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You are here: BAILII >> Databases >> England and Wales High Court (Family Division) Decisions >> London Borough of Islington v Al- Alas & Anor [2012] EWHC 865 (Fam) (19 April 2012) URL: https://www.bailii.org/ew/cases/EWHC/Fam/2012/865.html Cite as: [2012] Fam Law 943, [2012] EWHC 865 (Fam), [2012] 2 FLR 1239, 128 BMLR 1, (2012) 128 BMLR 1 |
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FAMILY DIVISION
Strand, London, WC2A 2LL |
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B e f o r e :
____________________
MAYOR AND BURGESSES OF THE LONDON BOROUGH OF ISLINGTON | ||
Applicant | ||
- and - | ||
CHANA ![]() | ||
1st Respondent | ||
-and- | ||
ROHAN WRAY | ||
2nd Respondent | ||
-and- | ||
JAYDA FAITH ![]() ![]() |
||
(through her Children's Guardian Dorothy Pottinger) | ||
5th Respondent |
____________________
Ms Jo Delahunty QC & Ms Kate Purkiss (instructed by Goodman Ray Solicitors) for the 1st Respondent
Mr Ian Peddie QC and Mr Christopher McWatters (instructed by S A Carr & Co Solicitors) for the 2nd
Respondent
Mr Vinod Sharma of BKS Legal Solicitors for the 5th Respondent
Hearing dates: 20th February – 26th March 2012
____________________
Crown Copyright ©
Introduction
The Law
"The triad becomes central to a diagnosis of NAHI when there are no other signs or symptoms of trauma such as bruises or fractures" [Para 65].
" Whilst a strong pointer to NAHI on its own we do not think it possible to find that it (the triad) must automatically and necessarily lead to a diagnosis of NAHI. All the circumstances, including the clinical picture, must be taken into account" [Para 70]
"..cases of NAHI are fact specific and will be determined on their individual facts" [Para 267].
'In my judgment, a conclusion of unknown aetiology in respect of an infant represents neither professional nor forensic failure. It simply recognises that we still have much to learn and it also recognises that it is dangerous and wrong to infer non-accidental injury merely from the absence of any other understood mechanism. Maybe it simply represents a general acknowledgement that we are fearfully and wonderfully made.'
"In the brief summary of the submissions set out above there is a broad measure of agreement as to some of the considerations emphasised by the judgement in R v Cannings that are of direct application in care proceedings. We adopt the following:
(i) The cause of an injury or an episode that cannot be explained scientifically remains equivocal.
(ii) Recurrence is not in itself probative.
(iii) Particular caution is necessary in any case where the medical experts disagree, one opinion declining to exclude a reasonable possibility of natural cause.
(iv) The court must always be on guard against the over-dogmatic expert, the expert whose reputation or amour propre is at stake, or the expert who has developed a scientific prejudice.
(v) The judge in care proceedings must never forget that today's medical certainty may be discarded by the next generation of experts or that scientific research will throw light into corners that are at present dark."
Background
13.3.09 'I undressed the baby and checked him from head to foot and had no concerns, I did not see any injuries and he seemed physically well'.
23.3.09 physical check of Jayden was carried out and records 'I was assisted in undressing him by Chana. The physical checks consisted of an all over body check and I saw no bruises or anything that caused me concern'
30.3.09 'conducted my checks on Jayden, I saw Chana undress and hold him and her interaction with him was appropriate. I completed a physical check on Jayden. This includes a front and back check and head to foot check. On being handled Jayden seemed fine and I saw no injuries on Jayden and appeared to be physically well on seeing his skin tone, weight and the way he was moving.' She was satisfied that the mother no longer required their services and so discharged her from their care.
14.4.09 "it was mainly Chana who replied to my questions although I can't recall clearly her exact response. I remember thinking how nice it was that both parents had come with baby, especially as they were so young. They looked very sweet together and came across as being very together….I had no concerns with them or Jayden. They handled Jayden well and seemed to interact well with him – both looking at him and smiling….They presented as a happy family and Jayden as a happy healthy baby. I had no concerns"
5.5.09 (Jayden's 6 – 8 week check) "I can't remember which parent carried Jayden into my room but it was Rohan who undressed him and put him onto the exam trolley. It was also Rohan who carried Jayden round to the GPs room once I was finished. However Chana was the one who I was mainly addressing my questions to and also she frequently smiled at Jayden, so this caused me no concerns. I measured J's weight, head circumference and length…I do remember that all of his measurements were normal. It is the policy of the Primary Care trust that all babies aged under one year are weighed naked. I saw no visible markings or injuries to Jayden. To me he appeared as a happy, thriving, well settled baby. Both of his parents appeared to interact well with him." Ms Gofton also spoke to Chana to ensure there were no concerns regarding possible post natal depression. Ms Gofton said she had no worries on that front.
2.6.09 "impressed by how caring he [Rohan] seemed of Jayden in that he was very attentive and gentle with him…her [Chana's] replies were all positive and she seemed very happy talking about her baby. I thought it very positive that she was breastfeeding and Jayden was in a good feeding routine…I had no concerns with him – he was clean and appeared happy. He was looking around and reacting well. He presented as a normal baby with no visible injuries or illnesses"
16.6.09 "On 16th June I didn't observe anything wrong with him. Again he presented as a clean and well cared for baby. He was looking around. He appeared settled. I can't recall on this occasion which parent handled him but I can say that I believe both parents to smile at him and interact with him well. The father, Rohan, asked appropriate questions about Jayden's feeding as he was worried he was now sleeping through the night whereas before he had been waking up for a feed. I reassured him that this was perfectly normal for a baby of Jayden's age. The mother Chana was not worried about anything and I saw no reason for her to be so. She was again quiet, unless spoken to, but seemed happy and responded appropriately to anything asked of her"
30.6.09 (this was a drop in clinic which parents' can attend) "Rohan predominantly handled the baby but Chana was attentive of Jayden and often smiled at him….I remember praising Chana for how well she was doing breast feeding and she was really happy with this praise – her whole face lit up. Again Jayden presented as a happy and settled baby. Both parents interacted well with him….Nothing from their demeanour caused me any worries" #
14.7.09 "Jayden was again accompanied by both parents and again nothing in their demeanour worried me. Both seemed happy and well adjusted…Jayden presented to me as a happy, healthy child and his parents appeared well adjusted and attentive of him" On that occasion a student nurse was present and Ms Welch said she oversaw and repeated everything that the student nurse did. It was a relatively short visit as it was only a weight check but she noted nothing of concern.
in his limbs.
