“F, during his contact, informed me that the only reason he remained in Britain was because of C2. F stated that he had spoken to his MI5 colleagues, and he had the option to go to Brazil or America and work there.”
“C1 was next assessed by a doctor on the date of his immunisations (20 April 2005 ). He underwent a general eight week check. It is documented that his head circumference at that time was 37 cm (2nd centile). His head control and muscle tone were satisfactory. His vision was satisfactory. C1 was reported to fix and follow. His general behaviour was satisfactory. Examination of his hearing, genitalia, hips and cardiovascular system were all normal. The GP reports that C1 was given a combination vaccine against diphtheria, tetanus, pertussis (whooping cough), polio and Haemophilus influenza type B infection (Pediacel combination vaccine batched C2034AA). This vaccine contains inactivated extracts of the five different organisms that cause the aforementioned diseases. In addition C1 was given the meningitis (C) immunisation as a separate injection.”
“My mother came over to our house to baby-sit, and my father and F began fixing our garage roof, which was a job they had been planning to do for some time. The hairdressers is about a five minute walk from my home. When I got back at about 4.00 to 4.15pm, my mother had just gone home. C1 was in his bouncy chair. I fed C1 at about 5.30pm and made up bottles and placed them in the fridge. I then had something to eat and got ready to go out. Before I went out, I again asked F if he was sure he did not mind me going out, and he was quite clear that he wanted me to go out and he seemed perfectly normal. After I had left the house, I remembered I had forgotten four cans of cider that I intended to take to my friend’s house, so I came back in to get them. Nothing was unusual in the house. C1 was in his bouncy chair in the living room and F was on the sofa watching TV. I returned from my girls’ night out at approximately 12 o’clock, to find police coming out of my house and to be informed that C1 was poorly and had been taken to hospital. I was shocked and confused, as he was fine when I had gone out.”
“The fixed brain weighed 780g and showed “bleeding below the middle covering” (subarachnoid haemorrhage) over each hemisphere, largely parallel with surface blood vessels and most obvious over the upper surface of the “front of the right side of the brain” (superior aspect of right frontal lobe), the “junction between the lobes at the front and the sides of the brain” (each sylvian fissure), and between the optic nerves and the midbrain. No abnormality was seen in the blood vessels of the Circle of Willis, and there was no gross abnormality of the “little brain” (cerebellum) or brain stem. Some minor subdural clot was present in association with the “membrane which separates the halves of the brain” (parafalcine subdural clot). Multimple “top-to-bottom (coronal) slices of the brain revealed no unequivocal haemorrhage within the ventricles, and no significant gross abnormality, other than apparent vascular congestion. Examination of the fixed cervical cord confirmed the presence of “blood outside the outermost covering” (epidural blood) in the posterior cervical and posterior and anterior lumbar segments, with possible subarachnoid haemorrhage in the mid-thoracic segment and blood in the epidural fat throughout the mid-thoracic to lumbar region.”
“The cerebral hemispheres are of lower attenuation than normal and there is almost complete loss of grey white differentiation. Some minor relative sparing of grey-white differentiation is seen in the medial occipital regions bilaterally, i.e. these appear to be the only areas of the brain that are less involved in the hypoxic process at the time of this scan. The generalised low attenuation and loss of grey white differentiation is secondary to extensive hypoxic-ischaemic brain injury. This, somewhat unusually, involves the basal ganglia, thalami and brainstem, and the fact that these areas are involved is likely, in my view, to reflect the severity of the injury. Other than the generalised hypoxic-ischaemic injury, no other focal brain abnormality has been identified. The cerebellum is also of abnormally low attenuation with reduced grey white differentiation. It is extremely unusual to see involvement of the cerebellum evident on scans in the majority of hypoxic-ischaemic brain injuries; the cerebellum is usually spared (in terms of scan appearances) in hypoxic insults due to events such as asphyxiation or when a patient has collapsed secondary to cardio-respiratory arrest from various causes. The ventricles are not enlarged and indeed are within normal limits for size, but the basal cisterns are partially effaced, suggesting a mild degree of brain swelling at the time of this CT scan, but see comments regarding lack of sutural splaying in this context below. High attenuation material (representing acute blood) is seen in a patchy peripheral linear distribution, consistent with peripheral subarachnoid haemorrhage in the sulci over the surface of the brain, in the Sylvian fissures and in the posterior horns of both lateral ventricles. Whilst severe hypoxic-ischaemic brain injury (from whatever cause) can lead to oozing of blood into the subarachnoid space, the amount of subarachnoid blood and its distribution on C1’s scan is, in my view, more in keeping with traumatic aetiology for the subarachnoid haemorrhage. In the region of the falx there is also some high attenuation material, consistent with acute blood. In some places this acute blood appears somewhat irregular in outline and this too is likely to be due to blood in the subarachnoid space. However, particularly posteriorly, the appearances are more suggestive of the presence of acute subdural blood lying adjacent to the falx, with blood extending inferiorly to layer over the upper surface of the tentorium slightly more on the left than the right. There is also a little high attenuation material seen in relation to the falx cerebelli, suggesting some posterior fossa subdural blood. It is not possible to estimate the age of any of this acute blood on the basis of the neuroimaging appearances alone, as blood can appear bright on CT scans from soon after an episode of bleeding for up to 7-19 days; very occasionally longer (but see comments regarding timing of injury below). In addition, over both frontal regions there is evidence of subdural fluid collections of a different appearance to the acute blood. These other collections are of low attenuation (i.e. are darker than the underlying brain). The low attenuation collection on the left is slightly larger than the collection on the right. Whilst traditionally low attention subdural collections would be most likely to have been thought of as chronic subdural haematomas (i.e. evidence of older episodes of bleeding), it is increasingly recognised that low attenuation subdural collections can be seen in the context of acute injuries when the arachnoid membrane has been torn, as this can allow cerebrospinal fluid to leak into the subdural space and either collect there or dilute any acute blood present. Given the extent of the rest of the brain injury, in my view it is most likely that the lower attenuation fluid seen represents the result of an acute injury which has involved tearing of the arachnoid membrane. The scan appearances therefore are in my view explicable on the basis of being the result of a single event. The lack of any pathological evidence of older bleeding or a subdural neo-membrane would, in my view, support this conclusion. The scan has also been photographed on bony windows. No fracture has been identified. There is no soft tissue swelling evident to suggest a recent impact injury against a hard or unyielding surface. There does not appear to be significant sutural splaying at the time of this examination. This suggests that, although some cerebral swelling is evident as the basal cisterns are effaced, this has not caused any sutural splaying and suggests that the causative event is likely to have occurred very close to the time of the CT examination, in my view, i.e. before major swelling has had the opportunity to develop. I note that the post-mortem skeletal survey (which I have not seen) was reported as showing some probable sutural splaying. Given the extent of the hypoxic-ischaemic brain injury evident on the CT scan, I am not at all surprised that there may have been some sutural splaying by the time of the post-mortem skeletal survey, as brain swelling would have continued to develop in the period between the CT scan and the time of C1’s death. Given the extent of the brain injury, it is my view, it is extraordinarily improbable that C1 would have behaved any way normally after causative event, and is likely to have become obviously and severely unwell at the time of the causative event.”
“It is not possible to manipulate the images to view details of the bones of the skull. On the soft tissue images no obvious scalp swelling is apparent. I cannot comment on whether there is a skull fracture or whether there is spreading of the skull sutures (sutures are the gaps between the plates of bone that make up the skull). I note that Dr Stoodley, who has seen bone windows for this study, did not find evidence of skull fracture or sutural widening. The brain is dark and featureless. The normally visible distinction between grey and white matter has been lost. Although the brain may be slightly swollen, normal fluid filled spaces are still visible around the base of the brain, and there is no herniation of the brain across intracranial compartments. There is extensive high attenuation (looks white on the images) material seen over the surface of the brain. This represents recent haemorrhage. Much of this blood is in the subarachnoid space. That is to say, it lies in the cerebrospinal fluid that normally surrounds and bathes the brain and extends into the folds and fissures of the surface of the brain. Some of the blood outlines the falx and the tentorium. These tough dural membranes project inwards from the superior and posterior aspects of the skull to lie between the cerebral hemispheres (falx) and between the forebrain and the hind brain (tentorium). They are covered with a more delicate layer, the arachnoid membranes. It is likely that this blood is subdural in location – lying between the layers of membranes. There is also blood within the ventricles – the fluid filled spaces in the centre of the brain. The subarachnoid space is in free communication with the ventricles and blood can travel from one of these regions to another. The subdural space is normally separate from the subarachnoid space and blood within this compartment is less mobile. There are collections of low attenuation (looks dark) fluid over the convexities of both cerebral hemispheres. These collections are separate from the subarachnoid space and are likely to represent subdural collections. That is to say, the fluid lies between the membranes on the inner surface of the skull. From the radiological appearances, the darker fluid could represent either (a) old subdural haemorrhage (because intracranial blood becomes darker in appearance with time), or (b) cerebrospinal fluid that has looked from the subarachnoid to the subdural space through a tear in the (delicate) arachnoid membrane. I note that at autopsy this was found to be bloodstained fluid without evidence of old haemorrhage. This supports the second possibility (leakage of fluid through a tear/tears in the arachnoid membrane).” 55. In his evidence Dr Stoodley told me that, at the time of the scan, the level of brain swelling was mild. How then do the neuroradiologists interpret that which they found at the scan? Dr Stoodley in his report said: “The pattern of acute haemorrhage (both subarachnoid and subdural) demonstrated on the scan is most likely to be due to head trauma, in my view. Any insult of sufficient severity which causes reduced blood and/or oxygen supply to the brain can lead to hypoxic-ischaemic brain damage and, as stated above, severe hypoxic-ischaemic brain injury from any cause can lead to patchy subarachnoid haemorrhage. However, in my view the pattern of subarachnoid haemorrhage seen on C1’s scans is much more likely to be due to a primary traumatic cause rather than to be due to a secondary phenomenon of hypoxic-ischaemic injury. Given that the scan was perform only a few hours after C1’s collapse, it would be very unusual, in my experience, to see this degree of subarachnoid haemorrhage in the context of a primary acute hypoxic event such as an apnoeic event. Although there is only a small amount of acute subdural blood seen on the scan, its distribution in the posterior interhemispheric fissure and posterior fossa is unusual in conditions other than head trauma. I note that there was evidence of a blood clotting abnormality (thought to be secondary to C1’s clinical condition). I am aware that brain injury itself can lead to clotting abnormalities, but it will be important to obtain expert haematological advice regarding the nature of C1’s acute clotting dysfunction. In any case, from the point of view of the neuroradiological appearances, in cases of intracranial haemorrhage secondary to blood clotting abnormalities, the bleeding usually occurs into the substance of the brain itself rather than being subarachnoid or subdural bleeding over the surface of the brain. The pattern of subdural blood is therefore also more in keeping with a primary traumatic cause rather than being due to any secondary effect. The degree of hypoxic-ischaemic brain injury evident on the scan performed at around 0200 hrs (i.e. within a very few hours of C1’s clinical collapse) is very extensive and involves almost all of both cerebral hemispheres, the deep grey structures, brain stem and cerebellum. In view of the extent of this injury, it is virtually inconceivable that C1 could have behaved in any way normally after the event which caused this degree of brain injury, and he is, in my view, likely to have become obviously and severely unwell at the time of the causative event. Very occasionally in clinical practice, a child who has stopped breathing for some reason at home or elsewhere is brought into hospital having been resuscitated by carers and/or paramedics. It is very unusual, in my experience, to see any degree of hypoxic-ischaemic brain injury in any of these cases on such early scans, and I cannot recall ever having seen such a degree of hypoxic-ischaemic brain injury as is seen on C1’s scan in such a clinical situation. Infants and children who stop breathing for various reasons or who, for example, suffer seizures are not infrequently resuscitated by carers and professionals with various degrees of training and experience. Those infants and children who have head scans following such events do not, in my experience, show the features demonstrated on C1’s scan. In addition, in such circumstances it would be extremely unusual to see this degree of change in the cerebellar hemispheres secondary to such a primary hypoxic insult. Evidence of hypoxic-ischaemic change in the cerebellum on scans is occasionally seen in cases of non-accidental head injury, especially in injuries toward the more severe end of the spectrum of severity. In my view, therefore, the head injury is likely to have been the cause of C1’s collapse and the reason he required resuscitation, rather than resuscitation being the cause of these appearances. Looking at all of the neuroimaging appearances and interpreting those in the context of a very acute sever clinical deterioration, the only reasonable explanation that I can put forward which explains all of these features is that C1 suffered an episode of head trauma. The types of head trauma that infants of C1’s age can be subject to are: (i) birth related; (ii) accidental head injury, and (iii) non-accidental head injury. The acute blood event is unequivocally recent and could not date back to the time of delivery, and I am unaware of any condition that could have occurred at the time of delivery which would lead to such a devastating and sudden clinical deterioration as occurred to C1 on April 22nd 2005. There is no history of accidental head trauma of sufficient severity to account for the neuroimaging appearances, and C1 was not of an age where he could have manoeuvred himself into position to have caused himself such harm. The neuroimaging appearances seen are, however, entirely consistent with being due to an episode of non-accidental head injury. This is likely to have involved a shaking or shaking/impact mechanism, although it would not, in my view, have been necessary for any impact to have occurred with an external surface. Majority medical opinion is of the view that what is required to produce such injuries is likely to be the repetitive backwards and forwards movement of the unsupported infant head which pivots on the neck.” (i) birth related; (ii) accidental head injury, and (iii) non-accidental head injury. 