Hypothesis: The death of Baby A may be attributable to a medical error in the NeoNatal Unit at the Countess of Chester Hospital

 Some weeks ago I described the complexities relating to the prosecution(s) and convictions(s) of Lucy Letby as a "complex matrix of competing hypotheses".

 See A complex spectrum of competing hypotheses

 In this post I want briefly to set out my hypothesis regarding the causation of the death of Baby A and the collapse of Baby B.

The hyptheses adopted by the prosecution was that Lucy Letby had murdered Baby A and had attempted to murder Baby B.

The jury (wrongly in my view) accepted that the prosecution's hypotheses were proven. Lucy Letby was (wrongly) convicted of the (supposed) murder of Baby A and Lucy Letby was also (wrongly) convicted of the (supposed) attempted murder of Baby B.

The hypotheses set out by the International Expert Panel were that there had been no murder of attempted murder.

My hypothesis is slightly different.

It is close to the hypothesis implicitly put forward by the International Expert Panel but specifically includes an element to the effect that there was a criminal act (or failure to act) at the Countess of Chester Hospital.

My hypothesis is that the death of Baby A may be the result of "gross negligence" by staff at the Countess of Chester Hospital and that the resultant death of Baby A may fairly be termed Gross Negligence Manslaughter.

 At this point in time I can only express it as a hypothesis ... a suspicion if you like.

On 7th June 2015 Babies A and B were born at the Countess of Chester Hospital.

The plan had been that the mother of Babies A and B would be delivered in, I believe, London due to the mother suffering from antiphospholipid syndrome. 

At least some forms of antiphospholipid syndrome are mediated by antibodies.

One effect of such antibodies is to predispose the person with antiphospholipid syndrome to thrombotic and/or thromboembolic events.

The sufferer from antiphospholipid syndrome is often given anticoagulants in order to reduce the risk from thrombi or emboli.

 My hypothesis assumes that the mother of Babies A and B had antibody-mediated antiphospholipid syndrome and was on an anticoagulant, very possibly warfarin.

It is well known that warfarin can cross the placenta and can cause warfarin embryopathy.

Similarly, late in pregnancy it is well-established that antibodies cross the placenta and provide a measure of immunological protection in the neonate.

In my view it is likely that both Babies A and B had antibodies (from their mother) which predisposed them to thromboembolic events but also had an unknown amount of warfarin which provided some measure of protection against such thromboembolic events.

It is likely (but I've seen no direct evidence that it happened nor its timing) that both Baby A and Baby B received (routine) Vitamin K in the Delivery Suite or in the NeoNatal Unit.

Vitamin K, simply speaking, reduces or removes the anticoagulant effect of warfarin.

 By giving Vitamin K (as I assume happened) Babies A and B were exposed to the unopposed risk of thrombotic and/or thromboembolic events from the mother's antiphospholipid antibodies.

The result?

Both Baby A and Baby B had thromboembolic events.

Baby A was, in a sense, unlucky with a thrombus or embolus affecting the brain stem or an important structure in the heart causing a fatal collapse.

The bizarre skin phenomena were tiny thrombi or emboli reaching the skin and breaking up or dissolving.

Baby B was, in a sense, lucky. There was a thrombus or embolus reaching a vital structure causing a collapse but the luck lay in the breaking up of the thrombus or embolus enabling resuscitation of Baby B to succeed.

Again the bizarre skin phenomena were tiny thrombi or emboli reaching the skin and breaking up or dissolving.

At the moment I can't be certain that either Baby A or Baby B was given Vitamin K.

I can find no mention of Vitamin K in the reports of the first trial of Lucy Letby.

But if Vitamin K was administered it seems to me to make the case for Gross Negligence Manslaughter.

Let me briefly explain my reasoning.

The Crown Prosecution Service Guidance on Gross Negligence Manslaughter is here:

 CPS Guidance: Gross Negligence Manslaughter

 The relevant part of the Guidance seems to me to be the following:

In order to prove the offence, the prosecution must therefore establish the following elements:

a) The defendant owed a duty of care to the deceased;

b) By a negligent act or omission the defendant was in breach of the duty which he owed to the deceased;

c) The negligent act or omission was a cause of the death; and

d) The negligence, which was a cause of the death, amounts to gross negligence and is therefore a crime;

 In my view the "negligent act" was to give Vitamin K (as I assume to have happened) Baby A and Baby B.

The predictable effect of giving Vitamin K was to increase the risk to Baby A and Baby B of thrombotic and/or thromboembolic events.

The results?

Baby A died, in my view due to Gross Negligence Manslaughter.

Baby B collapsed but was resuscitated.

Who might be the suspect(s) for the hypothesised Gross Negligence Manslaughter of Baby A?

It seems to me that Dr. B is a prime candidate.

From reports of evidence given at the first trial of Lucy Letby it seems likely that Dr. B was the consultant in charge of the care of Baby A and Baby B.

If anyone has knowledge of whether Babies A and B were given Vitamin K I would appreciate pointers to the relevant evidence.

At the present time this is a blog post expressing a hypothesis, not a report to Cheshire Constabulary of suspected Gross Negligence Manslaughter by Dr. B and/or others.