Dr Peters
Consultant for CATS (Children Acute Transport Team) since its inception in 2001. In his role he has been involved in the care of between 1,200 and 1,500 critically ill children each year, including on average about 30 serious head injuries.
Agreed findings at the post mortem
At the post mortem on August 3rd 2009 the following findings were made: External Examination
(i) Various marks consistent with therapy
(ii)No old or recent marks of injury
Internal Examination
Sub-scalp bruising on the right parietal/occipital region over an area of 5cm x 5cm. Associated sub-periosteal bleeding from the midline to the right over the occipital bone over 3cm x 1cm area. A thin film of subdural haemorrhage over both hemispheres [more on the left] adherent to the dura. Some thin film subdural haemorrhage involving the skull on the left side. A suspected underlying fracture on the right occipital bone.
Radiological Findings confirmed by later bone histopathology-
1. Left hand: 1st left metatarsal: Incomplete mid-shaft fracture. 2nd left metatarsal: Incomplete mid-shaft fracture and crack fracture towards the end of the bone. 3rd left metatarsal: Complete mid-shaft fracture.4th left metacarpal: Double complete shaft fractures.
2. 2 left ribs, costchondral area: Abnormal growth plates attributable to established rickets.
3. Left proximal humerus: Fracture of the proximal humerus between the growth plate and the bone (a metaphyseal fracture).
4. Left proximal femur: Fracture of the proximal femur at the interface between the growth plate and the bone (a metaphyseal fracture).
5. Right distal humerus in two places (old fracture).
6. Proximal humerus: Fracture of the proximal humerus at the interface between the growth plate and bone (a metaphyseal fracture).
7. Right mid-tibia: Old healed greenstick fracture and a complete fracture of the shaft.
8. Right parietal bone: A displaced fracture of the skull bone.
9. Right occipital bone: A traumatised fissure.
10. Left radius: Incomplete crack fracture of the shaft with rickets affecting the growth plate.
11. Left ulna: Rickets in the growth plate.
12 .Right radius: Rickets affecting the growth plate.
The Brain
Subdural haemorrhage, global ischemic injury, ischemic axonal injury and axonal injury to the pyramids and spinal nerve root axonal injury.
The Eye
Fresh retinal haemorrhages in both eyes with bilateral papilloedema (optic nerve head swelling). There was also subdural bleeding associated with the optic nerve.
The LA's case
Expert evidence
Pathologists
Dr Scheimberg
The majority of the post-mortems are babies, rather than children. In relation to the coroner post-mortems the majority have been babies between two and seven months old.
Dr Rouse
Dr Cary
Neuropathologists
Dr Colin Smith
(1) Acute subdural bleeding associated with focal intradural bleeding. This is seen in the cerebrum and also microscopically within the spinal cord. Within the spinal cord the bleeding extends along the spinal nerve route sheaths. The main pathology within the cerebrum is that of global ischemic brain injury. The ischaemia extends through the neocortex, hippocampi and deep grey nuclei and is associated with glial cytoplasmic swelling.
(2) Neutrophils (type of white blood cell) are seen overlaying the convexity. Dr Smith had considered acute purulent meningitis, but considered this neutrophilic infiltrate to be secondary to global ischemic brain injury. He was unable to demonstrate bacteria or fungi using special stains.
(3) The ischemic brain injury extends into cerebellum and brain stem and there is evidence of widespread ischemic white matter injury as highlighted by the beta APP staining. He considers this to be secondary to brain swelling caused by global ischaemia.
(4) Within the cerebellum and midbrain there are one of two foci, which suggest a more established focal ischemic injury in that there is more prominent neuronal loss and reactive gliosis associated with macrophage infiltration. This raises the possibility of a separate less prominent ischemic injury prior to the main collapse of the child.
(5) Prominent axonal spheriods seen within the medulla suggesting a hyperflexion/hypertension type injury, although they have to be interpreted with great caution due to the widespread ischemic axonal injury.
(6) Also of concern is the prominent beta APP immunostaining of spinal nerve roots at the lumbosacral region associated with haemorrhage extending along the dural sheath again these need to be interpreted with caution.
He concludes that much of the neuropathology is non-specific and global cerebral ischaemia can be caused by a wide range of insults ultimately resulting in some degree of cardiorespiratory distress. He reported that there were two aspects that concerned him to a possible traumatic origin in this case (1) the presence of axonal spheroids within the pyramids, and (2) significant axonal damage to the lumbosacral spinal nerve roots with associate dural sheath haemorrhage. Finally, in his written report, he notes caution that the findings he made need to be interpreted very carefully in view of the widespread ischaemic pathology.
(1) All three neuropathologists agreed the following lesions were present: Subdural haemorrhage (SDH), severe brain ischaemia, brainstem injury (axonal spheroids), spinal nerve route damage and meningeal inflammation.
(2) With respect to the meningeal inflammation the differential diagnosis is between inflammation reactive to the hypoxic ischemic injury and partially treated meningitis. Whilst all agreed the former was more likely, they also agreed the latter can't be ruled out.
(3) With respect to the evidence of the head trauma contemporaneous with the collapse all participants agreed that there was no evidence of fractures or gripping marks. Dr Smith is noted as saying the presence of SDH was indicative of contemporaneous trauma but he agreed there was no other evidence to support trauma at the time of collapse.
(4) With respect to the old axonal injury in the brainstem all agreed that this was not contemporaneous with the collapse. Dr Smith noted that no studies have demonstrated how long axonal spheroids take to develop or how long they retain their APP immunolabelling in children, particularly when they are secondary to global ischaemia. Dr Ramsay was concerned about the aetiology as the pattern, in his view, was not typical of traumatic axonal injury.