56. In his oral evidence Dr Stoodley was asked to respond to certain points made by Dr Squier in her evidence. Dr Squier had asked rhetorically why, if fluids which showed a higher attenuation in the subarachnoid space, when they had gone through a tear, if they did, in the subarachnoid membrane, then in the subdural space showed a low attenuation? She said she would expect to find the same level of attenuation and the fluid in both the subarachnoid and subdural spaces. Dr Stoodley answered that it was not blood but cerebrospinal fluid (CSF) that was passing from the subarachnoid space through the tear to the subdural space. He told me that if one sees an obvious difference in attenuation between the subdural and subarachnoid spaces, then one can be confident that there is abnormal fluid in the subdural space. 57. Dr Squier further questioned the hypothesis of a tear in the arachnoid membrane. She could not think why trauma could cause a tear at one point in the arachnoid membrane and not at others. Dr Stoodley said that he could not demonstrate a tear from the scan, but it was not difficult to see in this case the CSF in the subdural space. It is the CSF and not the clotted blood in the subarachnoid space which goes through the tear into the subdural space. CSF is not found in the subdural space in a healthy child. It is found only in the subarachnoid space. Thus, if CSF is seen in the subdural space on the scan, there must be a mechanism by which it gets to the subdural space, and in his opinion that is by a tear in the arachnoid membrane. 58. Dr Squier suggested in her evidence that the low attenuation could mean that what was seen in C1’s subdural space was a chronic bleed, possibly from birth. Dr Stoodley rejected that. The CSF in the subdural space could not be birth related for the reason that it is the subarachnoid and not the subdural space that holds the CSF. In a healthy child there is no subdural space. 59. Dr Stoodley was asked what would be seen on the scan if C1 had suffered a simple cardiac arrest. He told me that it would give rise to hypoxic-ischaemic damage. If that was all the scan had shown, then that would be consistent with cardiac arrest. If there had been a simple cardiac arrest, then the hypoxic-ischaemic damage would take much longer to show up on a scan, possibly days, but not within hours. The unusual feature in C1’s case is that if he had suffered a simple cardiac arrest, then according to Dr Stoodley it is surprising that the scan showed quite extensive hypoxic-ischaemic damage three or so hours after his collapse and also evidence of acute subarachnoid haemorrhage at that time. In his view, hypoxic-ischaemic brain injury would not give rise to scan evident, acute subdural haemorrhage. In patients that are scanned after cardiac arrest, in his experience, followed by resuscitation efforts, hypoxic-ischaemic damage is seen, but not either subdural haemorrhage or low attenuation collections. 60. Dr Squier told me that in a case of severe hypoxic-hypoxia, together with coagulopathy – that is to say that blood does not clot properly if it bleeds – and where resuscitation puts pressure into the veins, then blood vessels in the dura can leak into the subdural space. Dr Stoodley accepted that compression on the chest causes thoracic pressure. Nevertheless, in patients he has seen or known about, where there was simply cardiac arrest followed by resuscitation, what is not seen on the scan is subdural haemorrhage. That is his clinical experience. Dr Stoodley accepted that the extensive haemorrhage in the subarachnoid space could be secondary to either hypoxic-ischaemic injury or secondary to trauma. He agreed that the quantity of blood in the subarachnoid space was unusual in C1, but the large amount of blood in the subarachnoid space was not unique, in his experience. To him, the amount of blood reflected the degree of severity of the trauma. 61. Dr Squier raised another matter, namely that it was difficult to know and/or see whether the blood seen on the scan was within the falx, where there are many blood vessels, or whether it was adjacent to the falx. Dr Stoodley rejected that. From the scan he said it was not difficult to see. There was no intradural blood. He did not see on the scan any leakage of intradural blood into the subdural space. 62. Finally, as to overwhelming infection, he accepted that ischaemic injury can occur after, for example, meningitis, but ischaemic change in such a case is focal and not general. It is also very unusual in such a case to see haemorrhage into the subdural space unless there was a severe clotting disorder, or the venous sinuses (that is the veins that carry the blood back to the heart) were clotted with blood, and there was no evidence of that. 63. Dr Gawne-Cain in her report said as follows under paragraph headed: “Opinion”: 1. “The combination of radiological findings – cerebral oedema with subarachnoid and multifocal subdural haemorrhage – is very suggestive of a traumatic cause. The additional finding of retinal haemorrhages is also in keeping with trauma, and completes the ‘triad’. This pattern of brain injury and haemorrhage is one that we associate with a rotational acceleration/deceleration injury such as might be caused by shaking. It is believed that rotational acceleration/deceleration of the head results in (a) stretching and tearing of bridging veins passing from the brain to the skull causing small volume subdural and subarachnoid haemorrhages; (b) stretching and damage to nerve fibres in the brain stem causing apnoea of variable duration (cessation of breathing) resulting in hypoxic insult to the brain; (c) in severe cases, tearing of fibres within the brain substance, or shear injuries. That rotational trauma can cause such injuries is generally accepted. However, the strength and nature of the forces required to cause the injuries is more in dispute. Confession evidence exists that suggests that shaking alone is capable of causing brain injury [1] but confessions are not always reliable. It has been suggested that the rotational forces generated by shaking are insufficient to cause brain injury, but are greatly increased if there is impact at the end of the rotational movement [2]. Arguments revolve around whether the biomechanical models used in experiments are sufficiently true to real babies, and whether the impact needs to be with an external object or could be with the infant’s own back/chest [3]. Certainly in cases of this kind, evidence of impact is not always found [4], and this is one of the reasons prompting workers in the field to search for alternative explanations for the constellation of findings. Even if it is accepted that the ‘triad’ may be caused by shaking a baby, the presence of the ‘triad’ does not automatically prove that shaking has occurred, and other possibilities should always be considered. I retain rotational acceleration/deceleration injury as a reasonable explanation of the radiological appearances. 2. In this case, no history of shaking has been given, and it is necessary to explore other possible explanations for C1’s collapse. 3. Birth may cause intracranial haemorrhages. However, the bleeding and brain injury are too recent and could not be explained by a traumatic birth. This possibility is rejected. 4. Accidental Trauma: An accidental fall resulting in impact to the head, with a significant rotational element, might result in intracranial haemorrhage and cerebral oedema. The generalised pattern of haemorrhage and the lack of evidence of impact in this case would be atypical for an accident. No accidental injury has been described. This possibility is rejected. 5. Cardiac Arrest: We know from the medical notes and statements that there was a significant episode of cardiac arrest. Could a cardiac arrest on its own, from whatever cause, be responsible for all of the intracranial findings in this case? It could account for the extensive ischaemic damage to the brain. It might result in a small amount of oozing of blood into the subarachnoid space from damaged capillaries. It has been suggested that it might also account for subdural haemorrhages. This controversial hypothesis (or theoretical possibility) was advanced by Geddes et al [5]. It does not fit with our clinical or radiological experience of babies with hypoxic brain damage of any known non-traumatic cause. The hypothesis was considered and rejected in the Court of Appeal in 2005. C1 had a documented clotting abnormality, believed to be secondary to the hypoxia/cardiac arrest. Could this, added to the brain ischaemia, account for the intracranial haemorrhage? It might explain why the subarachnoid haemorrhage was extensive (rather than a tiny amount of oozing). However, if there were a significant amount of haemorrhage from reperfusion of damaged capillaries, it is surprising that there was no evidence of haemorrhage into the brain substance. Even with clotting abnormality, it is difficult to explain the subdural haemorrhages without some element of trauma. In this respect, the dark subdural collections over the cerebral convexities are very important. They do not represent recent haemorrhage alone, and thus cannot be the straightforward result of oozing from blood vessels, even if it is accepted that this could be caused by hypoxia and/or a blood clotting abnormality. In my opinion, the ‘bloodstained fluid’ is most likely to represent bloodstained cerebrospinal fluid that has leaked into the subdural space through a tear/tears in the arachnoid membrane and such a tear/tears would be caused by trauma. Thus I reject primary cardiac arrest, from whatever cause, with or without a blood clotting abnormality, as a cause of the intracranial appearances in this case. 6. Traumatic Resuscitation: It was suggested in the Coroner’s Court that the constellation of findings could result from a combination of cardiac arrest, clotting abnormality and a traumatic attempt at resuscitation by a non-professional. As discussed above, it is my opinion that some trauma occurred to account for the subdural collections, in particular the dark subdural collections. Cardiopulmonary resuscitation might cause certain rib fractures, but would not normally cause head trauma. I cannot see that resuscitation, even if inexpertly performed by an amateur following instructions over the phone, could cause traumatic head injury. However, if there was shaking in an attempt to revive, then it is plausible that intracranial haemorrhage might be caused. In the documents available to me, including transcripts of the extensive police interviews, no history is given of shaking to revive. This explanation is plausible but very unlikely. 7. Intracranial infection may be associated with brain ischaemia, subdural collections and small amounts of intracranial and subdural haemorrhage. The radiological pattern in this case is not at all typical of intracranial infection. It is my understanding that there is no clinical or post-mortem evidence for intracranial infection. This explanation is rejected as a possible cause of the injuries. 8. Choking or Aspiration: This has been advanced by some workers as a possible cause of the triad of encephalopathy, subdural haemorrhage and retinal haemorrhages. The hypothesis is not, at present, backed by clinical evidence or experience, and is not generally accepted. The details of the arguments for and against this hypothesis are best discussed by other experts, including clinicians. From the radiological perspective, even if it is accepted that choking could cause subdural haemorrhage, it would not cause leakage of cerebrospinal fluid into the subdural space and would not explain the dark subdural collections. This explanation is rejected as a possible cause of C1’s injuries. 9. Immunisation: That immunisation might cause encephalopathy and intracranial haemorrhage is a minority view, and is not generally accepted. I leave it to other experts to discuss to what extent this is plausible. From my radiological perspective, even if a reaction to immunisation could cause cardiac arrest, hypoxic brain damage and intracranial haemorrhage, it would not explain the dark subdural collections. This explanation is rejected as a possible cause of the injuries.” 64. In her evidence, Dr Gawne-Cain adhered to her conclusions. She told me that the radiological pattern in C1 is not at all typical of intracranial infection. There was no patchy change. Within infection one will not find extensive subarachnoid haemorrhage or dense subdural haemorrhage. When cross-examined by Mr Tillyard, she told me she would not expect to see the amount of subarachnoid haemorrhage with hypoxic-ischaemic damage. She would be surprised if the hypoxic-ischaemic damage had caused the amount of subarachnoid damage, but if it did, then the cause could be coagulopathy. So far as the falx was concerned, some of the blood she saw on the scan was adjacent to the falx. So far as the subdural blood found at post-mortem was concerned, Dr Gawne-Cain told me that she could not exclude the possibility that it had been caused by oozing of the blood vessels together with coagulopathy, but she was confident that CSF in the subdural space shows up on the scan as low attenuation. She told me that she thought it pretty unlikely, but possible, that the fluid seen in the subdural space was from leaky blood vessels because the scan was performed two or three hours after the event causing C1’s collapse, which is a very short time. She is used to seeing effusion occurring over days and not hours. In her neuroradiological experience, she had never seen subdural haemorrhage come after hypoxic-ischaemic damage. 