The Lee Review

Compared and contrasted to the prosecution and my own review of the clinical evidence and testimony

Many of you will be aware that a press conference was convened by Sir David Davis MP and Lucy Letby’s new barrister Mark McDonald at which Professor Emeritus Dr Shoo Lee delivered the report of an independent expert review committee that voluntarily gave their time and expertise to review the medical cases for each of the Countess of Chester Hospital (CoCH) neonates. I met with Sir David at his home during 2024 when he was embarking on this review of the Letby prosecution and he struck me as an intelligent and thoughtful man with an engineering and analytical background - someone who whilst being a politician was actually eminently suited to overseeing and understanding the often technical way that we science types work.

In this brief article I will look at two of the neonates that are included in the summary report from Professor Lee’s review committee, and I will contrast the prosecution and my own original position with theirs.

Child A/Baby 1:

Child A’s mother had anti-phospholipid syndrome (APS), an autoimmune disorder wherein the patient’s body mistakenly believes its own natural substances are infective and, as a result, leads to the creation of antibodies that attack the organs and tissues. In the pregnant woman this is further complicated by the fact that pregnancy itself is a weird and complicated immunological challenge wherein the foetal tissues and placenta are already being actively protected from immunological activation by the mother’s immune system. Put basically, the placenta and baby contain material that is 50 percent foreign to the mother because the foetus is a combination of both the maternal and paternal DNA, and during the pregnancy process the mother’s immune system goes through a dysregulation process that supresses immune response where it concerns the placenta and developing baby, while being alert for placental shedding into the mothers blood stream and cleaning up the remnants of that process in order to prevent inflammation and issues elsewhere in her body. When this immunosuppressive process breaks down, elevated maternal blood pressure and another autoimmune condition called preeclampsia can be the first sign that things have gone, sometimes fatally, wrong. The antibodies released by the autoimmune process that results from APS can cause blood clots to form in arteries and veins in many places including the legs (DVT), lungs (pulmonary embolus) kidneys (renal embolus) and spleen (resulting in splenic infarction). A large European cohort study found that between 5-40% of deaths in patients with APS result from these clots.

The Prosecution Position: The prosecution allegation before the jury during the first trial revolved around Dewi Evans’ claim that Child A died from complications caused by an air embolus injected by Ms Letby into an intravenous (IV) catheter. It was claimed this air embolus would have acted much like a blood clot, by blocking blood flow and causing the neonate’s collapse, resulting in the then unreported blotching or discolouration on Child A’s skin and his death.

My Original Position: As I noted in my original report on Child A, he and his twin Child B were born by emergency caesarean section (EMCS) after their mother, who had this APS autoimmune disorder, became gestationally hypertensive - that is, she had high blood pressure during pregnancy that can often be the first sign of serious trouble. This led obstetricians at CoCH to believe she was, or was becoming, preeclamptic. Preeclampsia was an outcome should not have been unexpected by her clinical team. A young girl develops Type 1 Diabetes Mellitus (T1DM) which itself is an autoimmune disorder. In her teens or early twenties she goes on to develop Systemic Lupus Erythematosus (SLE or Lupus) and, in later life, she tragically develops an autoimmune thyroid disorder. This occurs because, as we have known for many years, one autoimmune disorder often leads to another... and another... and... so on. The autoimmune mechanisms such as aberrant Natural Killer (NK) cell biology that cause disorders like APS, T1DM and SLE are the same ones most often involved in preeclampsia.

Preeclampsia is often an advanced sign of a poorly perfused placenta - that is, the placenta that feeds and nourishes the developing baby is receiving inadequate blood supply from the mother. Babies born to mothers with gestational hypertension are often smaller than a normal baby because the effect of hypertension is to restrict blood flow to the baby and, by extension, to limit foetal growth - what we describe as small for gestational age or SGA babies. Approximately 1 in every 10 mothers has some form of hypertensive disease during pregnancy. While the rate of SGA babies born to mothers who do not have hypertension during pregnancy is around 9.8%, this increases to over 15% (1 in 7) for mothers who have low-grade hypertension, 25% (1 in 4) for mothers with severe gestational hypertension, and 37% (1 in 3) for mothers like Child A’s who are showing signs of an autoimmune liver disorder known as HELLP syndrome.