(5) There was discussion of the relevance of axonal injury in nerve roots. Dr Smith notes that this aspect raised concern in relation to the traumatic episode, although recognised the need for caution particularly in the light of recent publications. Dr Ramsay considered such findings as generally unreliable indicators of spinal injury in the absence of other findings of spinal trauma. He also thought there were other abnormal findings in the spinal cord leading to the possibility of a more pervasive metabolic or other CNS process.
Dr David Ramsay
(1) In relation to the leptomeningeal inflammation Dr Ramsay considered, in his experience, that it was unusual to find this degree of inflammation purely in association with hypoxic ischemic brain injury. He said the appearance indicates that something is stimulating or irritating that part of the body and specifically with the pattern like this, an infection by bacteria. Dr Smith considers this is secondary to the brain injury which Dr Ramsay does not disagree with but his experience puts an infection higher than Dr Smith but did acknowledge 'At the end of the day, the possibility of infection, based on the clinical evidence, would seem to be unlikely'.
(2) Definite hypoxic-ischemic neuronal change is not visible in the spinal cord. Dr Ramsay said the findings of the hypoxic-ischemic neorons is fairly non¬specific and there are a number of explanations for why they should become red. He concludes it is caused by the 'bombardment of the nerve cells by the increased electrical activity in epilepsy can itself damage the neurons in this way'
(3) In relation to axonal injury he said the ability to identify abnormal axons has been greatly improved by the use of a specific technique referred to as beta-amyloid precursor protein immunohistochemistry, (usefully shortened to BAPP) which identifies where the flow of protein up and down the axons has been compromised or slowed down by some process. That process can be trauma, hypoxic ischemic injury and/or brain swelling. Dr Ramsay has sought to separate the two patterns of axonal injury; the classic form (the form recognised in unconscious patients for decades) and the more recent form, called the pleomorphic form, that reveals not only in trauma, but in other situations of brain injury unrelated to trauma, much more widespread but subtle damage to the axons. He said Jayden had both patterns, the pleomorphic form which did not surprise him due to the extent of the brain injury and swelling. The classic axonal swellings were restricted to the brain stem. He said save for one site they have an odd appearance which suggests they may have been around for some time, or there could be some other process that hasn't been recognised in the brain to account for them. In one site he said there were classic axonal swellings in one of the white matter tracks low down in the brain stem. He said the absence of siderosis and astrocytes, which he would expect to see if there was traumatic axonal injury, means that whilst trauma can't be excluded as a possibility these features are not seen. Dr Smith in his written and oral evidence was cautious about the significance of these as supporting a traumatic cause, he said in his statement and his evidence that they are an aspect that concern him as to a 'possible' traumatic aetiology.
(4) The concern about the significance of the axonal swellings to support trauma is supported by the view that his experience as a neuropathologist (which is supported by the experience of the clinicians) is that one would expect that after an injury is inflicted on a child that causes the triad and which causes axonal swellings localised to the brain stem is that the child is immediately and permanently unconscious. He said the clinical history does not fit with his experience of inflicted head injury in infants. He accepted that there is a debate in the literature about this 'but it's not very convincing yet'.
(5) In relation to the significance of the axonal damage in the lumbosacral part of the spinal cord he said the general idea is that when a child is violently treated that the rapid flexion, twisting and extension of the vertebral column stretches these nerve roots, causes the axons to be injured and therefore allows one to identify the sites of axonal injury. But he cautions against reliance on this on two grounds: Firstly, you need to know what the normal state of affairs in the infant's spinal cord is; it may be a normal finding, it has not been adequately explored in the medical literature. Secondly, you need direct evidence of trauma (e.g. fractures to the vertebrae, bruises to the tissue around the vertebral column, tearing of muscles), which were not present. The red cells in the nerve roots are common non-specific findings with an absence of an inflammatory reaction. Again Dr Smith is cautious about this aspect too in his written and oral evidence, referring to it as an aspect that concerns him as to a 'possible' traumatic aetiology.
(6) He expresses general caution about using cerebello changes to date injuries. He said whilst there are some features to suggest there are older injuries they could also be the result of acute events over the last three days of Jayden's life.
(7) In relation to the cause of the SDH being other than traumatic in cause Dr Ramsay said, referring to the Cohen/Scheimberg paper, that possibility still remains theoretical. His own view was that it is an evolving part of the medical literature, that there were good grounds to believe that under certain circumstances in severe hypoxic-ischemic injury such haemorrhages can take place, but that the acceptance of that as a mechanism is not wide. Dr Smith in his evidence said it was a 'great leap'.
Opthalmologists
Professor Luthert and Dr Bonshek
(1) Both described the eyes as being somewhat autolytic caused by the delay in the removal of tissue for fixation, the degenerative process causes the tissue to fragment and it can make it somewhat harder to interpret change.
(2) They confirmed the presence in both eyes of scattered retinal haemorrhaging that went as far as the equator and beyond, into the ora serrata. Professor Luthert said he 'found it difficult to be completely confident of precisely what was where, because things had moved around because of the disintegration' although the RetCam images clearly show that the haemorrhages are going beyond the equator and neither disputed the findings made by Dr Nischal.
(3) They agreed there was optic nerve sheath haemorrhage.
(4) The existence of papilloedema; this is a swelling of the optic disc (where the optic nerve comes into the back of the eye). Professor Luthert said its existence suggested to him that there has been 'significant and reasonably sustained increase in intracranial pressure'. There was an issue between the experts as to timing. There was no evidence of papilloedema in the RetCam images. Professor Luthert said in his view it takes time for papilloedma to develop so its absence would not exclude the existence of increased intracranial pressure, he said 'I do not find the absence of evidence of papilloedema when the RetCam images were taken as an indication that the retinal haemorrhages have not resulted from a mechanism, if you like, therefore secondary to raised intracranial pressure.'. Dr Bonshek agreed it was evident post mortem but said '..it is mild, and the pattern of bleeding seen pre-mortem at Dr Nischal's examination, and also even at post mortem actually, is not the pattern of bleeding one associates with papilloedema, at least not all of it.'
