not in a position to make a finding about whether he did behave in a sexually inappropriate way towards J. I find however that the mother, knowing of the allegation that the father had behaved in that way, failed to protect J from further contact with him.

Taken together, these findings about the mother’s treatment amount to serious and chronic neglect at a time when she was receiving considerable support through Social Services, as well as from her own mother, DA, and from friends and neighbours. Miss Davis and Miss Dewhurst, on behalf of the local authority, have rightly taken the view that it would be disproportionate to conduct an enquiry into each and every allegation about which there is documentary evidence that the mother was unable to cope, but I have heard enough to reach a clear conclusion. I conclude that this mother was simply unable to cope with the demands for caring for her children.

I turn to consider the evidence about the deaths of the two boys.

A number of experts have been asked to advise as to the interpretation of the medical and pathological evidence in this case. I have already referred to Dr Fowler and Dr White, consultant pathologists, who conducted the post-mortem examinations on respectively J and B. Both gave oral evidence before me. Dr Patricia Kenny, consultant paediatrician, was instructed to prepare a report by the police in order to prepare supplementary reports for these proceedings and give oral evidence. In addition I had the benefit of the opinion of Dr Cartlidge, consultant paediatrician and senior lecturer in child health, instructed to give a paediatric overview as to the cause of the boys’ deaths, Dr Robin Martin, a consultant paediatric cardiologist and adult congenital heart disease cardiologist based at the Bristol Royal Hospital for Children and the Bristol Heart Institute, Professor Nigel Klein, Professor in Infectious Diseases and Immunology at the Institute of Child Health and honorary consultant paediatrician at Great Ormond Street Hospital, Professor J B Leonard, formerly Professor of Paediatric Metabolic Disease at the Institute of Child Health in London and honorary consultant paediatrician at Great Ormond Street Hospital, and Dr Newbury-Ecob, a consultant geneticist and honorary reader at the University of Bristol, who was asked to advise as to the likelihood of genetic conditions playing any part in the deaths of either J or B. Of these five, only Drs Cartlidge, Martin and Newbury-Ecob were asked to attend to give oral evidence.

The expert evidence in this case has focused on a number of issues which I shall consider by reference to the following questions:

In the case of J, Dr Cartlidge thought it unlikely that an infection would cause a healthy child to die so suddenly. The only possibility was myocarditis, that is to say inflammation of the heart muscle. Whilst he thought it unlikely that J was suffering from this condition, he advised seeking the opinion of a specialist in infectious diseases and as a result Professor Klein was instructed.

Professor. Klein noted the history of hospital admissions on 1^st January and 3^rd January and in particular the diagnosis of chicken pox following the latter admission. J was found to test positive for the chicken pox virus, varicella zoster, in blood tests taken on 3^rd January and again shortly after death on 6^th January. Professor Klein commented that in general chicken pox is a benign condition, but can prove fatal in certain circumstances. He noted that viruses are relatively common causes of myocarditis and observed that myocarditis has been reported as “an extremely rare complication of chicken pox.” In this case, however, Professor Klein was unable to find any clinical or pathological evidence of myocarditis and he found no other evidence to indicate that a virus was responsible for J’s death. Professor Klein concluded that although J was suffering from varicella chicken pox when he died, he died with the infection and not because of it. He concluded that there was no evidence to indicate that any other virus or bacteria were responsible for J’s death.

There was, in Professor Klein’s view, also no evidence that any infection or infection-related process had contributed to B’s death. Dr Cartlidge noted there was no evidence that B was suffering from an overwhelming infection of the sort which might have been fatal. B was known to have been happy and playful at the time that he left his nursery at 3.30 on the day of his hospital admission, 1^st April. Neither his grandmother, DA, nor his mother had raised any concerns about B’s health that evening. On arrival at hospital, B’s white cell count, including his neutrophil count, was normal. Likewise his seroractive protein concentration was normal on the night of the admission to hospital. The post-mortem revealed no histological evidence of myocarditis and there was no evidence that B was suffering from this condition. Thus all the chemical markers for infection were normal in B’s case. Dr Cartlidge was unable to exclude the possibility that B had a minor infection at the time of his death, although the medical evidence indicated the absence of any serious infection. Dr Cartlidge is unaware of any infection that can cause a healthy child to die so suddenly.

Dr Cartlidge thought it unlikely that any inborn error of metabolism could have caused the collapse of these children but advised seeking the opinion of a specialist and as a result Professor Leonard was instructed. He reported that metabolic disorders, sufficiently severe to cause some unexpected deaths, do not manifest without prior illness. It would, said Professor Leonard, be most unusual to have two patients with the same metabolic disorder in the same family die without obvious symptoms. He noted that the mother’s general health is fine except for congenital hypothyroidism. Professor Leonard advised that a link has been established between sudden deaths and congenital hypothyroidism. In this case, however, the three children had all been screened for this disorder at birth and those tests revealed that they did not suffer from this condition. As the mother is otherwise healthy, Professor Leonard considered it unlikely that two of her children would suffer a dominant metabolic disorder. Similarly, as B and J had different fathers who were unrelated, recessive disorders can also be excluded.

Taken overall, as the mother is well and the children have different fathers, the likelihood of a genetic metabolic disorder is low. Professor Leonard observed that both B and J were healthy, growing and developing within normal limits. Neither child had any significant illness before the terminal event. No biochemical findings were apparent that could not be explained by the cardiac arrest. No relevant abnormalities were found at post-mortem. Professor Leonard therefore concluded that there was no evidence, either clinical or genetic, pathological or biochemical to suggest that B and J had inborn error of metabolism to account for their sudden fatal illness.

The expert evidence on the cardiac and genetic aspects of this case are particularly complex and, to a considerable extent, interrelated. A cardiologist, Dr Martin, was instructed at an early stage in the proceedings, but advised that an opinion should be sought from a specialist in genetics and as a result, Dr Newbury-Ecob was instructed, albeit at the cost of postponing the hearing. I shall consider their evidence in the following: first, cardiac disorders in general, then the diagnosis of Long QT Syndrome, generally, third the clinical diagnosis of LQTS in B’s case, then genetic abnormalities generally, then genetic factors in LQTS, then genetic diagnosis of LQTS in this case, and finally conclusions on cardiac and genetic factors.

