R v. Lucy Letby

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This website, along with all the scientific detail it contains, has been produced and compiled by a scientist with expertise in rare paediatric diseases. The author has no prior association with the Lucy Letby case.  The information provided has been thoroughly researched, and experts within the relevant scientific fields were consulted to obtain additional knowledge and insights.  

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R v. Lucy Letby

In 2020, Lucy Letby was charged with the murder of 7 infants and the attempted murder of 10 infants.  These children were all under the care of Lucy Letby in the neonatal unit at the Countess of Chester Hospital, in Chester, UK.  These attacks were reported to span the period running from June 2015 to June 2016.  At the time, nobody suspected Lucy Letby of wrong-doing.  It was only after the consultants who were running the neonatal unit became the subject of a critical report from the Royal College of Paediatrics and Child Health (RCPCH) that they went on to file a report with the police alleging the infant deaths were due to the actions of nurse Lucy Letby.  In all but one case, the infants received autopsies and the coroner found that they died of natural causes.  This website was created to present the science behind the claims made against Ms Letby.  The information contained herein reflects the basic scientific standards and findings relating to the claims made by the expert witnesses. Despite the requirement that expert witnesses should present full information on matters upon which they are called to testify, none of the information contained on this website was ever made available to the jury by the expert witnesses.

A Scientific Overview

Last update: 19.07.2023

The case against Lucy Letby lacked scientific evidence and is based on unverified hypotheses

Based upon published peer-reviewed research, and with the guidance, advice, and insights of other scientists, it is the view of Science on Trial that the scientific information put before the court by the expert witnesses is quite simply inaccurate, misleading, and in many instances false. The expert witnesses in this case are in all likelihood aware that the claims they have made lack the necessary scientific findings, and if they were to write these claims up and attempt to submit them for publication, their submission would be quickly rejected. 

Although we may not be privy to each and every element presented during proceedings, as scientists we are able to identify the scientific standards and research relating specifically to the scientific elements included in the case. Additionally, we can identify the proper methodology that should be employed when conducting a scientific investigation based upon clinical medical notes. A significant part of this type of scientific consultation involves extensive reviews of patient medical records, along with clinical reports of infants and children with rare diseases. This work necessitates the adoption of rigorous scientific investigative principles and protocols, along with an understanding of problematic variables such as observer bias, in order to yield a report that can be acted upon by the clinical team. Unlike a forensic investigation, such approaches have serious consequences to the health of specific patients if the conclusions made are erroneous or are scientifically unsubstantiated. Even where such an investigation involves patients with the same underlying conditions, great care is taken to recognise the significant influence of non-genetic factors which may alter outcomes. 

The claims made by the experts in this case were reviewed and the references upon which they relied to make such claims were sourced, analysed and cross referenced with the body of literature on the related topics. Based upon these factors, it is quite apparent that the quality of the scientific evidence is deficient and scientifically unfounded. For example, Dr Evans’ primary assertion is that some of the infants were harmed by air embolism, where air was deliberately injected into a vein, or through the stomach. Peculiarly, Dr Evans relies on a research paper from 1989 dealing with gas embolisms, which occur through the use of high ventilation pressures in preterm neonates. The cause of death due to gas embolism from high pressure ventilation differs substantially from the cause of death due to air embolism. It is never properly explained how the article Dr Evans references could ever have been used as a basis for describing air embolism using ambient air with 21% oxygen introduced through various tubes. The paper Dr Evans references describes air embolism caused by high pressure 100% oxygen being delivered to the lung with such force it caused an air leak in the lung. When demonstrating the symptoms of a given physiological state, it is necessary to demonstrate this state in multiple peer reviewed journal articles. There is no evidence supporting the finding of air embolism in any of the infants, as the expert witnesses rely on a journal article depicting gas embolism and not air embolism.

There was a failure to ensure conformity in clinical standards and terminology used by experts and medically trained witnesses

The unique physiological state of preterm neonates is such that we cannot look to a global presentation in order to determine clinical instability. Instead, we need to separate out physiological functions and make assessments of the general functional capacity of specific organ systems. An infant diagnosed with jaundice or admitted to the neonatal unit for ventilation is not clinically stable. Further, the heterogenous physiological differences present in premature neonates reflects a distinct clinical condition which cannot be reliably compared to the clinical picture relied upon from term infants.

Not a single expert appears able or willing to present any similar case involving a comparable setting, patient population and set of symptoms as scientific certainty. Given that in the case of every infant, the medical records report ‘possible sepsis’ and the symptoms described point to an infection of some nature, it is shocking that no infectious disease expert has been called upon to review these cases. In the absence of such an expert, there should be a proper explanation detailing why no investigation surrounding infectious diseases took place. This evaluation would require at minimum an assessment of the possible infectious disease pathogens that pose a risk to neonates during the perinatal period, where infection is associated with sudden unexplained neonatal collapse/death. This evaluation should be accompanied by an assessment of the factors relating to sepsis for each child and why an infectious disease was ruled out.

The indictment centres around claims from co-workers of the defendant, which assert the infants were stable prior to collapse. Where such statements are made and are based on clinical insights they must be defined, and the definition must be in present day use, and be widely applicable across the patient population being studied. In a medical setting, the absence of physiological phenomena equates to the term "stable". Thus, considering that a diagnostic test establishes parameters which define clinical significance, the use of terminology such as "stable" should be reflected by the absence of clinical issues in the patient’s medical notes. One does not assess patients on the basis of whether they are "stable". Clinical diagnosis is reached based on whether the patient exhibits signs of clinical instability. Despite this clear discrepancy, all the medical professionals who testified for the prosecution repeatedly referred to neonates being “stable”, “very stable” or “stable enough.” Indeed, it was stated that a child who was born at 23 +6 weeks gestation was “very stable” prior to experiencing a bout of sudden projectile vomiting. This child had apparently not undergone proper MRI brain scanning and was receiving a combination of Gaviscon, breast milk and formula via nasogastric tube. The condition of the infant does not reflect that of clinical stability where the child is unable to feed independently and where there is no relevant assessment of development of white matter brain injury, which is present in up to 50% of very low birth weight infants (Romero-Guzman & Lopez-Munoz, 2003; Agut et al., 2020).

