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You are here: BAILII >> Databases >> England and Wales Family Court Decisions (other Judges) >> T (A Child : fact finding) [2014] EWFC B115 (12 September 2014)
URL: http://www.bailii.org/ew/cases/EWFC/OJ/2014/B115.html
Cite as: [2014] EWFC B115
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IMPORTANT NOTICE
This judgment was delivered in private. The judge has given leave for this version of the judgment to be published on condition that (irrespective of what is contained in the judgment) in any published version of the judgment the anonymity of the child and members of her family must be strictly preserved. All persons, including representatives of the media must ensure that this condition is strictly complied with. Failure to do so will be contempt of court.
Case No: LQ14C00229
In the Family Court
In the Matter of the Children Act 1989
And in the Matter of Ti, Te, T (Children)
Date: 12.9.14
Before:
HHJ Swindells QC
Between:
Lincolnshire County Council
Applicant
-and-
TM (I)
TC(2)
MM(3)
Ti, Te, T (4) & (5)
Respondents
Mr Andrew Norton: for the local authority
Mr Justin Slater: for the 1st Respondent
Ms Samantha Dunn: for the 2nd Respondent
Ms Kristina Brown: for the 3rd Respondent
Ms Hari Kaur: for the 4th and 5th Respondents
APPROVED JUDGMENT
Judgment
HHJ Swindells QC:
Introduction
1. I am concerned with the welfare of three children: Ti who is 2 almost 3 and the twins, Te and T who are almost 1.
2. The mother of the children is TM, aged 30 (‘the mother’) and their father is TC, aged 23 (‘the father’). Their maternal grandparents are JM and MM.
3. On 8 January 2014 radio-imaging disclosed bilateral subdural fluid collections over T’s cerebral hemispheres. Care proceedings were issued on 28 March 2014.
4. The matter comes before the court for the finding of fact element of the final hearing to determine the non-accidental and perpetrator issues; the parents and the maternal grandmother being in the pool of potential perpetrators. The Schedule of Findings which the local authority seeks to establish on a balance of probabilities appears at TB1A/23-24.
5. The parents and the maternal grandmother deny inflicting any injury upon T.
6. I heard evidence via video or telephone link from the experts: Dr Stephen Chapman, Consultant Paediatric Radiologist & Paediatric Neuroradiologist; Mr Jayaratnam Jayamohan, Consultant Paediatric Neurosurgeon; Dr George Rylance, Consultant Paediatrician. I further had the advantage of reading the report of Dr Raina Liesner, Consultant Paediatric Haematologist, which was not challenged. I also heard evidence from two Health Visitors.
Background
7. On 20 November 2013 (‘the November episode’) the twins were with their parents whilst their sister was being cared for at the grandparents’ home. The parents say that at about 9 pm T was asleep in the pram whilst Te was awake and in her father’s arms.
8. The mother states that she went upstairs leaving the father with the twins. She heard T cry and the father call “come down quick.” The mother saw T in the father’s arms (Te was also in his arms) and that she was floppy. The mother took hold of her. T was pale, breathing but not crying. The mother in a panic called the maternal grandmother and on her attendance the grandmother called 999. In the transcript of the 999 call the grandmother said that ‘T was awake … and breathing but she’s gone all limp - going all over…she’s not responding to anybody…’
9. An ambulance was sent at 21.48 and the medics arrived by 21.54. T was taken by ambulance to hospital arriving at 22.18. with a history of ‘went limp tonight’. The presenting complaint was recorded in the hospital notes as follows: ‘episode of becoming pale & floppy at 9.45 pm. Was in pram & started crying & when dad picked her up – was floppy in limbs + pale on face. Was conscious & normal breathing. This episode continued for 2/3-4 min & T was normal when ambulance team arrived. No H/O fever, vomiting or diarrhoea; No H/O cough & cold; no H/O rash…feeding well…. T was noted as active and playful and handling well. .. this episode could be cardiac in origin…’ T was referred to a paediatric cardiologist for an Echo (ECG).
