England and Wales High Court (Family Division) Decisions

i)                    L who is now rising 12,

ii)                  M who is now aged five,

iii)                N who is now aged two,

iv)                P who is now aged 7months

Background

These Proceedings

Threshold

i)                    That K died as a consequence of cardiac necrosis caused by the deliberate administration or accidental ingestion of cocaine by or whilst in the care of

a)                  her mother, the first respondent, and or

b)                 her father [father 1], the second respondent, and or

c)                  her paternal grandmother, and or

d)                 her maternal grandmother

ii)                  that one or more of those four individuals alternatively failed to protect her from the administration or accidental ingestion of cocaine

iii)                that the children were exposed to emotional abuse as a result of domestic violence perpetrated by father 1 upon the mother.

i)                    Mother - filed 11^th May 2020:

a)                  Reserved her position as to whether cocaine ingestion was the cause of K’s death or whether her death was consistent with cocaine intoxication.

b)                 Accepted her own use of powder cocaine every 4 to 6 weeks during the 12-month period leading up to February 2019 but no use thereafter.

c)                  Accepted repeated consumption of cocaine by father 1 on a daily basis.

d)                 Accepted that K was exposed to and/or ingested cocaine whilst in the care of the mother, father 1 or paternal grandmother.

e)                  Denied deliberate administration of cocaine to K by herself.

f)                  Did not accept being knowingly responsible for culpably failing to protect the children from being exposed to drugs.

g)                 Accepted L was suffering significant emotional harm and that the children were likely to be suffering significant physical and emotional harm by virtue of their exposure to cocaine and domestic abuse in the form of loud arguments and volatility and occasional physical abuse by father 1 to the mother.

h)                 That she felt unable through fear of violence from father 1 to do more to protect K and the other children. She alleged that she has been consistently subjected to violence and threatened with violence throughout most of the relationship, whenever she tried to confront father 1 about his drug use or asked him to leave.

ii)                  Father 1

a)                  Accepted the presence of cocaine in K, that her death was consistent with cocaine intoxication but not that, on the balance of probabilities, cocaine was the cause of K’s death.

b)                 Accepted a limited role in caring for K, in the days and months preceding her death.

c)                  Accepted his own repeated consumption of cocaine in the 12-month period prior to July 2019. He denied being a dealer.

d)                 Denied administering cocaine to K or causing her to ingest, or any negligence in his or others care of her. He also denied negligently failing to protect her, his position was the same in relation to the exposure of the other children to cocaine or cannabis.

e)                  He accepted arguments between himself and the mother (which the children would have witnessed) and that she asked him to leave the property from time to time. He denied physicl abuse.

f)                  He denied that the children had suffered significant harm by virtue of being exposed to domestic abuse although accepted they may have suffered emotional harm as a result of hearing arguments.

iii)                MGM

a)                  Accepted the presence of cocaine in K’s hair and urine and awaited the cardiologist’s opinion in relation to cause of death.

b)                 She denied being involved in the care of K in the days or months preceding her death or playing any role in K being exposed to cocaine, whether deliberately or inadvertently.

c)                  She denied any role in the exposure of the other children to drugs.

d)                 She said she was unaware of drug use by the parents.

e)                  She agreed that the children had been exposed to domestic abuse between father 1 and the mother.

iv)                PGM

a)                  She accepted the presence of cocaine in K’s urine and hair  but awaited expert evidence in relation to the cause of death.

b)                 She accepted caring for K in the days and months preceding her death.

c)                  She accepted that the mother and father 1 had repeatedly consumed cocaine in the 12-month period preceding July 2019.

d)                 She denied consumption of cocaine herself and attributed her hair strand tests to environmental exposure.

e)                  She denied any role in K ingesting cocaine.

f)                  She denied any role in any of the other children being exposed to cocaine.

The Parties’ Submissions

i)                    The mother’s failure to give evidence should not lead the court to attach no weight to the mother’s evidence. A more nuanced approach is required given the mother’s situation.

ii)                  The medical evidence established that K’s death was caused by heart failure, arising out of cardiac necrosis, caused by ingestion of cocaine.

iii)                Hair strand testing evidence demonstrates that the mother, father 1 (repeatedly) and paternal grandmother had consumed cocaine, including smoked crack cocaine, in the 12-month period preceding July 2019. The Chemtox samples can be relied upon and the different results from Lextox can be explained, both by the fact that the hair sample was not the same (being separated by some 10 weeks growth) and by the possibility of interference.

iv)                The mother’s lies about her own use, means her account cannot be relied upon but her evidence about father 1 being a drug dealer is contrary to her interest.

v)                  The totality of the evidence supports the presence, on a regular basis, of drugs in the household of the mother and the paternal grandmother.

vi)                Hair strand testing of the children shows that they were exposed to cocaine. For L, this would be in the mother’s household and for M and K, in both the mother and paternal grandmother’s households.

vii)              Each of the adults knowingly exposed the children to risks associated with drug exposure and have culpably failed to protect them.

viii)            The evidence supports K’s exposure as having occurred whilst in the mother’s home. The medical evidence is more supportive of her ingesting the cocaine at some point after leaving nursery on 3^rd April but cannot rule out exposure during the day on the fourth, when in the care of the paternal grandmother and father 1. The symptoms of illness that she demonstrated on the third and fourth prior to being taken to the GP, are non-specific and do not pin down the timing of her exposure. None of the accounts of the adults explain how she came to ingest the cocaine that killed her. It is therefore difficult to identify how it occurred and perhaps does not matter precisely how. It is not a tragic accident, but a highly culpable event. Both the mother and father 1 culpably failed to bring their use of cocaine to the attention of the hospital. Had they done so, tests might have been carried out which could have prevented her death

ix)                The mother’s evidence can be relied on in relation to father 1’s drug dealing. His history in terms of his antecedents and his evidence are consistent with him being a drug dealer. The other evidence from L and the covert recordings supports this interpretation.

x)                  There was a level of domestic abuse in the parents’ relationship, but not to the extent that the mother now maintains where she says she was unable to address father 1’s frequent drug use and the consequent exposure of K to it. Her account has developed over time, with no reference to domestic abuse in her first interview. The other evidence from the maternal grandmother and L do not support a high level of violence, but rather a deteriorating relationship linked to father 1’s growing alcohol and drug use, but not one which prevented the mother from protecting the children. The absence of evidence from any other source undermines the mother’s account.

i)                      She does not now seek the return of the children to her care but accepts that a full psychiatric assessment of her will be required.

ii)                  The court should take into account her evidence and the reason for her failure to give evidence and the circumstances in which her evidence was given.

iii)                The timing of K’s ingestion of the cocaine which led to her death is difficult to determine, save that it occurred prior to her attendance at the GP on the fourth. The evidence, in particular the phone records, convincingly show that father 1 was present in the home on the evening of the third and overnight into the fourth. The court should not rule out the possibility that it was ingested during the period when K was in the care of father 1 and paternal grandmother. The lack of detail in their accounts and, in particular, their behaviour later that day is highly suspicious.  Their failure to seek medical attention for K, when they said they considered her to be very unwell, does not withstand proper scrutiny. The paternal grandmother’s failure to return the mother’s calls that evening is not properly explained; nor is the father’s failure to attend hospital. Did they know something, which was why they behaved as they did?

iv)                The mother’s behaviour in immediately taking K to the doctors is inconsistent with an individual who was concerned that a child had consumed illegal drugs. The evidence does not support the mother being aware of K having ingested cocaine

v)                  The Local Authority must prove that the Chemtox reports, which show an increasing and high usage in respect of the mother’s drug use, are more persuasive than the Lextox reports, which show a declining usage. The later Lextox reports are consistent with the earlier Lextox reports. The results provided by Chemtox, after the conclusion of the evidence are unsatisfactory and the court should rely on the better evidence of the Lextox reports. The Local Authority must prove that the mother interfered with her hair if the court is to prefer the Chemtox report. They cannot do that and it is improper to infer or speculate as to how the mother might have acquired the knowledge of how to influence a drugs test. By July 2019, when the directions hearing took place, she was unaware that a further drug test might occur, she undertook not to interfere with her hair and the opportunity to do so between the direction and the taking of the sample was limited. Her evidence should be accepted on this.

vi)                In respect of the mother’s account of father 1’s drug use, she has nothing to gain from this, her evidence has evolved but the court can still rely on it. Father 1 is dishonest, he denied drug use during an earlier assessment and was subsequently found to be using drugs.

vii)              The two youngest children’s hair samples show the presence of crack cocaine which L’s does not. L did not visit the paternal grandmother’s save on one occasion. It is more likely that the children were exposed to crack cocaine at the paternal grandmother’s home.

viii)            The evidence supports the conclusion that father 1 subjected the mother to serious and significant domestic abuse which prevented her from leaving the relationship or doing more to protect the children from exposure to his drug use. The chronology supports him having a violent aspect; he has been violent to previous partners, to his brother, to property, has convictions, his mother told another Local Authority that he had a violent character and the mother reported abuse to the paternal grandmother and his abusive behaviour is also evidenced by L and by the maternal grandmother  who saw physical damage to the property.