The importance of the underlying physiology of premature neonates was not properly highlighted by experts

In the case of R v. Lucy Letby, all but one of the infants fulfil the criteria for preterm birth, (<37 weeks gestation). There is no discussion about the multifactorial elements that combine to place the preterm infant at significant risk of death due to the disruption in foetal growth brought about by their premature birth (Sehgal et al., 2022; Schindler et al., 2017; Saigal and Doyle, 2009). Further, there is no discussion surrounding the significant body of evidence that demonstrates that extremely low birth weight infants (<1000 g) have a mortality rate of ~15% and that twin births, male gender and maternal complications are closely associated with an increased incidence of mortality and morbidity.   

In the present case, those infants who died did so after a period of excessive cardiopulmonary resuscitation, that exceeded the ILCOR guidelines. There is no discussion surrounding findings that preterm babies (born at <37 completed weeks of pregnancy) have a higher mortality, morbidity and risk of impaired motor and cognitive development in childhood than babies born at term (Heino et al., 2016). This is despite the fact that seventeen out of 18 infants described in the indictment were born before 37 completed weeks of gestation. Moreover, in England and Wales, the incidence of preterm birth is higher in multiples, where ~50% of all multiples are born at a gestational age of less than 37 weeks. Taking the infants included on the indictment, we find that eight of the eighteen infants were multiples, of which four infants were very preterm (<32 weeks gestation) and the other four were moderately preterm (32 – 34 weeks gestation). Among the single births, three infants were both extremely pre-term (<28 weeks) and extremely low birth weight (<1000 g). In England and Wales the incidence of perinatal death for very preterm infants in 2015 stood at ~ 8%.  

In three cases involving infants who died, it was reported that they were removed from ventilation support in the immediate period before death. There appears to be no clinical explanation for the removal of ventilation. Instead, there are reports within the notes of a deterioration in the hours prior to removal. There is no criticism of any of the medical treatment rendered to these infants despite the RCPCH report from that same time detailing that the consultants only held two ward rounds per week, the ward had insufficient senior cover, and there was a reluctance to seek tertiary level advice and escalate concerns in a timely manner. Rather, both the expert witnesses, Dr Evans and Dr Bohin, represent the conduct of the medical professionals responsible, for the patient’s care, as a reflection of the clinical standard. In many cases, the approaches and actions of the clinical team can only be described as inappropriate and demonstrative of an abject failure to apply the principles of diagnostic work-ups. Several infants are noted to require a lumber puncture, presumably to ascertain risk for meningitis. This does not ever occur because the infants die before the procedure is performed (see, Child C and Child D). In a separate incident, both the consultant, Dr Brearey, and the registrar, Dr Ventress appear unable to determine the cause of desaturations in an infant while on ventilation. Both clinicians determine that the cause of the desaturation must be equipment malfunction. Once the ventilator is changed and the same phenomena recurs, they appear to take no diagnostic steps other than to remove the child from the ventilator and reintubate her five minutes later. It is not clear whether the infant is being intubated prior to analgesia or muscle relaxant infusion, though that is apparently the case.

The role of medical supervision and its contribution to the condition of the infants in the case was not covered by experts

The testimony of the medical professionals should be carefully reviewed to ascertain whether they exhibit the requisite competence in regard to the application of biological reasoning to clinical care. A key claim that is made to justify removal from ventilation support is that the infant is ‘fighting the ventilator.’ Whether this term is clinically appropriate, given its usage for adult populations, is a matter that does not appear to be questioned. However, many medical professionals exhibited a disregard for the serious impact neonatal pain plays in the health and welfare of preterm infants. There are numerous occasions in which extremely preterm neonates are intubated without any analgesia, and/or both the delivery of analgesia was delayed. In other instances, there were two infants who underwent intubation and were not administered surfactant. There was no assessment as to whether these failings contributed in any significant manner towards their deaths. However, it is apparent that two infants succumbed to complications associated with lung injury (Child D and Child K).   

There appear to be significant inconsistencies with regard to ventilation strategies and approaches. Despite the fact that morphine 100-mcg/kg bolus followed by 10 mcg/kg/h continuous infusion for 7 days or less (median duration of exposure in the treatment group was 77 h) showed no detrimental long-term neurological effects (Simons et al., 2003), there were reported claims of infants fighting the ventilator and this was used to justify their removal from ventilation. There was little investigation as to why this phenomena was apparent in very preterm infants, and in one representative case, Dr Gibbs removed an infant from the ventilator and she died ninety minutes later (Child I).  Removal from the ventilator was not discussed as a factor in assessing the cause of death.

There is no discussion surrounding the predicted outcomes for the population of neonates in the indictment. For example, the experts fail to reconcile the finding that up to 50% of extremely preterm infants fail extubation, even when extubation criteria are met, such as the level of ventilator support and respiratory function parameters. In a study of 3343 extremely low birth weight (<1000 g) neonates who received mechanical intervention, 2867 (85.8%) survived to discharge. Mortality was associated with exposure to a greater number of mechanical ventilation courses (Jensen et al., 2015). In this case, three of the infants are classified as extremely low birth weight, however there is little discussion of the unique physiological circumstances confronting such infants, and whether mechanical ventilation represented a particular risk factor in terms of their clinical prognosis.

Much weight is given to the coincidental element that Ms Letby was present for some of the events characterised as ‘sudden collapse.’ Records not presented to the court, nor referenced by the experts, reveal a pattern of stillbirths and perinatal deaths that for a five year period follow the exact same trend. Indeed, there were a significant number of stillbirths that occurred alongside the perinatal deaths in the period between June 2015 – November 2015. When establishing a cause of biological phenomena, it is not permitted to manipulate or massage the data. Thus, the greatest insight into the “sudden collapse” of the infants in this case required a thorough review and comparison of the symptoms, and circumstances of all the infants on the ward during that same period. It does not appear that any such review took place.