10. T was seen by the GP the following day and low haemoglobin was noted.
11. On 8 January 2014, after a missed cardiac clinic appointment, T was presented at hospital by the parents for the appointment. T’s head was noted to be ‘bigger than average.’ From the records T’s head circumference had been measured as 34.1 cm (ie 2nd centile) on 7 October 2013 and 36.4 cm (ie 9th centile) on 12 November 2013 but on 8 January 2014 was found to be 42.5 cm (ie 97th centile). The hospital notes record ‘floppy episode – Nov 13; no further episodes; no other concerns; feeding well, growing normally… HC – 42.5 cm (> 98 tile)…bossing of head engorged veins; AF soft (big)…’
12. A CT scan was carried out which disclosed fluid collections over both cerebral hemispheres.
13. The following day an MRI scan was taken of T’s brain and spine, which confirmed subdural fluid collections over both cerebral hemispheres. A skeletal survey found no other injuries. There were no retinal haemorrhages.
14. A repeat MRI scan on 2 April 2014 showed that the subdural haematomas had almost completely resolved.
15. On 7 April 2014 T was admitted to hospital with an elevated anterior fontanelle but in the context of her having vomited.
Expert Evidence
Dr Chapman
16. In his report dated 16 May 2014 Dr Chapman made the following findings from the CT scan taken on 8 January 2014. There were fluid collections over both cerebral hemispheres. These were largely located towards the front of the head and the left collection was larger than the right. The fluid was of slightly higher attenuation than the normal cerebrospinal fluid in the lateral ventricles and subarchnoid space. The sulci were not prominent over the front part of the brain, implying that the fluid collections were having some compressive effect on the brain. The lateral ventricles were slightly larger than would be expected for a child of this age. There was no skull fracture or scalp swelling to suggest a recent impact against a hard surface.
17. The skeletal survey on 9 January 2014 showed that there were no old or recent bony injuries. There was no radiological evidence of an underlying medical condition. He noted that children with glutaric aciduria type 1, a metabolic disorder and a rare cause of subdural haemorrhages, often have other brain MRI evidence of the disease which T did not.
18. The MRI scan on 9 January confirmed the subdural fluid collections and that the collections over each cerebral hemisphere comprised 2 collections of different signal intensities separated by a membrane. There was no abnormality of the brain itself or of the spine or spinal cord. A chronic subdural haematoma predisposes to further haemorrhage but the further haemorrhage does not necessarily require further significant trauma.
19. The MRI scan taken on 2 April 2014 showed that the subdural collections had almost completely resolved with just a tiny residual left sided collection of subdural fluid. The ventricle remained slightly dilated.
20. He concluded that the neuroimaging demonstrated bilateral chronic subdural haemorrhages. According to a 2005 epidemiological study (referred to below) the majority of subdural haematomas at T’s age are due to inflicted head trauma and the pattern of change here suggested shaking as the mechanism. Shaking typically results in recent multifocal haemorrhages and/or chronic subdural haemorrhage extending over both cerebral hemispheres: Kemp et al ‘Neuroimaging: what neuroradiological features distinguish abusive from non-abusive head trauma?’ Arch Dis Child (2011) 96:1103-1112.
21. While the age of the haematomas cannot be determined with any accuracy it is highly unlikely that they were a birth injury. The literature shows that birth related subdural haemorrhages resolve by four weeks and none re-bleed: Whitby et al (2004) ‘Frequency and natural history of subdural haemorrhage in babies and relation to obstetric factors. Lancet 363: 846-851; Whitby et al (2005) ‘Clinically silent subdural haemorrhages – NAI or not?’ Pediatr Radiol 35:S102 (“the Sheffield Study”).
22. As to timing, subdural haemorrhages become fluid after about 3 weeks. It is also widely accepted that membrane formation also takes about three weeks before becoming visible on neuroimaging. The appearances on 8 January and 9 January imply an injury sustained prior to mid December. Given that the subdural haematomas had not only become fluid and formed membranes but had also increased in size, it is more likely than not the initial onset was some weeks prior to mid December.
