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Based on the evidence available, it is not possible for Dr Evans to reach the conclusion that air embolism was a cause of death

There are numerous issues with Dr Evans’ claims surrounding air embolism and they should be addressed before any matter concerning his expert opinion is relied upon by the court. Dr Evans uses none of the basic standards required to make his determination that the cause of death in any of the seven cases is due to air embolism.

The expert opinion is not reliable

It is the assertion of Dr Evans that the vast majority of infants in this case experienced symptoms that are attributed to air embolism. Moreover, Dr Evans’ forensic investigation began a number of years after the autopsies were performed. The autopsies established a cause of death for each infant. The reports did not conclude that air embolism played a role in the events leading to death. Additionally, there is little conformity with regard to the findings from the autopsies. Only two infants reveal similar conditions at death and these are unrelated to air embolism.  Child C and Child I revealed hypoxic ischaemic damage to the heart and other organs. These are not findings attributed to air embolism, but rather point to some event that caused inflammation in the myocardium. There are a number of issues with regard to Dr Evans’ investigative procedure, and these should be subject to proper scrutiny, as per Criminal Practice Directions CPD V Evidence 19A Expert Evidence 19A.5: “factors which the court may take into account in determining the reliability of expert opinion, and especially of expert scientific opinion, include: 'whether the expert's methods followed established practice in the field and, if they did not, whether the reason for the divergence has been properly explained.’”

Relevant information was not factored in to Dr Evans conclusions

The absence of bodily fluids to conduct specific metabolite and molecular testing guarantees that an investigation, as performed by Dr Evans, which rejects autopsy findings, is based on his opinions and little else. The importance of blood being taken at the time of death cannot be overstated. In a hypothetical case involving a pair of twins with one survivor, a blood sample from the deceased twin could be used in a whole battery of molecular investigations, and these could inform the investigator of physiological outcomes that occurred in the surviving twin. One cannot obtain a better control in a biological study than a genetically identical twin. The number of twin pairs in the case reflects a missed opportunity to gain insight into the occurrence of the symptoms described. It is curious that Dr Evans fails to investigate the increased prevalence of multiple births in this case. Recent studies into causes of sudden postnatal collapse reveal that 25% of fatal collapses occur in babies born as a twin pair. Indeed, this case involves a disproportionate number of twin pairs, and this is a pattern that should have been investigated further by Dr. Evans. The finding that in the first days of birth, twins born in the same pregnancy exhibit similar symptoms within a 24 hour period is indicative of an organic origin which has its roots in the womb environment. It is fantastical to take the higher incidence of twin births, associated with complications, and attribute that to wrongdoing, when such a phenomenon is consistently reported in the literature.

The basis of the claims are unfounded

In reaching his conclusion that air embolism was the cause of death in every instance, Dr Evans relies upon the review of clinical notes and a selective interpretation of some autopsy radiographs and images. Clearly, for Dr Evans’ opinion to stand as a conclusion that is scientifically valid, it requires that he cannot also tolerate the conclusions made in the five cases where a cause of death was determined by autopsy. Moreover, Dr Evans was working in the dark regarding the most crucial factors which could provide significant clarity in the cause of death. The failure of medical doctors to collect any serum or bodily fluid samples at time of death prevents a thorough assessment of the molecular underpinnings associated with the death of the infants. There is a distinction between the skills required for the delivery of medical treatment and the skills employed by scientists when conducting an investigation. In the former case, the practitioner has wide latitude to make decisions as to what treatment approaches to apply. In the case of a scientific investigation, the approach adopted cannot be subjective. The aim of an investigation is to uncover the causative elements through a systematic analytical process. It appears that Dr Evans has applied his medical treatment approach to conducting a complex scientific investigation into the collapse of 18 infants, without any regard for the stringency such an investigation demands. Dr Evans is unconcerned by the lack of molecular evidence in the case, which is likely due to his failure to understand the level of precision that is required to make a determination of air embolism or any other condition as a cause of death. The molecular evidence is essential to the determination of cause of death, and it is on a par with evidence such as a footprint, fingerprint or DNA sample left at a crime scene (Cunningham, 2017).    