Appropriate expert evidentiary standards were not met by expert witnesses

A scientific investigation, which will necessarily rely on an investigator to make conclusions based on clinical records, must demonstrate that the underlying approach used to reach their findings is supported within their field of expertise. For example, if there were any initial suspicion that the sudden collapses were due to a genetic disease, but upon preliminary testing it is identified that there is no genetic aetiology that could suitably describe the sudden collapses, then one must still identify a control group of some other kind to compare the findings.  This is in order to establish whether their findings are truly unique. Clearly, the control group in this case would be all the other neonates on the ward during the same period.  

The absence of expert evidence could be viewed as demonstrative of the unique nature of the allegations made in this matter. The problem with this idea, though, is that the experts have failed to report on actual evidence that directly opposes the claims they have made, and in some cases this shortcoming reveals a failure in either expertise or honesty. For example, Professor Hindmarsh testifies that there are no studies detailing the adsorptive properties of insulin, which is the tendency for insulin to adhere to most any surface. This is untrue. There is a significant body of research relating to this phenomenon, and upon review it shows that such adsorptive properties of insulin to the venous lines can result in a decrease of insulin delivery by as much as 70%. There is further evidence that insulin forms bonds to the bag delivering the ternary parenteral nutrient (TPN) solution and/or dextrose saline solution, and this can reduce the delivery of insulin by as much as 60%. The increased binding to plastic surfaces is compounded by research which reveals that insulin added to TPN and/or dextrose solutions is unstable and results in a decreased bioavailability of insulin by ~40%. This finding persists over at least 24 hours. Professor Hindmarsh fails to make any of this important and relevant empirical evidence available to the jury, and fails to give it any consideration in his testimony.

Causes for discordant insulin and c-peptide levels were not revealed to the court by experts

Professor Hindmarsh fails to explain the core differences between neonatal physiology and paediatric physiology. He fails to explain findings that demonstrate discordance between c-peptide and insulin concentrations in neonates owing to the increased binding of insulin to erythrocytes (Puukka et al., 1986) and the increased concentration of proinsulin relative to insulin. In addition, he makes no mention of the fact that both infants who reportedly showed increased plasma concentration of insulin were at significant risk for the production of autoantibodies to insulin. Child F was treated with insulin in the days prior, which is related to the production of autoantibodies (Liu et al., 2023), while Child L was born to a mother who was seriously unwell and had a diagnosis of gestational diabetes.  

Gestational diabetes is associated with hyperinsulinemia The production of maternal antibodies to insulin in response to maternal insulin treatment can result in insulin readily crossing the placenta. It was identified that 24% of umbilical vein cord blood contained non-human insulin, demonstrating the transfer of exogenous insulin from the mother to her infant in utero (Lindsay et al., 2004). A later study showed that more than half of the infants of mothers with insulin-dependent diabetes have maternal insulin autoantibodies (mIAAs) at birth, and the close correlation between the mIAA levels in the newborn infant and those in the maternal circulation verifies the claim that the IAAs in cord blood represent transplacentally transferred antibodies. These mIAAs could form complexes with the infant’s endogenous insulin, thereby prolonging the half-life of insulin. Pregnancy, in general, induces non-immunoglobulin transfer of maternal insulin into foetal circulation, and this tendency is increased at the time of delivery in both diabetic and non-diabetic mothers (Ronkainen et al., 2008).

Despite the fact that Professor Hindmarsh is an Emeritus Professor, based at University College London Hospital (UCLH), there is nothing to suggest that he has any involvement with hypo/hyperglycaemia pathways in preterm neonates at either UCLH or Great Ormond Street Hospital. Nor does he possess any advanced or specialist knowledge in the assessment of assays used to test C-peptide and insulin. It is provided that “The expert must be able to provide impartial, unbiased, objective evidence on the matters within their field of expertise. This is reinforced by Rule 19.2 of the Criminal Procedure Rules, which states that an expert has an overriding duty to give opinion evidence which is objective and unbiased.” Where a witness refers to a single blood test result and suggests that there is only one way the result can occur, which is through poisoning, this must be more than the expert’s simple opinion, especially in light of the significant body of evidence and empirical data showing that such a claim by a witness is strongly associated with wrongful convictions (Marks, 1999). Professor Hindmarsh stated that a blood test with an insulin concentration of 4657 (units not given pmol/L or mU/L) and very low c-peptide could only occur due to exogenous administration. Remarkably, he then leaps to a conclusion that this insulin must have been administered via dextrose/TPN solutions. This is a stunning claim to make, not least when a concentration of insulin of 4657 pmol/L or 4657 mU/L, would kill two grown men. Yet the infant, who was both very low birth weight and very preterm, recovered without any sequelae in just a few hours.

Professor Hindmarsh fails to provide examples of such discordant insulin/c-peptide levels in clinical case studies, despite the fact that such evidence does exist. Villaume et al (1982) detailed a case of spontaneous hypoglycaemia in which very high plasma insulin (18000 pmol/L) but low normal plasma C-peptide levels occurred. This case could not be attributed to exogenous insulin administration as it otherwise would have been. The mechanism in Villaume's case is unknown: the authors postulated that reduced removal of (endogenous) insulin by liver and peripheral tissues but normal removal of C-peptide produced the observed results. Such a finding likely occurred in the case of Child F, where he presented with increasing signs of jaundice and increasing levels or creatinine and urea, which results in shifts in the glomerular filtration rate in the kidney.  Where both liver and renal function is disturbed, the concentration of insulin in the blood would be increased owing to a reduction of insulin metabolism and breakdown occurring via hepatic and renal routes.

With regard to Child L, the fact that studies demonstrate 50% of infants born to mothers with gestational diabetes have mIAAs in their circulation at birth (Ronkainen et al., 2008) suggests that such a scenario must be considered when hypoglycaemia is identified at birth, as was the case for Child L. The presence of mIAAs in the neonate’s circulation would explain the diminished response to dextrose infusion. The availability of insulin bound to mIAAs would be dependent on the affinity of the antibody for insulin. Moderate to high affinity mIAA binding would result in a pool of insulin being released slowly over time, resulting in persistently low blood sugar. Once all the insulin is released from the antibody complex, the antibodies will be degraded and hypoglycaemia is unlikely to recur. This phenomenon has been observed in several autoimmune conditions.