23. Within the clinical history there was an event on 20 November 2013 during which T experienced a short lived collapse in which she was floppy for 2 minutes. In his opinion, this could be the occasion when she sustained the acute subdural haemorrhages that subsequently became chronic. The event could be explained by a head injury which caused subdural haemorrhages but probably little or no brain injury because of the short lived nature of the event. Bilateral subdural haemorrhages are much more in favour of acceleration/deceleration (ie shaking) than impact.
24. In his oral evidence he accepted that where there was no evidence of hypoxic ischaemic brain swelling, no tears within the brain, no retinal haemorrhages and no other injuries such as bruising or damage to the spinal column and where there is only evidence of subdural haematomas, as here, such cases represent a challenge for the expert. This was exacerbated by the fact that what he was looking at on the images was historical and not an acute stage.
25. He had relied upon an epidemiological study carried out by the British Paediatric Surveillance Unit which reviewed 186 infants aged 0-2 years with subdural haemorrhage or fluid collections presenting in a 1 year period: Hobbs C et al. Subdural haematoma and effusion in infancy: an epidemiological study’ [Arch Dis Child 2005; 90:952-955]. 106 (57%) were due to no-accidental injury. If those with known accidents, medical conditions etc are excluded then the figure rises to 86% due to non-accidental injury. However, in 17 (9%) the cause was undetermined. In 85% of the cases due to abuse, there were other injuries. He acknowledged that it was an old paper and was at a time when children were not so extensively investigated as now but currently this is all the data we have.
26. Although the 9% of children in the UK in respect of whom no conclusion can be reached as to causation is a significant figure and has to be a possibility in this case, he had looked at the majority cause which is inflicted injury and at the fact that November episode was a significant episode which provided for the possibility of injury. If there had been no evidence as to when the subdural haematoma was caused, the reasonable possibilities would have been inflicted trauma or simply an unknown cause. The November episode where the symptoms which T presented, in his view, were consistent with head injury and tipped the balance of probability towards an episode of inflicted trauma. This was the only occasion when T evidenced neurological disturbance and was consistent with the radiological period for the injury and with the period when her head circumference went from normal to an increased circumference.
27. He said that on imaging alone one could not exclude birth related subdurals but the current conventional wisdom was that they would resolve by four weeks of age and do not recur. He accepted that data is based upon a small number of children, several 100s, where there is no evidence of small subdurals becoming chronic subdurals, but that there maybe one in a 1000 or 5000, where it may occur – we do not know. He further noted that birth related subdurals tend to be sited at the posterior fossa and are not bilateral.
Dr Rylance
28. Dr Rylance in his report dated 8 June 2014 deferred to Dr Chapman in relation to the presence of subdural collections and accepted that the subdural haematomas of chronic and repeated nature were responsible for the scan appearances and the reason why T was found to have a larger than expected head circumference in January 2014. He further accepted Dr Chapman’s timing that the initial and subsequent bleed on each side of the brain must have occurred more than 3 weeks prior to the CT scan of 8 January 2014.
29. In his view, the episode of floppiness and pallor which affected T on 20 November was a significant clinical change, albeit relatively short lived – approximately 5 minutes before a return to normal. It is the only time that such a change was evidenced in her and makes it more likely than at any other time for the cause of the episode of bleeding into the subdural space.
30. He expressed the view that it was extremely likely that T did not have a pre-disposition to easy bruising/bleeding through having a coagulation disorder but recommended a comprehensive coagulation test investigation, which was undertaken and reported upon by Dr Liesner, who excluded a severe coagulation disorder as causative of the subdural haemorrhages, which Dr Rylance accepted totally.
31. He had, however, further noted that the test carried out for glutaric aciduria type 1 had not been the appropriate investigation. He had recommended that a non- invasive urinary organic test be requested and to include a blood test for acyl carnitines via a heel prick, although he acknowledged that negative tests would not exclude the presence of glutaric aciduria. A skin biopsy would not produce a false negative but this is a more invasive procedure and would take time.