i)                    The evidence supports the conclusion that K ingested cocaine  at the mother’s home, whilst under her care and control; that it was her cocaine (she being a significant consumer) probably kept in her bedroom drawer and at all times under her control. It explains why she lied and lied again as to her true levels of drug use and why she has made serious allegations against father 1.

ii)                  Father 1 has suffered the loss of his daughter and his children. The court should not lose sight of the emotional impact on him and the effect it may have had on his recall.

iii)                Father 1 has not sought to compel the mother to give evidence and does not invite the court to draw inferences against her, but rather to urge the court not to rely on her evidence, against him. The mother clearly could have given evidence even though she is unwell. The court therefore should give little, if any, weight to her written evidence which has not been challenged by cross examination, in respect of which there are many inconsistencies which are now unexplained and where to ensure fairness for father 1, who has been rigorously cross-examined, caution should be applied to the mother’s evidence.

iv)                The court should bear in mind that she would have been cross-examined on, amongst others, the following points: why she initially gave accounts on 6^th April and shortly thereafter which pointed to father 1 being absent and playing no significant role in childcare; why she spoke well of him in initial accounts; why she only makes allegations against father 1 after her first interview and after she has taken legal advice; why she only mentions father 1’s role in drugs during her interviews in July after she has been arrested for murder; why she made no reports of domestic abuse to any health professionals, to police or any other authority; how the maternal grandmother was never aware of it; why she made no drugs allegations against father 1 when it was initially disclosed that K had cocaine in her system; how her account can be relied on  when she repeatedly misled the court as to her own drug consumption; what she may have said to L to influence her account.

v)                  Father 1 gave evidence and his evidence should be relied on. He should be given credit for attending and giving evidence remotely, whilst still unwell. His evidence has been rigorously challenged and it is hardly possible to fairly compare his evidence with the mother’s.

vi)                The evidence does not support father 1 living at the property or spending considerable time there, particularly as a primary carer. Her initial accounts are most likely to be accurate: the account given to DC Lockstone is a reliable account and does not place father 1 as living in the property, or being present in the property at the time cocaine was probably ingested. Her later accounts which draw him into the household have not been tested. He is unlikely, therefore, to have left cocaine at the property which K consumed. As the principal occupant, the cocaine was more likely to be the mother’s. Father 1 has been frank about his drug use, whereas the mother has not been. This should lead the court to conclude it is more likely the mother who was the source of the cocaine. The mother’s developing case of seeking to attribute blame to father 1 is an attempt to distance herself and to seek an excuse for her behaviour

i)                     Considerable reliance is placed on the expert evidence as to the significance of K’s symptoms in terms of timing the ingestion of the cocaine.

ii)                  The weight of the evidence relating to the timing of the ingestion of cocaine, points away from the three-hour window when the paternal grandmother was caring for K between about 1.20 and 4.30 on the fourth. She is not therefore culpable for K’s death. Even if the court concludes she is a drug user (which is denied) and her house is used for drug consumption, it does not make her culpable for K’s death.

iii)                K’s symptoms of a tummy ache, vomiting, a high temperature, puffy eyes are not non-specific, when one knows that she died of cardiac necrosis caused by cocaine ingestion. All of them are said by the medical experts to be consistent with cocaine ingestion and oedema arising from deteriorating heart function. Both Dr Hawcutt and Prof Bu’Lock considered the clinical picture supported the ingestion of cocaine at some point after K left nursery and prior to the grandmother’s arrival on the fourth.

iv)                The scientific and medical evidence together, pointed to her consuming the cocaine between two and three days prior to her death. In particular the detection of BZE in urine, but its absence from blood on the 5^th, was consistent with consumption on 3^rd April, when she was taken ill in the evening.

v)                  The evidence does not support there being a significant deterioration in her condition between the mother leaving to take L to the hospital and her return. The mother said when the grandmother arrived that she would take K to the doctors later that day.

vi)                Her account of the day of the fourth can be relied upon. She is a caring granny who would have taken K to hospital had she been aware of an incident which put K at risk.

vii)              The drug testing results from Chemtox are not consistent with Lextox. The paternal grandmother is clear that she did not use cocaine and the court should rely on her account. She is also clear that she did nothing to interfere with her hair. There is nothing to show that she was aware that one could cheat a drugs test. The drugs tests and the drug mapping support the conclusion that the lodger and the father were both heavy users in her household and this explains her  Lextox hair strand test results which Dr Cirimele accepts are consistent with exposure rather than consumption. She was unaware of the extent of their drug usage in her house. The historic evidence is hearsay and double hearsay which does not support any recent link between the paternal grandmother and drugs. Evidence dating back to 2002 is of little or no probative value now, particularly when it is hearsay or double hearsay. The covert recordings do not suggest she knew anything about K ingesting cocaine.

viii)            She is the only person who willingly gave evidence and she should be given credit in terms of her credibility for this.

i)                    A more nuanced response to the mother’s failure to give evidence is required and the authorities support this. One cannot simply give no weight to her evidence.

ii)                  The evidence establishes that the mother and father 1 had periods of high conflict in their relationship. However, the evidence of a seriously abusive relationship is questionable. She did not report any domestic abuse to her GP, or to her health visitor and her allegations arose only in her interview with the police on 16^th July 2019. Much of her earlier evidence, for instance about the dog biting father 1, could have gone further and made allegations but did not. The maternal grandmother knew nothing of it, albeit she was aware of a toxic relationship between the two. Is the evidence sufficient to establish the mother’s case that she was so fearful of father 1 that she was unable to leave him, unable to prevent him storing cocaine at her home and  unable, by reason of fear, to protect the children from his behaviour? The children did suffer significant emotional harm as a result of exposure to conflict in the relationship but the court should be cautious about making findings to the extent the mother alleges.

iii)                The evidence supports the conclusion that father 1 sold cocaine; L’s interview; the mother’s evidence of his activities; his previous convictions; the evidence of the covert recording in particular his admission of ownership of the paper wraps. The court can also conclude that the paternal grandmother knew of father 1’s dealings; there is no other interpretation for the covert recording conversations. She condoned the mother and father 1’s use of drugs by caring for the children so they could consume. She was relaxed about discussing drugs with her son. The evidence of her familiarity with drugs and ease around them should inform the court’s assessment of the hair strand testing. The Chemtox results can be relied upon and the court should note that these hair strand samples were taken when the parties had almost no notice of samples being taken  due to the police interest in cocaine  having been involved in K’s death. The drug mapping which found traces of cocaine all over the paternal grandmother’s home supports a picture in its entirety which supports the Chemtox results being accurate.

iv)                The court should also conclude that the Chemtox results for the mother were accurate for the same reasons. Her evidence of her own drug use and that of  father 1 has been inconsistent and variable and cannot be relied on save that it accepts cocaine use. This also includes crack cocaine which was found in mother’s hair, the grandmothers’, the father’s, the lodger’s, Q’s and M’s.

v)                  Medical evidence as to the timing of the ingestion was not clear. Prof Bu’Lock’s evidence did not clearly indicate any particular timing and nor was it conclusive as to K’s symptoms during the day of the fourth. The evidence of father 1 and paternal grandmother as to the fourth and their responses in the evening of the fourth should be rejected. However, what the consequence of that is, uncertain. All that can be said for sure is that K came into contact with the cocaine at the mother’s home. The court should not go further than saying that K ingested the cocaine at some point between teatime on 3 April and the mother’s return home at about 4:30 PM.

vi)                Father 1’s evidence as to his activities on the night of the 3^rd/4^th was wholly unreliable, but the evidence is not sufficiently clear for the court to conclude that K came upon the cocaine at some point overnight on 3^rd April and before the arrival of the paternal grandmother at 11 am

vii)              The evidence supports a conclusion that it was father 1’s activities that resulted in cocaine being in the house.

viii)            The evidence demonstrates that the mother sought to protect father 1 in the early days of the police investigation. She was not forthcoming with evidence about his activities until July 2019. She failed to protect the children during her relationship with father 1 if her account of the extent of domestic abuse is rejected and she protected him thereafter. The paternal grandmother also failed to protect the children if she was aware of the extent of father 1’s drug dealing and the use of cocaine by the parents.

The Law

The burden and standard of proof

Drug Testing

i)                    a detailed chronology.

ii)                  a schedule of matters agreed and not agreed between the medical experts.

iii)                a schedule of drug testing results.

i)                    Dr Cirimele

ii)                  Professor Forrest

iii)                Dr Hawcutt

iv)                Dr Ashworth

v)                  Dr Cary

vi)                Dr Palm

vii)              Prof Bu’Lock

viii)            The paternal grandmother

ix)                The maternal grandmother

x)                  Father 1

The Medical Evidence

i)                    Dr Michael Ashworth - Consultant Paediatric Pathologist and Special Cardiac Lead at GOSH

ii)                  Dr Nat Cary - Consultant Forensic Pathologist

iii)                Professor Robert Forrest - Forensic Toxicologist

iv)                Dr Dan Hawcutt - Consultant General Paediatrician and Senior Lecturer in Paediatric Clinical Pharmacology

v)                  Dr Lina Palm - Consultant Paediatric Pathologist

The minutes of the meeting appear at E308. A schedule of points agreed and not agreed was drawn up following the meeting.  It addresses a number of specific questions.

i)                    What is the relevance of the hair-root testing results?