Child A went without fluids for between one-third and half of the day shift due to tissued IV cannula and the resulting insertion of an initially malpositioned but reinserted umbilical venous catheter (UVC). Child A’s fluid balance was in severe deficit during his first day such that, along with the reasons for his surgical birth, the potential implications of his mother’s autoimmune disorders, and the fact that his charts showed a gradual decline during much of the day, there were sufficient reasons for concern regarding his wellbeing even before Ms Letby arrived on the ward that evening. It was a miracle that he was not SGA (he was born at 1.66kg which is slightly higher than the 1.5kg average weight of a 31 week gestation premature neonate). It should not be forgotten that Child A was cared for on the unit and in the same room as his sibling, Child B, and another child identified as Baby Jacob. Baby Jacob twice developed severe sepsis from hospital acquired bacterial infection while in the same nursery room and during the same 8 day period that Child A, B and C were present, and in which Child A, C, and one week later, Child D, died.

Child A was the first of this group of neonates to be treated for suspected sepsis, and my original position when reviewing the documentation and testimony and writing my article was that a sequence of three things led to Child A’s demise: (i) that Child A acquired a bacterial pathogen that was already present in fixtures, fittings and possibly even in the air of the CoCH neonatal unit, (ii) that this infection, even once suspected (as had been noted by Dr Beech), was not properly and competently treated, because (ii) the medical staff present lacked the competence required to care for these at-risk neonates.

The Lee Review Position: The reviewers for Child A noted that the mother not only had APS, but also an uncharted but nonetheless common complication of liver issues during pregnancy, cholestasis of pregnancy. Cholestasis of pregnancy occurs when bile that is usually stored in the gallbladder builds up within the liver and results in that bile being released into the bloodstream, sometimes causing the outward appearance of jaundice (yellow/orange skin and yellowing of the sclera of the eyes). They identify the potential for the mothers antibodies to have passed via the placenta and into Child A, potentially resulting in thromboembolism, which is more likely where there is infection. Given that Child A’s suspected sepsis and antibiotic bolus were both administered shortly after birth, and before he was sent to the neonatal unit, the presence of infection may very well have been a contributory factor. The reviewers noted that two central line catheters were present, without infusion, for at least four hours, and report that it is possible, and not uncommon, for these to develop a clot at the tip of the catheter that, when infusion is recommenced, can detach and travel through the baby’s blood stream to vital organs and the brainstem. They contend such a clot was Child A’s primary cause of death - that it travelled from the catheter tip and likely lodged in the brainstem, causing the sudden crash only minutes after the IV infusion was reinstated and resulting in the inability to resuscitate. They support this contention with evidence from the post mortem of Child A that disclosed recent non-occluding clots in the vasculature of the liver, showing Child A had had a thrombotic event in close proximity but prior to the time of death. They also identify the possibility of foetal vascular malperfusion, and note that it often results in sudden collapse 1-2 days after birth.

Outcome: Unlike the Prosecution and Dewi Evans’ position, which I believe I described at the time as requiring quantum leaps of logic, my original position was neither antithetical to or in contradiction with the evidence placed before the jury, nor with the findings of the Lee Review empanelment. While the post mortem findings for Child A were not available to me at the time, I had identified and discussed many of the contributory factors relied upon by the Lee Reviewers to draw their eventual conclusion. I therefore support their findings and believe both theirs and my own view of the evidence is clinically and legally more reasonable than that of the Prosecution and Dewi Evans[1].

That said, I strongly believe two things played out that affected the jury’s view of that evidence. First, it was presented in an intentionally fragmentary way such that I could see nothing put before the jury that was laid out, similar to my article for Child A, in complete and chronological order. The prosecution approach of chopping and changing witnesses who would take the stand briefly to evidence some fragment of the whole story, be stood down while other witnesses did the same, only to retake the stand later in the proceeding to adduce yet more fragments was confusing at times even for those of us who are legally trained - but imagine what it was like for a jury of non-legally or medically trained people. Second, that the jury, like the rest of us, were kept in the dark regarding both evidence that did not suit the Prosecution’s version of events (the post mortem report, the full ramifications of the mothers medical conditions etc.) and that knowledge of these things should have, as it did for me, update their belief regarding the process and causes for Child A’s demise.