32. The blood and urine tests have not been carried out. In his oral evidence, he said that, because the wrong test had been done, he would have gone on and done the right test, but he was not making a strong case for the test. In his view, it was exceedingly unlikely that T was suffering from glutaric aciduria type 1. Because of her age now he would have expected that she would be showing early signs of glutaric aciduria in terms of her speech, degree of stiffness and muscle tone. In the early stages a child who has glutaric aciduria would have difficulty in co-ordinating speech and in swallowing and feeding and stiffness in the arms and legs making it difficult to manipulate items.
33. There were no signs of glutaric aciduria type 1 in the comprehensive assessment of T carried out by the health visitor on 3 September 2014. A good development assessment would give a 50/50 chance of seeing some clinical signs. There may well be imaging signs as they develop before the clinical signs but imaging signs were absent in T’s case. Adding all the evidence together, this provides quite a lot of reassurance that T does not have glutaric aciduria type 1 although one cannot exclude the possibility totally. In the great majority of cases most children with glutaric aciduria do not have subdural haematomas and where they do the subdural haematomas are almost always unilateral rather than bilateral. He said that her appearance would be different if she had glutaric aciduria. The head circumference would have increased considerably more than the trajectory on T’s centile chart. She would have had bossing of the bones at the front of her head ie a domed appearance of her face, which would give a different appearance from hydrocephalus. The bulge in her fontanelle on 7 April was entirely different and was not relevant.
34. He said that neither low iron nor a Vitamin D deficiency leads to subdural haemorrhage.
35. He considered the possibility that the subdural haemorrhages were unexplained but, on balance, cautiously concluded that it was more likely than not that the cause of T’s injuries was inflicted injury.
Mr Jayamohan
36. In his report dated 19 May 2014 Mr Jayamohan stated that, whilst there remained a theoretical possibility that very rarely a child may sustain birth related subdural haemorrhage which, instead of reabsorbing and disappearing, may stay to cause a chronic subdural haemorrhage which may or may not become symptomatic, this was exceptionally rare and there was no evidence that T had a symptomatic birth related subdural haemorrhage.
37. He went on to state that from a neurological perspective there were no neurological findings which would support non-accidental injury being the more likely diagnosis than any other in this case and he, therefore, placed the case into the unknown category.
38. In his oral evidence, he initially said that in the first expert’s meeting (referred to below) he had supported the agreed position that the most likely cause of the initial haemorrhage was inflicted trauma. He said that there was nothing from a neurological perspective which supported trauma and so he had based his conclusion upon the epidemiological study, Hobbs C et al, that statistically the most likely cause of a subdural haematoma in a child with normal bleeding and no metabolic cause was inflicted injury. The November episode where T became markedly unwell was probably brain dysfunction and this logically fitted with the proposition that it was inflicted injury.
39. He said that glutaric aciduria was a very, very rare disease. In the 100s of children he has examined he has never had a child diagnosed with glutaric aciduria. As the chances of T having glutaric aciduria are extremely low, an invasive skin biopsy would not be warranted.
Expert Schedule of Agreement
40. A meeting took place between Dr Chapman, Mr Jayamohan and Dr Rylance on 10 June 2014, which produced a Schedule of Agreement as follows.
(1) T suffered bilateral chronic subdural haemorrhages over both cerebral hemispheres. On each side there were two collections of different intensity suggesting there had been two episodes of haemorrhage on either side.
(2) Only the first of the bleeds required an explanation as the second (rebleed) in the presence of chronic subdural haematomas may arise from minimal or no trauma.
(3) The most likely cause of the initial haemorrhage was inflicted non accidental trauma in the absence of any results that indicate a likely underlying cause for a propensity to bleed easily or develop subdural haemorrhages.
(4) In the absence of any results from investigations, the most likely mechanism was shaking.
(5) The level of force can not be ascertained other than it would have involved a level of force significantly greater than normal handling and the rough and tumble of situations with siblings.
(6) The most likely timescale for the cause of the event was between early/mid November to mid December.
(7) It was recommended that the necessary coagulation test be undertaken together with a blood an urine test for glutaric aciduria 1. If the testing revealed coagulation abnormalities consistent with a propensity to bleed easily or likely glutaric aciduria 1, this would provide a potential and probable explanation for the haemorrhages irrespective of nay clinical discrepancies.