65. As to how the CSF got from the subarachnoid space into the subdural space, she told me that a tear in C1’s subarachnoid membrane is the best explanation there is because not enough time had elapsed between the event causing the collapse and the scan for effusion to occur. There was no evidence of old blood in the subdural space and there was no inflammation. Mr Tillyard suggested to her that in C1’s case there may have been asymptomatic bleeding at birth. Dr Gawne-Cain said that if that was so, then there would be hemosiderin staining, which there was not. 66. Mr Edwards He told me that he frequently looks at scans to make clinical and operative decisions. If he is to operate, he has to interpret from the scan the size of haematoma which he may have to remove. At paragraph 3.9 he reviewed the scan. His findings are similar to those of Dr Stoodley and Dr Gawne-Cain. He told me that any fluid seen in the subdural space is pathological and not a naturally occurring fluid. C1 did not show symptoms of cardiac arrest because there was subdural haemorrhages and because of the low attenuation. For there to have been oozing of vessels into the subdural and subarachnoid spaces, then the haematoma would have been increased in size. The amount of swelling of the brain was modest at the time of the scan. 67. As to the arachnoid membrane, he told me it is very delicate. One can actually see through it. The most likely point of tearing would be at a point where the blood vessels traverse the subdural space. A tear would allow the CSF to pass through from the subarachnoid space to the subdural space. There was no other explanation for the presence of CSF being in the subdural space than that it got there through a tear in the arachnoid membrane. He told me that, in his opinion, subarachnoid bleeding can occur in the presence of both brain swelling and coagulopathy. He has seen a similar amount of blood in other cases of trauma. Furthermore, in C1’s case the degree of subarachnoid haemorrhage was no worse at the time of the post-mortem examination than it was in the scan. Thus, as the clotting anomaly was not corrected for at least three and a half hours after the scan (that is to say, by the administration of fresh frozen plasma) were the subarachnoid haemorrhage to be a direct result of oozing from the encephalopathic brain, he would have expected to see an increased amount of subarachnoid haemorrhage present. 68. So far as intradural bleeding was concerned, he saw from the scan that the blood was adjacent to the falx. Furthermore, the post-mortem photographs showed the same. He did not accept that the subdural blood was a result of hypoxia together with coagulopathy and/or that attempts at resuscitation would lead to the presence of haemorrhage in the subdural space. He told me he had never seen oozing from the dura. In his report at paragraph 5.03.16, he said this: “I am not aware of any clinical cases in which subdural haemorrhage of this appearance was seen in the context of a non-traumatic hypoxic-ischaemic encephalopathy. This is supported by the medical literature: a paper by Byard et al (2007) reviewed 82 infants and children who underwent autopsy for proven non-traumatic hypoxic ischaemic encephalopathy. None were found to have a subdural haematoma at autopsy. I am aware of the more recent abstract presented at a recent neuroradiology conference. The authors undertook a retrospective case note and imaging review of all infants under the age of three years, dying in the emergency department or admitted to the paediatric intensive care unit after a cardiorespiratory arrest, over a six year period. Of the 60 children evaluated, 45 had a combination of post-mortem examination, CT brain imaging or both. None of these infants had a subdural haematoma. It should be noted that the abstract would have been subject to peer review, but the full details of the study have not been published. In my opinion it is unlikely that the subdural haematomas seen in this case have arisen from a non-traumatic cause.”
“Coagulation tests were also checked and in Dr Collins’s report [E379] it is stated that they were received in the laboratory at 11.11 on 23.4.05, which is some time after the initial collapse, hypoxic and hypothermic episodes and a period of acidosis and hypotension (F17). The results are reported as follows: prothrombin time 15 seconds (prolonged), activated partial thromboplastin time 32.8 seconds (within the normal range) and fibrinogen 0.8 g/L (NR 2-4 g/L). A thrombin time, a measure of functional fibrinogen, was correspondingly prolonged at 19.6 seconds. These are also recorded in a laboratory report (F100). Dr Collins has concluded that these results are compatible with the clinical picture of collapse and hypoxia, reflecting an early form of disseminated coagulation which is a condition in which a trigger (such as hypoxia, infection or inflammation) activates the coagulation cascade systemically and causes consumption of clotting factors and platelets resulting in prolonged clotting tests and decreased platelets. This seems the most likely explanation of the abnormal coagulation tests in this child.”
“C10 There are two coagulation test results for C1: one which shows a normal fibrinogen and one taken later which shows a significantly low fibrinogen in association with a prolonged prothrombin time and normal activated partial thromboplastin time. Given the clinical picture of collapse, hypoxia, hypothermia, hypotension and acidosis, these tests are compatible with a progressive consumption coagulopathy, secondary to the clinical state and not the cause of it.” 71. At G265 she concluded that there is no evidence, either clinical or laboratory, that C1 had a bleeding diathesis that would predispose him to subdural and retinal haemorrhages. In her evidence she agreed with Mr Edwards that the platelet count of C1 was not low enough to cause spontaneous haemorrhage. She agreed that coagulation would be brought about by hypoxia, and a simple cardiac arrest might have triggered a clotting disorder. Septicaemia would have to be severe and overwhelming to cause coagulopathy. The antibiotics administered at about midnight to C1 would not have reversed an infection. She said that there was no evidence of any overwhelming infection. The post-mortem examination showed to her no evidence of infection. 72. Dr Giogrande agreed with Dr Thomas’s report. He told me that in respect of Mr Edwards’ seeking clarification at paragraph 5.04 of his report as to the severity of C1’s coagulopathy, he would say that the blood sample indicated a mild coagulopathy. Both haematologists agreed that C1 had abnormal clotting results, which showed evidence of coagulopathy which was secondary to the clinical state of C1 and not the cause of it. Dr Thomas further explained that the effect of coagulopathy is to make the sufferer more susceptible to bleeding and to bleed for longer but not any faster. 73. The Neuropathologists Dr Smith and Dr Squier examined microscopically a number of brain and spinal cord sections taken at the post-mortem examinations. They also examined macroscopically the brain by way of digital images taken at the time of the post-mortem examination. Dr Squier, in her report of31 January 2008 , summarises the pathological findings acute brain swelling, acute subarachnoid haemorrhage, axonal APP expression consistent with impaired blood and/or oxygen supply, axonal swellings in spinal nerve roots, subcortical splits, acute intra and subdural bleeding, fresh spinal extradural bleeding, and haemorrhage into the base of the pons. 74. As I understand it, the only disagreement between Dr Smith and Dr Squier is as to the causation of the axonal swellings and the spinal nerve roots, to which I will come in due course. Both are agreed that the swelling of the brain, as at the time of the scan, was mild and that the brain swelled after the scan, so that at death the brain was seen to be swollen with a tight dura and brain herniating through cuts in the dura. Both agreed that there was more subarachnoid haemorrhage than usual. Dr Smith said it was far in excess of what he had seen in his experience. Dr Squier described it in her evidence as “very extensive, particularly over the cerebellum”
“The pattern of spinal cord nerve root axonal injury, however, does not appear to be ischaemic in origin. I am aware of focal nerve root injury being described in the setting of brain swelling (unpublished observation) and the brain was swollen in this case. Equally, focal nerve root injury has been described in the setting of trauma. I will attempt to interpret the neuropathological findings in relation to the specific question of whether or not there has been trauma in this case. It is important to note that there is no external evidence of trauma in this case. Much of the neuropathology is non-specific and can be attributed to the coagulopathy demonstrated by haematological investigations. I am, however, concerned by the focal subdural spinal cord bleeding associated with axonal damage within nerve roots. In my experience, this is frequently seen in alleged cases of non-accidental injury, and the cases of focal nerve root injury associated with cerebral swelling do not have surrounding haemorrhage present. I can find no evidence of any non-traumatic disease process within the brain or spinal cord which would account for the sudden collapse of this infant. It is, however, possible that a vast majority of the neuropathological changes seen may have developed secondary to a non-neurological collapse in this infant. As noted above, however, I do have concerns regarding the focal subdural bleeding in relation to nerve roots which at one level is associated with focal axonal injury. In summary, there is nothing from neuropathological examination of this case which would allow a definitive diagnosis of non-accidental injury to be made. Equally, there is no evidence of any neurological disease to account for the sudden demise of this infant. In summary (in response to specific questions stated in correspondence 12.10.07): In summary (in response to specific questions stated in correspondence 12.10.07): 1. “C1 has developed global cerebral ischaemia (lack of blood to the brain) resulting in irreversible brain injury and brain swelling. The cause of the sudden collapse cannot be definitively ascertained by neuropathological examination. 2. C1 has died as a result of lack of blood flow to the brain and subsequent brain swelling. This does not, however, account for his sudden collapse. 3. The potential causes of sudden collapse at this age are numerous. For example, there has been an undiagnosed cardiac cause for collapse which would produce much of the subsequent neuropathological features. However, I am concerned by the focal spinal cord pathology which, in my opinion, is suggestive of an episode of trauma. I cannot give an alternative explanation for such a lesion in the absence of trauma. 4. In my opinion, trauma is the most likely cause of sudden collapse and subsequent brain injuries, but I cannot exclude the possibility of non-neurological causes for sudden collapse (such as cardiac). 5. As above”. 77. In his oral evidence, Dr Smith said that axonal swellings in the spinal nerve roots can be associated with trauma. They can also be associated with a swollen brain, but in such a case one does not see bleeding into that area. In trauma nerve damage and bleeding is seen. In cases of a swollen brain with no trauma, the swelling is a slow process and, importantly, haemorrhages have never been described. 78. Dr Squier told me that the removal of the spinal cord at post-mortem examination is often a traumatic procedure and that the bleeding may be a post-mortem artefact. As to that latter matter, she accepted, when cross-examined, that any bleeding could not have been a post-mortem artefact because, as per Dr Smith at GQ24 and 25, the BAPP accumulation is an active process which requires cellular energy, i.e. it will not occur after death. Dr Squier told me that pulling out the spinal cord at post-mortem examination could cause the axonal damage. Dr Smith told me that the removal of the spinal cord would not necessarily cause axonal damage but, in his experience, the technique of removing the spinal cord is not an explanation for the bleeding around the damaged nerve roots in the spinal cord. Dr Smith told me that the presence of damage to the nerve roots has no relevance to coagulopathy. He believes that it is a coincidence that there was damage to the nerve roots and there is also localised bleeding. Furthermore, it was a remarkable coincidence that blood had gathered at the site of the damaged nerve roots and nowhere else in the spinal cord. If, as was suggested by Dr Squier, there was leakage of blood as a result of the coagulopathy, he was careful to say that the localised area of bleeding around the nerve roots must be cautiously interpreted. 79. Dr Squier was struck by the position of the axonal swellings, i.e. they occurred at the point where they crossed the dura and where fresh bleeding occurred. Into this she factored C1’s coagulopathy. But, as she said at GQ120/121, she could provide no explanation for these swellings, and that it would be unsafe to make a diagnosis of trauma. “I simply do not know how to interpret this finding”
“There is no key provided to identify exactly which images were made of which eye, but examination of the digital images on the CD provided by Dr Leadbeatter shows that there is extensive optic nerve sheath haemorrhage involving both optic nerve sheaths. This appears more severe at the proximal ends of the optic nerve (i.e. in the region immediately behind each eye). Here is macroscopically visible blood within the orbital soft tissue adjacent to each optic nerve and further back within the orbital fat. No views of the anterior surface of the eyes are provided, so I am not able to comment on the front of the eyes, conjunctivae and corneas. The eyes have been opened in the coronal plane, and a diagram provided on the copy of the neuropathology request form confirms that this is approximately at the equator of each eye (the mid-point from front to back). There is extensive bleeding over the surface of the retina of each eye in all retinal areas. There is widespread retinal thickening due to oedema and, in addition to post-mortem retinal folding, there also appear to be broad perimacular folds present in both eyes. Widespread intraretinal bleeding amounting to retinoschisis (splitting of the retina) is evident along the cut margins of the retina of each eye. Haemorrhage in the posterior portions of the eyes, associated with the perimacular folds, obscured the optic nerve heads in both eyes so that these structures are not visible. In one of the eyes – it is not indicated whether this is the left or the right in the information provided to me – there is quite marked detachment of the anterior vitreous gel which can be seen appearing to ‘billow out’ behind the lens. Some blood can also be seen trapped within the interstices of the various vitreous compartments. Given the way in which the eyes have been opened (in the coronal plane) there is no opportunity to examine the anterior chamber structures macroscopically. The lenses appear to be macroscopically normal.”