Agreement:

a)                 Drugs will only enter the hair root via the blood supply so is evidence of ingestion rather than contamination.

b)                 Drugs found in the hair root is evidence of ingestion in the days before the sample taken (1 to 5 days or so) but not possible to be more prescriptive about a timescale.

c)                  Cocaine found in the hair root represents drugs circulating in the blood and not contamination described by Dr Cirimele by sweat from other individuals or other bodily fluids.

d)                 If someone had taken an acute overdose of cocaine, Professor Forrest agrees with Dr Cirimele that one would expect to find more cocaine or metabolites in the hair root analysis.

e)                  As no cocaine or benzoylecgonine was found in fluid extruding from the thawed liver that suggests that a few days have elapsed and the concentration at the time of the acute illness was not particularly high.

ii)                  What aspects of K’s final illness, collapse and death are:

-          compatible with having been caused by cocaine ingestion, or

-          incompatible with or an unlikely consequence of cocaine ingestion?

Agreement:

a)                 Cocaine exposure caused injury to the heart (evolving ischaemic necrosis in the left ventricle and the heart septum both mainly on the endocardium but also within the deeper zones of the myocardium and multifocal contractions and necrosis, local myocyte damage associated with acute inflammation and mononuclear cells which are not that acute).

b)                 No evidence of increased scarring to indicate a longstanding process (as would expect to see in cocaine induced cardiomyopathy).

c)                  The findings are not explained as a consequence of resuscitation as K was in a collapsed state for 1 hour before she was declared deceased and these changes to the heart would not appear in that time.

d)                 The myocardial necrosis is the cause of the collapse as that set in place a heart rhythm disturbance.

e)                  The clinical presentation and pathological findings are consistent with cocaine ingestion.

f)                   If K had ingested a toxic amount of cocaine, more than a minimal amount of cocaine two or three days before, it is entirely possible that there would have been some detectable in the liver but not necessarily so.

Disagreement?

Although, when looking at the totality of the evidence Dr Hawcutt agrees, on the balance of probabilities, that cocaine ingestion caused the heart damage that led to death, he expresses the opinion that there is nothing in the clinical picture that is unique to cocaine intoxication but there is also nothing that points to sepsis.

Dr Palm also said, “the post mortem findings in themselves are really nonspecific, the pathology is there but their interpretation is not straightforward, and I have no clear course to explain what happened to K and I have no alternative diagnosis to offer either”.

iii)                Are there any known diseases, illnesses or other conditions which could adequately explain K’s final illness and death?  In particular, (a) has sepsis been ruled out, and (b) is resuscitation a possible cause of the necrosis?  In relation to any other possible cause, please indicate factors which will assist in assessing its likelihood.

Agreement

iv)                No infection identified in life or since death that provides an explanation.

v)                  Resuscitation not a likely cause of the necrosis

vi)                No inflammatory focus or of myocarditis (inflammation of the heart that can be seen after viral infections).

vii)              No other possible cause for the necrosis has been identified.

Disagreement

Dr Ashworth of the view that the necrosis “could conceivably be the result of hypotensive episodes or something profound like that but isn’t necessarily specific for cocaine and there were no other features, there was no chronic change, no fibrosis. I wasn’t particularly impressed with the inflammatory reaction and so on. So, I think its damage and it is of more than a few hours duration, probably not much more than a day or so, but other than that I’m not sure that I can be more specific than that”.

1. Do the other experts agree with Dr Hawcutt’s opinion:

‘[…] I am therefore of the opinion that, on balance of probabilities, the most likely series of events is that K ingested cocaine in the day or so before the bloods were taken […].’ [E264, p.10 of 32, para. 1.14]

Agreement

Yes, subject to the following qualifications:

(a)   The levels found are not a cocaine overdose just sufficient to intoxicate.

(b)   Children may be much more sensitive to the negative effects of cocaine.

(c)    Benzoylecgonine is a major metabolite of cocaine, is detectable for longer in urine than serum after ingestion of cocaine. You are more likely to detect cocaine or benzoylecgonine in urine than you are in a simultaneous blood sample. The benzoylecgonine finding without cocaine in urine probably reflects ingestion sometime in the 48 hours or so before the sample was taken and that would fit in with the negative result for benzoylecgonine or cocaine in the serum sample collected at 14:18 hours on the 5th of April.

(d)   Normally speaking, the presence of BE without cocaine in urine would probably suggest ingestion in the ‘48 hours or so’ or ‘day or so’ before the sample was collected.  This would also fit with the negative result for BE and cocaine in the serum sample. (Prof. Forrest, 9H)

(e)    However, urine production was probably decreased, which might make interpretation of test results more complicated and might increase the duration during which there would be a positive urine sample after ingestion.  (Dr Hawcutt, 10D)

(f)     The urine sample represents, on the balance of probability, the ingestion of cocaine a day or so before the urine sample was taken.

(g)   The absence of cocaine in the fluids from the thawed liver is suggestive of there not having been a massive or large overdose of cocaine, but is consistent with there having been a small overdose or ingestion of cocaine. (Prof Forrest at 15G-H, correcting Dr Cary at 15D, Dr Cary agreeing at 16A)

(h)   Cocaine can be fairly ephemeral, and if K had ingested a toxic amount of cocaine, more than a minimal amount of cocaine two or three days before it is entirely possible that there would have been some detectable in the liver but not necessarily so. [Professor Forrest 15G]

2. If ingestion of cocaine were the primary cause of or a contributory factor to K’s death, what, if anything can be deduced in relation to the quantity of cocaine ingested and the timing of this?

Agreement

See above

3. What is the possible relevance of the other drugs (Diphenhydramine, Amitriptyline, Fluoxetine and Lido) detected in K’s hair-strand testing?

Agreement (no disagreement with the views expressed by Professor Forrest)

(a)   Cannot draw any conclusions from Amitriptyline or the Fluoxetine due to ease of contamination.

(b)   Diphenhydramine is unusual to find in a child’s hair and may have been given to K as a sedative.

(c)    Lidocaine concentrations are not high so unlikely to have made any contribution to the mechanism of K’s death and might be as a result of contamination

L, M and N

4. Is there any possible explanation for the hair-strand testing results of L, M and N other than exposure to or ingestion of cocaine?

Agreement (as between Professor Forrest and Dr Hawcutt)

(a)   Unlikely to be contamination after hair samples taken as the washings were re-analysed.

(b)   Unlikely to be laboratory error.

(c)    Likely to be exposure to or ingestion of cocaine.

5. In relation to these hair-strand testing results, is it possible to distinguish between exposure and ingestion?  What factors militate for and against each method?

Answer

Professor Forrest explains why distinguishing between exposure and ingestion is difficult but does not answer the question [see pages 19 and 20 of transcript].

In an email on 14 April 2020, Professor Forrest said that the hair of a child living in an environment contaminated with drugs (smoked or in powder form) may be directly contaminated.  A child may also ingest drugs through drugs being on hands which have touched drug contaminated surfaces and which are then placed in that child’s mouth.  Normal care of a child by an adult whose hands are contaminated with drugs may result in drugs entering the child’s body.

6. What are the possible and likely consequences to children of the ages of L, K and N of chronic exposure to cocaine and cannabis in quantities and over periods equivalent to those which led to the hair-strand testing results.

(Responses given by Professor Forrest and Dr Hawcutt at the experts’ meeting did not answer the question)

(a)   No clinical evidence that any exposure the children had has caused harm that has reached the threshold for medical attention.

(b)   A child can live in a household where there are adults smoking cannabis and using cocaine and suffer no apparent specific physical ill-effects.

In an email on 14 April 2020, Dr Forrest said he considers this question is best answered by a practitioner (including a paediatrician) with experience of families where children are cared for in an environment where drugs are being used. The consequences to children of exposure to drugs depend on a number of factors, not just the toxicology.

i)                    12^th of September 2019

ii)                  10^th December 2019

iii)                11^th of December 2019

He also provided 2 expert reports dated 20 March 2020. He has subsequently provided further answers to questions raised after his evidence was completed along with print-outs or copies of notes of the actual results obtained.

i)                    Cocaine is the parent drug and metabolites of it include;

a)                  Norcocaine; a metabolite.

b)                 Cocaethylene; this is created when cocaine is metabolised with alcohol.

c)                  Benzoylecgonine (BZE); this is a metabolite but can also be produced outside the body.

d)                 AEME; this is a product of crack cocaine and is created by its burning and ingestion and metabolisation in the liver. It is unique to crack cocaine.

ii)                  You cannot tell from the levels detected what the amount consumed was or how frequently it was consumed as the test result is a mean. One can say whether the results are consistent with exposure to (contamination) or use of the drug and whether the use was occasional/rare, regular or heavy.

iii)                When drugs are present around the household or in the environment i.e. due to poor housekeeping, on surfaces, direct contact with the powder, smoke, et cetera they can get onto the outside of the hair strand. However, this sort of external contamination is generally removed during the decontamination procedures used prior to the analysis of the hair sample. Drugs which are smoked can also be passively inhaled or drugs can be ingested accidentally if left around the household or on surfaces.

iv)                Children have a low body mass and as such the dose required to attain the same concentration in a child will be less than that in an adult.