Histopathologist
Professor Malcolm
(1) The effect of the vitamin D deficiency goes beyond simply the impact on the bones.
(2) Calcium is controlled by the endocrine system and is borrowed from the bones to support the rest of the body.
(3) When he wrote his textbook in 2001 rickets was rare in developed countries.
(4) In the last few years there has been a significant increase in rickets, both congenital rickets and potentially nutritional rickets.
(5) Congenital rickets would appear to be the most severe because it starts pre-birth.
(6) There is a difference between low vitamin D or vitamin D deficiency as shown by testing the blood and rickets, which is an alteration of the growth and structure of a bone. One leads to the other but the two are not the same.
(7) Jayden had moderate to severe rickets.
(8) In cases Professor Malcolm has come across this case is as severe as he has seen since the 1 970s when rickets were very common in children in Glasgow, where he worked. Since then he has only seen one of the severity seen in Jayden, although gives the caveat that his experience is distorted by the fact that he looks at bones from dead children so it cannot reflect the severity in the population as a whole.
(9) He agreed with other witnesses that expressed surprise at the presence of this type of rickets in a child as young as 4 1/2 months. He said there has to be a reason for identifying rickets. As can be seen in this case not all clinicians are attuned to the presence or absence of rickets
(10) There is no objective way of evaluating the strength of the bone, you don't know how much force is required to inflict any damage; it can only
be inferred.
(11) He found it very surprising that the mechanisms causing the fractures had not produced any visible signs such as bruising.
(12) He did not see any fractures to the ribs.
(1) In the CCC a central plank of the Crown's case (and Dr Cary and Dr Peter's evidence) was that the recent haemorrhage around the skull fracture and the fissure were advanced as evidence of recent injury of some kind to the healing fracture site prior to admission to UCLH. In his evidence at this hearing Professor Malcolm confirmed that this haemorrhage took place within 24 hours of death; namely when Jayden was at GOSH. He agreed the relatively fresh haemorrhage implied trauma of some kind to those particular sites which on that timing cannot be related to the parents care.
(2) The evidential foundation for his opinion on timing. He accepted that rickets affected the healing process, although not in the first stage as calcium was not needed. In relation to the timing of the older fractures he accepted that the evidential foundation for his timing (6 or 10 weeks) when looking at Jayden's particular circumstances was not very strong although he maintained his position that none of the fractures could be birth related.
(3) The failure to conduct any tests on the strength of the bone. He accepted the bones may be less robust than in normal infants and that rickets affects all the bones, but he could not see how the healed right humeral fracture and the recent tibia fracture could be down to handling Jayden. He said the tibia is probably the strongest bone in the body and he considered it was difficult to see that a transverse mid shaft fracture of the tibia in a non mobile infant could be down to rough handling and rickets. He said a cortical fracture of the humerus requires significant trauma; he said looking at the cortex of the bone there is sufficient bone there that he thought it would take quite a degree of force to actually cause it to fracture completely. His rationale for that view was that he has examined the histological sections; he looks at the bone thickness, both in children and in adults. He did not apply that analysis to the skull fracture.
(4) He agreed there were a number of factors that affected bone strength; diameter; cortical thickness; and collagen strength. He said the only difference when you look at the strength of a bone with and one without rickets is the amount of calcium present within that bone. Beyond that one cannot assess the strength of the bone without doing a whole series of mechanical tests which he was not aware of ever having been done.
(5) In relation to the skull fracture he said rickets would have very limited effect on the strength of the skull, if anything it would make it more malleable. He did not agree that the existence of craniotabes would make the skull more likely to fracture. Firstly, because if you reduced the calcium in the skull you make it more flexible, therefore less brittle. Therefore, in his view, it would require greater force to fracture the skull in a four month year old, but he accepted there was no sign of external injury. Second, he relied on a paper by Teresa Chapman and others in 2010 when they reviewed 47 children in Seattle with proven rickets and found no skull fractures. He said this was one of the few papers in the world that has looked at this. They were all under the age of 2 years, there were 6 under 6 months and there were no fractures noted in any non-mobile child. However he accepted that he did not know whether the study differentiated between congenital or acquired rickets, as he agreed that would make a difference to the severity of rickets. He thought they would all have to be moderate to be diagnosable on an x-ray. Also the study did not make clear what the difference in time was between diagnosis and taking part in the study as the parents or carers may have behaved very differently if they knew their child had rickets. Finally, it is not clear what images were done on the children, whether there were full skeletal surveys.
(6) The metaphyseal fractures are not, in his opinion, affected by rickets as calcium is not present in the growth plate. He said they are caused by a twisting or rotational mechanism. In relation to their existence he said much of the literature was based on radiological evidence rather than pathological evidence. He said on several occasions he had been asked to look at a metaphyseal fracture that appeared on an x-ray which, in fact, wasn't a metaphyseal fracture. Again relying on the Chapman study he said none of the children in that study suffered from classic metaphyseal fractures. He was asked about a 2008 study by Russell Chesney in 2008 which stated that 'Patients with metaphyseal lesions and/or rib fractures are sometimes said to have 'pathognomonic findings' of either rickets or abuse. Fractures at these locations are found in a wide variety of inherited and metabolic disorders as well as in cases of trauma', he said that was written in 2008 and prior to the Chapman paper he would have accepted that as it was the best they had, but he doesn't accept it now because of the Chapman paper.
(7) He did not accept Dr Cohen's view regarding the existence of the traumatised fissure. He said she did not mention or see the granulation which he said is the crucial diagnostic feature, it is the healing tissue which is what he sees in the fissure and why he believes it is traumatised. He said it is not particularly obvious and he may have seen it because of his expertise.
(8) He was not able to say whether the massage conducted by the parents on Jayden could be responsible for any of these fractures.
(9) He said he could not gainsay the paediatric evidence that such fractures may not cause pain and so may not be detected by the carer. He said he found it surprising that there were no bruises relating to mechanism by which the fractures occurred but did not profess expertise in this aspect.