“Examination of the sections prepared in the Cardiff laboratory reveal that there is very extensive retinal haemorrhage affecting all retinal layers and all retinal areas in both eyes. There is some degree of autolysis, which may be a reflection, in part, of the considerable damage to these retinas. There is extensive pre-retinal blood, as well as subhyaloid (beneath the vitreous) bleeding and focal bleeding into the vitreous. Many areas of retinal detachment, with subretinal blood, are present and, in some areas, there are small foci where there has been retinal pigment epithelium (RPE) detachment with sub-RPE bleeding. However, much of the RPE in both of the eyes is detached by artefact. There is extensive vitreous detachment. Whilst vitreous detachment may occur due to post-mortem artefact, in both of these eyes it is associated with, in the area of the vitreous base, detachment of peripheral anterior retina and ciliary body. Here some areas of haemorrhage beneath the detached ciliary body epithelium are evident, indicating that this is an ante-mortem phenomenon. Somewhat oblique cuts have been prepared through the histology blocks which include anterior segment. Here the anterior chamber of each eye can be seen to contain proteinaceous exudates, but no blood. There is some artefactual detachment of the corneal endothelium and some artefactual lifting and detachment of corneal epithelial cells. There is no evidence of conjunctival, subconjunctival or episcleral haemorrhage. The cornea, iris and lens do not appear to have been disrupted, but the histological view is quite restricted because of the orientation of the tissue blocks. In both eyes there is extensive bleeding within the sclera in the area of the vascular circle of Zinn adjacent to the optic nerve insertion into the eye. In the left eye this bleeding is linked to a focus of choroidal haemorrhage. In the central retinal vein of the right eye, at the optic nerve head, there is a collection of blood clot adherent to the vessel wall. In two veins within the orbital tissue adjacent to the right eye there is also more blood clot. In further sections prepared in the Manchester laboratory, this clot is seen to extend to the branching point of a large vein. Many of the peripheral nerves within the orbital tissue adjacent to both eyes contain blood beneath their external sheaths. Bleeding has also occurred free within the orbital fat and within the eye muscles. There is very severe optic nerve sheath bleeding (most marked in the anterior parts of the nerves) with intrasheath blood, subdural and subarachnoid bleeding, and bleeding external to the optic nerves.” 82. As I read Dr McCarthy’s report at G54, he is in agreement with those findings. As I understand their evidence, there is no disagreement between them as to the nature of the injury in C1’s eyes. Dr Bonshek put it this way, at G77: “In the case of C1, whilst extensive and severe retinal haemorrhages are a major feature, other significant findings present are: perimacular folds, retinal detachment, retinal oedema, vitreous detachment, RPE detachment and haemorrhage, choroidal haemorrhage, scleral haemorrhage, haemorrhage beneath the ciliary body epithelium, anterior chamber exudates, optic nerve, sheath haemorrhage and orbital haemorrhage, and acute inflammatory cells within the conjunctive eye.” 83. The ophthalmologists are also agreed as to the likely cause of these injuries. Looked at in isolation, they told me, the causes of retinal haemorrhage are numerous. But there is no history of accidental trauma. No natural cause of the retinal haemorrhages has been identified. Coagulopathy and CPR may be associated with retinal haemorrhages, but in these situations the bleeding is typically in the posterior retina and is limited in extent. Although there was a blood clot within two orbital veins of the right orbit and within the central retinal vein within the right eye, Dr Bonshek understood that C1 suffered from secondary coagulopathy. He found no clotting elsewhere. The post-mortem and histology report give no description of excessive/intravascular clotting elsewhere in the body. C1 was given fresh frozen plasma. Dr Bonshek thus interprets the blood clots to be due to coagulopathy. Meningeal coccal meningitis and septicaemia have been described as associated with retinal haemorrhages, but in his opinion there was no evidence of any infection. Birth is a recognised cause of retinal intracranial bleeding, but with C1, he said, the retinal bleeding was recent. 84. Dr Bonshek said in his report that the injuries were not caused by resuscitation. The view of the working party of The Royal College of Ophthalmologists was that CPR alone was very unlikely to cause retinal haemorrhage, even if carried out by unskilled people. Dr Bonshek also excludes the injuries being caused by C1’s immunisation. [See G80]. Most experts, Dr Bonshek said in his report of30 July 2007 , agree that the combination of retinal haemorrhage, subdural haemorrhage and acute encephalopathy, is very suggestive of NAI, if other causes cannot be identified. Taking all the findings, both ocular and non-ocular, Dr Bonshek is left with NAI as the most likely cause of the irregular findings. Findings within the eyes and the orbital tissues are at the severe end of the spectrum in cases which he has examined. In his opinion, the likely mechanism for the injuries was shaking. Dr Bonshek was careful in his report to state that the “triad” of injuries cannot be taken in isolation as conclusive of C1’s death, but it is a strong indicator. He told me that he was at a loss to find a credible alternative explanation for the findings within the eyes and associated structures of C1. 85. Dr Bonshek explained to me how, in both eyes, the epithelium structure was lifted and haemorrhages were beneath it. The epithelium is a single layer of cells between the retina and the choroid. In C1’s left eye the choroid itself has had haemorrhages, but there were also haemorrhages in the fat, muscles and nerves outside each eye. The retinal haemorrhages were seen two hours after his collapse, which was very quick. In his opinion, the retinal haemorrhages had occurred at or before C1’s arrival in hospital. His coagulopathy occurred after his brain was damaged. He told me that the combination of retinal haemorrhage, optic nerve haemorrhage and subdural haemorrhage is quite closely associated with trauma, however that trauma may have been caused. He also told me that the presence of perimacular folds in both eyes is an indicator of the severity of the injury but it was not an indicator whether the injury was accidental or not. There was no evidence of infection over the surface of the brain in C1. As I have said, he told me that the findings in C1’s eyes were very suggestive of trauma. If no history of accidental trauma was given, then non-accidental injury was left as the only possibility. 86. Dr McCarthy in his report, on3 January 2008 , posed three questions: (1) Is this non-accidental injury of a shaking/impact aetiology; or (2) is this accidental injury with impact aetiology; or (3) are the brain swelling subdural haemorrhages, ocular and optic nerve haemorrhages secondary to an event in which there was a spontaneous cardiac arrest, of undetermined cause, and there was subsequent coagulopathy and resuscitation? At G255 Dr McCarthy sought to answer his questions: “The reports provided by Dr Steven Leadbeatter and Dr Richard Bonshek are both extensive and detailed, and refer to various descriptions of causation contained in Medical Literature. There is an abundance of Medical Literature on this subject. However, in my opinion, there has been little true scientific progress in the last five or so years regarding the pathophysiological causation of the features seen in this so-called triad. In this case the minor injuries that have been noted, and in particular I refer to the small bruising to the left side of the back of the scalp and the small areas of bruising below the jaw, have been attributed to the acts of resuscitation and the subsequent coagulopathy. In this respect, if this is the case, then there is no unequivocal evidence of any impact injury to his child. The possibility of a soft impact is also considered wherein no actual bruising has been caused. This can neither be included nor excluded. Thus, in the absence of any definite impact injury to the head of this child, one has to consider the possibility that the subarachnoid haemorrhage, the cerebral encephalopathy and the haemorrhages into the eyes have been caused during an act of shaking injury. This child was eight weeks of age and prior to Wednesday20th April 2005 , was in apparent good health and thriving. This child received multi-agent vaccination on the20th April 2005 from which time the child was said to be more sleepy than usual. This is clearly subjective and is not amenable to verification. However, in terms of causation of the type of haemorrhage, brain swelling and lesions identified in this child at the time of admission to hospital, I believe that the temporal association with vaccination is merely coincidental. I know of no peer reviewed literature which would suggest that this triad of features can be caused by vaccination. Turning now to the suggestion that the encephalopathy, the subarachnoid haemorrhage and the retinal haemorrhages were a consequence of a cardiac arrest of unknown cause with subsequent coagulopathy, this similarly falls into a category wherein there is no verified peer reviewed literature to indicate that this is an event that occurs or can occur with any frequency. I know of no verified accounts of cardiac arrest resulting in the triad of features as seen in this child. This suggestion appears to be based on a hypothetical situation and perhaps has been reinforced by fairly recent medical literature, which hypothetically regards the features of the triad as being secondary events subsequent upon some other causative event. These have variously been suggested as Pertussis infection, bouts of continuous coughing, retching and vomiting, and other non-specific events that result in raised venous pressure within the brain and within the eyes. Apnoeic events and trivial injury have also put forward as suggestions, as have other events. … Regarding the wellbeing of this child and the history given, it is highly unlikely that this child would have been able to function to any normal extent following the development of the brain swelling, subarachnoid haemorrhage and retinal haemorrhages. Therefore, it is entirely likely that these findings developed at or very close to the time that the haemorrhage occurred, i.e. the history given that this child was sleeping in the bath at 20.00 hours and then took a small feed at 21.00 hours, indicates that the child could not have been suffering these devastating injuries at that time. The paramedics attended at 23.20 hours and it is entirely likely that these injuries occurred shortly before that time. In final conclusion, therefore, I would agree with the report that has been issued by Dr Richard Bonshek, and in particular the statement that Dr Bonshek has made on page E437 where he says: ‘I am at a loss to find a credible alternative explanation for the findings within the eyes and associated structures of C1”
“I agree that the numerous marks found on post-mortem examination…” (That is a reference to the bruising on the exterior of C1) “…could be attributed to attempted resuscitation. Also the finding of two bruises on the underside of the chin and bruises on the anterior abdominal wall could be secondary to consumptive coagulopathy rather than representing genuine non-accidental bruises. Finally, the microscopic rib fracture not seen on any other examination but found on post-mortem histological examination also could be attributed to attempted resuscitation.”