v)                  Children’s hair is more porous and thinner than adult hair and so is more susceptible to absorbing drugs which are present in the environment. Their hair is thus more likely than adult hair to show the presence of drugs which are derived from their environment.  Because of the porosity of the hair environmental contamination from drugs is more likely to permeate and remain in the hair. Results from testing the ‘wash’ of the hair of children rarely produces evidence of drugs.

vi)                Adult hair can be contaminated by external exposure and then the results from the wash will have more significance and the values for the parent drug and metabolites will have more significance in indicating consumption or contamination.

vii)              Comparisons between individual’s hair samples are also difficult to draw. The growth rate of adult hair varies considerably both between individuals but also within an individual. Thus a 12-cm segment of hair from one individual may represent an entirely different period of time from a 12 cm segment of hair from another individual. If their hair growth were at the extreme ends of the ranges with one growing hair very quickly and the other growing hair very slowly a 12 cm strand might represent a difference between 17 months to 8.5 months and thus (applying an average growth rate of 1cm per month) comparing what applying an average growth rate of 1 cm per month might appear to represent the same time period for two individuals might in fact be very different time periods indeed.

viii)            Environmental contamination can come in many forms. It may of course come, in the case of cocaine, from the presence of powdered cocaine itself which the child may touch and transfer to its hair. Dr Cirimele also included, within his description of environmental contamination, a child ingesting cocaine powder by touching powder which was present on a surface, including toys and then putting their hands in their mouth. However, cocaine and its metabolites would also be present in the environment from the sweat or urine of an adult who had consumed drugs. Sweat or urine could be transferred from the hands or body of an adult onto the hair of a child. Environmental contamination could also come from crack cocaine being smoked with the smoke landing on the child’s hair. Direct ingestion could also take place by the child breathing cocaine smoke. Smoke particles or their residue could remain after smoking had ceased which could be responsible for contamination or (it seems to logically follow) ingestion. Thus, whilst test results might in broad terms point to environmental contamination they might also reflect an element of ingestion.

ix)                 Contamination of adult hair from the environment was less likely because adult hair was less porous. However, it could occur.

x)                  Dr Cirimele emphasised that making comparisons between the results obtained from the children’s hair strand tests were difficult because there were so many variables. The differences between one child’s metabolism and another, their body weight, their hair type, the duration and frequency of exposure all made direct comparisons or extrapolations difficult. He said there were no controlled studies to his knowledge. He did say that in general terms the older the child the lower the level of contamination was likely to be because there was less direct physical contact and less likelihood of hand to mouth transfer.

xi)                Lidocaine is a well-recognised cutting agent for cocaine.  He believes that its presence in the test results for K could be attributed to Lidocaine being administered during her treatment.

i)                    K:

a)                  The presence of cocaine along with the detection of its metabolites is suggestive of exposure to cocaine. The concentration at the root end is low and medium at the tip end suggesting repeated exposure to cocaine within the time period covered.

b)                 The quantitative difference between the results obtained referred to in the September statement and in the February 2020, statement are explicable by the different sites where the hair samples were taken from.

c)                  Both suggest external contamination given the distribution pattern with increasing concentration the tip to the root end.

d)                 The presence of cocaine could be due to exposure via passive inhalation or surface contamination (i.e. being in an atmosphere where cocaine was being smoked, through sweat or direct contamination such as the tablet/drug powder being in contact with the hair).

e)                  Drug metabolites can be detected in the hair of young children even if the drug has not been ingested and can be explained by a contaminated environment (poor housekeeping, smoked drugs such as crack or cannabis by others) or by sweat transferred by the hands of drug users. However, K could have ingested drugs also.

f)                  The decreasing pattern makes it more likely the exposure was due to external contamination than actively incorporated drugs from blood because the oldest hair sections are the more contaminated when compared to more recent hair sections which have been less in contact with the contaminated environment.

g)                 If K was ingesting cocaine as a result of accidentally picking it up the amount of ingested cocaine should be significant enough to disrupt the observed decreasing pattern.

h)                 The detection of cocaine and cocaine metabolites in the root samples were consistent with the results obtained referred to in the September 2019 statement. They suggest she was not overexposed to the drug at a time closer to death (by over-exposure this means no significant change in exposure).

i)                   Cannabis, opiates and amphetamines were not detected.

j)                   Occasional repeated exposure to amitriptyline, fluoxetine and Lidocaine over the whole of the period but external contamination or sweat transfer is a possible contributor of a part or major part of the drug presence.

k)                 Occasional exposure to levetiracetam, ketamine but cannot exclude external contamination as a probable contributor

ii)                  The mother:

a)                  Repeated and increasing and heavy use of cocaine from mid May 2018 to mid-May 2019.

The test results were queried as a result of the way they were presented in the report and in particular there was concern by the mother’s team that they had somehow been reversed. Eventually the original results were provided in handwritten form which confirmed the figures given in the report. The mother submitted that the court should be cautious about accepting these results given the way in which they were presented and the fact that they indicated an opposite pattern of use to both of the Lextox reports.

b)                 Cannabis heroin and amphetamine methamphetamines not detected.

iii)                Father 1 x 2:

a)                  Active cocaine use suggesting repeated and heavy use during the period early March to July 2019. Decreasing usage within the more recent times.

b)                 Cannabis, opiates and amphetamine not detected.

iv)                The paternal grandmother:

a)                  Occasional use of cocaine within the period mid May 2018 to mid-May 2019. External contamination not suggested as sole reason for drug presence.

b)                 Cannabis, heroin and amphetamine not detected.

v)                  The maternal grandmother x 2:

a)                  Suggestive of occasional exposure to cocaine between early July 2018 to early January 2019. Stop in drug exposure within more recent months

b)                 Cannabis, heroin and amphetamine not detected.

vi)                Q:

a)                  Occasional exposure to heroin or external contamination within the 10-month period from September 2018 to early July 2019.

b)                 Occasional use of cocaine.

c)                  Occasional exposure to cannabis. External contamination suggested. Possible presence in atmosphere where drug being smoked.

vii)              R:

a)                  Active cocaine use suggested. Repeated use within the three-month period from early April to early July 2019. Decreasing use over period May to July.

b)                 Occasional use of MDMA.

c)                  Cannabis and opiates not detected.

viii)            L:

a)                  Suggestive of exposure to cocaine during the period of time covered by the hair test. Presence could be due to exposure via hair surface contamination from tablet/drug powder being in contact with the hair, cocaine present in atmosphere from being smoked, sweat from the hands of drug addicts.

b)                 Fluoxetine detected in one section of hair suggesting exposure possibly once to this drug.

ix)                M:

a)                  Suggestive of exposure to cocaine over the period covered. Presence could be due to exposure via hair surface contamination from tablet/drug powder being in contact with the hair, cocaine present in atmosphere from being smoked, sweat from the hands of drug addicts.

b)                 Amitriptyline and fluoxetine exposure during the time period covered by the test. The distribution pattern for both drugs along the hair shaft suggest external contamination as a probable contributor

c)                  Cannabis opiates and amphetamine not detected.

i)                    In respect of the maternal grandmother he did not regard the difference in results as significant because his laboratory tests for smaller quantities and the amount detected by his laboratory were under the levels which Lextox test for. Thus, he maintained his view that the maternal grandmother’s test results were consistent with occasional environmental exposure which either ended in January 2019 or which was at such a low level they were not detected by his tests.

ii)                  In respect of the very divergent results obtained for the mother and the paternal grandmother he identified that his samples had been provided some two months (in fact 10 weeks) prior to those tested by Lextox. He therefore posed the question of what had occurred during that period of time which might have affected the results. Clearly one issue he was concerned about was whether the hair had been treated in any way which would have affected the presence of drugs in the hair. In particular he focused on the fact that the Lextox results detected BZE in the hair of both the mother and the paternal grandmother which he said was inexplicable by normal processes. BZE would be present in hair either through ingestion or environmental contamination but would always be associated with the presence of the parent drug i.e. cocaine. He said all of the literature and his understanding was that if BZE was present through environmental contamination there would be higher results for the parent drug. However, BZE presence alone could be explained by the application of hair treatments which had eradicated the presence of cocaine but left traces of BZE which is not a true metabolite but can also be created through the application of alcohol or bleach

Dr Forrest

i)                    The concentration of BZE in sample AM serum three is not high but it does indicate that cocaine has entered K’s body at some point. The way in which it entered the body cannot be determined.

ii)                  Any child being cared for in an environment where cocaine is present may well have cocaine and/or BZE in their hair and possibly in their blood. The mere presence of cocaine and/or its breakdown products in hair, or in low concentrations in blood or urine does not necessarily imply deliberate administration of cocaine to the child.

iii)                There is likely to have been ingestion of cocaine within a day or so of collection of the blood sample. The hair analyses indicate K is likely to have been in an environment where cocaine is present for about eight months preceding her death.

iv)                Children are not little adults they differ in the ways in which their bodies handle drugs. The results for their hair is relatively low and is less likely to reflect ingestion although deliberate ingestion cannot be excluded. Nor can the occasional deliberate administration be excluded.

i)                    He agreed with most of what Dr Cirimele said when it was put to him. He deferred to Dr Cirimele on the contamination of the hair root issue because he accepted that it was Dr Cirimele who had actually cut the hair in order to test it and so if he thought there was a possibility of contamination arising from the lack of a clear delineation between the hair root, envelope and hair he deferred to it. However, he also said that whilst it may be more likely contamination, it did not rule out ingestion.