In his report, Dr Martin states that unexpected deaths in children can have many causes. He advised that cardiac causes of death can be divided into three groups: (1) underlying structural heart disease, (2) inflammatory or genetically-determined disorders affecting the heart muscles such as myocarditis or cardiomyopathy and (3) heart rhythm disorders, in particular what are termed channelopathies – inherited conditions that render the individual susceptible to fatal ventricular rhythm disturbance. Channelopathies include a group of conditions called Long QT Syndrome, (hereafter “LQTS”), and a rare group of conditions calledCatecholaminergic Polymorphic Ventricular Tachycardia, (“CPVT”). In this case, post-mortem examination of J and B excluded the presence of underlying structural heart disease and myocardial histology did not show any evidence of heart muscle inflammation or cardiomyopathy. With both children, therefore, this only leaves the channelopathies as a potential cardiac cause for their deaths.

Dr Martin gave some background information about channelopathies. LQTS and CPVT are conditions related to mutations of genes that control the passage of ions across the membranes of the heart muscle cells. The largest study so far would predict that 5 to 10 per cent of Sudden Infant Death Syndrome cases have an alteration of one of the LQTS genes that may either result in death due to ventricular arrhythmias, or may represent a predisposing factor that may be lethal in combination with other risk factors, such as hypoxia or overheating. Dr Martin reminded the court that neither J nor B was an infant, but sudden death from LQTS and CPVT can also occur in older children.

As Dr Martin explained during his oral evidence, in cardiac arrest there are two main rhythm changes. In the first, called asystole, there is no electrical activity; the pumping action of the heart stops and the ECG shows a flat-line. In the second, the heart goes into a disorganised rhythm, known as ventricular fibrillation or ventricular tachycardia. The heart becomes uncoordinated and does not work as a pump. Each portion of the heart is trying to contract at different times, so it stops pumping blood. Most heart conditions, including LQTS, would normally present with disorganised rhythm associated with heart muscle problems. Asystole is an arrest of rhythm commonly recognised in other causes, rather than in LQTS, and is much more likely to be due to respiratory cause or hypoxia. Dr Martin agreed with Miss Judd, however, that a cardiac arrest, unless treated, “all ends up in asystole.” In such circumstances, he agreed that one may not know if someone who presented with a heart that had stopped beating altogether had experienced an arrest which started with a disorganised rhythm.

LQTS is so called because it is marked by the lengthening of what is called the QT interval on the ECG, although not all long QT intervals are caused by LQTS. A long QT interval is thus a pointer to LQTS, but not diagnostic of it. The diagnosis of LQTS is dependent on a number of factors: (1) the ECG findings, (2) the history of circumstances of the death and/or previous history of any unexplained blackouts or faints, (3) family history and (4) DNA analysis. Dr. Martin stated that excluding a cardiac cause of sudden unexplained death can be difficult and the likelihood of a channelopathy being the cause of death would be estimated from careful review of the four areas cited above, coupled with an assessment of the alternative causes. Often, a diagnosis of LQTS can be made on the basis of the ECG findings alone, but death is the first sign of LQTS in an estimated 10 to 15 per cent of cases and where an ECG has not been obtained prior to death, a diagnosis has to be based on other findings, including genetic findings, if available. The circumstances of the death may also be important. Dr Martin observed that death during sleep has been recognised as occurring with some types of LQTS. He also stated, with regard to the ECG findings, it is important to realise that at least 10 to 15 per cent of people with LQTS may have a normal ECG.

Prior to the development of genetic testing, various diagnostic criteria for LQTS were developed, one of which was helpfully set out by Dr Martin in a table in his report. Measurement of the QT interval on the ECG is a crucial part of these diagnostic criteria. This interval is typically measured in leads 1 and B6 and then corrected for heart rate using a formula known as Bazett’s formula. The interval is the time measured from the start of the Q wave to the end of the T wave on the ECG and can be expressed in seconds or milliseconds. Relevant normal values after correction for the interval are as follows: for children and adolescents, over 460 milliseconds equals a prolonged QT interval; 440 to 460 equals borderline prolongation. For women, in excess of 460 milliseconds equals a prolonged QT interval and between 450 and 460 milliseconds equals a borderline interval. Dr Martin explained that the criteria are applied by allocating a particular score to certain factors, thus a corrected QT in excess of 480 milliseconds in children scores three points, a corrected QT of between 460 and 469 scores two points, etcetera. Where family history definitively identifies a member of the family as having LQTS, a score of one point is added. Where a member of the immediate family had died under the age of 30 from an unexplained sudden cardiac death, a score of 0.5 is added. There are a number of other factors for which scores are added, but none are relevant to this case. A strict application of these criteria leads to a diagnosis of LQTS if there is a score of more than three. Dr Martin stated that whilst it is not a precise diagnostic tool, a patient who scores over three is usually made the subject of a diagnosis. However, Dr Martin stressed that this is not a firm rule and it is necessary to consider the whole clinical picture.

B underwent a number of ECG examinations after his admission to hospital on 1^st April. On analysing the first ECG, taken at 14.34 on 2^nd April, Dr. Martin observed that the QT interval in leads 1 and B6 was 440 milliseconds and the corrected QT interval, using Bazett’s formula, was 610 in lead 1 and 604 in lead B6. The T-wave morphology was abnormal with notching in leads B4, B5 and B6. The next ECG produced for Dr Martin was curiously unnamed, but appeared similar to the other, correctly named ECGs within B’s medical records. It was taken at 21.47 on 3^rd April; that is to say some 30 hours after the initial ECG and showed signs of a bradycardia with a heart rate of 69 beats per minute. There are various other abnormalities considered by Dr Martin to be consistent with ischemia. The QT interval was 460 in lead 1 and 480 in B6, with corrected QT of 493 and 515 respectively. Similar appearances were noted on a number of subsequent ECGs taken prior to B’s death.

Following B’s admission to hospital, A was subjected to ECG analysis which revealed no abnormality. In addition, an ECG analysis was carried out on the mother on 3^rd April. In her case there was a borderline prolongation of the QT interval, but Dr Martin noted that at the time the mother was taking an antidepressant and a tranquiliser that had both been associated with some prolongation of the QT interval in some individuals, particularly in over-dosage.