“I agree that many of the findings could be related to a prolonged period of circulatory arrest and resuscitation with consequent consumptive coagulopathy. Many of the mentioned pathological findings may explain the mode of death but they do not account for how the original collapse that precipitated hospital admission occurred. Possibilities that might explain such a collapse include: (a) A specific natural cause. (b) So-called ‘near miss’ Sudden Infant Death Syndrome (now called apparent life-threatening event – ALTE). (c) Shaken Baby Syndrome. A) A specific natural cause A very through post-mortem examination and subsequent second neuropathological and eye examinations failed to identify any natural cause or non-traumatic disease process within the brain or spinal cord which would account for the sudden collapse of the child. Therefore, I think that a specific natural cause was not the cause of the sudden collapse. B) ‘Near Miss’ Sudden Infant Death Syndrome C1 was in an age group where natural deaths of obscure causation are known to occur. In some cases the infant is discovered after the initiation of whatever process it is that leads to death but before death has actually occurred (‘near miss’ SIDS). Although resuscitation might be successful, there may be serious consequences if the heart has stopped beating for a significant period of time. However, in such cases extensive retinal haemorrhages and other brain damage seen in this child are not found, and I think that this was not the cause of C1’s sudden collapse. C) Shaken Baby Syndrome Shaken Baby Syndrome (SBS) is a widely recognised diagnosis in the medical literature. The medical components of SBS include retinal haemorrhage, subdural or subarachnoid haemorrhage and associated fractures with a paucity of external physical findings (Caffey J. The whiplash shaken infant syndrome: Manual shaking by the extremities with whiplash-induced intracranial and intraocular bleeding, linked with residual permanent brain damage and mental retardation. Paediatrics 1974; 54: 369 -403). The presentation of SBS originates from a mechanical injury, which results in angular rotation of the infant’s head sufficient to crate acceleration and deceleration forces of the type frequently encountered in major automobile collisions. The clinical presentations vary from a pure shaking incident, where the child is violently shaken; blunt force injury, where the child is thrown or receives a blunt impact injury to the head; and, finally, as a component of other injury in the battered child syndrome. Many reports have offered evidence that shaking alone can produce life-threatening injuries in infants (Alexander R, et al: The incidence of impact trauma with cranial injuries ascribed to shaking. Am J Dis Child 1990; 144: 724 – 726; 3. Gilliland MGF, et al: Shaken babies: some have no impact injuries. J Foren Sci 1996; 41: 114 – 116; 4. Lazoritz S, et al: The whiplash shaken infant syndrome: has Caffey’s syndrome changed or have we changed his syndrome? Child Abuse Neglect 1997; 21: 1009 – 1014). Further support for the latter claim comes from the statements of perpetrators and other witnesses and the lack of evidence of impact. The relative incidence of brain injury due to the shaking or the impact injury remains unknown; in many cases both forms of injury may be present. However, despite the debate over the exact mechanism of injury, the classical findings of retinal haemorrhages, subdural haematoma, and brain damage cannot be fully explained by any other medical entity. The SBS apparently results when a young child is shaken by holding the thorax, shoulders, or abdomen. This shaking must be done by an individual much larger than the child, usually an adult, in order to achieve sufficient acceleration of the body of the child. During the shaking it is assumed that the head can be whipped back and forth because of the relative inability of the infant to control its neck muscles and because of the relatively large mass of the head in relation to body. This mechanical instability perhaps explains why whiplash-shaking deaths are uncommon in children older than one year. In addition, the infant skull has the flat base and still not developed fossae (that typically hold the adult brain in place) permitting more rotation to the brain than in adults during acceleration-deceleration. Finally, the underdeveloped myelinisation of the neuronal axons of the child’s brain predisposes to laceration of long neurons which is a typical injury/finding in SBS. The victim of the SBS may have bruising over the upper extremities, neck or the chest where the child was held and shaken. However, bruising is more the exception than the rule. Old or new fractures of the long bones and/or ribs may be present in the shaken baby syndrome but they represent associated secondary injuries which indicate that the child has been abused during his/her life and not primary injuries due to the primary effect of shaking forces. Retinal haemorrhages have been rarely documented after resuscitation. (Wissow LS. Child abuse and neglect. N Engl J Med 1995; 332: 1525-31; Odom et al. Prevalence of retinal haemorrhages in paediatric patients after in-hospital cardiopulmonary resuscitation; a prospective study. Paediatrics 1997; 99: E3). Studies addressing this issue have not shown as association between retinal haemorrhages and cardiopulmonary resuscitation in the absence of pre-existing brain trauma, seizures, tumours, sepsis, severe dehydration or coagulation defects. (Gilliland MG et al. Are retinal haemorrhages found after resuscitation attempts? A study of the eyes of 169 children. Am J Forensic Med Pathol 1003; 14: 187-92; Kantor R. Retinal haemorrhage after cardiopulmonary resuscitation or child abuse? J Pediatr 1986; 108: 117-32). An experimental study using piglets could not induce retinal haemorrhages through resuscitation (Fackler J et al. Retinal haemorrhages in newborn piglets following cardiovascular resuscitation. Am J Dis Child 1992; 146: 1294-6). The severity and type of retinal haemorrhages and other pathological findings in this case, as Dr Bonshek concluded, indicated severe trauma due to non-accidental injury. As for the impact of the vaccination of C1 and whether this could, in whole or in part, explain the injuries that C1 subsequently displayed, I confirm that I am not aware of any literature linking routine immunisation with pathological changes found in the brain and retina of C1, but this is not my area of expertise and I defer to Dr G Debelle’s comments in his paediatric overview. Taking into account all clinical, imaging and pathological findings and opinions, I think that C1 had collapsed and later died due to a non-accidental head injury. He showed a combination of findings which indicate inflicted injury by shaking.” (b) So-called ‘near miss’ Sudden Infant Death Syndrome (now called apparent life-threatening event – ALTE). (c) Shaken Baby Syndrome. A) A specific natural cause B) ‘Near Miss’ Sudden Infant Death Syndrome C) Shaken Baby Syndrome 90. In his oral evidence, he confirmed that nothing he had seen or read altered his opinion. In relation to the bruises on the back of C1’s skull, they could be attributed to the three causes as set out in Mr Edwards’ report at paragraph 5.03.1, namely a blow to the back of the head on a mattress or carpet; pressure on the back of the head due to resuscitation; and post-mortem artefact. Dr Vujanic was taken to task by Mr Tillyard for not mentioning this opinion in his report. Dr Vujanic told me that post-mortem artefact could be excluded. Contact with a soft surface was more likely than bruising following resuscitation attempts, but he did not rule out the latter. He agreed with Dr Smith that the hypoxic-ischaemic injury was second to the cardiac arrest, but that the whole picture had to be looked at. 91. So far as Prolonged QT Syndrome was concerned, it was a theory, with no firm, confirmed evidence. He agreed that there may be a connection between cardiac arrest and Prolonged QT Syndrome, but that in babies who die after cardiac arrest from Prolonged QT Syndrome there are no retinal haemorrhages seen, and certainly not the degree of retinal haemorrhages suffered by C1. He concluded his evidence by saying that the retinal haemorrhages in C1 were seen within two hours of his admission. One hour of resuscitation, even with coagulopathy, was very unlikely to cause the retinal haemorrhages. 92. Professor Risdon in his report at G95 sets out the history. He sets out the reports of Dr Stoodley and Dr Bonshek, and at G101 his comments were as follows: 1. “Both Drs Stoodley and Bonshek are of the opinion that baby C1 had suffered brain injury resulting in his collapse and unconscious state on admission to hospital, and that the injury had been sustained shortly before his admission. Both rejected the concept that the child’s death was in any way related to the routine inoculations he had received shortly before his death. 2. I would agree with this conclusion. I know of no concrete evidence linking routine immunisations with intracranial pathology of the type seen in this case. Head injuries and sudden unexpected death from other causes often affects children of this age, and this is also the time at which immunisation is given. The two events may well be temporally related, but not in a causal sense. 3. Dr Bonshek did not think that the retinal haemorrhages were related to resuscitation. 4. I entirely agree with both Drs Stoodley and Bonshek that this child had died as a result of a head injury, the characteristics of which indicate an inflicted nature. 5. The triad of findings that most authorities involved in child protection would regard as indicative of a shaking or shaking impact injury, namely intracranial haemorrhage (subdural and subarachnoid haemorrhage), retinal haemorrhage and encephalopathy, were present in this case. 6. Dr Stoodley refers to a minority medical opinion that this triad of findings can occur in situations other than non-accidental head injury. They have suggested factors such as aspiration of milk during feeds, choking, vomiting, paroxysmal coughing or gastro-oesophageal reflux. Dr Stoodley remarks that these opinions are in the main expressed by those who do not have day-to-day involvement in a clinical or radiological management of infants or children who suffer from these conditions and that the opinions expressed by these practitioners is not supported by everyday clinical experience. 7. I would wholly endorse this opinion and would note that the characteristics of the individual components of the triad are of great importance in distinguishing those cases due to non-accidental injury. 8. Shaking or shaking/impact involves severe rotational acceleration/ deceleration forces that have the effect of causing the brain to rotate within the skull. This ruptures small communicating veins on the surface of the brain that are the source of the subdural haemorrhage. These haemorrhages are important only as an indicator of the mechanism of injury. They do not form significant space occupying lesions, as do the more extensive collections of blood (subdural haematomas) mostly seen in older patients. The subdural and subarachnoid haemorrhages in this case clearly form only thin films as indicated by the post-mortem photographs. 9. The retinal haemorrhages associated with rotational acceleration/ deceleration injuries are typically extensive, involve all layers of the retina and are usually associated with haemorrhage around the optic nerves, all features that were present in this case. Retinoschisis and perimacular folds are also features characteristic of this type of injury. 10. Detailed neuropathological examination can indicate evidence of trauma to nerve cells and their extensions within the brain. These may be in addition to changes caused by hypoxia and ischaemia that are almost invariably present in babies who survive on life support. There may also be evidence of previous head injury, and for both these reasons I await the expert neuropathological report by Dr C Smith with interest. 11. Because non-accidental injury is often a repeated phenomenon by abusing carers, the presence of more than one head injury or evidence of non-accidental injury in other systems of the body are often regarded as useful additional factors in distinguishing between accidental and non-accidental injury. 12. Dr Bonshek mentioned the presence of haemosiderin in the optic nerve haemorrhages as a possible indicator of previous injury in this child and, like me, looked for possible further confirmation of previous head injury from the report by Dr Smith. 13. The fact that apparently non-accidental injury has occurred to the sibling of this child could be taken as evidence of further abusive behaviour by a carer. 14. I can see no reason to link this child’s death with resuscitation. The child was only resuscitated after he had collapsed. Resuscitation would not cause subdural or subarachnoid haemorrhage.”