ii)                  The issue of the urine or serum sample took up some considerable time. There were a number of possibilities as to what had happened including contamination from an earlier sample, laboratory error in labelling, contamination when the sample itself was taken and cocaine being given to K whilst at the hospital (this would explain the presence of BZE in a later blood serum sample and not in the earlier sample). He thought that it was unlikely that the sample had been erroneously labelled or contaminated by the testing equipment because the procedures existed to prevent this and there was nothing to support this. Nor did he think that the issue of background noise in gas chromatography testing was a likely explanation for the result. His abiding opinion, (and he was robustly challenged on all of the possible alternative explanations),  whether the sample was urine or serum and taking account of all of the issues relating to the possible problems with the sample was that the reading obtained by Dr Patterson represented the presence of BZE within the body at the time it was taken and thus represented some form of ingestion of cocaine by K in the period of days immediately preceding her death.  He acknowledged that the value given would be affected by whether the result was interpreted by reference to the values relevant to serum or the values relevant to urine but it was inescapable that BZE was present ‘more than minimal but not substantial’. The absence of cocaine being detected in the sample was consistent with the half-life of the parent drug cocaine and its metabolite BZE. He said it would be expected that the half-life of cocaine would lead to it being undetectable in blood something like 10 hours after its consumption and that it would disappear from urine more quickly than its metabolite BZE would.

iii)                He said one must be very careful about making assumptions about how much cocaine was ingested and when K was exposed. He emphasised the limitations of toxicological testing and what could be extrapolated from test results. He said that the presence of low levels of BZE in the urine sample in his opinion suggested consumption between 3 to 5 days prior to the test. He noted that issues such as dehydration or low blood sodium might have meant that K was producing more concentrated urine which would have led to the BZE being detectable in it for longer.  If it had been consumed more recently it is more likely that other samples including from the liver would have shown its presence. He said that what he knew of the description of K’s reported illness did not depict her as a child acutely ill or severely ill which would be more consistent with an overdose level. The lack of research or evidence of how much cocaine would need to be consumed to lead to this damage, and how children processed cocaine meant it was difficult to say much about the quantity that K may have consumed. He said it would be more than a trace but not necessarily very much. There are so many variables in relation to children and their sensitivity. He couldn’t say the type of cocaine consumed, how much, how frequently and/or the circumstances of consumption. His opinion was most likely oral ingestion but he accepted it could have been ingested by any of the mucous membranes including through the nose and eyes. He did not consider that the toxicological or other evidence pointed to the amount ingested being indicative of an overdose.

iv)                His view in relation to the very divergent results obtained by Lextox and Chemtox were that there were a number of reasons which could explain them including the application of hair products, differences in the testing methodology and reporting of the laboratories, errors in the process of reporting including the hair being tested from the wrong end. He said that studies showed that there could be widely varied results reported by different laboratories in respect of hair which theoretically represented the same time period. He did think that the results for the mother and paternal grandmother were at the far limits of the differentials he had seen. Having looked at the results for father 1 from Chemtox and Lextox he said that the differences noted there were within the normal range of differences reported. He did not think there was a need to seek explanation for the differences other than that.

Lextox Drug Testing Results

i)                    Dyeing: they do not test the sample to see if it has been chemically treated but it is subjected to 2 visual inspections. The first is undertaken on the physical hair sample itself to see if there is any visible dye line or if the hair appears of an unnatural colour. A further inspection is then undertaken on the hair liquid as sometimes when dye is used it can leach out and discolour the liquid extract. Section 53 of the LexTox report would record any observations as to evidence of dyeing.

ii)                  The use of the sample submission form contains a declaration as to the use of hair treatments.

iii)                Chemical treatments such as perming, or straightening cannot be determined.

iv)                The visual observations may not note the use of any chemical colour treatment, where the hair is dyed a similar colour to the natural hair colour or where a chemical hair treatment does not cause discolouration.

v)                  Lextox are UK accreditation service accredited and reporting scientists are members of the Society of Hair Testing.

i)                    The maternal grandmother: The cocaine concentrations measured in the six distal hair sections can be considered as low in the view of what can be expected in recreational users, suggesting occasional exposure of the maternal grandmother to cocaine within the oldest time period covered by these hair section tests (approx. between early-July 2018 to early- January 2019). The general pattern is suggestive of a decrease and a stop in drug exposure within the more recent months before sampling.

ii)                  The mother: tested positive for the cocaine metabolite BZE in all 12 hair sections analysed covering the period July 2018 to the end of July 2019. Cocaine and cocaethylene were detected in the six oldest hair sections. The Findings are more likely than not due to cocaine use. The levels of cocaine detected are in the medium range in the oldest two sections and in the low range in the remaining sections.

iii)                Father 1:  tested positive for cocaine and three cocaine metabolites BZE, norcocaine and cocaethylene in all five hair sections analysed covering the period end February 2019 to end July 2019. On the balance of probabilities, the findings are more likely than not due to the use of cocaine. The levels of cocaine detected are in the high range in the oldest section and in the medium range in the four most recent sections.

iv)                The paternal grandmother: she tested positive for BZE in all four hair sections analysed covering the period end July 2018 to end July 2019. As cocaine has not been detected the use of cocaine cannot be confirmed. It is likely that insufficient cocaine has been incorporated into the hair to be detected, especially in cases where chemical hair treatments have been used. Whilst the use of cocaine cannot be confirmed it would not be expected for a cocaine metabolite to be detected without cocaine in cases of exposure. However, on the balance of probabilities the results obtained are more likely than not due to the use of cocaine. The levels detected are in the low range.

v)                  The maternal grandmother. There is no evidence the MGM has used cannabis or cocaine in the time period end July 2018 to end July 2019.

vi)                The children:

a)                  L: present in the five oldest hair sections is the metabolite BZE. Cocaine was also detected in one other section.  The results indicate that L has either ingested cocaine or passively inhaled cocaine smoke. A cannabis constituent was also detected in the three oldest hair sections. That indicated L had either ingested cannabis or passively inhaled cannabis smoke. It was not possible to detect how they entered her body but passive inhalation or accidental ingestion or a combination of the two were possible.

b)                 M. Cocaine was detected in all 12 hair sections. BZE was detected in the 11 oldest hair sections. Wash solutions were negative. The results indicated that M had either ingested cocaine or passively inhaled cocaine smoke. A cannabis constituent was detected in the six oldest hair sections and the 12 wash solutions were negative. The results indicated M had either ingested cannabis or passively inhaled cannabis smoke. The levels detected were in the low range. It was not possible to detect how they entered her body but passive inhalation or accidental ingestion or a combination of the two were possible.

c)                  N. There was no evidence that N had ingested or recently been exposed to cannabis or cocaine.

Professor Bu’Lock:

Thus, it would appear that the presence of cocaine was pervasive at the family home over a significant time frame and it is likely the children were exposed to it for much, if not all of their lives.

was not one which was supported by the evidence (in terms of the length of their exposure) but nor was it one which was inappropriate to make given the instructions she had been working under. It not surprisingly led to a firm response from Miss Isaacs in particular which was both understandable and justified but did result in time being consumed with the expert on a factual issue which was for me to determine not the expert. Notwithstanding this excursion Professor Bu’Lock’s evidence was illuminating and invaluable in terms of understanding the likely physiological process which ultimately led to K’s death.

i)                    K's terminal decline and demise were consistent with a child in a low cardiac output state with no evidence of sepsis or other likely cause for her decline detectable in life or at autopsy.

ii)                  It seems most likely (on the balance of probabilities) that the heart damage induced by recent cocaine ingestion was a significant contributor to her low cardiac output and other symptoms, and ultimately led to her death. Whether  there were other contributory occurrences / events prior to her admission or not, it seems likely that had the possibility of cocaine ingestion been disclosed at any stage in K's hospital presentations, medical and other management may well have been different and K might well still be alive today.

iii)                K's blood gases and blood chemistry investigations also showed that her body was struggling to perfuse her organs properly with a blood lactate level of 4.4 which is really quite high. Lactate is a chemical released as a product by cells that are working without adequate oxygen supply or by damaged tissues. However, the level of acid in her blood (pH 7.413,) was normal which meant that to a point her body was compensating-

iv)                The other abnormality was a low sodium level (126) which is unusual and was unexplained. It can be due to excessive fluid intake or extreme salt loss but there is no evidence of either of these. I gather from my learned pathology colleagues that it can also be seen in cocaine toxicity. [This last observation led to a series of questions being asked of the professor and the production of a number of papers on the issue of cocaine toxicity.]

v)                  As detailed in P 16 of APPENDIX 1, the ECG strips recorded (K42-46) during the resuscitation do NOT suggest that there was an abnormal heart rhythm at least once K had lost her cardiac output. Rather there was 'pulseless electrical activity" (PEA). The significance of this will be explained

vi)                There was no evidence of structural heart disease (the heart was normally formed) but the myocardium of the left ventricle (muscle of the main pumping chamber to the body) was damaged when looked at under the microscope (H1560)

vii)              K died because her heart ceased to be able to pump sufficiently efficiently to support her circulation. Autopsy examination showed the presence of damage to the muscle of the left ventricle of the heart which had likely occurred at least a day or so before she died. This is of a pattern consistent with blood vessel damage and areas of reduced perfusion to the heart muscle likely due to blood vessel spasm or blockage and is consistent with the effects of cocaine on the heart muscle.