A poor understanding of the aetiology of human diseases limited the scientific investigation undertaken by experts

It is a fundamental aspect of human biology that all diseases and disease states proceed by established mechanisms on a molecular level. Every diagnostic description has a mechanism which occurs at a molecular level that ultimately brings about the observed symptoms. In some cases, the symptoms we observe are a by-product of that mechanism. They are not the direct result. Any scientist should be able to reason that the epiphenomena, the observed disease symptoms, are a manifestation of a number of chemical reactions and molecular interactions that occur within the cell and between cells throughout the body. There is an assumption that the reason that scientists have yet to develop a cure for a particular disease is because we do not understand how or why the disease manifests itself. A significant contributor to instilling this belief can be found in the medical community. Patients are often left in a state of bewilderment when a doctor informs them that scientists do not know why a given biological event occurs. However, this is more the perspective of a medical doctor than it is the reality of a scientist’s knowledge. Science is not so much about knowing as much as it is about reasoning. In this submission, we systematically go through the claims made by the experts in the case and explain why these claims cannot be put before a jury, as not even a scientist would be able to reason about their underlying hypotheses, simply because hypotheses are more conjecture than established fact. Where possible, we attempt to tackle the reported clinical phenomena on a mechanistic level, which is a more logical and reductive approach than simply placing faith in a particular cause of death based solely on subjective experience.    

There is no way to effectively understand what the evidentiary standard was in bringing this case to trial. Based upon the lack of direct scientific evidence, it is apparent that it was not brought based on the findings of a forensic investigation. Still, we believe that in the face of the multitude of experts insisting on the outcomes arising from deliberate harm, it would be an act of recklessness to fail to call for a trial on the issues. The expert witnesses appearing before the court did so in full knowledge that the scientific standard they applied to this case falls far below that which is required of any person who asserts that their expertise is grounded in experimentally-derived biological science. It is particularly problematic that the experts overrode the presumption that the infants died of natural causes, given that 6 of the infants underwent an autopsy where the cause of death was determined to be natural. In its simplest form, before one can even begin to conduct a murder investigation and hear evidence derived from that investigation, there is a requirement to provide an explanation for the findings made at autopsy. This marks the initiating step in deciding as to the claim asserted by the medical doctors, when they reported to Cheshire Constabulary that Ms. Letby is England’s most prolific female child murderer. In order to even conduct such an assessment, one would at the very least need to re-examine the bodies.

Remarkably, the consultant, Dr Gibbs claimed that he suspected Ms Letby of murder in 2015. He not only failed to properly lodge this complaint, but he also failed to ensure the proper collection of serum and blood samples after the death of the patients. Additionally, it appears that Dr Gibbs failed to notify the coroner that he had firm suspicions that the infants were the victims of murder. It is also the case that the hospital failed to lodge the deaths with the Child Death Overview Panel, which would have conducted an independent investigation at that time. Despite claiming he held concerns beginning in June 2015, Dr Gibbs failed to take the necessary steps to ensure the proper preservation of the body after death, permitting the heating, bathing and holding of the infants for hours after the loss of all vital signs of life. The treatment of the bodies after death, combined with the lack of blood and serum samples collected at the time of death compounds the inherent difficulty in determining the cause of death. These shortcomings mean that there is no appropriate refutation of the autopsy findings, and nor can there be, given that the bodies were not exhumed for re-examination.

An investigation in defiance of the basic scientific method poses a significant risk to the reliability of the evidence presented

From the outset, this case proceeded by pure scientific speculation, and introduced employees of the same organisation that employs the defendant (The National Health Service) to testify to the validity of the forensic investigation performed by an expert who solicited the role as an investigator (Dr Evans). The indictment concerns the deaths of seven neonates (down from 8) and a further 15 charges of attempted murder. In only two cases is there evidence that might be deemed to have some scientific validity. Those are the charges relating to insulin poisoning. However, contrary to their intended purpose, if the expert witnesses were to apply the actual scientific rigour required of them, they would recognise that the two cases of insulin poisoning are so scientifically unlikely that it leads one to assume that the entire case is based on flawed scientific logic.  Admittedly, we do not know what the legal standard is for changing cause of death, but Ms Letby should not be treated to such an unusual situation where a criminal trial is used to disprove the findings of the pathologist who performed the autopsy, and the coroner who confirmed the findings. Simply put, that is what has occurred in this matter. There is no refutation of the recorded cause of death. Instead, there is an immediate disregard for the autopsy findings, except for those which lend support to the claims put forth by the expert witnesses. 

When confronted with a probable rare disease, there is a certain approach one must take to determining whether there is one primary condition which leads to diverse, partially overlapping outcomes, or whether there are wholly distinct entities at play. It appears the medical experts failed to determine either of these possibilities. There is no proper analysis of the overlapping symptoms, the time of appearance, nor any effort to characterise reported physiological phenomena. This is despite the emerging theme surrounding the instability of the infants concerning the fact that the vast majority were very premature infants (<32 weeks gestation) or extremely premature (<28 weeks gestation) and that such infants have inherently unstable autonomic nervous system reflexes.

In every case what is being described is the interplay between the inherent instability of the infants and some other force. That other force may have been a viral infection or some other birth complications. There is circumstantial evidence, based upon the symptoms described and onset of the those symptoms, that strongly implicates a viral infection as playing the primary function in the death and destabilisation of the infants. We are not seeking for any person to simply take us at our word. Rather, Science on Trial was formed to enable individuals who are interested in the science behind this case to gain an understanding of the manner in which the British criminal justice system wilfully and deliberately disregards basic tenets of the scientific method. This is achieved through the invitation of unqualified medical doctors, with limited experience in scientific investigations to conduct complex forensic examinations with little more than radiographs, and essentially no toxicology, blood testing or genetic data.

Science on Trial, how does it stack up?