The basic scientific standards for air embolism have not been met

Dr Evans provides no evidence that is supported in the field of forensic science which points to air embolism as a cause of death. Moreover, there is an abject failure to provide the court with the minimum scientific standards required to determine air embolism (Banjanowski et al., 1999; Bolliger and Thali, 2015; Jorens et al., 2009) . It might surprise the reader, as it did us, that none of these scientific standards have been investigated by Dr Evans, and nor can they be because such an investigation must occur at the time of autopsy. Furthermore, there is no supporting evidence which shows that air embolism can cause such a wide array of physiological outcomes as reportedly occurred in the infants. Desaturations are weakly associated with air embolism, but are highly prevalent in premature infants due to their immature brain development, which delays the onset of respiratory control. In cases of air embolism, desaturations occur in the immediate two minute period prior to fatal cardiac arrest. Therefore, in those instances where desaturation occurred absent a fatal cardiac arrest, they cannot be attributed to air embolism. This means that Dr Evans cannot rely on the occurrence of desaturations to support his air embolism theory where they are not associated with death. These foundational issues must be addressed before tolerating the assumption that Dr Evans’s expert opinion is based upon a standardised and thorough scientific investigation into the cause of death.

Air embolism as a cause of death

The heart is the key organ that reveals air embolism

It is necessary to provide a simple description of air embolism, as this will facilitate a greater understanding of the autopsy approach described in this report. Air embolism consists of an interruption of the circulatory system by bubbles of air (or other gas) that gain access to the circulation, usually through the venous side. An air bubble forms in the blood and enters on the venous side where it moves towards the heart.  The venous system contains deoxygenated blood which is high in CO2, and this blood is returned to the heart such that it can be pumped through to the lungs where the CO2 can be exchanged for oxygen. The air bubble contained in the blood enters the heart through the vena cava (superior or inferior), and becomes trapped in the right ventricle, blocking the pulmonary artery. This air block causes air embolism. The air usually remains in the right side of the heart, pulmonary trunk and arteries. The air rarely emerges on the pulmonary vein side. Death is usually immediate, but can be delayed by up to about 2 hours.

Almost the only mechanism of death is 'pump failure of the right side of the heart. Air fills the great veins, right atrium and right ventricle, causing the blood to become frothy, which prevents it from being pumped on by the heart in systole because air is compressible. Air will not penetrate the pulmonary capillaries in any quantity unless some vascular shunts are present. The frothy blood will not be seen in the left side of the heart except in cases of dysbarism (where ambient air pressure changes at a pace too rapid for the human body to adapt, see decompression sickness).

Air embolism can only be determined using the correct autopsy method

A determination of air embolism requires the performance of a specific autopsy.  A consequence of the autopsy is the identification of multiple key findings which provide an overall consensus that death was due to air embolism. The figure provides an overview of the autopsy approach that must be performed in order to make a determination of air embolism. This protocol is fairly simplistic, when performed by a pathologist.  In the case of the infants at CoCH, it does not appear any such investigation was performed. It should be noted that a peer reviewed article cited by Dr Evans describes some of the findings required in this autopsy approach. However, Dr Evans fails to identify any of these findings in his investigation. Despite not finding key elements attributed to air embolism, Dr Evans proceeds to use radiographs and other images of dissected organs to support his air embolism theory. The basic standard for the detection of air embolism, in medicolegal matters, does not permit a determination of air embolism by radiographs and dissected organs. Air embolism can only be diagnosed at the time of autopsy and through a positive determination and analysis of extracted air from the right ventricle. Recently, Magnetic Resonance Imaging (MRI) and Computed Tomography (CT) approaches have been combined with autopsy to confirm air embolism (Christian Jackowski et al., 2004), however no such methodology has been used by Dr Evans. An autopsy for air embolism requires the following: 1. Posterior to anterior dissection, with clamping of major veins and arteries. The organ is removed from the body and submerged in water, the clamps are removed and the specimen is observed to detect the presence of air bubbles. An exception to this approach is the mesenteric vasculature. These vessels stay intact in the body and water is poured into the abdominal cavity and the specimen is observed for bubbles. It must be noted that air contained within smooth muscle structures as the large intestine, bladder or gut, are not indicative or determinative of air embolism. 2. The lungs are similarly inspected for any occurrence of tension pneumothorax which may resemble air embolism. Thus, any pathological findings in the lungs, such as pneumonia, pneumonthorax, or immaturity of the lung should raise doubt as to air embolism as a cause of death. 3. The key organ for establishing air embolism is the heart. This should have been made abundantly clear in Dr Evans’ reporting to the court. Without findings of abnormal quantities of air in the heart, it is impossible to assert air embolism as cause of death.  The figure below provides an overview of the autopsy approach that must be performed in order to make a determination of air embolism. 