B’s corrected QT interval of over 500 would have scored three points using the diagnostic criteria set out above. In addition, again on the basis of those criteria, Dr Martin agreed with me that the death of J meant that a score of 0.5 should be added to B’s score. The mother’s borderline QT interval fell just short of the level which would have added a further point to B’s score on these criteria. Applying the criteria strictly, therefore, B exceeded the level at which a definite diagnosis of LQTS would be made. Dr Martin stated, however, that one has to look at the whole clinical picture. The ECG changes in B were not specific to LQTS. A long QT interval is not diagnostic of LQTS. Other explanations might account for the long interval, for example, hypoxia or neurological damage. Dr Martin observed that, in the case of someone who has had a cardiac arrest, one has to be very wary of making a diagnosis, unless the changes seen have been established as being persistent.

In his report, Dr Martin, noted that in the multiple ECGs following B’s cardiac arrest, there was evidence not only of significant QT prolongation, but also of ischaemic-looking ST and T-wave changes. In the opinion of the treating physicians at the time, the QT prolongation, consistent with the CT changes, were thought to be likely to be attributable to ischemia from the cardiac arrest and the severe neurological injury that was sustained. Dr Martin commented that it is indeed recognised that hypoxia and ischemia can cause all these ECG findings and in particular that neurological injury can cause QT prolongation. Thus, on the balance of probabilities, Dr Martin concluded that the ECG changes in B are “most likely to be secondary to the cardiac arrest and the severe neurological injury.”

In the experts’ telephone conference, Dr Martin described the long QT interval in B’s case as “quite severe” and said that the changes observed were “more extensive than you usually see.” He reiterated that he attributed these changes to the neurological damage in cardiac arrest, but added that it was unusual and outwith his normal experience, pointing out that he did not get asked to see ECGs on patients in such circumstances. He noted that B had effectively died and been resuscitated again and that this was “a fairly extreme example of resuscitation and there is not much information on this point.” In answer to Miss Judd, he confirmed that the interpretation of the long QT interval as attributable to a combination of ischemia and neurological damage was something he had gleaned from the literature, since he did not usually see children with neurological damage in his practice.

Dr Martin then considered the medical history of the boys. J suffered from a chicken pox infection at the time of his death and Dr Martin remarks that fever can sometimes be associated with sudden death in individuals with LQTS. He noted that they were both found collapsed during sleep. Death during sleep has been described sometimes as occurring in cases of LQTS, although Dr. Martin said that it is rare to find children dying at this age. He observed that both cardiac arrests were asystolic arrests, that is to say the heart stopped beating completely; as stated above, in channelopathy the cardiac arrest is usually associated with the irregular rhythm disturbances – ventricular tachycardia or ventricular fibrillation. As mentioned above, however, Dr Martin agreed with Miss Judd that every cardiac arrest, unless treated, ends up in asystole, and he agreed that one may not know whether someone who presents with a heart that has stopped beating altogether had experienced an arrest which started with a disorganised rhythm. He agreed that it was not possible to say how the cardiac problems in J or B had started. It depended on how long the effective pumping of the heart stopped. The longer you go from effective beating, the more likely it was to end up in a flat-line. In J’s case, he had apparently been dead for some time before the paramedics arrived. Thus it was possible that the asystole had been preceded by a spell of irregular rhythm disturbances. In B’s case, on the other hand, this seemed less likely, given that it was possible for his heart to be revived. He accepted, however, that it was not known how long B’s heart had stopped beating and it was conceivable that he could have had a cardiac condition 30 minutes before he was discovered by the first responder.

Turning to the family history, and specifically that of the mother, Dr Martin concluded that the borderline QT prolongation on her ECG may be a normal finding or it could relate to her medication. He added that “whilst the ECG findings seen in the report are in the normal population and are certainly not diagnostic of LQTS, it is not possible to exclude the diagnosis.” Overall, however, he concluded that there was no clear evidence of heart disease in the immediate family. He was asked about the medical histories of some distant relations of the mother. Her great-grandfather is said to have died of a heart attack at the age of 30. On her father’s side, there was a cot death of a cousin. Dr Martin observed that he suspected that if one looks at most families, one would find family members this removed where this sort of incident had occurred. Whilst one can never rule out the possibility that these events might have some bearing on the diagnosis of the boys’ condition, Dr. Martin commented that “the further you get away from the individual, the less likely it is to be relevant.”

At this point, it is necessary to consider the question of genetic analysis. In answer to Miss Judd, Dr. Martin acknowledged that, when analysing the family history, it had to be remembered that, at any one point, one might have a gene mutation but no symptoms. Furthermore, it was possible that symptoms might be expressed later in childhood or in adulthood. It was possible, furthermore, for the presentation of symptoms to skip a generation and it was possible that one might not see symptoms in more than one generation, notwithstanding that all have the gene. Thus before reaching any conclusion on whether the children suffered from a heart abnormality, I turn to consider the evidence of the expert geneticist.

Before considering Dr Newbury-Ecob’s opinion and evidence, it is helpful to summarise the types of genetic inheritance, drawing largely from the helpful passage in Professor Leonard’s report. Inherent diseases are defects in the genes and the diseases they cause are inherited in four different ways.

Understanding of the human genome has increased enormously over the past 20 years. It is still increasing and there is still much to be learned. In cross-examination by Miss Davis, Dr Newbury-Ecob observed that genetic analysis was an art rather than a science. It is, she said, a common misconception about genetics that it is black and white. On the contrary it is very much an art based on the assessment of a number of different factors. The process of making a diagnosis of a genetic condition involves a number of factors, both clinical and molecular. The absence of information from a genetic testing does not exclude a genetic condition. With the advent of genetic testing, possibilities for diagnoses increase and the number of undiagnosed patients is going down, although as Dr Newbury-Ecob observed in cross-examination by Miss Judd, there are still a number of genetic conditions that doctors are not yet able to diagnose. As yet, however, genetic testing is not sufficiently reliable to establish conclusively that a genetic condition has been excluded. Furthermore, and of relevance to this case, there is a paucity of information about LQTS in children of this age. In answer to a question from Miss Judd, Dr Newbury-Ecob accepted that very few children were tested genetically at this age, because this is not the age at which death from LQTS normally occurs.