Child F/Baby 6:

Child F’s mother also gave birth to twins (Child E and F), delivered premature at 29 weeks 5 days (29⁵) by emergency caesarean section (EMCS). Child F required resuscitation at birth, and because of mild respiratory distress was intubated, ventilated and received surfactant to prevent alveolar collapse shortly thereafter. While he was 1.434kg at birth, within the first 24-40 hours he had lost approximately 10% of his birthweight. This is not unusual, but is something that we are keenly aware of to ensure that the baby’s weight recovers within a very short time. Child F’s time at CoCH was marred by contradiction - he was in good condition yet he needed resuscitation and intubation, he was hyperglycaemic and shortly thereafter hypoglycaemic, he was doing well and had no unusual readings yet even as evidence for sepsis was becoming more apparent, was still only considered to have suspected sepsis. And, according to most in the mainstream media who sought to portray Ms Letby as the insulin-poisoning baby murderer, he had either categorically never been prescribed insulin or they remained entirely silent as to whether he had been prescribed the drug... or, as one single journalist begrudgingly wrote, he had been prescribed a tiny dose. Given that the dose involved was 0.2units/kg/hr via a syringe driver, it might sound to adults like a tiny dose. However, for a neonate, it is actually quite a significant dose that would see the premature 1kg baby potentially receiving almost 5 units of insulin over a 24 hour period. At around 1.3kg after the initial drop in birthweight, Child F would receive around 6.25 units over a 24 hour period - a not inconsiderable dose. Rather than receiving a single subcutaneous dose of a couple of units like an adult diabetic might - to be gradually taken up by the lymphatic system, Child F received his insulin infusion directly into his blood stream (intravenously) for around three hours, receiving in total around 0.8 (80%) of a whole unit. There were other interesting issues such as the insulin test that was 1.3 at 5:56pm when the blood was drawn and sent to Royal Liverpool Hospital, but had returned to the previous level of 1.9 only four minutes later at 6:00pm even though, aside from taking blood, no actual treatment had been performed.

The Prosecution Position: The now infamous prosecution allegation was that Ms Letby had ‘doped’ or poisoned one of the intravenous (TPN) feed bags in the unit fridge that had been pre-prepared and sent up by pharmacy, with insulin. To support this claim they produced a test result showing that Child F had high insulin values but low c-peptide levels, which they said indicated the presence of administered exogenous (not naturally occurring or from outside the body) insulin.

My Original Position: My original take on the Child F situation was to identify the many contradictions and identify situations and circumstances that might have led to Child F potentially receiving insulin incorrectly. After all, it happens all the time in hospitals that some variation of the wrong patient receives the wrong dose of the wrong medication at the wrong time via the wrong route - in nursing we teach something called the five ‘rights’ that must be present before you administer any medication to a patient... simply substitute ‘right’ for every ‘wrong’ in my previous sentence and you will understand what I mean. In this case I observed that Child E, Child F’s twin, had been receiving insulin infusions prior to his death and it was possible that medication and TPN feeds labelled for Baby Surname had been mis-administered to the other Baby Surname. While babies are given dual labels (one on their wrist and another on their ankle) and nurses are supposed to scan the code or patient number on these labels prior to administration, it would not be the first time that a quick look to check it said the right surname has resulted in such a seemingly simple mistake. In fact, we saw an example during the first Letby trial where the unnamed nurse who was responsible for Child F at one point admitted co-signing as having witnessed administration of a medication that was documented as having occurred at 2am during a different shift - and which therefore she could not have actually seen because she was not present during that other shift.