“In my opinion, C1 suffered a single episode of inflicted traumatic head injury, with sudden collapse with hypoxic encephalopathy, hypothermia, retinal haemorrhage and subdural haemorrhage on the surface of the brain and in the cervical and lumbar area, the latter being possibly due to post-mortem artefact. The absence of any scalp swelling fracture does not lessen this possibility as the proposed mechanisms of injury do not involve linear impact onto a hard surface, nor does the apparent difference of opinion about the spinal nerve root damage. No other cause for his collapse and death, such as infection, vaccine-induced encephalopathy, near-miss Sudden Infant Death Syndrome, neurovascular anomaly, inherited metabolic disease or primary coagulation defects could be identified. I accept that the external bruising and the microscopic rib fracture may well be secondary to coagulopathy and efforts at resuscitation. However, the extent and distribution of the retinal haemorrhages and distribution of the subdural blood is consistent with inflicted traumatic head injury. In addition, the suddenness of the collapse is consistent with inflicted traumatic head injury.” 96. In his evidence, Dr Debelle told me that C1 suffered a single event, causing almost immediate collapse. He agreed that hypoxic-ischaemic damage could arise from cardiac arrest, but you cannot just block out all the other factors, i.e. intracranial and ocular findings. Mr Tillyard put to him the hypothesis of cardiac arrest, hypoxic-ischaemic damage, coagulopathy and resuscitation leading to oozing of vessels into the subdural and subarachnoid spaces. Dr Debelle was not dismissive, but in his opinion the subdural haemorrhage and subarachnoid haemorrhage were present (that is to say, looking at the scan) before there was evidence of hypoxic-ischaemic damage. He agreed that the degree of blood in the subarachnoid space was unusual in a setting of NAI. He agreed that the idea of a tear in the arachnoid membrane was a fairly recent one, within the last two years. If septicaemia was present in C1, he would not expect C1 to behave normally and then suddenly collapse. He could find no evidence of overwhelming infection. There was no evidence of suffocation. He accepted that Prolonged QT Syndrome can be the cause of cardiac arrest, but that in C1’s case it is inconsistent with the presence of subdural and subarachnoid haemorrhage. Babies with Prolonged QT Syndrome do not have subdural, subarachnoid and retinal haemorrhage. It was extremely unlikely that C1 was suffering from that syndrome. 97. Dr Robert Sunderland made it clear in his evidence that he did not believe that shaking, as opposed to shaking followed by the head impacting on a surface, could cause the injuries seen in C1. He plainly believes that the “shaking hypothesis” is wrong. He referred to research papers at H1 and again at H16, which involve neck injuries in children involved in frontal collisions in road accidents. He referred to an email at H29, which he says sets out the biomechanical case that shaking does not cause trauma in infants. In his report he said that he could not exclude trauma, but he had cited mechanical research that questions the shaking theory. He could not exclude suffocation. But this he subsequently retracted in cross-examination. He could not exclude infection, by which he said in his evidence he meant septicaemia. What led him to septicaemia was C1’s raised white cell count and seeing the presence of petechiae on C1’s tummy. As I understand his evidence, he did not suggest that C1 was a SIDS baby. In his evidence-in-chief he explained that a SIDS baby was a dead baby who was, in life, completely normal and where at post-mortem examination no abnormality was found. Thus C1 could not be a SIDS baby. I shall refer later in this judgment to further aspects of the evidence of Dr Sunderland. 98. The Triad I adopt, with respect, the descriptions given by the Court of Appeal, Criminal Division, in its judgment on21 July 2005 in R v Harris, Rock, Cherry and Faulder[2005] EWCA Crim. 1980 , at para 63-65: 63. “As already stated, when the three elements of the triad coincide for some years conventional medical opinion has been that this is diagnostic of NAHI. Typically the brain is found to be encephalopathic; blood is found in the subdural space between the dura and the arachnoid subdural haemorrhages; and there are retinal haemorrhages. There may also be other pathological signs such as subarachnoid bleeding and injuries at the cranio-cervical junction. Further, there may be injuries to nerve tissue (axonal injuries) and external signs of broken bones, bruising and other obvious injuries such as extradural oedema (bruising). Determining these findings requires medical experts from a number of different disciplines interpreting often very small signs within the complex structures of an infant’s brain and surrounding tissue. 64. The mechanism for these injuries is said to be the shaking of the infant, with or without impact on a solid surface, which moves the brain within the skull, damaging the brain and shearing the bridging veins between the dura and the arachnoid. The shaking may also cause retinal haemorrhages. In the sense that the explanation for the triad is said to be caused by shaking and/or impact it also is a unified hypothesis, albeit that each element is said to be caused individually by trauma. 65. The triad of injuries becomes central to a diagnosis of NAHI when there are no other signs or symptoms of trauma such as bruises or fractures.” 99. The Court of Appeal, Criminal Division, then went on to consider the unified hypothesis, i.e. Geddes III. At paragraphs 66 to 67, the Court of Appeal said: 66. “Dr Geddes and her colleagues, following research into almost 50 paediatric cases without head injury, proposed that the same triad of injuries could be caused by severe hypoxia (lack of oxygen in the tissues) which in turn led to brain swelling. The hypothesis was that brain swelling combined with raised intracranial pressure (ICP) could cause both subdural haemorrhages and retinal haemorrhages. Thus, is was argued that any incidents of apnoea (cessation of breathing) could set in motion a cascade of events which could cause the same injuries as seen in the triad. It will be appreciated that there are many events which could accidentally cause an episode of apnoea. 67. In Geddes III the unified hypothesis was summarised as follows: ‘Our observations in the present series indicate that, in the immature brain, hypoxia both alone and in combination with infection is sufficient to activate the pathophysiological cascade which culminates in altered vascular permeability and extravasation of blood within and under the dura. In the presence of brain swelling and raised intracranial pressure, vascular fragility and bleeding would be exacerbated by additional homodynamic forces such as venous hypertension, and the effects of both sustained systemic arterial hypertension and episodic surges in blood pressure.’ Thus, it was suggested that all the injuries constituting the triad could be attributed to a cause other than NAHI. We understand that this paper has been much cited in both criminal and civil trials since its publication.” 100. How then do the local authority, the guardian and the father put their cases about C1, now that all the evidence, both written and oral, has been given? I shall attempt to summarise them. The Local Authority The overwhelming medical evidence is that the abnormalities found in the brain and eyes of C1 can only be fully explained by him suffering an episode of trauma, probably shaking. Between paragraphs 22 and 63 of their written submissions, Miss Mifflin and Miss Williams analyse the medical evidence. In paragraph 64 they submit that the court needs to be able to find an explanation that fits all the abnormalities found in C1. The only cause that fits all is trauma, and, in the absence of accidental trauma, that leaves only inflicted head trauma. Taking into account all the circumstances both medical and non-medical, they submit that the court is drawn to the inevitable finding that C1 was assaulted by the father on the night of22 April 2005 by shaking and/or shaking impact. 101. Mr Furness, having analysed the medical evidence between paragraphs 12 and 19 and the lay evidence at paragraphs 20 to 25 of his written submissions, submits that the various causes of collapse, which he sets out in extenso at paragraph 26, have been excluded, leaving only inflicted head injury, and that injury was caused by the father shaking C1 at or about 10.30pm on22 April 2005 . 102. The fundamental points made by Mr Tillyard and Mr Parsley are to be found between paragraphs 12 and 20 of their written submissions. Thereafter they too carefully analyse the medical evidence. They rightly draw attention to what they describe as “the wider canvas”, namely the evidence of the father’s devotion and care of C1 and C2, his love for the mother and the good home conditions. (See Re B, Children[2006] EWCA Civ. 1186 ). I have set out the evidence upon which they rightly rely. They go on to make the point that in the light of the doctor’s beliefs in 2005 about C1’s death, had the father shaken C1, surely he would have let sleeping dogs lie and not challenged them to come up with a cause for C1’s death. The father’s obsession with immunisation was not the action of someone who knew full well why C1 had died. Mr Tillyard and Mr Parsley submit that the improbability of the father inflicting injury on C1 is “very high indeed”, and why on this particular night when (I paraphrase) there was nothing untoward in himself or about C1? 103. They then submit that there are alternative explanations to the supposed triad of signs. They invite the court to start with what happened in 2005 and 2006. Dr Leadbeatter and Dr Davis both came to the conclusion that they could not exclude Sudden Infant Death Syndrome as being the cause of death, and that the bleeding that was found at post-mortem and on the scan was attributable to the abnormal coagulation, the prolonged period of hypoxia, together with attempts to resuscitate over a period of about an hour. They submit that this cannot lightly be dismissed as being plainly wrong. Dr Leadbeatter and Dr Davis are both very experienced experts in their field, and had in mind the possibility that this may have been an inflicted non-accidental head injury. SIDS does occur, and when it does, the baby’s heart stops and there follows an hypoxic-ischaemic insult to the brain. What is unusual in this case is that after such a long period of time, the child is resuscitated and is then kept alive for another 15 hours. When C1 arrived at hospital, he was clinically dead, and it was Dr Vujanic who said that it was a miracle that they revived him at all. This is very unusual, notwithstanding the evidence of Dr Risdon that it was likely to give rise to very unusual intracranial findings. Mr Tillyard and Mr Parsley went on to submit that: “Both doctors explained to the court in some detail their conclusions and the basis upon which they were reached. We would submit that they were well thought out and are supported in many respects by the other experts in the case. (a) The widespread hypoxic-ischaemic brain injury was secondary to cardio-respiratory arrest, with a prolonged period of no cerebral blood flow. It is a non-specific finding and in itself does not indicate trauma. (b) C1 had a coagulation abnormality, together with a prolonged period of hypoxia, together with resuscitation. Under such circumstances the blood vessels in the brain may become leaky and the blood flow through them is re-established reperfusion injury. This becomes the more likely the longer there has been a failure of blood and oxygen supply because it damages the linings of the small blood vessels. (c) Most of the bleeding seen on post-mortem is around the blood vessels. There are small areas of bleeding with few cells getting out. There are not large collections of blood that you might have expected had any of the blood vessels ruptured. In our submission, this supported the idea that the abnormal coagulation was causing blood to seep from the blood vessels into the subdural and subarachnoid spaces, and that it was causing the retinal haemorrhages.”
“What has changed? There are no new facts. The only difference is the evidence from the neuroradiologists and the ophthalmologists. If there is an alternative explanation for their findings or there may be, the verdict of the Coroner should carry some considerable weight.” 104. So having carefully analysed all the matters, Mr Tillyard and Mr Parsley conclude in this way: 48. “We accept that the court cannot look at individual components of the trial in isolation, and that the court has to take an overall view of the evidence. However in doing that, a thorough investigation of each individual component of the triad needs to be carried out, and it is only when all other causes have been realistically excluded and the only remaining explanation is trauma that the court should find the case proved. 49. There are other non-traumatic explanations for all the findings in this case. There is a wide diversion of medical opinion as to how valid each of the explanations is. When the wider canvas is put in the balance as it should be, we submit that the court cannot be satisfied that those explanations, taken together and individually, are so improbably the cause or the findings as to leave shaking the only acceptable explanation. The evidence cannot be regarded as sufficiently cogent as to overcome the improbability of this father killing his son.”
“I have provided some related comment in my answer before question 32 (Re Dr Sunderland’s 3.14). I believe that I may have seen microscope slides from the case to which Dr Sunderland refers. The case I have seen has been presented by Prof Luthert to eye pathology meetings and I have been given the opportunity to review them. This is a case of bacterial meningitis and bacterial meningitis is a rare but recognised cause of retinal bleeding. The cases which have been reported in the literature, however, have not shown such extensive retinal bleeding as found in the case shown by Prof Luthert. It remains the case that the case mentioned by Dr Sunderland (and shown by Prof Lutert) did have meningitis. I am not aware that C1 had meningitis.” 109. Accordingly, since C1 did not suffer from meningitis, this one case provides no support whatever for Dr Sunderland’s supposition. Furthermore, when cross-examined by Mr Furness, he agreed that the presence of petechiae as on C1 frequently happened with children suffering from disseminated intravascular coagulopathy. I agree with Mr Furness’s submission at paragraph 17.6 that the presence of petechiae on C1 is a non-specific sign. There is a further factor which points away from infection. Dr Thomas told me that antibiotics were administered to C1 at about midnight. At just after 11.00 am on 23 April the blood was analysed. There was no sign of infection. If infection had been present, one dose of antibiotics would not have reversed it. The blood culture was negative for infection. 110. Finally, the overall effect of the evidence of the father and the mother and MGPs is that up to the time of C1’s collapse in the late evening of 22 April, C1 was a well and thriving baby. In my judgment, the evidence on this issue is all one way. I find that C1 did not collapse as a result of and/or die from any infection, for the simple reason that the evidence drives me to the conclusion that there was no infection. 111. Reaction to Immunisation I wish to say that it is a very natural and understandable reaction that when a child suddenly dies within a short span after he has been immunised, a parent or parents might conclude that the only explanation for the child’s death was an adverse and fatal reaction to that immunisation. But, I must emphasise, no medical expert has given any credence whatsoever to such a belief. Therefore I have to say, on the evidence, that I am driven to rule it out as a cause of C1’s collapse and/or death. 112. QT Syndrome The parents went to see Professor Peter Fleming, Professor of Infant Health and Development Physiology in the Department of Neonatral Medicine at St Michael’s Hospital in Bristol. It is apparent from his letter of24 October 2005 to the parents that he spent a lot of time explaining to them that it was unlikely that C1 had died as a result of his immunisation. At the end of his letter he wrote the following passage: “There are some very rare conditions which can contribute to sudden and unexpected deaths in infancy and which can be precipitated by minor stresses; for example, infections or immunisation and which are not detectable post-mortem. The most important of these is a group of conditions called the Prolonged QT Syndrome in which there is an abnormality of the electrical conduction system in the heart, which may cause sudden death, particularly under such circumstances. Although from your description it sounds extremely unlikely that C1 suffered from this condition, my recommendation would be that your new baby should be checked for this condition by having an ECG, an electrical recording of heart activity. In order to be certain that this will identify Prolonged QT Syndrome, the ECG must be done when the baby is at least two weeks of age.” 113. Very late in this case there was a flurry of emails just before the start of the hearing before me about Prolonged QT Syndrome. All the medical experts said that it was outside their field of expertise, but that certain findings were not consistent with cardiac arrest following QT Syndrome. What is QT Syndrome? It is a genetic complaint. It has been explained by Professor Fleming in that passage of the letter that I have just read out. Furthermore, an article by Dr Skinner, a Paediatric Cardiologist in Auckland, New Zealand, which is to be found at GQT20, describes the syndrome. The presence of the syndrome can lead to cardiac arrest. 114. Mr Tillyard and Mr Parsley at paragraph 46 of their written submissions submit that Prolonged QT Syndrome is raised as part of the father’s case not to prove that this was the cause of collapse, but to show that there are conditions which can lead to cardiac arrest, and this particular cause has not been excluded in C1’s case. 115. I accept the submissions of Miss Mifflin at paragraph 58 to 63 and of Mr Furness at paragraph 19 of their written submissions. There is no evidence that C1 suffered from Prolonged QT Syndrome. Professor Fleming thought that C1 having QT Syndrome was “extremely unlikely”
“Extensive hypoxic-ischaemic change, involving the thalami and cerebellum are occasionally seen in the context of trauma, including more severe cases of suspected inflicted head trauma. I am occasionally asked to give opinions regarding intracranial pressure monitoring in children who have suffered a hypoxic-ischaemic insult following non-traumatic cardiorespiratory arrest from which they have been resuscitated, but have never seen such extensive changes manifesting on a scan taken within three hours in this patient group. There is extensive subarachnoid haemorrhage present particularly over the cerebral convexities (3.0/04). In the absence of any identified vascular pathology or evidence of cerebral vasculitis, in my opinion the most likely cause of the subarachnoid haemorrhage in this case is trauma. Although in hypoxic-ischaemic encephalopathy, particularly in the presence of a severe coagulopathy bleeding can occur, it would be unusual to see a subarachnoid haemorrhage of this extent. I am also of the opinion that the degree of subarachnoid haemorrhage is no worse at the time of post-mortem than it was on the scan performed at 2.00 am on the23rd April 2005 . As the clotting anomaly was not corrected for at least three and a half hours after the CT scan, were the subarachnoid haemorrhage to be a direct result of oozing from an ‘encephalopathic’ brain, I would have expected to see an increased amount of subarachnoid haemorrhage present.”