Essentially, the scientific “proof” in this case amounts to the conflation of gas embolism with air embolism, and the reliance on one single publication from 1989 which details the consequences of gas embolism. However, this is not the same phenomenon that Dr Evans uses in his assessment of cause of death. Dr Evans contends that these infants, with wildly different autopsy findings, died due to air embolism and not gas embolism. The evidence Dr Evans relies on to prove air embolism is from a paper detailing a wholly distinct phenomena called gas embolism. This alone demonstrates how woefully out of his depth Dr Evans was in conducting his investigation. That other experts joined Dr Evans in support of his flawed reasoning should not be used to contort scientific evidence and speculate that these individuals know any more than the average lay person. It appears self evident that none of these individuals had ever seen or experienced a case of air embolism deliberately carried out by a third party. Nor did any of these individuals conduct research in the area of air embolism. Rather, Dr Evans adopted a hypothesis which defied the principles of the scientific method and each witness sought to provide an interpretation of a handful of radiographs to boost Dr Evans’ claims. If it were somehow possible to determine cause of death using radiographs and photographs of dissected organs, then surely there would be no need for autopsies. We appear to have been asked to accept that the autopsy findings should be disregarded and replaced by interpretations of radiographs by individuals who had no involvement in the autopsies. 

There is great concern that the scientific claims made by the experts are not grounded in logical scientific reasoning and that the individuals who carried out the investigation were not simply deficient in their approaches, but further, that they went against basic scientific investigative standards. The consideration of such claims poses a real threat to the integrity of both the role science plays in society, and its role in the delivery of justice within the legal system.

It has taken many hours to put together this material and I could produce reams more. What is presented here is a fraction of the information this case brings up for a scientist. It is of great concern that by reducing the deaths of the infants concerned into a spectacle of confusing and dubious claims, we are effectively undermining the functioning and integrity of our legal system. We cannot as a group of people, however committed, make a determination of guilt on the back of scientific claims that are totally baseless. I fear this is precisely what has happened in this case. In an ideal world, only the highest quality evidence would reach the court. Nobody outside the realm of science can reasonably be called upon to judge the scientific basis of claims made by individuals asserting they are experts, but whose claims are purely speculative and unsupported by peer-reviewed scientific evidence. It falls on us, as scientists, to maintain the integrity of our discipline by speaking faithfully to that which our fellow scientists present in peer reviewed studies. I hope this information will be received as a good faith effort to ensure truthfulness in science.

Mortality rate at the Countess of Chester Hospital

It has been repeatedly claimed that the number of deaths at CoCH increased in 2015 and 2016, and the implication was that these two years were unique in the number of infant deaths. However, the original announcement made regarding the investigation into infant deaths at the Countess of Chester Hospital contained no statement surrounding an increased incidence of mortality. In the years following 2015 and 2016, the rates of perinatal death continued to increase.  

  • DCS Nigel Wenham stated on or around 18 May 2017 that: “Cheshire constabulary has launched an investigation which will focus on the deaths of eight babies that occurred between that period [2015-2016] where medical practitioners have expressed concern”

  • The cumulative infant mortality rate at the Countess of Chester Hospital for 2015 and 2016 was lower than the national average.

  • There is an unusual trend in the pattern of stillbirths and perinatal deaths.

  • The number of perinatal deaths in 2017 and 2018 was higher than in 2015 and 2016, but Lucy Letby was not on the ward in these years.

The expert evidence is not scientifically valid and in accordance with Criminal Practice Direction V Evidence 19A.6 Expert Evidence: it is not sufficiently reliable.  


Scientific Claim

The infants died by air embolism

Air embolism is not a vague or unclear cause of death to arrive at in the case of the sudden collapse of an infant. What is very clear is that the terms “sudden” and “collapse” are being used to restrict the investigation to air embolism as the cause of death. However, sudden postnatal collapses are defined entities and there is little discussion of how the findings in this case relate to sudden infant collapse (Blair et al., 2006; Miyazawa et al., 2020; Neagu et al., 2021; Oei et al., 2018; Quinton, 2014; Reyes et al., 2018; Schindler et al., 2017). The basis for a determination of air embolism as a cause of death is not a standard definition, and nothing about the definition given is unique to air embolism. Air embolism cannot be determined as the cause of death in these cases as there is nothing reported by the expert witnesses which finds that air embolism even occurred. 

The court may not be unaware that the only way that air embolism can be determined is either through autopsy, applying Richter’s method, or in living patients through the use of MRI or Computed tomography (CT) (Bajanowski et al., 1998; Divekar et al., 2004; Melvinsdottir et al., 2022). Neither approach was used in this case. The symptoms that Dr Evans claims are suggestive of air embolism are not supported in the body of literature reporting on air embolism. Further, the only citation to have been made relating to research in the field of air embolism is not relevant to these cases. Dr Evans references a publication from 1989 regarding gas embolism due to extensive mechanical ventilation in neonates. There is no suggestion that Ms Letby used mechanical ventilation as a weapon, nor is this being claimed. Clearly, the root cause of embolism due to mechanical ventilation differs from the claimed cause of air embolism due to deliberate harm. In the latter case, the accusation is that air was able to enter the circulatory system through the deliberate injection of air into venous lines going into the infant.