Dr Liesner
41. In her report dated 23 September 2013 Dr Liesner considered the results of blood tests performed on T on 26 August 2014. These tests, in her view, have adequately excluded a severe coagulation or platelet function disorder as a cause of spontaneous subdural haematoma.
Further experts’ meeting
42. In his oral evidence Mr Jayamohan looked through various photographs of the twins, which had been taken in early November [1A/C47-49; 52-65] (‘the photographs’) and, therefore, predated the November episode. Whilst expressing caution about using social photographs rather than medical photographs, he nevertheless noted that T showed signs of a change of head shape and ‘sun setting’ (looking down) and expressed the view that T was showing signs of raised intracranial pressure.
43. He went on to say that this put the November episode out of the picture as the original causative event. In his view, this made trauma a less likely explanation. In the light of this evidence, his view reverted to that of his report, namely that it was more likely that this case fell into the unknown category. He pointed to the fact that, in his view, this case had unusual features including the disappearance of the subdural by April 2014.
44. Later in cross examination he speculated that there may have been multiple traumatic episodes before and after the November episode and referred to the literature: Adamsbaum et al ‘Abusive head trauma: judicial admissions highlight violent and repetitive shaking [Pediatrics 2010; 126: 546-555]. In this study authors compared 29 cases in which the perpetrator confessed to violence towards the child with 83 cases in which there was no confession. In the 29 cases of confession, shaking was described as repeated from 2 to 30 times because it stopped the infant’s crying. He noted, however, that there was no evidence in this case of T incessantly crying or of either parent getting to a stress point. Furthermore, there was no evidence in relation to an earlier event or events of encephalopathy. Had there been, his expectation would have been that the parents would have responded by taking the child to hospital as they did on 21 November.
45. In the light of Mr Jayamohan’s evidence in relation to the photographs, a further experts’ meeting between Dr Chapman, Dr Rylance and Mr Jayamohan was set up for the evening of 9 September 2014. I was provided with a transcript of their discussions.
Timing
46. Mr Jayamohan said that from his interpretation of the photographs there was significant evidence that T was showing signs of raised intracranial pressure at the time the photographs were taken, in particular the frontal bossing of the forehead and the ‘sun setting’ of the eyes. In his view this evidence showed that the child had subdural collections for at least two weeks, and possibly longer, prior to the photographs being taken in early November. He said that this ‘takes out’ the November episode as the potential initial event for the causation of the subdural collection.
47. Dr Rylance said that he had been convinced by the photographs that the child had raised intracranial pressure and he agreed with Mr Jayamohan that this altered the timing completely as the child had to have a pre-existing cause for a raised intracranial pressure.
48. Dr Chapman deferred to his clinical colleagues on the interpretation of the photographs. He agreed that if the photographs were taken in early November, there had to be an event which occurred sometime between birth and the date of the photographs.
49. They considered the head circumference measurement taken on 12 November (which provided a contra-indication to the conclusion of raised intracranial pressure based on the photographs). Both Mr Jayamohan and Dr Rylance concluded that it was the measurement which was probably wrong. They put this down to the sort of measurement error, as in fact occurred in the most recent health visitor’s report (referred to below).
Causation
50. Mr Jayamohan said that he felt that, now that the November episode could not be regarded as the initial causative event, they had ended up with a diagnosis of trauma based upon epidemiology studies such Hobbs et al (2005) without any direct evidence such as documented encephalopathy or a similar event to support the diagnosis of trauma above an unknown cause.
51. He expressed his concerns as to the unusual features of T’s case, in particular the fact that the subdural had disappeared in April. Dr Chapman could not think of a case he had actually seen where chronic subdural haematomas had resolved but did not think that this would cause him to change his diagnosis. Dr Rylance accepted that chronic subdural collections might be unlikely to disappear rapidly when they had been present for some time.
