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Injection of air into the gut

Air in the body cavity of infants has alternative antecedents, where the associated evidence relating to sudden collapse is not presented

In the cases of Child H and Child P, both infants had pneumothorax. Dr Evans did not make an effort to explain how the symptoms of air embolism can mimic those of pneumothorax. Given that pneumothorax is a differential diagnosis of air embolism, the failure to make this information apparent to the court constitutes a deliberate effort to avoid providing the full body of evidence surrounding the claims made in this case.  For air embolism to occur, the following must be present: a direct communication and a differential pressure gradient between the source of air and vasculature favouring the passage of air into the circulation. Risk factors for intracardiac air embolism are trauma, vascular interventions, barotrauma from mechanical ventilation or resuscitation and air leak syndromes (Jorens et al., 2009).  It is highly relevant that all the causes of air embolism in neonates require vast quantities of air to enter the body cavity and then exert pressure on different organ systems.  There is no discussion by Dr Evans as to how the action of a ventilator, which forces pressurised air at 100% oxygen into the lungs, or excessive CPR - in which air is pushed in without resistance due to the loss of circulation - could be replicated by the injection of air into a vein or through a nasogastric tube.  Dr Evans not only fails to demonstrate that the autopsy reports contain the necessary findings to demonstrate air embolism, he also fails to explain how the actions of Ms Letby could have mimicked the accounts of air embolism upon which he relies to prove his theory. 

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Examples of air embolism

In the sample case, Intracardiac Air Embolism (ICAE) was diagnosed after a thorough retrospective review of the chest radiographs performed during the sudden onset of cardiopulmonary deterioration.  Given that air embolism is characterised by air lock in the heart, positive findings must be made in the heart (Kalane et al., 2018).  There is no description of air in the heart made from Dr Evans. Instead he focuses on air collecting in other parts of the venous system or in the body cavity more generally.  It is not possible for him to allege that the infants died from air embolism without identifying an actual route of air entry and then quantifying the composition of the air.

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Example 2

In the second case, a Serial Chest radiograph at 24 hours, 60 hours and 72 hours of life showed presence of pneumothorax (right), pulmonary interstitial emphysema and pulmonary oedema at separate times. These findings were resolved by the end of the fourth day.  On the fifth day, while stable, he developed severe bradycardia (HR <60 beats/min), hypotension (mean BP <16 mmHg) and desaturation requiring extensive Cardiopulmonary Resuscitation (CPR). A chest radiograph taken at the time of resuscitation demonstrated the presence of air in the right and left side of the heart, inferior vena cava and hepatic veins. Despite receiving extensive CPR, the baby died.  The findings in this case do not mirror that of air embolism described by Dr Evans, notably the decrease in heart rate, and the desaturation preceded the need for CPR. There is a need to clarify the actual antecedents of air embolism in the neonatal population, as Dr Evans asserts that any set of symptoms he describes are sufficient to determine air embolism.

A recent study demonstrated that systemic air embolism is associated with CPR

In neonatology, reports of air embolism are confined to incidental case reports, and no neonatal post-CPR CT/MRI series exist.  A cohort study of unsuccessfully resuscitated non-trauma adults (sudden cardiac arrest, thromboembolism, n = 247) by Shiotani et al. showed that intravascular air was detected in 71% of post-mortem CT scans.  In a study involving the use of CPR in 56 neonates,  Halbertsma et al., 2015, showed that a similar proportion of neonates exhibited intravascular air in MRI/CT imaging.  However, these findings were not identified at the time of autopsy, suggesting that the observation of intravascular air was due to CPR and not from any event characteristic of accidental or non-accidental air embolism.

CPR and preterm neonates

Halbertsma et al., performed a prospective cohort analysis of neonates who were resuscitated either post-partum or during their stay on the neonatal intensive care unit (NICU), analysed  between 30 July 2007 and 31 January 2014. The neonates were included if they had received chest compression during the study period.  Of the infants studied, n = 43 (77%) received chest compressions in the delivery room.  For n = 13, chest compressions were required during NICU admission (due to e.g. intubation procedure complicated by hypoxia and subsequent bradycardia).  The study revealed that when chest compressions are performed for more than 5 minutes, the mortality rate is 80%.  This increases to 94.7% because four neonates later had their care withdrawn.  The study lends support that neonates requiring excessive CPR may be non-viable.  The finding draws significant doubt on the claim that the failure to resuscitate the infants at CoCH was specific to air embolism.  It appears that any event requiring CPR in the neonatal period is associated with mortality.  This study casts serious doubts on claims made by Dr Evans regarding the significance of the failure to resuscitate the infants.