Dissection of the heart and analysis of extracted air

A thorough investigation of the heart is a necessary  requirement in the autopsy approach to identify air embolism. Dr Evans reporting to the court does not provide any information on the autopsies concerning abnormal quantities of air in the heart.  This is but one essential finding required to assert air embolism as cause of death.

Removal of air from the right ventricle

The autopsy procedure requires that removal of the heart is performed under water, to prevent the loss of air from the chambers of the heart. An aspirometer is used to extract the air from the right ventricle. A syringe needle is attached to the end of the aspirometer.  The right ventricle is pierced using the needle and the air is collected by the aspirometer.

The presence of air in the body cavity is not confirmation of air embolism

The finding of air in the body cavity of the infants cannot be attributed to air embolism. Following death, It was reported that the infants were bathed and then in many cases warmed. When blood is warmed in a body that has no circulatory pressure (as in a dead body) the gases in the blood will begin to shift owing to the decreased pressure in the vasculature. In turn, the gas in the blood becomes less soluble and this causes bubbles to form.  The treatment of the infants following their demise could have caused bubbles to form in the vasculature.  This is another reason why it is not possible to determine air embolism by reviewing x-ray images alone.

Skin mottling is unrelated to CPR and points to viral infection

Dr Evans described the mottling observed in some of the infants as being indicative of air embolism.  The closest description of such skin manifestations is observed in parechovirus/enterovirus infection, and is demonstrative of sympathetic nervous system arousal.  The mottling occurs due to adrenaline. Adrenaline in the nerve terminals can constrict arteries to change blood flow. This can happen when the brain gets inflamed and is a way to divert oxygen to the brain. The binding of adrenaline to its receptors on arteries results in vasoconstriction and subsequent changes in blood flow patterns. The relative discolouration of the skin is a function of blood flow patterns.  Where constriction of arteries occur due to the release of adrenaline, the distal limbs, such as the legs, will exhibit a noticeable pallor, and the local pooling of blood in other areas of the body can make them appear swollen and discoloured.  


The medical doctors at CoCH described a fluctuating colour pattern in the neonates. The cause of these changes is the relative saturation of adrenaline binding to receptors on arteries. The colour changes recede because the adrenaline and the receptor complex have a relatively short half-life. Loss of adrenaline activity will cause a return of the normal skin colour.

Adrenaline plays a core role in regulating heart rate and may have been the cause of the increased incidence of tachycardia observed in the neonates, and even the primary factor initiating cardiac arrest. The release of adrenaline from the adrenal gland occurs in response to environmental and physiological stresses.  In nearly all the cases at CoCH, the infants first presented with moderate-severe tachycardia.  Ultimately, adrenaline is a fast acting hormone, which can rapidly cause changes in blood flow, heart rate, and metabolism.  The release of adrenaline is a compensatory mechanism experienced upon contracting infectious disease and through environmental stressors.  Adrenaline release in response to invasion by infectious pathogens plays a primary role in dampening the innate immune response (Kox et al., 2014).  This serves an important function, as excessive innate immune  reactivity due to host infection is associated with cytokine storms.  Cytokine storms describe a massive molecular event due to upregulation of proinflammatory cells and the release of pro inflammatory factors. When left unchecked, innate immune reactivity can cause disseminated intravascular coagulation, resulting in internal bleeding and death (Yang et al., 2021). 

Skin manifestations due to changes in blood flow, apnoeic events and sudden death are features of Covid-19 infections.  The appearance of transient skin manifestations in the context of infectious diseases may reflect an attempt to limit innate immune reactivity through the release of adrenaline, in order to prevent the onset of a lethal cytokine storm.  However, adrenaline release must be carefully regulated because it is equally associated with tachycardia, due to increased peripheral vasoconstriction, pulmonary venoconstriction and reduced left ventricular compliance.

Air in the spinal cord is related to excessive force due to CPR

When an infant stops breathing, there is a loss of the pressure-volume relationship occurring during respiration. Likewise, the loss of heart rate causes a loss of effective blood perfusion. Cardiopulmonary compression will result in a recurrence of the pressure-volume relationship minus biological resistance. Thus, compression on the chest will result in the air pumped through the mouth being forced in opposition to its concentration gradient, which will likely result in thoracic and lumber accumulation of air. If the infant is not respiring, the inspiration of air is occurring without sufficient expiration. This increases the risk of air embolism, as the air will always move to the area of lowest concentration. The line of air in the spinal column of one infant is a condition called pneumorrhachis. In this condition, the air is observed in the lower thoracic and lumbar area and is indicative of the direction of dissection. Its occurrence is due to aggressive CPR, as was the case in above figure, which was taken from the post-mortem radiograph of a young infant (Krupik, 2012).