Scientific Claim

Injection of air into the stomach can cause death by air embolism

There is no evidence that an infant can be injected with air which would result in "splintering" of the diaphragm. A search for the terms "splinter" and "diaphragm" on Pubmed, the online search engine for life science publications, returns four results, all of which refer to foreign objects causing the formation of a splinter. This term appears to have no medical basis. There are 24 results returned for "splinting" and "diaphragm", of which only one might be relevant, and concerns gastric perforation in neonates which results in pneumoperitoneum (air in the abdominal cavity). However, this study deals with infants presenting with oesophageal atresia (Maoate et al., 1999) - a birth defect resulting in the oesophagus terminating prior to entry into the stomach - and tracheo-oesophageal fistula, where the windpipe is connected to the stomach. It is claimed that air injected into the gut via a nasogastric tube causes a splinting of the diaphragm sufficient to limit the regulation of breathing. There is no evidence to support such a claim. If an infant requires gastric feeding, this is an indicator of a greater physiological issue owing to prematurity. In the case of Child C, Dr Evans asserted that the infant died from Ms Letby injecting air into a nasogastric tube. Child C was born with an air bubble in his stomach - something that was observed on x-ray shortly after birth. This bubble worsened over time and the description of the events that follow are suggestive of a condition termed pyloric atresia.  This condition occurs when there is a blockage in the stomach that prevents gastric emptying. Interestingly, Dr Gibbs made suggestions about a potential blockage, but there was apparently little to no diagnostic work performed to identify what, if any, treatment should be given.  Pyloric atresia is associated with significant mortality, especially when left untreated (Zecca et al., 2010).  Suggestions from the defence that the abdominal bloating occurred due to CPAP appear unfounded, given that abdominal bloating from CPAP typically does not occur until at least 4 days after treatment is initiated. (Jaile et al., 1992).  However, the usage of CPAP may have worsened the condition, although the greatest issue was the failure to ascertain the cause of the black aspirates and the associated gaseous formation in the gut and bowel. Despite being aware that Child C had air in his stomach soon after birth, Dr Evans claimed that Lucy Letby was responsible for the massive amount of air found in the infant’s stomach and bowel.  It would have been next to impossible for Ms Letby to inject air into the infant via the NG tube, and this is supported by Boyle's law, which states that pressure is inversely proportional to volume. This means that one needs increasing amounts of pressure when trying to move air from a large volume to a small volume, such as a syringe into a very fine tube.  The force would be such that it would likely introduce an air lock in the nasogastric tube which would prevent more air moving through it. Ironically, the phenomenon that Dr Evans says would happen by injecting air into the vein would actually happen in the NG tube. Further, Dr Evans repeatedly claims that the cause of oxygen desaturation and breathing issues, as reported in the clinical notes, is due solely to air embolism.  If this were the only cause of such events, then surely breathing abnormalities would rarely be reported in the preterm population.  In actual fact, Dr Evans and Dr Bohin fail to address the significant complications associated with premature birth relating to the control of breathing. Nor do they address the impact of ventilation approaches on preterm breathing. Multiple studies demonstrate that apnoeas are common in preterm neonates and they play a major role in determining survivability of preterm neonates (Crawshaw et al., 2018; Dassios, 2023; Erickson et al., 2021; Miyazawa et al., 2020; Sehgal et al., 2022).


Scientific Claim

The blood test for insulin is confirmation of insulin poisoning

In both cases where it is alleged that Ms Letby poisoned infants with insulin, the claim is based on a single blood test that showed alarmingly high levels of insulin and nearly non-existent levels of C-peptide. These levels are so high as to warrant greater questioning. The blood testing conducted in this case does not resemble the standard of testing required in other comparable cases (Marks and Richmond, 2008). The experts fail to consider effects such as the Hook effect, which yields false negatives and could easily explain the low c-peptide concentrations observed. Dr Evans does not refer to other cases of insulin overdose or contamination to demonstrate that the testing used is sufficient to assert that the infants were poisoned with insulin (Hawdon et al., 1995; Ihlo et al., 2011; Liu et al., 2023; Marks, 2005; Shen et al., 2019; Taylor et al., 1982).


Scientific Claim 

The medical doctors bear no responsibility (Child C)

There are three cases that should be more appropriately scrutinised regarding the reported reasoning for removing children from ventilation and breathing support. In two cases, there is clear evidence that Dr Gibbs played a pivotal role in making life or death decisions. They represent the only two deaths in this case where it is clear that the actions of one individual, taken consciously, resulted in the death of two children. In the third case, it is less clear what the clinical basis was for removal from breathing support but there was apparently no consultant oversight into the care and decisions being made for the child. In early June 2015, Child C collapsed and was resuscitated, demonstrating signs of life such as spontaneous breathing. It was the assertion of Dr Gibbs that Child C would be brain damaged. It is not clear whether Dr Gibbs gathered this information from sonography, MRI scanning or some other means, as no evidence was presented to support this statement. As a direct result of the claims put forth by Dr Gibbs, the parents consented to giving the infant analgesia, sufficient to depress respiratory effort, until he passed away. It appears that the analgesia played a primary role in the end of life of this infant. It is improper to make any person responsible for this outcome when Dr Gibbs was the prescribing doctor.  


Scientific Claim

The medical doctors bear no responsibility (Child I)

In a second case, concerning Child I, Dr Gibbs removed the Child from the ventilator at 12:45 am, despite her showing signs of seizure activity (lip smacking, posturing) and she had repeated periods of apnoea. After removing the child from the ventilator, Dr Gibbs left the ward and returned home. At 2:10 am, Child I was pronounced dead. Given that 85% of sudden infant deaths occur during the night time hours, it is shocking that a child would be removed from a ventilator at night when fewer clinical staff will be available to assist. Further, for extremely preterm neonates (<28 weeks gestation), it is widely understood that it is a significant challenge to wean such infants from mechanical ventilation. Many studies have found that predicting successful extubation is an exceedingly difficult task, and the rationale given that the infant was ‘fighting the ventilator’ should have warranted a proper investigation into the source of the infant’s agitation. For ventilated preterm infants with evidence of asynchronous respiratory effort, neuromuscular paralysis with pancuronium reportedly has a favourable effect on intraventricular haemorrhage and possibly on pneumothorax. (Cools et al., 2005).


Scientific Claim

The medical doctors bear no responsibility (Child D)

In a third case, (Child D) efforts were made throughout the day to remove the infant from CPAP, repeatedly resulting in rebound desaturations and a return to CPAP. In this same interval, the child’s C-reactive protein (CRP) levels increased, indicating that she was experiencing the initial stages of adaptive immune system activation. This indicates that the infant was in the early stages of an infection. Despite this confounding picture of increasing adaptive immune activation, the infant was removed from CPAP in the early hours of the morning. There appears to have been minimal clinical review regarding this decision, and the child was ultimately pronounced dead some hours after breathing support was removed. There is no discussion as to whether the removal of preterm, or critically ill, infants from mechanical ventilation and/or breathing support can be conducted in the manner described in these cases.