LQTS is a genetic disorder caused by a number of different genes. There are a wide number of possible variants in a gene at any given point on the gene. To date, twelve different genes have been identified as positively affected in LQTS. In answer to Miss Judd, Dr Newbury-Ecob said that ten years ago there were about four genes that had been so identified, but more had been discovered and it is likely that there are more, as yet unidentified. Of the twelve that have been identified to date, five are the most common and responsible, it is believed, for 95 per cent of the cases of LQTS. One of these genes is known as KCNH2. In her report, Dr Newbury-Ecob observed that post-mortem molecular analysis in cases of Sudden Infant Death Syndrome had detected mutations or variants in long QT terms in 8 to 12 per cent of cases. In particular, the KCNH2 gene variants have been identified in patients in cases of Sudden Infant Death Syndrome. In such cases the variant leads to heart arrhythmias, triggered, dependent on the gene and variant involved, by a number of factors, such as arousal, noise, emotion, exercise or sleep.

On the other hand, 54 per cent of individuals with a long QT genotype remain asymptomatic. Not all variants have significant functional consequences. The laboratory can now look at the type of sequence change and predict how likely it is to affect the way in which the gene works. Geneticists use the term “pathogenic”, for a variant that will clearly affect function, and “non-pathogenic where the relationship is not established”. In the case of a pathogenic mutation, the abnormal gene product affects the normal potassium channel delaying repolarisation of the heart ventricle and leading to the changes in the QT intervals seen on the ECG. Identifying a variant does not by itself lead to a conclusive diagnosis of LQTS. Dr Newbury-Ecob said that in order to establish the genetic cause of LQTS in any particular case, it is necessary to identify first if there is a variant of any of the genes associated with LQTS and secondly, whether that variant is pathogenic, i.e. a cause of LQTS. Establishing pathogenicity of a variant or mutation includes wider family studies. If a mutation is said to be segregating with a disease phenotype or history of sudden death, it is considered to be more likely to be pathogenic than if it was found in unaffected family members. Dr Newbury-Ecob emphasised that LQTS is principally a clinical diagnosis. If the clinical signs are borderline, one attaches no significance to the presence of a variant. If the clinical signs are strong, the presence of a pathogenic variant does not add to the strength of diagnosis. The purpose of the testing is not to confirm the diagnosis, but to provide screening for other family members. Dr Newbury-Ecob said that it was difficult to say if this approach led to families with LQTS being missed. In order to answer that question, families would have to be followed over a very long time. Families can be evaluated now, but it may be that the significance of those observations will only become apparent in 20 years. “We do not have robust, long-term, case-controlled studies of these variants.”

Dr Newbury-Ecob stated that she was most comfortable with a diagnosis of LQTS where there was a long QT interval, in the presence of a relevant family history in which multiple members of the family had LQTS, coupled with a mutation that is both associated with LQTS and located at a point on the gene associated with pathogenic consequences.

This is an area of very fast pace of change, because of the rapid development of the genetic technology, such that with every case tested, a new variant found has to be subject to a process of evaluation.

In this case, genetic testing was carried out in a sample of B’s blood on the five genes most commonly associated with LQTS. Four of the genes were entirely normal, but analysis of the KCNH2 gene showed a variant and furthermore a new variant which had never been seen before. Dr Newbury-Ecob observed, however, that a variant in the KCNH2 gene is a relatively common finding. In answer to Miss Davis, she said that about 4 per cent of the population showed some kind of a variant, although it is unknown how many of those are pathogenic. The KCNH2 gene consists of 16 exons spanning 19 kilobases that is to say 19,000 letters of genetic code. Many potentially benign polymorphisms of this gene have been described, as well as many that are pathogenic.

The variant seen in this case is novel and has not been previously reported in either normal controls or cases of LQTS. Dr Newbury-Ecob added, however, that this does not exclude it as a pathogenic mutation. To establish pathogenicity, the laboratory looks, first, to see whether the variant has been described previously in patients with a genetic condition, secondly, how the type of variant is predicted to work, and, thirdly, the location of the variant in relation to the gene function.. Databases have been established around the world which laboratories can examine to assist with this analysis. All these factors will be considered before the laboratory reports if the variant has been functionally significant or not.

In this case, Dr Newbury-Ecob reported that the laboratory prediction of the variant found in B is that it is unlikely to be pathogenic, i.e. a cause of LQTS. If a variant changes the type of amino-acid, it is more likely to be predicted as functionally significant and therefore pathogenic, but the position in this case of the amino-acid sequence change was in the region of the gene with a lower likelihood of being associated with pathogenicity. In addition, Dr Newbury-Ecob said that it is in the regions of genes that are “highly conserved,” that is to say have been present throughout evolution, with which more critical functions and changes tend to be associated. Variants that occur in these conserved regions are more likely to be worrying and pathogenic. The gene in question here does not come in a conserved region. There is therefore no reason to think that this variant would cause LQTS by itself.

The genetic testing carried out on J was much less comprehensive than on B. The laboratory was only required to ascertain whether he had the same variant in the KCNH2 gene identified as in B. It was found that he did not have this variant. This process was possible using DNA protracted from tissue post-mortem. Whilst this is not as useful as testing on fresh blood samples, in this case there was no reason to have any doubt as to the quality of the DNA obtained from J’s tissue. It is relatively straightforward to look for a known change in the family by examining a post-mortem tissue, but very much harder to embark on a full genetic screen if only post-mortem tissue is available. As a result, it is not known whether J had any other genetic variants, merely that he did not have the same variant as found in B.

In cross-examination by Miss Judd, Dr Newbury-Ecob said that about 10 per cent of people with LQTS have a negative finding on genetic testing. The reason for this is that either the type of LQTS is caused by an as yet undiscovered gene or that the technology may have missed disorders in known genes. The pick-up rate in known genes is not 100 per cent. Furthermore, Dr Newbury-Ecob commented in her report that while the KCNH2 variant detected in B may not cause LQTS by itself, the possibility that it may have an effect on the LQ interval leading to a susceptibility or risk of arrhythmias in the presence of other factors, either genetic or environmental, cannot be discounted. It is potentially the case that a variant may be non-pathogenic in certain circumstances, but pathogenic in other circumstances, for example in the presence of other pathogenic variants. That is believed to be the model in many common diseases, such as heart disease and cancer. People inherit variants which may make them vulnerable in the presence of other genetic variants or environmental factors.