I proposed that there were several issues not limited to: (i) use of the incorrect test or a test used by an untrained or inappropriate person or on the wrong equipment - supported by the fact that the test used at Liverpool Royal Hospital to test the blood was specifically not supposed to be used by the hospital analyst for the purpose that the prosecution sought to use it for during the trial; (ii) a medical misconception unsupported by research regarding the belief that high insulin/low c-peptide means exogenous insulin administration and murder/poisoning - as supported by the research of Prof Vincent Marks; (iii) that previous research and cases have shown that tests for one type of insulin (for example, porcine insulin) may show wildly variable results when used to test for horse or human insulin; and (iv) the clear physiological evidence of sepsis that doctors were barely acknowledging as ‘suspected sepsis’, and that sepsis actually causes insulin/glucose dysregulation (there are studies actually showing that the body will release vast amounts of insulin to be used in its secondary role as a broad and non-specific anti-inflammatory agent, and that some tests during sepsis will show the high insulin/low c-peptide result during sepsis). My conclusion rested on Child F being another victim of pathogenic nosocomial bacterial infection and sepsis.

The Lee Review Position: The Lee reviewers described Child F as borderline for intrauterine growth restriction (IUGR), a condition that means he was receiving insufficient nutrients in the womb due to either a poor quality placenta or poor quality blood flow, and would not have grown to the size that we might have been expected. I find this particular diagnostic statement odd given that the average foetal weight at the start of 29 weeks gestation is around 1.1kg, and at the start of week 30 (the end of week 29) is 1.3-1.4kg. It is possible the reviewers had access to a customised growth chart for Child F that predicted a larger weight, but such a chart was not included in the bundle presented by the prosecution and does not appear to have been disclosed to the jury during the trial.

The Lee reviewers highlight my own identification of sepsis (actual sepsis, not suspected sepsis), and identify that the CoCH doctors should have administered higher glucose infusions earlier. They also identify the issue that administration of bolus doses of glucose, as the inexperienced CoCH doctors had ordered, causes insulin surging (or yo-yo-ing) and actually amplifies the hypoglycaemic effect. They also identify another issue that I discussed at length in my own article, that in order for the TPN bag to be poisoned with insulin it would have to have been in multiple bags, because Child F actually received TPN from two different bags over the course of the day. In following first principles, the Lee reviewers actually found that the c-peptide level was not unusually low for a neonate (within the 20-45^th centile), that Child F’s potassium levels were normal (insulin decreases potassium), that Child F’s glucose levels would have been much lower had exogenous insulin been present, and point to studies showing that the insulin/c-peptide ratios are completely different and imbalanced for neonates and that the immunoassay used are, as I had posited, unreliable due to such things as the interference of sepsis, but also due to the presence of antibiotics in the bloodstream. They conclude that Child F suffered from poor medical management of hypoglycaemia and the hypoglycaemia was, as I had suggested, the result of sepsis.

In conclusion

What we see from Professor Lee and his team of highly qualified experts is the thorough and thoughtful analysis that should have occurred prior to the first Letby Trial. Unlike the tendentious, biased and self-aggrandising reports and testimony of Dewi Evans, we see a report that, not unlike my own substacks for each neonate, has considered all of the evidence available to them. Note that they had even more material to consider than was made available to me at the time, from which they have drawn conclusions that actually describe the signs, symptoms, observations and outcomes for each infant. Their primary report that I will come to review more fully in the next few weeks, focuses heavily on poor medical management and infection - the pathogenic bacterial sepsis and NEC that appear to have been infesting the unit and infecting the neonates. Their report, along with much of the recent evidence of allopathic (doctor-caused) harm not only dispute the prosecution claims in every case, but actually suggest people other than Ms Letby should have faced charges for their conduct in treating these babies. We can only hope that reason prevails and Ms Letby’s life is restored to her in short order - and that the public are properly told how this ill-conceived injustice was allowed not only to occur in the first place, but was allowed to persist by our Court of Appeal.

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I have been neglecting my Substack of late due to the overwhelming need to work, sometimes 12-15 hours each day, in order to maintain my income and keep my extremely tenuous academic post. As described in two previous posts, I have been regularly attacked for my involvement in research on issues related to Covid and the Letby trial. I have even had official complaints made to my university employer by such people as retired nurses who are clearly so enamoured of the mainstream media baby killer narrative that they see my work as ‘supporting the baby killer’. The only upshot of such complaints is that I may unfortunately have a lot more time available for my substack reports… but whether my family will eat and pay its bills is another matter.

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Thank you

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[1] Leaving aside that it seems Evans has chopped and changed his so-called clinical and expert opinion on these cases.