Scientific Claim

Air embolism can cause a subcapsular liver haematoma

Subcapsular Liver Haematoma (SLH) is commonly associated with complications in preterm neonates, and is associated with excessive CPR, sepsis and birth trauma. There is no evidence that SLH occurs as a result of air embolism. In addition, liver organ failure is a symptom of untreated enterovirus infection, which can either be causal or simply co-occurring (Fuchs et al., 2013; Grapin et al., 2023; Wang et al., 2001; Yuri et al., 2018). It appears that there were two x-rays performed in the case of liver damage and the second (after death?) showed the haematoma. Given that SLH can occur in utero, it may simply be that it worsened as part of the deterioration of the baby's condition. In a recent review, (Liakou et al., 2022), researchers profiled 433 cases of SLH from the literature and found that most cases are preterm, with very high rates of mortality (>80%). SLH was described by Singer et al., 1998, and was linked to premature neonates. The group reviewed 755 perinatal autopsies and found that hepatic subcapsular haematomas were found in 52 (6.9%) cases, including 31 stillborn foetuses and 21 liveborn infants. Sepsis was associated with 62% of the cases with hepatic subcapsular haematomas.


Scientific Claim

The lack of elevated C- reactive protein indicates that the infants were not experiencing any infection

C-Reactive Protein (CRP) is part of the humoural, adaptive immune system. It recognises altered self and foreign molecules based on pattern recognition. Thus, CRP is thought to act as a surveillance molecule for altered self and certain pathogens. Infants born to term overcome the lack of adaptive immunity through supplemental protection afforded by maternal antibodies which are transferred through the placenta. The transfer of maternal antibodies to the foetus occurs throughout the third trimester, and is likely linked to protecting the developing nervous system from infection. This means that preterm infants substantially lack the transplacental transfer of maternal antibodies. This may explain why these cases are so clearly impacted because they lack adaptive immune responses and maternal antibodies. This may also explain the claims that the infants appeared to become suddenly unwell. In a term infant, the maternal antibodies will detect pathogens and activate the adaptive immune response. The first element of this process is the release of CRP from the liver. However, in the case of a preterm, the lack of immune surveillance results in a delayed response to pathogenic infection. The diminished immune response may permit invading pathogens to colonise the infant without detection, resulting in a sudden decompensation only when the pathogenic load is high enough to initiate the innate immune response.

Dr Dewi Evans 

In May 2017, Cheshire constabulary announced that at the request of medical professionals, it was opening an investigation into the murder of babies at the Countess of Chester Hospital neonatal unit.  The alleged murders occurred in the period running from June 2015 up to June 2016.  During this same period, the Countess of Chester had high levels of stillbirths.  A retired paediatrician, Dr. Dewi Evans, approached the National Crime Agency and suggested they should invite him to participate in the investigation.  Dr. Dewi Evans is not a pathologist or forensic scientist and he has no experience in the investigation of mass murder in a hospital setting.  Dr Evans disregarded the findings of the pathologists who performed the autopsies, instead developing his own theories as to how the infants died. He made his claims based on a review of the clinical record and on images taken at autopsy.  Despite having no new evidence, Cheshire Constabulary accepted the medical rationale of Dr Evans and charged Lucy Letby with seven murders and 10 attempted murders.  

Injection of air into the vein

Child A, B, D, E and M

Dr Evans claimed that he found evidence that some of the infants died or were injured by having air injected into their veins. Dr Evans said this caused an air embolism, which resulted in cardiac arrest. Venous air embolism is a rare event which has drastically decreased since the use of surfactant to remove the fluid in neonatal lungs (Divekar et al., 2004; Hemedez & Gündoğan, 2019; Jorens et al., 2009; Kalane et al., 2018; Lanfranco et al., 2017; Sarantopoulos & Lew, 2004). The decrease in the use of 100% oxygen when ventilating infants has decreased the incidence of air embolism. The symptoms Dr Evans associates with air embolism are not correct. He took his theory on air embolism from dated scientific papers and articles on decompression sickness. There are key symptoms that are associated with air embolism, but they are not described in this case. The symptoms of air embolism include: tachyarrhythmias, wheezing, decreases in end-tidal carbon dioxide (ETCO2), and both arterial oxygen saturation (SaO2) and tension (PO2), along with hypercapnia (Mirski et al., 2007). Despite these clear descriptions, only desaturations were described as symptoms that were detected in Dr Evans' analysis. In many cases, there was clear evidence that the CO2 levels were within range, in spite of the fact that changes in CO2 are a crucial finding in air embolism.

Insulin poisoning

Child F and L

Two of the infants were reported to have hypoglycaemia within the first few days of birth.  Both infants were premature and they were both the result of separate twin pregnancies.  Dr Evans claimed that Lucy Letby poisoned the infants with insulin. This claim was made on the basis of a single blood test for each child. The reason Dr Evans claims the blood test for insulin proves that Lucy Letby poisoned the infants is because they tested the concentration of insulin and C-peptide. C-peptide and insulin are produced from the same molecule, proinsulin, in an equal ratio.  The blood test showed high insulin and very low C-peptide.  This led to the faulty assumption that the insulin being measured must have been delivered exogenously. The discordance in the ratio of insulin to c-peptide was used as a basis to suggest that the insulin measured in the blood tests was delivered exogenously. There are a number of issues with this faulty reasoning. A blood test, such as the one used in this case, cannot be the only evidence used to make a determination of insulin poisoning. In neonates, especially premature neonates, it has been identified that the >70% of the insulin in the blood is actually proinsulin and its metabolites. Given that insulin is formed from proinsulin, they share sequence similarity. This means that a blood test for insulin may also detect proinsulin, which may be misreported as insulin. There are numerous confounding variables that the expert witnesses fail to discuss or make the court aware of. These place serious doubt on the reliability of the insulin tests being used to imply that the infants were administered exogenous insulin.

Force feeding milk

Child G 

In one particular case, an infant born at 23 weeks gestation started to projectile vomit immediately after being fed. These vomiting episodes were accompanied by instances of low blood oxygen levels (desaturations). It is reported that Lucy Letby fed the infant 45 ml of formula, breast milk and Gaviscon. However, Dr Evans alleged that at the same time she also injected air into the infant’s stomach via a nasogastric tube. Dr Evans claimed an estimated 100 ml of stomach contents was aspirated from Baby G and that this confirms that Lucy Letby injected air and milk into the infant’s stomach in an attempt to murder the infant. Dr Evans also confirms that at around this time, the infant’s C-reactive protein level had risen from 0 to 200. C-reactive protein is an immune response protein which is released by the liver upon infection. The increase in CRP is a strong indicator that she was experiencing an infection. As a consequence of the increased CRP, the infant was prescribed additional antibiotics. There is strong evidence that excessive antibiotic usage in preterm is deleterious to the development of enteric nervous systems. Dr Evans failed to demonstrate that the indicators of infectious disease observed in Child G were not causative in her presentation of desaturations and vomiting.