“The only other possible cause of a low attenuation collection in the subdural space is a ‘chronic’ (old) subdural haematoma. These would typically be at least two weeks of age. Chronic subdural haematomas of this age are invariably associated with a subdural neomembrane. Such a neomembrane was not found on post-mortem examination. Furthermore there was no evidence of old haemorrhage on the post-mortem examination. In addition to this the low attenuation collections had significantly reduced in size at the time of the post-mortem examination. This would be consistent with the fact that the low attenuation collections are of bloodstained cerebral spinal fluid, rather than clot, as the blood stained spinal fluid would have been dispersed by the progressive brain swelling that occurred in the hours after the CT scan. In my opinion, in this case the only possible explanation for this finding is an acute traumatic event.” 120. At paragraph 5.05.27, Mr Edwards tells me that in his clinical practice he regularly examines the fundi of infants and children with both head trauma and non-traumatic cases of raised intracranial pressure, and in his clinical experience he has only ever seen retinal haemorrhages that affect all areas of the retina in the context of inflicted head injury. At paragraph 5.05.2 he states that there are three possible explanations for the pathological sequence of events, namely: (i) “A single event which caused hypoxic-ischaemic encephalopathy and the intracranial spinal and retinal haemorrhages; (ii) an event which causes HIE followed by a secondary event resulting in bleeding; that is to say, a pre-existing or secondary acquired encephalopathy; and (iii) a primary bleeding disorder leading to HIE.”
“It is my opinion that a traumatic event is the only single event that could lead to both hypoxic-ischaemic encephalopathy and the bleeding seen. There are three possible causes of trauma in this age group. Firstly that it was related to birth injury: this can be discounted as there is no suggestion either from the clinical history (C1 was completely well up until the day of his collapse), the radiological findings (none of which was an ‘old’ injury) and the post-mortem findings which showed no evidence of ‘old’ bleeding that could date back to the time of birth. The second possibility is that the trauma was accidental. However, no accidental trauma was reported by either parent or the maternal grandmother who were the only people in sole charge of C1 prior to his death. Furthermore, C1 was non-ambulant; therefore, even the ‘trivial’ falls occasionally put forward as explanations for findings such as these can be excluded. By deduction, the only possible traumatic cause of C1’s injuries that remain is therefore inflicted head injury.”
“Removal of the spinal cord is often a very traumatic procedure, and I believe that the bleeding may be an artefact induced by removal of the cord.”
“The factors were severe hypoxic-ischaemic brain injury, coagulopathy and pressure caused by brain swelling”. 125. The Ophthalmologists Both Dr Boshek and Dr McCarthy were in agreement, so I will not repeat their evidence. They found not only extensive and severe retinal haemorrhage, but also other significant findings which I have set out above. The effect of their evidence is, in my judgment, that their findings in relation to C1’s eyes can only be explicable as a result of trauma. Both doctors recognise the need for caution and considered all the alternative postulated causes, and none of those alternative causes could result in the ocular findings in C1’s eyes, in their opinion. 126. Paediatric Pathologists Both Dr Vujanic and Professor Risdon are in agreement that the cause of C1’s collapse was a non-accidental inflicted injury for the reasons each gave in their evidence, and which I will not repeat. 127. The Paediatricians Dr Sunderland accepted in his evidence that his view that shaking could not cause the injuries seen in C1 is a minority view. He accepted he relied upon biomechanical research evidence, specifically crash dummies. He conceded that this area was outside his expertise. I agree with the submissions of Miss Mifflin and Mr Furness that the opinions of Dr Sunderland are of much less value than they might otherwise have been because he is not really prepared to accept that the shaking hypothesis has any validity at all. He relied on biomechanical research, but no biomechanical consultant was called before me. Furthermore, as I have demonstrated, he was compelled to abandon suffocation as a cause, and his evidence relating to infection as a possible cause was shown to be, in my judgment, completely flawed. The fact of the matter is that Dr Sunderland’s evidence was not objective, but started from a preconceived position that shaking cannot cause the injuries seen in C1. 128. I am afraid that I have to say, when I stand back and look at the medical evidence as a whole, it is apparent to me that where the medical evidence of Dr Squier and Dr Sunderland conflict with the evidence of the other experts, I have to reject it, for the reasons I have given. Thus, in my judgment, the medical evidence, standing alone, does point strongly, at the very least, to inflicted head injury and to non-accidental inflicted head injury. 129. So that nobody can say that I have lost sight of or undervalued the “wider canvas”, all of which I put into the balance very much indeed, I have some comments to make on it and upon the lay evidence: 1. Dr Stoodley told me at G35 as follows: “Despite the force required being obviously inappropriate and having been involved in many cases of alleged non-accidental head injury, I am of the view that the majority of these injuries occur when an otherwise reasonable carer suffers a momentary loss of control, usually out of frustration at a situation such as being unable to settle an inconsolable child, without there being any intent to cause the child harm.”
“The child was playing on an activity gym and dad kicked (accidentally) the side of the gym, and a plastic tube from the gym hit the child on the side of the face.”
“I next saw C2 and his parents on the22nd June 2006 (22/06/2006 ) when C2 was 11 weeks and one day old. At this consultation C2 was in a baby seat and when I asked how things were going, F replied something like ‘All right until two days ago.’ This then opened our conversation regarding an incident two days earlier when F had C2 lying on the floor under a plastic baby gym, with tubing and some fabric covering and toys hanging down. F had walked past to the kitchen to make a drink. On return he had been going to pick C2 up and, while walking past, he accidentally kicked the baby gym which fell against C2’s face. I clearly recall that F was sure that his foot had not made contact with C2’s face and that it was in fact the baby gym. They informed myself that they had taken C2 directly to the A and E Department at the Heath Hospital on Tuesday evening, but that he had been discharged. I then documented the injuries as I saw them. He had bruising to the right side of the face from the peri-orbital area, from the nose area to the right ear. There was also bruising and swelling around the eye on the upper and lower lids. I did not inform the parents at this stage, but I had concerns whether a plastic toy could cause such injuries, as I was now seeing C2 with these injuries some two days after the event.”