In the experts’ telephone conference, Dr Newbury-Ecob stated that the presence of the KCNH2 variant increased B’s vulnerability. It is possible that the changes in the KCNH2 gene, which are known to affect the length of the QT interval, may, in the presence of other factors, genetic or environmental cause, or be associated with LQTS or some other cardiac abnormality. This is the subject of speculation and research, particularly in the context of Sudden Infant Death Syndrome. In her oral evidence,, Dr Newbury-Ecob developed this point. The variant observed in B indicated some sort of susceptibility that could not be identified. Saying that it could not by itself cause LQTS is not saying that this variant had no role in disease or death. There is research evidence that KCNH2 might play a role in some way in the presence of other factors, genetic or environmental. Up to 10 per cent of families where there is more than one variant in LQTS give rise to clinical problems, whereas a single variant, on its own, would not be expected to do so.

From examination of family photographs, Dr Newbury-Ecob noted no features in A, J or B suggesting that there was any underlying genetic syndrome. Photographs of the mother, however, as a young child, revealed some mild dysmorphic features. In addition, the mother suffers from a congenital hypothyroidism and has an IQ in the borderline range. Dr Newbury-Ecob also noted that the mother’s head circumference is on a low centile compared to her weight and height, suggesting that she has relative microcephaly. Dr Newbury-Ecob considered it possible that these four features – dysmorphic facial features, congenital hypothyroidism, relative microcephaly and borderline learning difficulty – are linked genetically. The mother has not however been subjected to any investigation to establish whether or not there is such a link.

Following the production of Dr Newbury-Ecob’s report, Dr Martin confirmed his provisional that it was unlikely that J and B’s deaths were caused by a cardiac condition. “Whilst it is difficult to completely exclude a cardiac cause of death, there is no evidence of an inherited cardiac disorder, and it is more likely that their deaths relate to the non-cardiac causes described by Dr Cartlidge.” In oral evidence, Dr. Martin that, as Dr Newbury-Ecob had found no evidence of a genetic role in the death of either child, “we are back to clinical diagnosis and judgment concerning the nature and cause of the boys’ deaths.” The fact that genetic testing was undertaken and no pathological mutation found made it “a very, very low chance of either chance or either child having LQTS,” although he added that “no test or clinical assessment completely excludes it.” However, in answer to a question from Miss Judd as to how many channelopathies there are, Dr Martin said: “I do not think we know for sure; new ones are being discovered all the time.” He accepted that there are undiagnosed channelopathies, although they are thought to be rare. Although Dr Martin is not a geneticist, I attach some weight to his answer to Miss Davis: “to be fair, there are quite possibly a whole host of genetic conditions we know nothing about,” and his comment to Miss Judd that, “this is very much a developing area …. there is still a lot we do not understand.”

At the end of her report, Dr Newbury-Ecob concluded that there was no evidence from the family assessment of any inherited condition that could explain the deaths of either J or B. In her opinion, the KCNH2 variant in B was very unlikely to be the cause of death. In her oral evidence, Dr Newbury-Ecob agreed that she could not really go any further in saying that there is no evidence of a genetic condition playing any role in the death of this child. These tests carried out did not add to the evidence already available. Dr Newbury-Ecob again reiterated the point in her report that the variant observed in B indicated some sort of susceptibility that could not be identified. Saying that the variant could not by itself cause LQTS is not the same as saying that it had no role in disease or death. She agreed with Miss Judd that whilst KCNH2 is very unlikely to be the cause of B’s death, it might be associated with his death in some unknown way, or alternatively could be an incidental finding in no way related to his death. Dr Newbury-Ecob said she did not feel there was any evidence either way.

Dr Kenny defined petechiae as pinpoint units of bleeding, tiny haemorrhages in the thin walled venules of the circulatory system.

A scattering of petechiae was seen on J’s upper chest on the occasion of his first admission to hospital on 1^st January, although not on either of his subsequent admissions, including the admission on 6^th January when he was discovered lifeless. Examination of B, conducted around midnight on 1^st April following his admission to hospital, showed petechial bruising on the left side of his chest above the nipple and on the left side of his face. The photographs taken of B about two hours later and again at about 7 o'clock in the morning show possibly more widespread petechiae and other marks on his chest and, in particular, in Dr White’s phrase, a “fairly florid” pattern of petechiae on the left side of his face, stretching between his eye socket and crossing his upper cheek to his hairline.

In addition to the marks clearly visible on the left side of the face, the photographs taken on 2^nd April showed faint marks on the right side of his face. Dr. Kenny believed that these too were petechiae. In the course of the hearing, the police disclosed for the first time a full set of photographs taken during the post-mortem examination, in which the marks on both sides of the face are discernible, although those on the left still more pronounced than on the right. Dr White, at post-mortem, had concluded that the marks on the right side of the face were not petechiae. He thought it more likely that they were freckles. Until he gave he gave evidence, he had not had an opportunity to examine the photographs of B taken in the hospital. On close examination of those photographs, he conceded that there may have been some petechiae on the right.. He said that he and his colleagues had examined these marks during the post mortem but “could not convince themselves that they were petechiae.” Having seen the hospital photographs, that remained his view.

There was a considerable amount of evidence given concerning the interpretation of petechiae. Dr Trevelyan, not called as an expert but as a witness of fact who works as a consultant paediatrician in a busy general hospital, said that she saw petechiae quite often in her role as a paediatrician. Dr Kenny, in her report, said that petechiae can arise for medical reasons, in which case they are usually generalised over the whole body. They are seen in infectious diseases in association with inflammation to venules, most commonly in meningococcal septicaemia, but also more specifically in viral infections. J, of course, was suffering from chicken pox in early January 2011. Petechiae can also however be caused mechanically by the application of pressure that restrict the venous return of blood to the heart. In this context they have been associated with asphyxiation and consequently were the subject of much comment by the experts in the course of this hearing.

Before considering the expert evidence on this point in greater detail, it is important to establish, if possible, whether the petechiae seen on B by Dr Macintosh were present when B was admitted to hospital.