viii)            Pulseless Electrical Activity (PEA), also known as (Electro Mechanical Dissociation; EMD), is relatively common in children as part of the process of dying…… This is because if, for example, a child's breathing has been so poor or stopped for a period of time, the heart muscle is severely deprived of oxygen and cannot pump efficiently….. It can occur for example if there is nothing in the circulation for the heart to pump eg if there has been massive haemorrhage or severe dehydration; and hence there is 'hypovolaemia'….. In addition, it is often seen when there is a massive imbalance in the blood chemistry eg rising acid levels, or if there are other circulating toxic substances which prevent the heart muscle from responding to any electrical activity by pumping. This is usually at the end stages of a severe illness.

ix)                Pulseless Electrical Activity refers to cardiac arrest in which the electrocardiogram shows a heart rhythm that should produce a pulse, but does not. Pulseless electrical activity is found initially in about 55% of people in cardiac arrest.!" … Pulseless electrical activity leads to a loss of cardiac output, and the blood supply to the brain is interrupted. As a result, PEA is usually noticed when a person loses consciousness and stops breathing spontaneously.

x)                  Cocaine is known to cause constriction ('spasm") of blood vessels, which is why it was used e.g. to stop nosebleeds, … and this can occur inside or outside the heart. It can therefore cause 'myocardial infarction' i.e. areas of muscle death or damage. In adults this is more usually at the large vessel level but it is more likely than not, given the toxicology and hair root analysis results, the cause of the abnormalities of the left ventricle noted at the first autopsy.

xi)                I understand from the pathology reports and joint pathology statement that this damage likely occurred a day or two before K died and possibly even before she came to hospital.

xii)              Acute Cocaine toxicity, potentially in combination with a number of other drugs including antidepressants which are known also to cause heart rhythm disturbances, could have led to some sort of collapse prior to K being brought to medical attention. This is speculation, but her presentation was extremely atypical especially in the absence of sepsis. Although there was no evidence of a true 'dilated cardiomyopathy' in K, when this develops related to Cocaine it is likely to be as the result of serial insults and damage to the heart muscle over time. K was only 3. Cocaine does also however acutely alter the stiffness and contractile function of heart muscle (Refs 1 & 2) and would therefore leave it vulnerable to, for example, a drop in oxygen levels related to reduced consciousness level and breathing effort. It is noteworthy that throughout K's terminal admission her consciousness levels fluctuate, she is in the main tachycardic (increased heart rate) and pale and cool (hypothermic).

xiii)            It is also noteworthy that despite what appears to have been vigorous and competent resuscitation for over an hour, at no time was there ever any evidence of return of consciousness or of effective heart activity. I have attended hundreds of paediatric cardiac arrests over my career. Whilst ultimately it may not be possible to successfully restore and sustain useful heart activity, it is quite frequent that there is some, even temporary, return of spontaneous circulation and or consciousness even if that cannot be maintained. It would appear that this did not occur despite the absence of administration of any sedation. This implies that what happened terminally to K was a catastrophic failure of the circulation at the end of a much longer deterioration, albeit one that was not readily susceptible from the blood differences and observations undertaken throughout her last stay in hospital and indeed only an hour or so before she collapsed.

xiv)            I would therefore suggest that there is evidence of a significant period of what is known as 'low cardiac output' over the entire duration (and possibly prior to it) of K's final admission, mainly evidenced by her cool peripheries ('hypothermia) and persistently elevated lactate level. Externally it might have been manifest solely otherwise by her puffy eyes. Internally there is evidence that the additional fluid administered to K was in fact pooling in and around the lungs, heart and in the abdomen, rather than being 'pumped forward' around the body. This 'low output state' where the heart function and cardiac output is barely enough to provide for the metabolic demands of the body, was variably compensated for by K and her medical and nursing carers until her terminal collapse. This is not uncommon in children, who often seem to 'cope' until almost the end and then collapse very dramatically and sometimes terminally.

xv)              Cocaine ingestion in small children is well recognised in the literature as a cause of acute toxicity including fever, seizure or shaking / jerking, heart rhythm disturbances and sometimes death (Refs 3-8). The shaking and jerking are from increased nervous activity in the brain but may not always represent true seizures. They can also represent distress / agitation (Ref 8) and disturbed consciousness. There may be specific heart muscle injury from ischaemia (reduced blood supply from increased sympathetic nervous system activation, as well as increased heart rate and heart muscle oxygen demand). However, there are also more indirect effects on the heart muscle due to constriction of the blood vessels of the body causing increased resistance to blood flow around it and higher blood pressure, which reduces the heart’s ability to relax and fill. This can cause back pressure on the lungs and other organs and fluid retention. Cocaine also directly affects the chemistry of the heart muscle cells and therefore increases the risk of dangerous heart rhythm disturbances (usually ventricular tachycardia or fibrillation).

xvi)            With reference to whether there was / is any evidence of a familial cardiac problem, I have reviewed the extremely thorough examinations from my expert colleagues at Great Ormond Street (L1-16) for the 3 remaining siblings and it is clear that nothing has been found. Therefore, on the balance of probabilities, a primary (ie not drug related) underlying heart condition in K seems highly unlikely.

i)                    From my review of the extremely extensive bundle and supplementary materials, I can draw no other conclusion than to say that therefore I agree with the pathology experts that cocaine exposure caused the damage to K’s heart some days before her death. I can conceive of no other reasonable explanation of these findings

ii)                  This heart damage would have been very difficult to detect directly in life and her clinical presentation, particularly in the absence of a full history from the family, was therefore obscure. K was appropriately treated for the most likely diagnosis ie sepsis, but did not respond as expected, with a persistent lactate likely related to her ongoing low cardiac output state.

iii)                It is not clear precisely what precipitated her ultimate collapse but it would seem most likely that there was either a preterminal respiratory arrest or indeed a heart rhythm disturbance which went undetected and undetectable or that her heart simply ‘ran out of steam’. The rest is well documented.

iv)                My specific opinion is that it is extremely likely (certainly more than on the balance of probabilities) that K died as the result of adverse cardiac effects from exposure to Cocaine (+/- other medications) around the time she was brought to hospital on 4^th April 2019

i)                    Cocaine induced heart problems in children is limited to 2 or three cases over her career. Where she has been working for the last 20 years she has seen perhaps one case more recently which was in the last 5 to 6 years and that child did not die but rather suffered brain damage as a result of the drug having been cut with quinine and so responsibility for the child eventually passed to neurologists.

ii)                  An unknown cause is a diagnosis of last resort. Adopting a differential diagnosis leads one to seek to exclude other causes. In this case it would be very unusual not to be able to identify a reason for death in an apparently otherwise healthy three-year-old.  There has to be a reason and it is seeking to identify that reason.

iii)                The difference between K’s x-ray on admission and her CT scan at autopsy was that the latter showed significant fluid accumulation within the body. The significance of this was that it pointed to the heart not operating efficiently and circulating the fluids to support the blood pressure but rather the fluids collecting in the chest and abdomen.

iv)                She further expanded upon the effect of cocaine upon the circulatory system explaining that in stimulating the brain it caused blood vessels to constrict to ensure blood went to the core organs but it could overstimulate them causing restriction of the blood vessels supplying the major organs thus leading to an inadequate blood supply. In children whose blood vessels were unaffected by disease it was likely to impact the small blood vessels more which would affect the individual muscle cells and the area around them depriving them of oxygen and energy causing them to die or be damaged. Although the effect of cocaine is short lived and would wear off by the time the blood supply is restarted the cells may have died. The muscle in the endocardium is particularly vulnerable because it has the poorest blood supply and is affected on each contraction.

v)                  One would expect to see some acute symptoms after ingestion but the damage to the heart muscle would take some time to cause her to deteriorate.

vi)                The medical literature did not show that children exposed to cocaine died in the way K did nor did they show a more than minimal mortality associated with acute cocaine exposure. Prof Bu’Lock wondered whether the lack of testing in England masked greater prevalence. She noted that children who survived might still have heart damage, but you simply didn’t know. She accepted that there was no known association between living in a cocaine contaminated environment and death.

vii)              Cardiac necrosis in a child with a previously healthy heart is very rare. She has been contacted perhaps five times in 20 years in relation to cardiac necrosis.

viii)            Children’s complaints about how they are feeling are difficult to interpret. They often complain of tummy pain when the source of the pain is elsewhere. Other symptoms caused by cocaine ingestion might distract from any effects it was having on the heart. Heart pain is very good at making people vomit. It is though non-specific.

ix)                Children tend to be robust and keep going even with reduced heart output until they suddenly collapse. In particular whilst children are awake the body produces chemicals which continue to stimulate the heart. When a child falls asleep when their heart is in low output the stimulant chemicals are removed and can lead to the heart function dropping below the threshold at which it can sustain effective circulation. The presence of excess fluid causes further work for the heart to circulate blood. This can then result in PEA. The inability to restart K’s heart is consistent with a primary cardiac problem rather than a respiratory or infective cause.