“I next saw C2 who was accompanied by both parents. Also present was my registrar Dr Jo Saunders. Informed consent was obtained for an examination under child protection procedures from the baby’s father, F. They told me that he is a healthy baby who had been born at the University Hospital of Wales weighing 8lbs 8ox by an elective caesarean section. He had not required any special care. He had been breastfed for around seven days and subsequently commenced in bottle feeding. He is feeding well on SMA white cap and is now eleven weeks of age. I was told that at four to five weeks of age C2 had had bleeding from his nose and had also been taken to the University Hospital of Wales where he was seen on the Paediatric Unit and discharged. I was told ‘he had burst a blood vessel in his nose’. They went on to tell me that he has been developing well and now smiles and laughs. I was told that he has rolled from his back to his front last week, is holding his head up well and can move around on the floor. He will grab onto clothing when he is picked up. The family told me that on the evening of Tuesday 20th June his mother had been out for the evening and C2 had been in the care of his father. After his mother had returned at around 9.40pm, C2 was on the floor under his baby gym. His father told me that he had gone out of the room, and when he came back in he had caught his foot on the baby gym frame and had kicked the frame accidentally into C2’s face. Both parents had been present. They had noted swelling around C2’s right eye and had gone to A and E at the University Hospital of Wales at approximately 10.20pm where he had been checked over and sent home. Mum told me that the bruising had come out more yesterday and was actually a little less evident today. C2 had been fine since and had been feeding well. I specifically asked if C2 had any marks anywhere else before I commenced the medical. His mother told me before I examined him that he had a bruise on his right leg. The family thought that this was from his cot sometime last week, and told me that he kicks against the wooden cot bars. They also felt this could have occurred from a changing mat with metal framework which is clipped to the travel cot and is a piece of equipment with which I am not familiar. They also told me that he had a little mark on his left upper arm which they thought was from the car seat which is apparently difficult to use and was shown to me. Mum told me that this never looked like a bruise, but went on to tell me that, in her words, ‘it had initially looked like a love bite a couple of days ago’.” 139. The parents then told Dr Rawlinson about C1, and that the father attributed his death to immunisation. Dr Rawlinson then examined C2, whom she found to be a lovely responsive smiling baby, who handled normally. She found three areas of bruising, which she sets out at G62, which were as follows: “Head and Neck 1. There were blotchy patches of petechial bruising present over an area above and below the right eye and extending onto the eyelid and cheek. These patches of bruising were blue in colouration. There was slight soft tissue swelling present under the eye; there was a full range of eye movements, and no subconjunctival haemorrhages visible, although the sclera (white of the eye) looked slightly injected laterally. The bruising below the eye was in a roughly triangular distribution over an area approximately 2cm by 2cm by 2cm. Petechial bruising extended in a patch about 2cm above the right eye. There was therefore evidence of quite extensive petechial bruising to this area of the baby’s face some three days later. Right Leg 2. There was a linear brown bruise present on the anterior aspect of the right leg in the midline. This was approximately 3.6cm long with a distal linear extension of slightly lighter colouration. This was also brown in colouration and approximately 1.5cm long. Both parents told me that they thought this could be from his wooden cot bars or the metal frame of his changing mat in his travel cot. Left Upper Arm 3. In the midline of the left upper arm there were three small petechial bruises in a cluster. These appeared to be small linear petechial bruises. Whilst I was examining C2, his mother commented that they resembled a pinch mark and earlier had looked ‘like a love bite’. His father told me that this was from his car seat, which he then showed to me. Neck 4. There was a small red mark just below the nape of the neck posteriorly in the midline, which his mother told me had been present since birth and seems likely to represent a birth mark. I note that in Dr Papworth’s clinic notes of the previous day, she had also documented petechial bruising to the right face and the marks on the left upper arm, but there was no documentation of any bruising to the right lower leg.” 140. The father then produced the baby gym. He showed Dr Rawlinson how he had positioned the baby in the middle of the mat, but he had moved nearer to the right side of the gym. Dr Rawlinson noted that the baby gym had a hollow, lightweight, plastic, tubular frame, with material cover at the base and the legs, but no padding. The car seat was also produced. Dr Rawlinson explained to the parents that C2 appeared to be well developed mentally, but bruising in a young non-mobile baby raised significant child protection concerns and was not consistent with the explanations given, and that she was concerned that C2 had bruising on more than one area of the body. She told him that C2 would be admitted to hospital for further investigations. Towards the end of the consultation, the father became agitated. He wanted to know precisely when the investigation would be carried out. Dr Rawlinson said that C2 was likely to be on the ward for a week. C2 was admitted. Dr Rawlinson went on leave. 141. In her evidence, Dr Rawlinson told me that the police photographs of C2, taken on 23 June, were of poor quality from a clinical perspective. The pattern of bruising over C2’s right eye as she saw it upon her examination of C2 was over a large area. It was dark blue. Indeed, that is how the mother describes it. The bruise Dr Papworth saw was within the three linear lines below C2’s right eye. The bruise Dr Rawlinson saw to the right leg was readily noticeable. In respect of the arm and leg bruising, Dr Rawlinson was not given an explanation of a particular incident referable to the cause of the bruises. She was only given explanations of how they might have happened. 142. During her evidence, Dr Rawlinson was asked to explain how the father had demonstrated to her, with the baby gym, that the injury to C2’s face had occurred. She told me that this was all nearly two years ago. Nevertheless, she came out of the witness box and demonstrated with the baby gym. The father had placed the baby gym on the floor. He had stood at the front of the frame with the baby’s feet nearest to him, with C2’s head furthest from him. C2 had been lying on his back. The father had then walked forward and walked into the baby gym. Mr Tillyard put to her that the father told her that C2’s head, not his feet, was nearest to the father. Dr Rawlinson emphatically rejected that. She told me that from what the father had told her on 23 June and what she saw being demonstrated on that day, she could not understand how the injury had occurred. Dr Rawlinson told me that she had asked the father more than once during the examination whether his foot had hit C2’s face. The father was clear, she said, that his foot had not hit C2; it was the frame of the baby gym. Mr Tillyard pointed out to Dr Rawlinson in his cross-examination that she had made no note of asking the father whether his foot had hit C2. Dr Rawlinson could not explain why there was no such note. However, she did tell me that had the father told her that his foot had hit C2, she would have made a note of that. Further, in response to a letter from Rhiannon Jones, a social worker, she had written on9 August 2006 : “The history as given is as documented in my original report. Whether or not dad’s foot was ‘in contact’ with the baby gym (and the fact that I specifically asked whether his foot itself had hit C2), it is my opinion that the extent and distribution of the bruising to the face cannot be adequately explained. This does need to be seen in the context of the whole child, i.e. a non-mobile baby with evidence of bruising to three areas of the body.” 143. On 29 June, Dr Rawlinson met the parents again. She explained to them that the investigations had been normal, i.e. there was no medical reason for C2 to bruise more easily, but that unexplained bruising in a non-mobile infant raises significant paediatric and child protection concerns. In her statement at G65 she said: “In summary therefore C2 is an 11 week old non-mobile baby who appears healthy and is developing normally. He shows evidence of bruising to three sites of the body, some of which is petechial (tiny blood vessels). Further investigations have shown a normal coagulation screen and a normal CT scan of the brain, with no evidence of retinal haemorrhages on fundoscopy. The coagulation screen is normal, i.e. no medical reason for him to bruise more easily, had been detected at this time on baseline investigation. Such medical conditions are rare, and in any case both inflicted injury and bleeding disorder may coexist and the diagnoses are not mutually exclusive. I do, however, understand that his sibling C1, who died at eight weeks of age with a sudden unexplained death in infancy, was said to have abnormal coagulation following his collapse, but that this returned to normal before he died. I understand that Dr Collins, Consultant Haematologist at University Hospital of Wales, was involved in his management, and I will therefore write to him to ask if he feels any further haematological investigations in C2 are warranted. In my opinion, however, the pattern and distribution and extent of bruising around the right eye in C2 is not consistent with the explanation being offered of the incident with the baby gym, and although this may well have occurred, I do not think that this is the mechanism by which he sustained the bruising as seen. The fact that this baby has had three areas of documented bruising, including his face, is of concern. (Ref: Maguire, Archives of Disease in Childhood, 90(2) 196 – ‘Those who don’t cruise, rarely bruise”). It is generally accepted that a young non-mobile baby would not be able to bruise themselves by kicking against cot bars or changing equipment. The petechial bruising on the left upper arm was suggestive of a possible pinch mark. Overall therefore this presentation of unexplained bruising in a young non-mobile baby raises concerns regarding non-accidental injury.”
“I am also concerned at the history as given of C2 presenting at a few weeks of age to University Hospital of Wales with reported bleeding from the nose. This in itself is an extremely unusual finding in a young child and is in fact one of the ways in which imposed upper airway obstruction can present. (Ref: Child Protection Companion, Royal College Paediatrics and Child Health, April 2006). The hospital records of this presentation do need to be obtained as well as copies of the A and E attendance to the University Hospital of Wales with bruising around the eye in June 2006.” 144. As with C1, MGPs described both parents as loving and devoted. In 2005 the parents had taken part in three SUDI (sudden unexplained death in infancy) strategy discussions. Both parents told me they were overjoyed with the mother’s pregnancy and C2’s birth. The father, who the mother agreed was C2’s day-to-day carer as she had returned to work, told me that he had never had any difficulty with C2. When the health visitor visited C2, he was found to be a happy and thriving baby. 145. On4 May 2006 the father told me that when changing C2, he vomited and saw bloodstained vomit in the baby-grow. He told me that he saw no blood on C2’s nose. He called to the mother, who was upstairs at the time. She saw a streak of blood in C2’s vomit. She could not see any blood from his nose. The health visitor, who was due that day, came earlier, at the parents’ request. Both parents told me that Sue Field, the health visitor, suggested to them that the blood might have come from the nose. The father told me that the health visitor had said that many cases of baby’s vomiting involved vomiting through the mouth and nose. The records state that the cause of C2’s vomiting might have been overfeeding. As I have already recorded, on 11 May C2 was reviewed by Dr Papworth and all seemed to be well. On 20 June he was taken to the University Hospital of Wales. I have dealt with that and how the parents’ explanation was accepted. 146. On 22 June the parents brought C2 to see Dr Papworth as part of the CONY programme. During the mother’s cross-examination by Miss Mifflin she put to the mother a passage in the father’s police interviews where he said he did not want to take C2 to see Dr Papworth. The mother agreed that the father was reluctant to go. The father told me that he was not reluctant. He had been joking with the mother that if they took C2 to Dr Papworth, then in the light of the injury to C2’s right eye, they might be accused of assaulting C2. When he was cross-examined by Miss Mifflin, the same passage was put to him in his police interview. He agreed that when answering questions from the police, he had not been joking. 147. Both parents told me that the bruise to C2’s leg had occurred before the baby gym incident on 20June. The father told me that he first saw the bruise on the previous weekend. The mother told me that she had asked the father how it had happened. The father told her that C2 must have rolled against the bar of his cot or against the side of his changing equipment. Both parents agreed in evidence that neither told Dr Papworth of the bruise on C2’s leg. The mother had no explanation why they did not. The father, when asked about that, sought to say that it was Dr Papworth’s responsibility to notice it. The mother told me that she was present when the history was given to Dr Papworth. She agreed that Dr Papworth’s note that the baby gym “fell” on C2 was not saying that the gym was kicked into C2. The father told me that he believed he had told Dr Papworth that his foot and the baby gym had come into contact with C2’s right eye. 148. I now turn to recount the parents’ evidence of the baby gym incident. At about 7.30pm on 20 June the mother told me that she went out to her aqua aerobics, leaving C2 in the care of the father. There was no mark on C2’s face. At about 9.00 or 9.15pm she came home and came into the sitting room. She saw C2 lying under the baby gym, which was placed between the two settees. She saw the father come out of the kitchen door. She walked over to the table, shown on the plan with her marking – See E2238a. The small matchstick person represents C2 lying under the baby gym with his feet nearest the V, formed by the two settees, and his head closest to the kitchen door. The mother was unpacking her bag on the table with her back to C2 and the father. She heard a noise of the bells hanging down from the baby gym. C2 started crying. She rushed over to C2, who had been picked up by the father. C2 was upset and crying. The father was consoling him. Once C2 was quiet and asleep in the father’s arms, the mother noticed a redness on C2’s right cheek. The father told her that he had kicked the baby gym into C2. By the time they had taken C2 to the hospital, the mark was puffy and swollen. The mother told me she did not know which leg of the baby gym the father had kicked. 149. The father’s evidence was as follows. As the mother came into the sitting room, he went into the kitchen and came out again. The mother was unpacking her bag on the table. As he walked past the settee nearest the wall of the sitting room and kitchen, his left foot, more particularly that part nearest his little toe, connected with the bar of the baby gym on C2’s right hand side and nearest to C2’s hip. He actually gave it a forceful kick, and the baby gym and the foot hit C2’s face. C2 was on his back and slightly rolling to his right. The father believes that his foot did hit C2 because his left little toe was injured. 150. The father then came out of the witness box and stood in front of it to demonstrate to me what had happened. The baby gym was placed on the floor. C2, he told me, was lying with his head nearest to the father, slightly nearer the relevant strut. The father then walked forward “kicking” the strut. But what was immediately obvious to me and indeed to counsel watching the demonstration was that the baby gym, upon being kicked, was turned in an anticlockwise direction, and the strut, instead of moving in to where C2’s face would have been, moved in the very opposite direction; that is to say, out and away from C2’s face. The father did the demonstration again. This time it could be said that the strut might just have moved into C2’s face. Nevertheless, during his cross-examination by Miss Mifflin, the father again demonstrated twice what had happened. On each occasion the relevant strut of the baby gym moved out and away from where C2’s face would have been. 151. Causation of the Bruises All the experts relevant to these bruises told me that bruising to a non-ambulant child of C2’s age, i.e. two months as at23 June 2006 , was very rare. Dr Debelle told me that in his experience bruising was not a common experience and that studies had shown that bruising on a non-ambulant child was a rare event. Dr Sunderland agreed. Both accepted that one had to look not only at each bruise, but also at all the bruises together. Both told me that generally speaking they would expect the carers of a non-ambulant child to have seen how the bruising was caused. 152. Leg It is crucial to note that the bruising to C2’s leg was a linear mark which runs vertically up and down the front of his shin. Dr Sunderland told me that the rolling of C2 into the cot bars would not create enough momentum to cause such bruising. It was unlikely that a baby kicking out and his leg hitting the cot would cause such a bruise. Furthermore, it is an important point that the cot bars, as seen in the photographs, would have been at right angles to C2’s legs if he had rolled into them. The cot bar at right angles to the linear bruise would be most unlikely to cause such a bruise. Furthermore, Dr Sunderland told me that, to him, it was some sort of pinch mark. Dr Rawlinson did not consider the parents’ explanation to be satisfactory. She told me that cot-bound babies do not injure themselves. Mr Debelle said that the parents’ explanation was plausible, but bruising in infants was rare and it should have been witnessed. Both parents in their evidence were completely unable to relate the bruise on C2’s leg to any incident at all. The mother agreed in cross-examination by Miss Mifflin that C2 rolling into the cot bars was not an explanation of the bruising. 153. The Arm The mother described the marks on C2’s left upper arm as looking puckered and like a “love bite”