52. As to causation, Dr Rylance said that they do not know everything but the great majority of subdurals they saw were almost certainly as a result of trauma. He accepted that this was a statistical issue for the court to grapple with and that ‘this case was a little bit unusual and when something is unusual it does throw up uncertainty, which is hard to deal with’. He said that he did not think that it was necessary to have an encephalapathic episode to say that there was trauma. Bilateral subdurals of themselves may not cause brain dysfunction and, therefore, if you have brain dysfunction it is likely there was a traumatic cause, if no other cause is evident. All the other causes have been explained other than the unknown.
53. He described this as a very difficult area, particularly in the absence of retinal haemorrhages and hypoxic brain change. He said that the unexplained causation group is exceedingly small but it is very hard to know figures on this and he felt that it was ‘a somewhat statistical approach’ to causation with respect to those two possibilities: trauma and unexplained unknown. He nevertheless felt that the cause was trauma.
54. Dr Chapman said that the November episode had provided support for trauma as the cause but clearly if the photographs are accepted as showing a problem with the head circumference prior to 20 November, then that event cannot be used as evidence to support a traumatic aetiology on that day. So they were left with either the statistically greater trauma as the cause or the unexplained. As a radiologist, he could not differentiate one from the other.
55. Mr Jayamohan said that if the November event is taken out as the initial causation event and, if trauma is accepted as the most likely case based upon on epidemiology, multiple events would fit more with the history of no severe encepahalopathy. In his view, multiple shakes of a lesser level were more likely to explain the non presentation than a single traumatic event.
56. Dr Rylance said that he was marginally in favour of multiple episodes of trauma which were more likely to be two or three rather than a larger number. Repeated events may not have the same force as the one single event that causes a very significant reaction in the child. His final position was, however, that he did not know whether it was a one single event or a multiple.
Law
57. The legal burden of establishing the facts rests on the Applicant authority at all times. The standard of proof is the ordinary civil standard of the balance of probabilities; neither the seriousness of the allegation nor the seriousness of the consequences makes any difference to the standard of proof applied: Re B (Children) (Care Proceedings: Standard of Proof) [2008] UKHL 35.
58. Findings of fact must be based upon evidence, including inferences that can properly be drawn from the evidence and not suspicion of speculation: Re A (A Child) (Fact Finding: Speculation) [2011] EWCA Civ 12, per Munby LJ (as he then was). For a fact to be proved the judge must first decide whether or not it happened: Re B (above), per Lord Hoffmann.
59. Determining the facts is a difficult task which must be performed without prejudice or pre-conceived ideas. The court is guided by many things including the inherent probabilities, any contemporaneous documentation or records, any circumstantial evidence tending to support one account rather than the other and the overall impression of the characters and motivations of the witnesses: Re B (above), per Baroness Hale of Richmond.
60. As Dame Butler-Sloss P said in Re T [2004] 2 FLR 838 at 33:
‘Evidence cannot be evaluated and assessed in separate compartments. A judge…must have regard to the relevance of each piece of evidence and to exercise an overview of the totality of the evidence in order to come to the conclusion whether the case put forward by the local authority has been made out to the appropriate standard of proof’.
61. In assessing the expert evidence I must be careful that each expert has not trespassed outside the bounds of their own expertise but has deferred, where appropriate, to the expertise of the expert with the relevant specialty, and that, whilst appropriate attention must be paid to the opinion of medical experts, those opinions need to be considered in the context of all the other evidence. The medical experts are not the decision makers; it is for the judge, having analysed the whole of the evidence, including issues of credibility, to reach conclusions as to the facts which may vary from that reached by the medical experts: A County Council & K, D & L [2005] 1 FLR 851, per Charles J; Re S [2009] EWHC 2115, per King J.