On behalf of the mother, Miss Judd points out that the petechiae were not seen by any of the paramedics who attended at DA’s home, nor by any of the hospital staff, doctors and nurses who treated B following his arrival at hospital, nor by Dr Lajeunesse, when he conducted the limited examination of B at about 22.30. Of course, the focus of all medical staff was on saving B’s life. Miss Judd submits, however, that if the marks were present, it is surprising that they were not seen by any of the staff, given the fact that the marks to the left side of the face were comparatively florid and that medical professionals, paramedics and doctors were actively looking for marks or any other signs to assist them in diagnosing his condition.

Asked by Miss Judd how quickly the petechiae would have appeared after any episode of smothering, Dr White observed that if the victim was struggling to breathe, it would be expected that the petechiae would appear relatively quickly. He said that if it was correct that they appeared at hospital, as opposed to shortly after the time of an assault, it would not be possible to attribute the petechiae to any smothering. Dr. Cartlidgeagreed. Cross-examined by Miss Judd, he said that, if the petechiae were not present when Dr Lajeunesse examined B at 10.30 pm at hospital, it was “very unlikely” that the petechiae seen by Dr Macintosh at around midnight were attributable to anything that had occurred to the child prior to 20.15 that evening. He added, however, that if this had been a matter of his clinical responsibility, he would be questioning whether Dr Lajeunesse had missed the petechiae in the course of his examination.

Unlike Dr Cartlidge, I have had an opportunity of hearing Dr Lajeunesse give evidence. I find that his examination of B that evening was more than a cursory glance. He was expressly looking for signs, including petechiae, that might have assisted him in diagnosing what was wrong with B. I also consider it very significant that none of the paramedics, nor indeed any other medical professional. noticed any petechiae until Dr Macintosh’s examination. I agree with Miss Judd that the petechiae are very noticeable from the photographs and that it is very unlikely that they would have been missed. To my mind, this is a strong indicator that they were not present in the early stages of B’s treatment.

By the time of Dr Macintosh’s examination, B had been subjected to the most intensive resuscitation for a prolonged period of time. Might this be the cause of the petechiae that, as I find, appeared at some point after the admission to hospital? Dr Kenny was sceptical as to whether CPR can cause petechiae in children. She had never witnessed it herself and was unaware of reports of post-resuscitation petechiae in the scientific literature. Although Dr White had not seen cases in which petechiae had been sustained as a result of such resuscitation, he was aware that they had been described in the literature, although he acknowledged that this was a matter about which expert opinion was divided. Dr White thought that both the strength with which the resuscitation was administered and the period of time in which it had taken place would contribute to the presence of petechiae.

In closing submissions, Miss Davis makes the point that most, if not all, the resuscitation attempts had been completed by the time Dr Lajeunesse examined B. I acknowledge that point, but considering his evidence as a whole, and in the context of the other evidence, this does not cause me to conclude that he missed the petechiae and does not add weight to the suggestion that they were caused by an attempt at asphyxiation.

In addition, Dr White said in cross-examination by Miss Judd that petechiae could be seen after cardiac arrest, thus he could not exclude the possibility that distribution of petechiae on B’s face were attributable to the cardiac arrest that he had sustained. Dr Cartlidge pointed out that B had been through a period of extreme ischemia and was very acidotic following his admission to hospital. Such a condition would have a profound effect on his organs and it is possible that this ischaemic damage had contributed the appearance of the petechiae.

Furthermore, Dr White thought that in B’s case the distribution of the petechiae was not typical of what you would expect if caused by asphyxiation. Cross-examined by Miss Davis, he stated that, in cases of asphyxia, the most common place to find petechiae is around the eyes (i.e. on the outside of the eyelids) , on the inner surface of the eyelid, inside the lips and behind the ears. Those were what were described as the “classical distribution sites” for petechiae. These were typical sites because tissue pressure in those sites is less than elsewhere, so that there is no support for little blood vessels which are therefore liable to burst if there is an increase in venous pressure.

Dr White observed, in answer to Mr Cotton in chief, that petechiae per se were not diagnostic of anything. He described them as “an essentially soft sign.” I remind myself again of Dr Trevelyan’s observation about how frequently petechiae are seen on children.

On balance, I conclude that the petechiae were not present on B when he was admitted to hospital. For that reason, and because (1), the distribution of the petechiae on B’s face is not typical of asphyxiation and (2), the petechiae are, in any event, a non-specific sign, I find that the petechiae on B’s face are not evidence that he was smothered by his mother.

The scattering of petechiae on J’s chest on 1^st January was not in locations which, according to Dr White, are typically associated with cases of asphyxia. No petechiae were observed on J on his admission on 6^th January. I do not consider the petechiae seen on 1^st January to be a significant pointer to the cause of J’s death.

So far as B is concerned, Dr Cartlidge found no evidence of any general health problems, nor any developmental problems. B was a previously healthy child who died suddenly and unexpectedly at the age of four and a half. Dr Cartlidge described this as “very unusual.” J died suddenly and unexpectedly, aged 28 months. Dr Cartlidge described this also as “very unusual.”

Dr. Cartlidge considered that the evidence of a possible intentional airway obstruction in B’s case included: the fact that B was a healthy child; the fact that he had been well no more than half an hour before his collapse; the fact that he had collapsed suddenly without explanation; and the fact that his brother, J, had also collapsed and died suddenly without explanation. On the basis (which I have rejected above), that the petechiae were present on B on arrival at hospital, Dr Cartlidge concluded that they were consistent with, rather than diagnostic of asphyxiation, but stressed that his conclusion did not turn on the presence of the petechiae. Dr Cartlidge concluded that it is most likely that B died unnaturally and “smothering is probable.” He added, however, that “the medical evidence for smothering is not specific and relies quite heavily on the exclusion of other causes and an assessment of the case as a whole.”

So far as J is concerned, again Dr Cartlidge found no evidence of any general health problems, nor any developmental problems. Like his brother, J was a previously healthy child who died suddenly and unexpectedly, in his case at the age of 28 months. Once again Dr Cartlidge described this as “very unusual.”