Dr Cohen
Paediatric Neurologist
Dr Jansen
Endocrinologist
Professor Nussey
converted to an active hormone and the active hormone had some minor chemical changes done to it which make it active. Vitamin D has effects on, for example, the gut absorption of calcium. They regulate the wastage of calcium out of the body. Low concentration of blood calcium is called hypocalcaemia. It can be asymptomatic or it can be severe if there is a sudden lowering of calcium or very marked low calcium. Severe symptoms include seizures or spasms of the muscle, as many of the body cells are dependent on calcium for doing things. A deficiency of vitamin D in adults tends to cause mild hypocalcaemia and weakness of muscle and softening of the bones. In children where the bones are still growing it classically causes the condition called rickets, this gets its name from an old English word rick, which means twist. It also has other effects; it affects 3% of all the genes in the body. As a consequence the picture of the disease can be very variable; if you have 750 genes which are potentially affected by vitamin D, and each of those response elements within that gene are affected by 10 or 15 other factors, called transcription factors, these result in a very variable phenotype.
The conclusion of the article relied on by Professor Nussey states '...hypocapnia can certainly cause or worsen cerebral ischaemia, worsen outcome, and cause (direct or indirect) injury to other organs. The decision to institute hypocapnia for therapeutic purposes in the setting of acute brain injury should be undertaken only after careful consideration of the risks and benefits....it might be best limited to the emergency treatment of ICP or to acutely reduced brain bulk in the operating room in these settings, normocapnia should be re-instituted as soon as is feasible '
(i) The absence of any bruising noted, confirmed by the regular contact with various health professionals.
(ii) The variable ages of the fractures would be compatible with bone fragility of a degree that normal processes (such as putting an arm through a babygrow with a fractious infant) might produce the fractures, not because necessarily the force was excessive but because the bones were fragile.
(iii)The only injuries were to bone. Experimental evidence going back many years illustrates the extreme fragility of vitamin D deficient bones. Some of the studies describe the skull of babies who have got severe rickets as being parchment like.
(iv) There is some evidence (from a study conducted in Queensland) that entirely breastfed babies are less likely to be at risk of abuse.
(v) Vitamin D deficiency has an impact on fibroblasts and collagen type 1. It is not just limited to the growth plate and calcification. He considered it could have some effect in weakening the growth plate but was not aware of any study that had looked at that.
(vi) There was no reliable way of determining why some bones may fracture due to rickets and others don't as 'you would have to make some assumptions as to the torsional strength or cross strength of the bone and I don't see – because if you make that assumption then you're making an assumption about the strength and that's a perception.' He said there are cases in the literature of black American teenagers breaking the main bone of their legs during a seizure caused by the hypocalcaemia of rickets.
Paediatric Neuroradiologist
Dr Barnes
(1) Incomplete ossification in the skull called craniotobes (cranio means skull; tabes means softening of the skull).
(2) The front part of the ribs near the breast bone were abnormally thickened and widened at the growth centres. This is another finding characteristic of rickets, often referred to as 'rachitic rosary'.
(3) The growth centres in the upper part of the humerus at the level of the shoulder on both sides are irregular and fragmented, no bony or other reaction or swelling.
(4) In the lower portion of the baby's right humerus there is a transverse defect in the bone showing no swelling or healing reaction. This is consistent with a fracture or pseudo fracture. A pseudo fracture is a type of defect in the bone which is not considered to be a true fracture; it's a weak area and due to rickets that can cause a defect in the bone that is known as a 'Looser zone.'
(5) In the left humerus there are areas of irregular ossification or bone development in the shaft of the left humerus; a defect in the bone in abnormal areas of development of the bone that are weak.
(6) In the forearms on both sides there is bowing or irregular curving of the two bones in the radius and ulna. The growth centres of the ulna and the radius are very irregular.
(7) Within the hands there are irregularities, in particular the left fourth metacarpal which can be a fracture, pseudo fracture or a looser zone.
(8) Irregularity at the top end of the left femur, the growth centre is irregular.
(9) In the lower leg fibula and tibia in both legs the growth centres at the knee and ankle are irregular where there is incomplete calcium and phosphorous mineral deposition.
(10) The tibia and fibula are wavy and curved.
(11) In the right tibia there is an area of defect that could be a fracture, it has a very unusual appearance for a fracture. There is no swelling; there is little or no reaction to the bone or callous formation on the x-ray.
(12) There are a number of irregularities in the bones in the feet, particularly on the left.
In his evidence in this court Dr Barnes was able to point out many of these features to the court and the parties on the x-rays on his laptop. Some of matters listed above illustrate the point made by Professor Malcolm of the differences between what is seen on the images and what is seen under the microscope. For example the changes noted on the tibia and humerus, at (4) and (11) above are accepted to be fractures.
Paediatrics and Obstetrics
Professor Miller
(1) Of the main fractures identified on Jayden he considered if they were as a result of NAI there would be a high likelihood there would be bruising. He relies on two articles to support that view, McMahon and Matthew, both concluded that there was a strong association of soft tissue injury, including bruising, in infants who were abused and had fractures.
(2) Rickets is a systemic disorder that affects every bone in the body. Jayden vitamin D deficiency was very severe from the tests conducted. He questions the ability to accurately assess bone strength under a microscope in an infant who has rickets in the absence of proper tests being done.
(3) In his own clinical experience dealing with unexplained fractures and in reading the literature his view was that infants can incur fractures with minimal trauma because they have an intrinsic bone disorder, such as rickets. He relies on an article by Koo which concluded that physical therapy may result in fractures, although that study concerned only premature infants. He disputes the ability of Professor Malcolm to be able to distinguish between fractures as to which may be caused by rickets and what are not.
(4) He does not accept the view that classical metaphyseal lesion is specific to non accidental injury. In his experience he said he cannot tell the difference between what causes a metaphyseal fracture or what sometimes is not really a fracture but a healing metabolic bone disease or a variant or an irregularity, caused by the vitamin D deficiency. He distinguished the study conducted by Chapman as it did not include many children with congenital rickets and many of the children were older than Jayden, with the majority being over a year. The four children under 6 months did not have congenital rickets. He did not accept Professor Malcolm's analysis that as the growth plate did not have calcium there was no compromise in its strength. He said in rickets the metaphysis is grossly disorganised and there's abundant amounts of what is called non-mineralised osteoid that in his opinion puts that part of the bone at increased risk of being fragile.
