The Colin Norris case
The Colin Norris case is illustrative of the problems faced by the defence in relation to the lab test that identified the possibility of exogenous insulin administration.
There was a single lab result, in relation to a death, that revealed undetectable C-peptide with an insulin level of 12,408 pmol/L, combined with a blood sugar level of 0.6 mmol/L.
This was accepted by the jury as proof of exogenous insulin poisoning when combined with the evidence of the victim being in a coma before death, due to low blood sugar.
The test was clinical and could not be considered to meet forensic standards – no chain of custody for the sample and no repeat testing, for instance.
It was sufficient to convict.
It is possible that cases such as this convinced the defence that it was not possible to question the lab test.
Personally, I think this is mistaken. Each case should depend on its own facts.
It is the combination of the test with other supporting facts that pass the threshold for conviction. The clinical test in itself can only be viewed as strongly supportive (some will claim compelling) for the claim of exogenous insulin, and even then does not point to a particular perpetrator.
In the case of Colin Norris it was believed that hypoglycemia was extremely rare in elderly patients. This enabled the prosecution to link five additional cases to Colin Norris and claim a cluster.
Ultimately it was the cluster that led to the conviction of Colin Norris, combined with the index case for which a lab test result was available.
The case has been referred to the CofA by the CCRC and is under consideration.
The reason for referral is the development of scientific knowledge which impacts on the prevalence and understanding of hypoglycemia in elderly patients. New expert evidence now means the cluster of deaths may in fact be natural deaths.
Once the cluster falls away (if that is what the CofA decides) then only the index case with the lab result remains.
At that point there could be a number of possible perpetrators of the index case, not just Colin Norris as the statistical cluster is no longer present.
In the long term this may be helpful to the Letby case, where for some reason the likelihood of hypoglycemia in the two neonates was not eliminated as a possibility (based on my understanding of information in the public domain).
In the Letby case the lab result led to the expert witnesses constructing a narrative to make the lab result ‘make sense’ in relation to the surrounding facts, rather than considering whether it was in fact the lab result that was wrong given the surrounding facts.
If the case of Child L fell away, which is possible, then there would be less support for Child F. In the case of Child F the lab result sits uncomfortably with the fact of the TPN bag changes. There was also quite a discrepancy between the lab blood sugar level and those recorded by the neonatal unit. The lack of a chain of custody for the sample and the possibilities of lab errors becomes more realistic if natural explanations for the neonatal hypoglycemia exist.