Dr Cartlidge considered J’s earlier hospital admissions on two occasions to be significant. On 1^st January, J had been well when he went to bed, but two hours later found unresponsive and jerky, with blue hands, feet and face. On admission to hospital some 50 minutes later, he was fully conscious and afebrile, but with petechiae over his chest and upper neck. In Dr Cartlidge’s opinion, this episode considered in isolation would support a diagnosis of a fit, although he noted that the evidence of a fever was weak and the temperature taken in hospital over 37.9 degrees Celsius was not usually sufficient to trigger a febrile fit. So far as J’s second admission to hospital was concerned on 3^rd January, Dr Cartlidge noted that once again J had been well or reasonably well at the time he went to bed. Several hours later, he was found pale with staring eyes and possibly twitching of his hands. On admission to hospital, J was found to be suffering from chicken pox, but was very energetic and afebrile. In those circumstances, Dr Cartlidge ruled out the possibility that he had suffered from chicken pox encephalitis on this occasion. Once again Dr Cartlidge considered that this episode, taken in isolation, would not be of significance. However, when considered in the light of the later events, he considers that the admissions to hospital on 1^st and 3^rd January were concerning. The events that are said to have taken place on those occasions were similar to later events in J’s and B’s lives that resulted in their deaths. However, J’s clinical features on both 1^st and 3^rd January were not typical of a cardiac arrhythmia. Dr Cartlidge thought that smothering could have caused the clinical features in J on both 1^st and 3^rd January, as well as those described in both children immediately prior to their deaths. He therefore concluded that smothering was a plausible explanation for J’s death, but added again that medical evidence of smothering “is not specific and relies quite heavily on the exclusion of other causes and the assessment of the case as a whole.”

In his oral evidence, Dr Cartlidge said that in his clinical practice he had only come across two cases of children of this age dying without any known cause. He had no experience of two children from the same family dying in such circumstances and he was unaware of any epidemiological study of childhood deaths involving this age group. He was asked to consider a paper produced by counsel for the mother entitled, “Smothering children older than one year of age, diagnostic significance of morphological findings,” by Banaschak and Others (2003) published by Forensic Science International. This paper led Dr Cartlidge to reflect on how B, at the age of four and a half, would have been expected to struggle quite vigorously if an attempt was made to smother him. Cross-examined by Miss Judd, he acknowledged that it was more surprising that there were no marks on the four-year-old child.

In his oral evidence, Dr White said that the presence of physical signs of smothering would depend on the size and strength of the victim, the size and strength of the assailant and the method by which smothering was inflicted. In the case of child victims, the older the child, the more likely he or she was to struggle and the greater the likelihood of physical signs. Dr White considered that it was possible that B would have scratched himself in an attempt to prevent suffocation, but the fact that there were no scratch marks observed on B did not rule out suffocation as an explanation.

In passing, I remind myself that Dr White noted two small marks, bruises, on the top of B’s head during his post-mortem examination. He did not, however, suggest that they were indicative of a physical assault. The local authority did not ask the mother about these bruises, nor did they feature at all in the local authority’s case.

The striking picture provided by the consultant in emergency care, Dr Beardsall, was that B looked like he was sleeping, rather than suffering a life-threatening event.

Having found, as explained above, that the petechiae on B’s face were not present when he was admitted to hospital, I conclude that there is no clinical evidence of asphyxiation other than the fact that two children died suddenly with cardiac failure, for which no cause had been identified.

The doctors, of course, do not have the full picture. Only the court is in the position of seeing and hearing all the evidence. As other courts have repeatedly emphasised in the passages from reported cases quoted above, it is the judge alone who is able to evaluate all the evidence. In my judgment, there are a number of features in this case which undermine the local authority’s case that J and B were deliberately killed by their mother.

First, I consider it significant that no mark was found on either child that might have been linked to an attempt to smother him. I consider that this is a matter on which the court is entitled to take a view independent of the medical experts. I acknowledge Dr White’s point that the fact that there were no scratch marks observed on B did not rule out suffocation as an explanation, but to my mind it is significantly more likely than not that there would have been some mark on one of the children, particularly B at the age of four. The local authority does not confine its case to saying that B was attacked in bed. It is of course unable to be specific in any way as to where, when and how B was killed, if he was killed. Much of the focus of this case has, however, been on the proposition that he was smothered while asleep in his bed. Indeed, if he had been smothered when awake, it would be, in my judgment, even more remarkable that there was no mark on his body. At the invitation of counsel, I inspected the bed, currently in the possession of the police. It has a wooden frame shaped like a car, raised slightly higher than the mattress. Miss Judd concedes that it would have been possible for the mother to have smothered B on the bed, but submits it would have been much harder to do so than on a conventional bed and much harder to do so without causing him any bruising or other injury. I find considerable force in that submission. I consider it more probable than not that B, aged four, would have sustained some physical injury if smothered by his mother, and in particular smothered while lying on that bed.

Secondly, it is a notable feature of this case that, with one exception, the mother has given a consistent account about the events concerning the collapse of both boys. Miss Judd submits that if the history given by the mother about the three episodes involving J and the one involving B is false, it is extremely surprising that she has been so consistent about it, particularly given her limitations. I agree.

The exception concerns when she last checked B before finding him lifeless. On the evening she said variously that it had been two minutes previously and ten minutes previously. In oral evidence she said it had been before she last texted SB some 45 minutes beforehand. Miss Davis and Miss Dewhurst, understandably, attach significant weight to this inconsistency. In assessing the significance of this discrepancy, I bear in mind the mother’s learning disability and in addition that the initial comments made by the mother were at a time when she was in a state of distress. I also recall Dr Macintosh’s description of trying to get a history in a room full of people and that, while the order of events was clear, the timing was not. Furthermore, I take into account the fact that many people find it difficult to be accurate about timing. As Miss Judd points out, there have been several examples in this case: MP and EH, who were otherwise credible witnesses, were obviously mistaken about the timing of the phone call made by the mother to SB’s home, and the boys who saw B outside shortly before his collapse did not give consistent accounts as to the time when that incident occurred.

Save for this point, there is very substantial consistency in all the accounts given by the mother about the circumstances of the deaths of the children. Given the amounts of detail in the accounts, and the mother’s learning disability, this is to my mind a significant pointer to the truth of her account. I did not regard the discrepancy as to timing as significantly undermining the credibility of her account.