Jayden's birth
Professor Page
Biomechanics
Dr Van Ee
Mechanism
The parents
Discussion
The fractures and the fissure
(1) Classic metaphyseal fractures
(2) Skull fracture and fissure
(3) Fractures of the right tibia and humerus
(1) It appears the imaging relied on in that study was limited and did not include skeletal surveys which would capture any asymptomatic fractures;
(2) There is no detail given as to when the parents were made aware of the diagnosis of rickets and whether that would have affected the way they handled the child or the way the child behaved;
(3) There is no detail in the study of whether any of the children had congenital as compared to acquired rickets and the level of severity of the Vitamin D deficiency.
(4) The study acknowledged that some of the metaphyseal fractures seen had features 'closer to' the usual classic metaphyseal fractures.
(5) In an area where there is limited research and limited clinical experience in situations similar to those found in Jayden the court should be cautious in placing too much reliance on this one study.
(1) the sub scalp bruise;
(2) his view that the lack of calcium would make the skull more pliable and therefore less easy to fracture;
(3) the conclusions of the Chapman study that no skull fractures were noted.
(1) In addition to the matters outlined above about the Chapman study it did not, according to the report, include images of the skulls of those who took part;
(2) There is no evidential foundation, as I understand it, for saying that following a diagnosis of rickets some bones are more likely to fracture than others;
(3) The evidence in relation to previous brain injury is equivocal as between Dr Smith and Dr Ramsay;
(4) There is no evidence of any external mark consistent with such an injury;
(5) There is evidence as to the fragility of the skull bone during the post mortem which has not been challenged;
(6) The sub scalp bruising although indicative of a minor trauma did not support major trauma;
(7) Dr Cary's view was that such a fracture would require significant impact from the blunt force but there is no other evidence to support that.
(8) The timing of the bleeding around the fissure is within 24 hours which is when Jayden was in hospital.
(1) Whilst acknowledging his considerable experience and expertise Professor Malcolm lacks a comparator in this case due to the very limited number (only one other in the last 30 years) of a case as severe as the rickets were in Jayden in such a young baby;
(2) His analysis was of the uncalcified bone and therefore he was not able to consider ways of testing its strength and the extent of the calcium, if any, that was present in the bone. It is unfortunate that Dr Scheimberg's email request was not clearer as to what she required.
(1) There is no external evidence to support or indicate that Jayden was being assaulted by his parents; if anything the evidence all points the other way. That evidence is importantly not just self reporting by the parents but was witnessed by a range of professionals with whom the family had contact with on a regular basis over the four and half months he was in their care. Whilst such behaviour can't be ruled out it is unusual with this degree of 'visibility' by the parents and Jayden for something not to be noticed.
(2) There was no evidence of marks or bruises that could indicate that such abusive actions have taken place. Within the timeframes indicated by Professor Malcolm the child was very 'visible' to the professionals through the appointments he attended.
(3) The relatively unusual nature of Jayden's condition in the experience of the relevant experts and the literature which did not give them any reliable comparison with other similar cases.
(4) Whilst not scientific Dr Scheimberg, who is experienced in conducting post mortems of children of Jayden's age considered the bones (the rib and the skull) to be very fragile, in her experience and she compared them to newborn baby bones.
(5) I acknowledge that Professor Malcolm is the only expert histopathologist who specialises in bones but due to the particular circumstances of this case and for reasons outlined above I consider there are grounds upon which I can depart from his opinion.
(6) The evidence in relation to the traumatised fissure is now far from clear in the light of the timing of the fresh bleeding within 24 hours of Jayden's death. There is an issue about whether granulation was present which was not fully explored with Professor Malcolm. But in the light of the timing of the recent bleeding and my findings about the fractures I do not consider the traumatised fissure is more likely than not to be a result of inflicted injury.
Events leading to Jayden's death
Seizures or not?
(1) The description given by the parents of what they observed from about 5am on 22.7.09 has not seriously been challenged and I accept it. In their written closing submissions the LA set out what they said were inconsistencies in the various accounts given by the parents. Very little of what was set out was put to the parents in cross examination, or it was put in part to one but not the other. Considering the various accounts they have given (their police interviews, their oral evidence at the CCC, their statements in these proceedings and their oral evidence during this hearing) their account has remained broadly consistent. They describe how they found Jayden in his cot, laying to one side with his arms through the bars; the difficulties in feeding with his tongue stuck to the roof of his mouth; trying to engage him with his toys; the descriptions of him reaching out for the keys and drawing them to his mouth and that his eyes followed the toys and his mother. Their primary concern was that he was not feeding. Their prompt phone call to the hospital and the GP has not been disputed. Neither has their description of being able to feed and change him and not noticing any stiffness in his limbs. Their description of him shaking/shivering on their way to surgery accords with the description they gave the GP.
(2) The evidence from the GP both from the records and his oral evidence is not consistent with a child who has lost consciousness or exhibiting decerebrate posture. He conducted a full examination, observes Jayden as alert and observes him being undressed and dressed. They were with the GP for about 25 minutes, although he was not with them all the time. Even making allowance for the inexperience of the GP the description he gives is consistent with what was observed by the parents. The lack of any sense of urgency (although inexperience must have played a part in this decision) is graphically illustrated by allowing the parents to take Jayden to the hospital by public transport.
(3) The CCTV and stills of Jayden on the bus are consistent with the parents account and the GP's observations.