Injection of air into the stomach

Child C, I, O, P, Q

Dr Evans claims that air injected in to the stomach of infants, via their nasogastric feeding tubes, had a similar effect as air injected into the vein. He said that in some cases, air in the stomach would cause minor issues such as desaturations, and in other cases it would cause cardiac arrest and death. There is no evidence that injecting air into the gut could cause the death of infants. Air is pushed into the gut during cardiopulmonary resuscitation. Dr Evans fails to address the evidence that CPR in preterm infants is associated with systemic air embolism. Dr Evans cannot demonstrate that the findings he makes are anything other than artefacts associated with CPR. The failure to consider the impact of CPR as a contributing factor which increases the presence of vascular air results in Dr Evans overlooking additional information, which when given due consideration, may provide a more realistic explanation of the incidents reported in the case.

Attacking  organs with a sharp object

Child E, N, O

A number of children experienced internal bleeding (haemorrhage), which has few antecedents in the context of neonates. Dr Evans fails to consider any of the known causes of haemorrhage in preterm neonates, and Dr Bohin makes actual claims that fresh blood is not an indicator of haemorrhage. Given the complications associated with internal bleeding, it is unfathomable that any clinician would so freely dismiss the repeated occurrence of bleeding events in a neonatal population. Sudden bleeding in infants is typically associated with defects in blood clotting. Evidence of such defects can be determined from blood tests that measure Prothrombin time (PT), Partial thromboplastin time (PTT) and Fibrinogen. Alterations in these factors were identified in Child E, who experienced extensive haemorrhage. Dr Evans claims that the massive internal bleeding was due to air embolism and the interference of internal organs with an unknown piece of medical equipment. However, there is no evidence that such extensive bleeding is associated with air embolism, nor is it plausible to claim an unknown instrument was used when there is no evidence to support such a claim. It is apparent that both Child E and O experienced a hepatitis-haemorrhage condition, which has been associated with severe cases of viral sepsis (Grapin et al., 2023; Wang et al., 2001; Yuri et al., 2018). One possible explanation for the bleeding could be due to activation of the immature immune system upon infection. In some cases, the immature immune response can become out of control, causing a condition called disseminated intravascular coagulation (DIC) to occur (Gando et al., 2016; Popescu et al., 2022). In this condition, the immune system uses up the blood clotting factors and this causes the viscosity of the blood to change. The change in viscosity of the blood produces alterations in pressure in the vasculature, which can in turn cause devastating internal bleeding. No mention or explanation was made about the fact that pulmonary haemorrhage is diagnosed on the basis of haemorrhagic secretions, which are aspirated from the trachea, concurrent with respiratory decompensation that necessitates intubation or escalated support. This exact sequence of events occurred for Child E, and yet Dr Evans clings to his claims of air embolism as the cause of death. Child O was found to have extensive internal bleeding on autopsy, and this unclotted blood filled the peritoneal cavity.  In addition to the bleeding, the pathologist noted the presence of a hepatic subcapsular haematoma.  This was referred to as bruising of the liver.  On the basis of his review of radiographs and images of dissected organs, the expert witness Dr Marnerides, a pathologist employed by Guy’s and St Thomas’ NHS Foundation Trust, rejected the original autopsy findings and asserted that Lucy Letby caused the hepatic haematoma.  He provided no explanation of how this internal damage could be possible without causing extensive external injuries.  Dr Marnerides' testimony regarding Child O was quite possibly one of the clearest examples of an expert witness failing to inform the court of the major causes of subcapsular haematoma in the neonatal population. A basic search of the phrase “subcapsular liver haematoma AND neonate” into the life science research database yields 96 individual reports into this phenomenon occurring in the neonatal population. Compounding the inaccuracy of Dr Marnerides' claims is the fact that these haematomas were found to spontaneously rupture in preterm neonates.  Contrary to the expert’s claims that such occurrences are akin to a plant pot hitting one in the head in the middle of the desert, SLH was described as early as 1964, (Charif, 1964) and as recently as 2022 (Liakou et al., 2022).

Smothering, tampering, unknown

Child H. J, K

In some of the cases, it is unclear how Lucy Letby was even involved and what she is accused of doing to the infant. These cases provide only vague descriptions of the clinical notes. In the case of Child H, there are three allegations of harm, but no description as to how Ms Letby induced such harm. This case is particularly egregious, as the child was diagnosed with tension pneumothorax, which is associated with sudden infant collapse. In the case of Child J, Ms Letby is accused of inducing a seizure in a child by smothering, but no evidence other than the seizure activity is presented. In the case of Child K, the infant who died, after being transferred to another hospital, Dr Evans claimed Lucy Letby dislodged the endotracheal tube which was inserted to aide the child’s breathing. A meta-analysis of spontaneous extubation of endotracheal tubes (ETT) in neonatal units found that the most common cause of spontaneous extubation was agitation. The second most common issue was failure to properly fix the taping to secure tubing. Aside from these findings, it is apparent that there were delays in delivering analgesia to Child K. Extubation of ETTs often occurs with inadequate sedation, as failure to sedate the infant will result in activation of the gag reflex, which will result in displacement of the tube (Silva et al., 2023).

The expert witnesses provide far reaching misrepresentations of scientific and medical findings. In nearly all cases, the phenomena described by the expert witnesses have no basis in scientific fact, and were not observed by the witnesses themselves, nor any other expert in the field of scientific medicine. The claims presented are entirely hypothetical and the scarce scientific evidence they rely on to reach such hypotheses are either dated, not representative of the circumstances described in the case, or improperly interpreted due to faulty reasoning. Such efforts should not be permitted to stand as fact. No scientist would divert resources to investigating hypothetical claims that have no scientific basis, as there will naturally be little in the way of evidence to refute their findings.  One cannot defend against scientific claims that are wholly hypothetical, unvalidated, and implausible.


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