Thirdly, it is instructive to consider the earlier incidents involving J. The local authority suggest these incidents may have been incidents of smothering which the mother stopped short of causing lasting harm, but it must be remembered that J was not an infant but a child aged two years, four months. Had he been the subject of two attacks by his mother, it might, in my judgment, have been expected that there would have been some sign of apprehension towards her. The hospital staff and the paediatric ward noted, however, that there was good interaction between mother and son and no indication of fear on his part was ever mentioned.

Fourthly, I take into account the mother’s reaction to the collapse of the children. The local authority concedes that there is no definitive evidence about what is or is not a normal grief reaction. To my mind, looking at the evidence as a whole, her immediate reaction to B’s collapse was, for the most part, exactly what one would expect if her account is true. That reaction was one of extreme distress, described by MP, EH, TR, MM and AT. In hospital, her reaction was consistent with shock. She found it difficult to be heard in the presence of large numbers of friends and neighbours and the understandable grief expressed by her own mother, DA. So far as J’s hospital admissions were concerned, I do take into account the comments of the paramedics on one of the earlier admissions about her unusual reaction, but against that there is a description of her given by GW on 6^th January and the evidence from the 999 transcripts on that occasion was that she sounded upset. I also bear in mind that she suffers from a learning disability and that this may have affected her reaction and her affect. In cross-examination, and again in closing submissions, the local authority has emphasised the fact that the mother was at times refraining from taking her thyroid medication, but I consider that the evidence in support of the inference which the local authority invites me to draw – that this made her more prone to aggression - to be thin. Of greater significance perhaps, is that by failing to take her medication she may have become more lethargic. In addition, I note the comment of GW, who says she has known the mother all her life and describes her as not a person who really shows her feelings.

Overall, I accept Miss Judd’s submission that there is only limited evidence that the mother failed to show appropriate emotion about the deaths of her sons and such evidence as there is, is outweighed by evidence to the contrary.

Fifthly, there is, to my mind, a distinct implausibility about the local authority’s theory about what happened to B. The local authority’s case is that the mother had smothered B at some point in the period after her mother DA left the house. At some unknown point, the mother was seen dragging B into the house by a group of boys, all of whom were interviewed by the police and gave different times for this incident. Until 19.28 the mother was on the computer playing bingo and texting SB. It is difficult to imagine how she could have committed a prolonged attack on B during that period. It must follow that any attack can only have occurred after 19.28 on either side of the MSN exchange that took place between the mother and NF. If the evidence as to the mother’s internet usage is to be relied on, she was on her computer until 19.45. There was thus only a much shorter period when there was no evidence of her doing anything else.

There is, for obvious reasons, some uncertainty about the length of time required to smother a child, but broadly speaking it is thought to take something in the region of a minute. It is not something committed in a momentary loss of control. Having seen her give evidence, it is, to my mind, difficult to envisage this mother committing an act of violence on her child lasting the length of time required to asphyxiate it. It is equally implausible, to my mind, that she smothered B to silence him without realising the consequences of her action, having regard to the length of time needed to asphyxiate a child.

It is right that I find the mother guilty of significant acts of neglect of the children and that on occasions she over-chastised them, but to my mind these factors add little weight to the local authority’s case that she smothered the children, either deliberately or accidentally. The act of suffocating a child is very different from the type of conduct involved in acts of neglect.

Finally, and most importantly, having heard the mother give evidence, I find that she genuinely loved her sons. I acknowledge that she said on at least one occasion that she could kill B, but such a comment is uttered by most parents in exasperation at some time and is rarely indicative of a genuine wish to cause harm. In my judgment, her emphatic denials in evidence that she had killed her children were credible.

Miss Judd rightly points out that, whilst the various experts have pointed to the lack of evidence of any disease or condition that could have caused the death of either J or B, there is equally no evidence of smothering. She submits that it is no more likely that this mother smothered each child without leaving any signs, than that the child died of an unknown, probably as yet unrecognised, cardiac cause.

This mother has a variety of conditions which are likely to be genetic in origin. Dr Newbury-Ecob accepted that the new variant found in the KCNH2 gene, whilst not a cause of LQTS, might lead to a susceptibility or risk of arrhythmia in the presence of other factors, either genetic or environmental and might be associated with his death in some unknown way. Dr Martin noted that “there are quite possibly a whole host of genetic conditions we know nothing about.” The clear impression from his evidence is that the genetic understanding of cardiac disorders is still evolving.

I recall again the observations of Judge LJ in Canningsquoted above, in particular that “where there are one, two or even three deaths, the exclusion of currently known natural causes of infant death does not establish that the death or deaths resulted from the deliberate infliction of harm” and that “a great deal about death in infancy and its causes remain as yet unknown and undiscovered.” I also have in mind the observation of Butler-Sloss P in Re U, Re Bcited above: “The cause of an injury or episode that cannot be scientifically explained remains equivocal. Recurrence in itself is not prohibitive. The judge in care proceedings must never forget that today’s medical certainty may be discarded by the next generation of experts or that scientific research would throw light into corners that are at present dark.” Finally, I remember the wise words of Hedley J in Re R, also quoted above: “there has to be factored into every case which concerns a discrete aetiology giving rise to significant harm, a consideration as to whether the cause is unknown …. a conclusion of unknown aetiology in respect of an infant represents neither professional nor forensic failure. It simply recognises that we still have much to learn and it also recognises that it is dangerous and wrong to infer non-accidental injury, merely from the absence of any other understood mechanism.”

I have given extremely careful attention to the opinions of all the experts and Dr Cartlidge in particular. I acknowledge that there is a significant possibility that this mother was responsible for the deaths of the boys and my mind has fluctuated during the course of this hearing and in my subsequent deliberations. There may be in due course other evidence that bears upon this issue. Having considered all the evidence put before me, however, I find that the local authority has not proved on a balance of probabilities that this mother smothered either J or B.

The consequence of my finding is that, for the purposes of these proceedings, the court and the parties will proceed on the basis that the mother did not smother the boys. For the reasons explained above, however, I have found that the mother was responsible for significant acts of neglect of all the children and on that basis the threshold conditions under Section 31 of the Children Act are satisfied.