(4) The arrival at UCLH and Nurse Edward's observations are consistent with seizures. She is an experienced nurse, trusted by the Consultant Paediatrician. She immediately noticed something was wrong and observed tonic/clonic seizures and alerted Dr Sutcliffe. When he first saw Jayden and the parents he did not observe anything obviously wrong and finished off his other appointment. I consider it more likely than not that he gave reassuring words to the parents and that is what prompted the mother to phone her mother to say everything was fine. If Jayden had been unconscious or exhibiting decerebrate posturing Dr Sutcliffe as an experienced paediatrician would have noticed that. It is more likely that he was having fluctuating seizures. Nurse Edwards continued to observe what she considered were seizures and Jayden was seen by Dr Sutcliffe. He observed the abnormal movements and immediately made the referral to the resuscitation unit. It is of note that when he spoke to Dr Salt to warn her Jayden was on his way he said it was because of fitting. The subsequent suggestion by him that he observed decerebrate posturing at that time needs to be looked at in that context of the contemporary notes and recordings and what Nurse Edwards observed, which she was clear were seizures. I do not accept the suggested criticism of sending Jayden to the resuscitation unit rather than administering anti convalescent medication there (which they did not have) or requesting the resuscitation team to come to them. The unit was not far away and he sent a doctor with them.
(5) They were met by Nurse Leech in the resuscitation unit and she clearly realised something was wrong. She immediately realised Jayden needed to be weighed for medication and did so and took off his clothes. She did not observe any stiffness when she did that but did observe the seizures. Dr Salt soon arrived and between them they conducted their assessments. There has been a lot of evidence about the various scales to measure consciousness (AVPU and GCS) and how reliable they are particularly in such a young child. Standing back from that I consider what is important is that the form for the measure of the GCS being used they were familiar with using, they work as a team and are both experienced clinicians. Making all due allowance for the subjective element of these assessments I am satisfied, on the balance of probabilities, that they are broadly accurate. The significance is the deterioration between 11.35 and 12.20 when the score falls from 13 to 6.
(6) The fact anti-convulsing medication was administered immediately, followed by two more doses until the fitting appeared to subside.
(7) I have carefully considered Dr Peters evidence in relation to this and have weighed up his undoubted clinical experience in dealing with these cases but I am concerned that there is an element of his evidence that seeks to continue to justify his firm opinion formed at a very early stage as to the cause being due to some form of non accidental trauma. In my judgment he has had to try and account for the clinical picture ex post facto which in part does not sit comfortably with the early opinion he reached. Even making all due allowances for the difficulties in assessing consciousness the clinical evidence, from different sources, points towards repeated seizures.
(8) Dr Jansen, who has expertise in this field, both in terms of her qualifications and her clinical experience was instructed on behalf of the parents. She considered the clinical picture very carefully and had access to all the records. Her report carefully analyses the issues as she did when she gave her evidence. Her evidence is clear, and I accept it, that Jayden was suffering from seizures from at least 5am, that it rapidly became status epilepticus and was clearly refractory due to amount of medication required to control it.
(1) Dr Salt accepted that once Jayden was intubated the anaesthetists took effective control. The difficulty with that, and it may be in part due to the particular pressures of that day, is that there was no effective paediatric clinical oversight or driver in relation to the decisions made and events that afternoon. This was particularly when the effect of the muscle relaxants given to Jayden for the purposes of intubation meant that it would have been very difficult to monitor any continuing seizure activity. Dr Salt said when she was recalled that the dose of phenytoin given at 12 noon would have lasted 24 hours. That did not really deal with the point that there could be no certainty that it was actually working with Jayden, bearing in mind that he required three doses of anti convulsing medication prior to being intubated. Dr Peters suggested that this could be monitored by any changes in blood pressure or temperature. The difficulty with that is that there is evidence to support the fact that he was probably still fitting; Dr Runnacles notes in her statement that when she was contacted by Dr Salt about 5.45 pm there was raised blood pressure and she advised a further saline bolus. The clinical notes record morphine and medazalam (an anti convulsant) being prepared earlier on in the day but not administered. They were administered at 17.55. At 18.45 Dr Runnacles noted further seizure activity and administered lorazepam and a loading dose of phenobarbitone to control the seizure activity. All this points towards Jayden's fitting not having been adequately controlled during the afternoon. He was out of the effective direct clinical management of the Consultant Paediatrician.
(2) When he was intubated the second time the tube went too far down into his right lung, causing his left lung to partially collapse, as recorded on the post intubation x-ray taken between 14.08 and 14.12pm. Dr Shaw very helpfully produced the hospital records which show that she viewed the images at 14.34 and said she immediately phoned Dr Shaw to inform her about this. It appears more likely than not it was corrected soon after that (although his CT scan is timed at 2.39pm so it is unclear whether he would have been enroute at the time Dr Salt was alerted). In any event it appears this compromised his ventilation for at least 20 minutes. Dr Peters sought to play this down saying it happens regularly and suggested that it was in part due to gases from the stomach. The blood gas measurements taken at 14.24 showed Jayden's CO2 level had increased dramatically to 11.3 (twice the normal range). It is accepted that this will adversely contribute to his condition. It is unclear how or when this was corrected as there are no contemporaneous records about the management of this. The next blood gas was taken at 15.38 but that recording shows there was insufficient to measure and no attempt was made to take it again. The next one was not until 16.13 when the CO2 had dropped to 2.44 and remained at around that level for the next two tests taken at 16.17 and 17.17. Dr Peters has sought to rationalise this in two ways. First, by suggesting that there was no evidence that Jayden was hypoxic as the pulse oxymeter level was 100%. Professor Nussey said that only gave part of the picture. Second, that when considered in conjunction with the pH level it demonstrates that the body was self adapting to this change. Professor Nussey said that again only gives half of the picture. I prefer the evidence of Professor Nussey, whilst he may not have the same clinical experience as Dr Peters his expertise in considering the consequences of such changes is clear. As Dr Peters said 'It sounds like he [Professor Nussey] understands the chemistry better than I, but that translating into a clinically meaningful difference I just don't understand'. It is more likely than not, on the information I have, there was not proper management of Jayden's CO2 levels during this period and that both the high and low level are both likely to have contributed to his deteriorating condition.
The Triad
Retinal Haemorrhages
(1) Although Dr Bonshek in his report concluded that the findings were supportive of a traumatic cause he accepted in evidence that they could be caused by a very steep rise or spike in ICP. Unfortunately he had taken the history from a summary in the GOSH clinical papers, which did not have the full picture, which he was not aware of. When he was taken through it, in particular, the events around the time the retrieval team were dealing with Jayden he agreed there was a very steep rise in ICP that could cause the retinal haemorrhages. That was confirmed by Nurse Mogridge in her evidence.
