Blood gases and lactate — what natural deterioration looks like on the chart
Prosecution claim
Clinical-chart records including arterial blood-gas values, lactate trends, and oxygen saturation were used by the Crown's experts to describe deteriorations as sudden, unexpected, and more consistent with deliberate harm than with natural causes.
Counter-evidence
Natural clinical deterioration in critically unwell neonates produces characteristic blood-gas and lactate trajectories: rising lactate (reflecting anaerobic metabolism during tissue hypoxia), falling pH (metabolic acidosis), rising pCO2 (respiratory failure), falling base excess, and eventual oxygen-saturation instability. These trajectories are documented in the UK National Neonatal Research Database as the standard pattern for NEC, sepsis, overwhelming IVH, and cardiovascular collapse. The specific trajectories presented at trial are, on independent Panel review, consistent with natural deterioration rather than abrupt iatrogenic or deliberate events. A deliberate air embolism, by contrast, would typically show a characteristic abrupt-onset pattern rather than the evolving metabolic picture documented in the clinical charts.
The chart tells a story. The story the charts tell in these cases is of critically ill preterm infants decompensating along recognised natural-cause trajectories — not of abrupt, iatrogenic events.
What the jury heard
The jury was shown selected blood-gas and chart values and asked to weigh the Crown's expert interpretation of them. The full reference-distribution context — what these values look like in natural-cause deterioration — was not systematically presented.
What the Panel says
The Panel's case-by-case review walks through the blood-gas and lactate trajectories in the indicted cases and concludes they are compatible with natural-cause deterioration. The Panel's specific point is that the chart trajectories do not require a deliberate-harm hypothesis to explain them.
What independent experts add
- Rising lactate is the single most sensitive marker of tissue hypoperfusion in neonatal intensive care and is routinely present in NEC, sepsis and shock.
- Metabolic acidosis on blood gas is the downstream consequence of tissue hypoperfusion and is non-specific to cause.
- pCO2 rise with saturation fall is consistent with respiratory failure from any cause, including apnoea of prematurity.
- The 'sudden' adjective applied to deterioration at trial obscures the underlying picture: most acute decompensations in very preterm infants follow a documented 10-60-minute lead-in on chart values.
- Prof. Geoff Chase's physiological modelling addresses the insulin-value trajectories in Babies F and L specifically but the same methodology applies to the broader blood-gas evidence.
- The absence of the kind of abrupt, isolated pCO2 or saturation drop that would be pathognomonic of intravascular air embolism is itself evidence against the Crown's mechanism theory.