62. In Re U, Re B (Serious Injuries: Standard of Proof) [2004] EWCA CIV 567 Dame Elizabeth Butler-Sloss P further observed:
‘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 may throw light into corners that are present dark’
63. Cases in which it is alleged that a child has suffered injury as a result of shaking arouse great anxiety. This was recognised in the case of R v Henderson; Butler; Oyediran [2010] EWCA Crim 1269. The words of Moses LJ are apposite, albeit he was applying the different criminal standard of proof, when he said
‘Experts…must reconstruct, as best they can, what has happened. There remains a temptation to believe that it is always possible to identify the cause of the injury to a child. Where the prosecution is able, by advancing an array of experts, to indentify non-accidental injury and the defence can identify no alternative cause, it is tempting to conclude that the prosecution has proved its case. Such temptation must be resisted. In this, as in so many fields of evidence, the evidence may be insufficient to exclude beyond reasonable doubt an unknown cause. As R v Cannings [2004] EWCA Crim 1, para 177, teaches, even where, on examination of all the evidence, every possible known cause had been excluded, the cause may still be unknown.’
64. Citing the above passage, Hedley J in Re R (Care Proceedings: Causation) [2011] EWHC 1715; [2011] 2 FLR 1384 at [10] went on to say:
‘ The temptation there described is ever present in family proceedings too and, in my judgment, should be as firmly resisted as the courts are required to resist in criminal law. In other words, there has to be factored into every case which concerns a disputed 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…’ see also Re JS [2012] EWHC 1370 [44], per Baker J.
65. The unusual facts of Re R provide an illustration of this process. Three possible causes for a head injury to a baby had been identified by the experts: a perinatal event; a non-accidental injury and a aetiology which was neither known nor understood. There were considerable difficulties with the cause being either of the first two causes and Hedley J found on a balance of probability that the cause was one of unknown aetiology; non- accidental injury and a perinatal event being each less probable.
66. I bear in mind the comments of Baker J in Re JS (above) at [46] in relation to the triad of intracranial injuries:
‘As was explained by the Court of Appeal in the case of R v Harris and others [2005] EWCA Crim 1980 the medical diagnosis of non-accidental injury has for some years been based on what is called the triad of intracranial injuries consisting of encephalopathy, subdural haemorrhage and retinal haemorrhage. For many years the coincidence of these injuries in infants was considered to be the hallmark of non–accidental injury. As was made clear in the Harris case, however, the presence of this triad was a strong pointer to, rather than diagnostic of, non-accidental injury. In each case the court must carry out a thorough investigation of the facts. In many cases the child will have suffered other injuries, for example, bone injuries. In other cases some of the elements of the triad may be missing. But having examined all the evidence the court may still conclude that the child suffered non-accidental injury’.
67. It is also important to guard against a reversal of the burden of proof as occurred in M (Child) [2012] EWCA Civ 1580 where the first instance judge had found that ‘absent a parental explanation, there was no satisfactory benign explanation, ergo there must be a malevolent explanation.’ Ward LJ stated that this conclusion did not necessarily follow, unless, wrongly, the burden of proof had been reversed and the parents were being required to satisfy the court that it was not accidental injury.
Analysis
Non- accidental injury
68. Whilst appropriate attention must be paid to the opinion of medical experts, especially where they are experts of eminence as they are in this case, I remind myself that I must consider very carefully their opinions in the context of all the other evidence.
69. The picture presented by the wider canvas evidence is that the parents are in a settled relationship well supported by extended family members, in particular the maternal grandparents. The universal evidence of the health visitors was that the parents are loving, caring parents with good interaction with their children; parents who have given no concerns as to the level of care they were providing for their children. The evidence also is that the maternal grandparents are lovingly and appropriately engaged in the lives of their grandchildren. This is a case where there is no concerning evidence of neglect, substance misuse, financial or housing difficulties or violence or criminality or mental health difficulties. Importantly, there is no evidence of incessant crying by T leading to any evidence of frustration on the part of either parent. This is a very positive picture which, in my judgment, provides a highly relevant context to the determination I have to make.
70. As acknowledged by the cases referred to in paragraphs 65 to 68 and by the experts themselves, we are in an area of notorious scientific difficulty, especially where the only findings are of chronic subdural collections without the other features of the triad or any skeletal or other injuries.