(2) I accept Professor Luthert's analysis about the significance of the papilloedema and the optic nerve swelling.
(3) Professor Luthert had direct experience of a case where there were retinal haemorrhages similar to the pattern seen in Jayden where there had been no trauma.
(4) I preferred Professor Lutherts more cautious approach to the conclusions that can be drawn from the existence of retinal haemorrhages and their formation. He drew a very clear distinction between cause and mechanism.
(5) The case is complicated by the impact of the changing CO2 levels between 2 – 6pm on 22.7.09 and the effect those changes would have had on the blood vessels, possibly making them more likely to burst. Both Professor Luthert and Dr Bonshek agreed this could have been a relevant factor.
(6) Finally, it is important that the time of Dr Nischal's observations are factored in. He saw Jayden nearly 30 hours after he had been admitted to hospital and the detailed clinical picture was not known by Dr Nischal.
Encephalopathy
(1) It is agreed by all the experts who operate directly or indirectly in this area, and Dr Peters who is an experienced clinician, that the expected and typical presentation in this type of case if it had been caused by trauma of some kind would be immediate collapse. As Dr Peters said in his evidence in the CCC "one would expect that after an injury is inflicted on a child that causes the triad and which causes axonal swellings localised to the brain stem that the child is immediately and permanently unconscious." There have been references to different scenarios in the literature but that is not the experience of those who gave evidence. On any view Jayden' s presentation and history in the first part of 22.7.09 was not an immediate collapse or loss of consciousness.
(2) In the light of my findings about the impact of Jayden's rickets on his bones, the lack of any injury to the ribs (or any other sign of relevant external trauma), in the particular context of this case, where the mechanism of shake and/or impact has been the mechanism that has been put forward (both in the CCC and in this hearing) is relevant. As Dr Scheimberg said "..we know from the fresh bleeding in the fracture site which happened while he was in hospital. So obviously he is a very fragile child"
(3) I accept both the evidence of Dr Jansen and Professor Nussey that Jayden's low calcium levels would affect him in the two ways they describe; adverse impact on his immunity system and make him more likely to have seizures.
(4) I have made my findings about Jayden's presentation during the morning of 22.7.09. The primary cause of his seizure is unknown; the most likely contender is probably a form of febrile seizure which although there was no raised temperature due to his calcium levels, he was more likely to seize with a much lower level of infection. That could either have been related to his flu or possibly meningitis; the latter was never ruled out (through a lumbar puncture) although the clinical signs were not readily apparent. The low level infection cause is supported from a number of other sources: raised white blood cell count, raised CRP, the inflammation of the brain. Dr Ramsay considered an odd feature was the degree of leptomeningeal inflammation in the subarachnoid space purely in association with hypoxic-ischemic brain injury. This indicates that something was stimulating or irritating that part of the brain raising the possibility of an infection and specifically with a pattern like this, an infection by bacteria. Whilst none of these features would be enough on their own, taken together they provide support for that being the primary cause for the seizures. Jayden had been unwell with flu type symptoms for a number of days.
(5) The seizures were not effectively treated until just before 12 noon, some 7 hours after changes were first noticed in Jayden.
(6) It is more likely than not that Jayden carried on seizing, undetected for some, or all, of the afternoon between 2 and 6pm on 22.7.09. I have outlined my reasons for that above. This is likely to have contributed to the infarction of the brain.
(7) The difficulties with both the intubation tube and the changed CO2 levels are also likely to have contributed to the hypoxia and the adverse consequences that flow from it.
(8) I accept the evidence and analysis of Dr Jansen and Professor Nussey in relation to these aspects as they bring together the important twin features of the clinical expertise and also the knowledge of the wider impact of these changes on the different systems that operate in the body.
(9) The evidence in relation to axonal damage is complex. Both Dr Smith and Dr Ramsay have considerable expertise in this area, Dr Ramsay gave a detailed account of his experience. Dr Smith said that he had not seen axonal swellings outside motorbike accidents or admitted shakes however he conceded a non– traumatic cause was a possibility, he said it needed to be considered in the context of the overall ischemic damage Jayden suffered. He agreed axonal damage is not diagnostic of inflicted trauma. He said in his oral evidence and his section 9 statement the existence of the axonal damage raised the 'possibility of trauma'. In relation to damage in the lumbosacral part of spinal cord being an indicator for trauma Dr Ramsay had two important caveats to that: First, you need to know what the normal state of affairs in the infants spinal cord is and it has been seen in infants who die in situations where there is no suspicion of trauma, which Dr Ramsay had direct experience of. Second, traumatic injury to the spinal cord would leave signs of direct evidence of trauma (fractures to the vertebrae, bruises in the tissue, tearing of muscles) which is not present in this case. Red cells were present in the nerve roots; that is, in his view, a non-specific finding. In relation to the other axonal injury Dr Ramsay said that Jayden had both the classic axonal injury (which is established to be linked to trauma) and the plemorphic form (which can be related to other situations of brain injury unrelated to trauma). The presence of the pleomorphic form is not surprising in the context of severe ischemic injury but the classic axonal swellings are restricted to the brain stem and had, what he considered to be, rather peculiar appearance in all but one site. This suggested to him they had been around for some time. He said the only classic axonal swellings were those in the inferior cerebellar penduncle, which he agreed could indicate trauma, but would be associated with the child becoming 'immediately and permanently unconscious'. Dr Ramsay also considered the absence of siderosis (haemosiderin at the sites of the haemorrhages) and astrogiolsis (no reaction to the astrocytes) are relevant as contra indicators from the cause being trauma. Bearing in mind the caution Dr Smith gives to these indicators and the caveats outlined above from Dr Ramsay I do not consider they do any more than indicate the possibility of trauma but have to be looked at in the context of all the other evidence in this complex case.
Sub Dural Haemorrhage
Conclusion
General matters