Child A and Livedo Reticularis

Dr Evans' failure to conduct a proper investigation is evident from his review of Child A and B. These infants were born to a mother with antiphospholipid syndrome - a condition associated with stillbirth and placental issues. Although maternal APS (mAPS) is not associated with adverse events in newborns, there are a number of case studies that suggest there are circumstances where mAPS may be a harbinger of physiological challenges in neonates. In a case study, "a male, preterm born twin infant, whose mother had been diagnosed as primary APS, developed thrombocytopenia, livedo reticularis, pericardial effusion and thrombosis of the left subclavian and external jugular veins concomitantly with severe respiratory tract infection soon after his delivery, that culminated with his death two months after the birth, in spite of the large spectrum antibiotic therapy and all supportive measures.” (Robin and Santiago, 2006). 

Subsequent to the infant’s death, blood testing revealed the infant had high antibody titers associated with APS, which suggests that his demise was linked to an enhanced autoimmune response associated with APS. This case is highly relevant to Child A and further highlights the difficulties in determining cause of death without any blood and serum samples. It is notable that the infant in the case study was a premature, male twin, who exhibited physiological challenges immediately after birth, and he was described as having Livedo reticularis. It is essential that the court be exposed to case studies, such as that presented here, as they raise serious doubt as to the reliability of Dr Evans’ claims.

Skin manifestations and air embolism

The  ‘rash’ described by the medics is not a rash at all.  A rash is regulated by a local histamine action, which is released due to local inflammation of the tissue. The skin manifestations described in the infants appears to be linked to blood circulation and is, at best, a skin manifestation.  It is apparent that the skin manifestation observed in the infants is called livedo reticularis and is associated with a wide number of conditions. What seems not to be understood is that livedo racemosa is what occurs in decompression sickness and this is a distinct entity from livedo reticularis. “The pathology of livedo racemosa is well described as a thrombotic/embolic occlusion of arteries. This concept of arterial occlusion suggests that the decompression-associated livedo racemosa may be also caused by arterial gas embolism.” In the paper quoted above, it was confirmed that decompression illness is associated with livedo racemosa. This same skin manifestation cannot be what was observed in the infants, because Livedo Racemosa occurs due to an air embolism in the arteries. However, Dr Evans asserts that Letby injected air via the lines going into the infant. None of these lines were arterial lines. Further, the expert witness describes air in the venous system in the lungs and brain. In short, the air embolism and rash theory does not stack up because the claim by the prosecution expert is that air is injected into the veins, but the skin manifestations that occur in decompression sickness and air embolism occur due to air in the arteries. The paper concludes: “In conclusion, in diving medicine the term cutis marmorata/livedo reticularis is used incorrectly for describing the actual pathology of livedo racemosa.” (Harris et al., 2020).  Skin manifestations similar to those described in the infants routinely occur in enterovirus and parechovirus infection.   Despite sepsis being a differential diagnosis of air embolism, Dr Evans makes no mention of other physiological changes that might result in the skin manifestations that were reported.

Dr Evans fails to consider a differential diagnosis

The differential diagnosis for air embolism include:  * Acute myocardial infarction * Heart failure * Tension pneumothorax * Septic shock * Ischemic stroke None of the differential diagnoses for air embolism were discussed by Dr Evans, nor was any effort made to explain how they were ruled out, especially in the infants who exhibited lung complications, such as pneumothorax.  Dr Evans’ failure to explain why differential diagnoses were not more fitting to the cause of death/harm makes it difficult to determine whether the investigative approach taken was appropriately rigorous. Dr Evans should at least have provided an explanation as to why none of the differential diagnoses are not more applicable to the cause of death when compared to air embolism.

If air embolism substantial enough to have caused death is present, frothy blood will be quite evident oozing from the ventricular lumen, almost invariably the right. If this is apparent, however, it will almost certainly already have been seen on the pre-autopsy radiograph.

Bajanowski et al., 1999

"Proof of Fatal Air Embolism"