71. Looking at the overall evidence of the experts, it was clear that they all, quite properly in my judgment, felt unease at putting forward a diagnosis of trauma based solely upon a 2005 statistical study without any supporting evidence. The November episode as the initial causative event had provided some evidential support which at the time of the first experts’ meeting had been enough to tip the balance of probability in favour of an agreed diagnosis of trauma. However, at the second experts’ meeting both of the clinicians, Mr Jayamohan and Dr Rylance, agreed that the photographs provided compelling evidence that there was raised intracranial pressure which predated the November episode and, therefore, eliminated it as the initial causative event.
72. There was, however, a head circumference reading of 12 November taken by a health visitor, which contradicted that view. The probability of an error in the measurement was, therefore, raised by Dr Rylance and Mr Jayamohan and fully explored with the two health visitors who gave evidence.
73. I have to say that the potential for error was amply demonstrated by the acknowledged error recently made by one of the experienced health visitors. She frankly admitted that she had muddled the twins’ measurements. This had resulted in plunging T’s measurement, on the face of the record, down from her 98th centile to her sister’s 50th centile (a glaring mistake which she subsequently amended).
74. The health visitor who took the head circumference measurement on 12 November was a student health visitor and not an experienced practitioner. It was clear on the face of her recordings in the head circumference chart in T’s Red Book that she had made an error at the second week. She had initially marked the circumference at 36.1 cm, which she had crossed out and re-marked at 34.1 cm. I regret to say that this did not give me any confidence that her measurement on 12 November could be relied upon as accurate. In the light this unsatisfactory and disquieting evidence as to the reliability of health visitor recordings, I find that the head circumference measurement on 12 November was probably wrong and I prefer the evidence of the experts as to the presence of raised intracranial pressure as shown in the early November photographs.
75. All three experts agreed that the evidence of pre-existing intracranial pressure ruled out the November episode as the initial causative event and, therefore, as supporting evidence for their original consensus diagnosis of trauma. The loss of this evidential prop tipped the balance of probability for Mr Jayamohan against a diagnosis of trauma in favour of unknown cause. Its loss left Dr Chapman unable to differentiate between trauma and the unexplained as the cause. Dr Rylance still marginally inclined in favour of trauma but hedged his view with so many doubts and uncertainties that I could not regard his hesitant conclusion as a ringing endorsement for a diagnosis of trauma.
76. Given their entirely proper doubts on the issue of causation once it solely depended on a statistical approach, I was troubled that their discussion moved on to speculate about the possibility of multiple traumatic events. There was not an iota of evidence to support such a possibility which, in my judgment, rendered this speculation a wholly unsafe foundation for the erection of the balance of probability. It is perhaps timely at this point to remind myself that the experts are not the decision makers in these difficult cases. The case law is clear that it is for the judge, having analysed the whole of the evidence, to reach conclusions as to the facts which may vary from that reached by the medical experts.
77. I accept the evidence of Dr Liesner, which rules out a coagulation disorder as a possible cause for T’s subdural collections.
78. This leaves four possible causes of T’s subdural collections: a birth related event; a metabolic disorder; non-accidental injury or an aetiology which is unknown or not yet understood.
79. I am satisfied on all the expert evidence that it is extremely unlikely that T has the metabolic disorder of glutaric aciduria type 1 or that the chronic subdural heamatomas were birth related.
80. For the reasons I have set out above, there are considerable difficulties with the cause of non-accidental injury based solely upon relatively old statistical data. All the experts, however, have acknowledged that this case presented unusual features, for example the almost total disappearance of the chronic subdural by April 2014. Mindful of the guidance of Hedley J in Re R (above) I, therefore, find on a balance of probability that the cause was of unknown aetiology; non–accidental injury being a less probable cause, particularly when viewed against the wider canvas evidence.
Threshold
81. It follows that the threshold is not met for the purposes of s 31(2) of the Children Act 1989 and I accordingly dismiss the local authority’s application for a care order.
82. I wish to make abundantly clear in this judgment that I totally exonerate the parents and the maternal grandmother.
83. I should also add that, in the light of the original expert consensus that the subdural collections were traumatic in causation, no criticism can or should be levelled at the local authority for issuing the care proceedings in order to safeguard the children’s welfare.