x)                  Although low-sodium levels can cause damage to the heart they have to be very substantially below the levels that were noted in K. She was appropriately treated for suspected SIADH low sodium. Her reading was 126 and it would have to drop to 103 in order to have an impact on the heart muscle cells.

xi)                K’s appearance with puffy eyes is consistent with heart failure or heart damage but other things obviously can cause it and where it is linked to poor circulation tends to start from the feet; gravity plays its role.

xii)              Had cocaine been identified as a possible problem it would have led to greater consideration of the cardiac issues. She could have been transferred to a cardiac centre where her circulation could have been supported artificially and her blood oxygenated away from the body.

xiii)            Lactate or lactic acid is produced by muscles which have an inadequate oxygen supply. It alters the acidity of blood making it less efficient and is a warning sign about the supply of blood and oxygen to the body. High lactate is an indicator that K was very significantly ill before she came to hospital. The usual range is below 2 and K’s was above two and above four which is a source of serious concern. One would expect it to reduce if the child had an infection which was being successfully treated with antibiotics. Her CRP wasn’t elevated and her white count came down quickly which is inconsistent with infection.

xiv)            The evidence suggests that K’s oxygen saturation levels were being monitored and the alarm went off because the monitor could not detect her oxygen saturation levels as her pulse had ceased.

xv)              The ECG strips show the CPR but don’t show any resumption of normal heart output when they pause CPR to check whether there is any activity. It is not possible to tell from them whether there was a heart arrhythmia. This is used incorrectly to describe an abnormal rhythm. Arrhythmia means no rhythm. The presence of the ECG trace shows electrical activity in the heart but no resumption of circulation. Adrenaline would not have caused the damage - the only perfusion to the heart is from the cardiac massage. Adrenaline administered in resuscitation wouldn’t have time to cause the damage seen.

Dr Hawcutt:

Dr Jacques:

Dr Ashworth

i)                    Examination of the heart, which had already been extensively dissected revealed no abnormality. Although the tricuspid and mitral valves were not present he was able to say that they could not have been abnormal as the rest of the heart would have shown changes in its appearance had they been so. Overall his examination of the heart showed no abnormality or pre-existing condition.

ii)                  He reviewed the slides taken for microscopic examination. This included the slides taken at 22 May post-mortem and the slides taken at 10 April post-mortem.

iii)                In respect of the 22^nd May slides they showed autolysis with the loss of much of the nuclear detail. No myocyte necrosis was identified and nor was inflammation. There was a focal mild increase in fibrous tissue in the endocardium. There was a mild increase in interstitial collagen at the insertion of the posterior aspect of the right ventricular wall into the interventricular septum but no discrete scarring.

iv)                In respect of 10 April slides, I set out what he reported in full. It has been the subject of considerable focus in the course of the hearing.

The original sections of myocardium taken by Dr Palm at the time of the post-mortem examination have been reviewed. They show small foci of sub- endocardial haemorrhagic myocyte necrosis on the left-ventricular aspect of the inter-ventricular septum. There is no associated cellular reaction. No similar changes are seen in the extra pieces of myocardium examined, but the degree of autolysis means that small such foci may not have been detectable.

Conclusion:

Minor non-specific changes in the myocardium. Small foci of sub- endocardial necrosis left-ventricular aspect of interventricular septum, possibly resuscitation related. There is no evidence of chronic ischaemic damage (in the form of fibrosis) in the myocardium and there is no myocarditis.

“When I say no inflammation what I mean is not significant inflammation which indicates a longer process of the body starting to react to try to heal the necrotic tissue damage. I did see small spots of inflammation (reactive cells) which was the beginning of the process of the body reacting, but it was minimal which is why one can say the process hasn’t been on-going for that long’

‘I did see cellular reaction-I was referring to myocarditis when the reporting Dr Palm’s report says there is ‘no associated cellular reaction’

This seems somewhat hard to reconcile with the use of the expression ‘no associated cellular reaction’ particularly if one accepts (as I do) that myocarditis is defined by inflammation commencing in heart tissue which causes myocyte damage/necrosis of the heart tissue. In this case Dr Palm said this was not myocarditis because the sequence was reversed in that in K’s heart myocyte damage/necrosis had occurred and this had resulted in the commencement of an inflammatory response as the body sought to deal with the death of the heart muscle cells.

Dr Cary

i)                    There is no evidence of any underlying natural disease that caused or contributed to cause of death or indeed the cause the clinical features at the time of presentation. Detailed neuropathological examination of the brain did not reveal evidence of a cause of death.

ii)                  Microscopic examination of sections of the heart revealed multifocal myocardial necrosis in both the left and right ventricles. These are associated with exposure to stimulant substances such as adrenaline and can also be seen as the result of ingestion of stimulant drugs including cocaine.

iii)                There was a single piece of evidence, namely the analysis of a urine sample, which suggested cocaine was ingested in the time period around the time of admission.

iv)                It is apparent that over the many months leading up to death there has been repeated exposure to a multiplicity of drug substances including cocaine. It is not possible to distinguish between exposure as a result of ingestion (whether through passive inhalation of smoke or through swallowing) and exposure of the hair directly as a result of a contamination including by the sweat of another person or persons.

v)                  The opinion of a consultant paediatrician and further analysis of the hair roots were to be sought to further clarify matters.

Dr Palm

i)                    Investigations included a whole-body CT scan, naked eye and microscopic examination, specialist neuropathological examination (by Professor Jacques), microbiological and metabolic screening studies. These did not reveal a pre-existing congenital or acquired natural illness or medical condition that could have caused or contributed to K’s death.

ii)                  There was no evidence to indicate an ongoing overwhelming infection or sepsis. The examination of the brain showed no morphological evidence of meningitis or encephalitis.

iii)                There was no external traumatic injury, bruise or other sign to suggest physical abuse. There were no internal traumatic injuries to any organs.

iv)                Non-specific internal findings of generalised vascular congestion, pleural and peritoneal effusions, acute thymic involution and diffuse pulmonary haemorrhagic oedema were consistent with an acute mode of death and likely due to acute heart failure.

v)                  Naked eye examination of the heart including the heart muscle was normal. However, on examination under the microscope some abnormalities were revealed which I shall set out in more detail below. The heart muscle showed features of spotty myocyte necrosis associated with an inflammatory infiltrate, areas of contraction band necrosis and evolving ischaemic myocardial necrosis. There was no evidence of structural heart disease, myocarditis, vasculitis or signs of a cardiomyopathy.

vi)                The toxicology screening which detected cocaine and BZE in hair and BZE in one blood serum sample, together with the clinical history and the cardiac pathology strongly suggested her death may have been a result of acute cocaine toxicity.

Sparse eosinophils, neutrophils and mononuclear cells are observed in the interstitial myocardial tissue of the right ventricle, in areas associated with localised myocyte damage and acute inflammation. Multifocal contraction band necrosis and areas of evolving ischaemic necrosis are seen in the left ventricle and in the interventricular septum, both subendocardially and within the deeper zones of the wall. Small areas of myocardial ischaemia and haemorrhage are seen in the ventricular myocardium close to the AV node; otherwise the AV node is histologically unremarkable. The features are in keeping with cocaine-related myocardial damage superimposed by systemic hypotension. There is no evidence of myocarditis, fibrosis, cardiomyocyte hypertrophy or disarray, giant mitochondria, increased proliferative activity or other features to suggest a cardiomyopathy. The epicardial and intra-myocardial arteries are unremarkable. There is no microscopic evidence of atherosclerosis, granulomatous inflammation or vasculitis.

i)                    Sparse eosinophils, neutrophils and mononuclear cells are observed in the interstitial myocardial tissue of the right ventricle, in areas associated with localised myocyte damage and acute inflammation. The heart muscle is the myocardium. It consists of muscle cells which are called myocytes which contract. In the right ventricle she found areas where the myocytes were virtually dead. These were surrounded by inflammatory cells which were part of the body’s response to the damage to the myocytes. Neutrophils are the white blood cells which fight against infection. Eosinophils are also a white blood cell which is part of the immune system. Mononuclear cells are also a subtype of white blood cell which are there to clean up around a damaged area. Neutrophils and eosinophils are the early responders from the bone marrow to damage with mononuclear cells arriving later. The standard texts refer to a period of 12 to 24 hours for neutrophils to be seen following a myocardial infarction. The mononuclear cells take longer. Some studies may refer to 6 hours for the cells to appear, but mainstream is 12 to 24 hours for the earliest appearance. These white blood cells were present around the damaged myocytes and in the interstitial tissues which support the heart muscles and nerves. She said they were unmistakable to a pathologist and could not be confused with myocarditis. She described this as spotty areas of necrosis. This damage would need the passage of at least 12 hours to become detectable on microscopic examination. Whilst one might see neutrophils and eosinophils with other conditions the presence of the mononuclear cells was only consistent with damage to the myocytes. The spotty necrosis might represent damage caused by the toxic effects of cocaine. It could not be consistent with resuscitation efforts because neither sufficient time elapsed for the inflammatory response to develop (in one hour or less) and nor did K’s heart output ever recover so as to allow blood circulation which could have carried adrenaline

ii)                  Multifocal contraction band necrosis and areas of evolving ischaemic necrosis are seen in the left ventricle and in the interventricular septum, both sub-endocardially and within the deeper zones of the wall. The inner part of the heart muscle in contact with the blood (the wall of the chamber) is lined with the endocardium and under that the heart muscle is quite vulnerable to low oxygen levels. This is called the sub-endocardial area. It is more vulnerable to low oxygen levels than the outer areas because the blood vessels which supply it pass through the outer layers of muscle (Professor Bu’lock added that every time the heart contracts the blood supply to the sub ended area is restricted). The interventricular septum is the part of the heart which separates the left and right ventricles Two different types of necrosis, were seen in this area. Firstly, contraction band necrosis, which is the death of cardiac myocytes obvious under microscope as bright pink bands. This could be caused in the last hour of life. (I think she was referring to death of the cell by hyper-contracture) This is not linked to the resuscitation either as although they could theoretically be caused by the resuscitation process, if K did not regain cardiac output, they cannot be attributed to it. This could be due to hyper-contracture (the cell bursting) or to vaso-constriction (lack of blood supply and thus oxygen).  Evolving ischaemic necrosis is muscle tissue which is dying as a result of a lack of oxygen. It is acute; recent and developing. It might be a function of the heart efficiency deteriorating secondary to the other damage or it could be directly related to cocaine. It is not associated with the presence of white blood cells responding as the damage is still developing. However, ischaemic damage does also require cardiac output in order for it to evolve. As K did not regain cardiac output after her collapse, it is not likely related to the resuscitation. One might not see a white blood cell response to evolving ischaemic damage if the heart is not sustaining normal blood pressure.

iii)                Small areas of myocardial ischaemia and haemorrhage are seen in the ventricular myocardium close to the AV node; otherwise the AV node is histologically unremarkable. The atrioventricular node is cited within the right atrium very close to the atrium and ventricle. It is where the heart pacemaker cells reside which give the heart its rhythm and so is part of the electrical conduction system of the heart. Myocardial ischaemia is also a description of damage or necrosis due to lack of oxygen. This was also associated with some bleeding where the blood was leaking out of the blood vessels. Although the damage did not involve the AV node itself its presence in that region could possibly have affected the electrical signals and thus contributed to arrhythmia.

iv)                The features are in keeping with cocaine-related myocardial damage. Cocaine is toxic to heart cells. It can damage individual cells and can cause myocardial infarction and evolving ischaemic damage. It might also cause coronary artery damage in the form of thrombosis in adults. In adults if cocaine has been used for a long period of time and the adult has survived the areas of the heart which have sustained necrosis become scarred. It is called cocaine induced cardiac myopathy. Heart cells do not replace themselves. Dead cells simply become scar tissue. Damaged areas of the heart prevent it functioning properly. They could induce an abnormal heart rhythm. A damaged left ventricle (more so than right ventricle) can induce an abnormal rhythm even with unhealthy AV node. A damaged heart affects the efficiency with which it is pumping blood around the body and the body responds by targeting the blood at essential organs. If the efficiency of the heart drops too low it eventually ceases to be able to provide sufficient oxygen to the heart itself degrading its efficiency even further and eventually leading to a collapse.

v)                  Superimposed by systemic hypotension, systemic hypotension describes the effects on the heart caused by low blood pressure related to the reducing efficiency of the heart and the final collapse.

vi)                There is no evidence of myocarditis, fibrosis, cardiomyocyte hypertrophy or disarray, giant mitochondria, increased proliferative activity or other features to suggest a cardiomyopathy. The epicardial and intra-myocardial arteries are unremarkable. There is no microscopic evidence of atherosclerosis, granulomatous inflammation or vasculitis. This identifies and excludes a large number of underlying conditions which might manifest similar features. After the toxicological results were received the coroner required a special post-mortem to be undertaken. This was done with Dr Cary. At that post-mortem they decided that it would be prudent for cardiac pathologist to look at K’s heart and the slides.

a)                 The finding that I initially could not explain was the heart microscopy, the heart examination showed what I described as evolving ischaemic necrosis in the left ventricular and the heart septum, both mainly on the endocardium but also within the deeper zones of the myocardium. And there were also multifocal contractions band necrosis, and more importantly local myocyte damage which was associated with acute inflammation, and I have also mentioned mononuclear F cells, which are not that acute. There was no evidence to suggest any increased scarring to indicate that that was a longstanding process as one would expect to see, in, for example. cocaine induced cardiomyopathy? 00:26:13].

i)                    It is not uncommon for a post-mortem to be unable to establish a medical cause of death. One looks for a clinical pathological marriage. K’s case is a complex case on the pathology alone.

ii)                  Sepsis or other forms of acute infection are not straightforward to detect post-mortem. One looks for an established inflammatory focus an organ such as the lung, heart or brain as well as general in inflammatory response including an enlarged spleen for instance. This evidence should be corroborated by microbiology from blood or other material. Only when both are found can one diagnose sepsis. The use of antibiotics and antiviral drugs may eliminate any viral or bacterial infection post-mortem. However, one would expect samples taken during life and prior to the administration of such drugs to grow cultures or otherwise demonstrate an infection. In K’s case there was no evidence in her organs of the inflammation one would expect with infection and her blood samples taken during life did not grow any cultures consistent with an infection. However, one cannot exclude sepsis.

iii)                K did not have myocarditis. It is completely different under the microscope. In myocarditis an inflammatory process causes the death of the myocytes. Thus, under the Dallas criteria you can diagnose myocarditis if you have inflammation and myocyte damage or you can have borderline myocarditis if there is evidence of inflammation without myocyte damage. You cannot diagnose myocarditis based on myocyte damage alone. In K’s case the process was the other way round. The myocyte damage or necrosis had occurred first and was being followed by an inflammatory response.

iv)                In general, myocardial damage and its resolution is slightly slower in children than in adults. In adults by 48-hours there would be a significantly florid inflammatory response.  In broad terms the upper end for the damage seen in K’s heart is 36 to 48 hours.

v)                  Dr Palm accepted that her conclusions were not consistent with what Dr Ashworth said in his report, although she sought to explain how it might be that he had expressed himself as he had. She stood by her conclusions and confirmed that Dr Cary had seen the slides and confirmed what she saw.

vi)                Adrenaline can cause damage to the heart myocytes in the same way that cocaine can. However, in order to do so the adrenaline has to reach the tissues. As K never regained cardiac output after she collapsed it is hard to explain how adrenaline could have caused the damage.

vii)              Two sets of slides were made which were microscopically examined. The first set were produced on 10 April and were of good quality. They do not deteriorate after they have been taken. The second set were taken at the second post-mortem and were of poor quality as the heart tissue had deteriorated in the six-week-old interval.

Factual Evidence

The Mother

Father 1

 Paternal Grandmother

The Maternal Grandmother.

 Discussion and Evaluation

Conclusions

i)                    K died as a result of ingesting cocaine in the mother’s home at some point in the afternoon or early evening of 3 April 2019.

ii)                  That cocaine was brought into the house by father 1 in connection with his drug-related activities and carelessly left in such a way and in such a quantity as to be ingested by K.

iii)                The mother was well aware of father 1’s bringing of cocaine into her home and of it being processed there. She did not do anything effective to prevent this but this was not through fear of father 1 but because of the nature of the relationship between the two of them and her own involvement in recreational drug use. Given her generally protective nature in relation to the children it seems most probable that she turned a blind eye or persuaded herself that sufficient precautions were being taken to protect the children. This was to kid herself. Given the nature of father 1 it was a risk that any reasonable person ought to have identified and taken steps to actively protect the children from.

iv)                Although the disclosure to the hospital staff of the possibility of cocaine might have led to medical action which would have prevented her death I’m not satisfied that the possibility of K having ingested cocaine would have been on the mother’s radar given the non-specific nature of the symptoms, the fact that she had not witnessed anything herself and the doctor’s suspicion of sepsis. Doubtful though I am of father 1’s reliability I am prepared to accept that he loved his children and had he known that K had ingested cocaine he would somehow have indicated this although that is a very fine balance given his determined efforts to distance himself from responsibility and to protect his own skin. On balance he is sufficiently self-absorbed and sufficiently unaware of much relating to his children’s health and welfare that I’m not sure it would have occurred to him that he might have left some cocaine around and one of his children might have ingested it. However, given his primary responsibility for having carelessly left the drug available to be ingested this is perhaps of only marginal importance.

v)                  The paternal grandmother does not bear any direct responsibility for K’s ingestion of cocaine. It was not ingested in the time she was caring for K with father 1 on 4 April. She was not present in the home when it was ingested. She does though bear some indirect responsibility in that she was the head of a family who were steeped in Class A drug misuse and had been for many years. She was well aware of father 1’s activity as a supplier and I am satisfied knew that he processed drugs both at her premises and inevitably at the mother’s. She also was well aware of his deteriorating alcohol abuse and it was a self-evident risk that in handling drugs in either her property or in the mother’s property there was a real risk that careless handling would leave drugs in the environment where they might be ingested by children. The frequent presence of K and M in her own home her cavalier attitude to the presence and consumption of drugs by father 1, by the lodger by her daughter plainly represented a risk to them which is reflected in the environmental contamination of their hair part of which is attributable to presence in her premises. It is luck rather than judgment on her behalf that no harm came to them.

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CHRONOLOGY

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