Thrombosis in preterms — an underconsidered natural-causes explanation
The prosecution’s claim: Several indicted collapses were attributed at trial to air embolism as the cause of sudden deterioration with skin colour changes. The framing treated air embolism as the leading explanation for circulatory events with mottled skin appearance.
Prosecution claim
Several indicted collapses were attributed at trial to air embolism as the cause of sudden deterioration with skin colour changes. The framing treated air embolism as the leading explanation for circulatory events with mottled skin appearance.
Counter-evidence
Thrombosis in extremely preterm infants is a well-documented natural cause of sudden circulatory collapse, and central venous catheters are a specific risk factor — every indicted baby with a central line was, by definition, at elevated thrombotic risk. In two of the indicted cases thrombosis is not a speculation but the Panel's conclusion. Child A, the Panel finds, died from thrombosis: the mother had anti-phospholipid syndrome, a recent non-occluding liver thrombus was found at post-mortem, and catheters had been left unperfused for up to four hours. Child B collapsed from thrombotic emboli arising from a central intravenous catheter that was kinked and had not been heparinised, potentially aggravated by the same maternal anti-phospholipid syndrome; her D-dimer was 6219 and her platelets 103. In neither case did the Panel find any evidence of air embolism. (Thrombosis is not the Panel's finding everywhere: Child E's death, for instance, it attributes to a massive gastrointestinal haemorrhage.) A proper differential-diagnosis workup on each suspicious collapse would have included imaging and laboratory testing for thrombosis. Much of that workup was not done at the time.
Key point: A preterm baby with a central line in place who collapses is at risk of thrombosis as a first-line diagnosis. Air embolism should be much further down the differential, not at the top of it — and in Children A and B, thrombosis is what the Panel found.
What the jury heard
Air embolism was presented as the leading explanation for collapses with skin-mottling; thrombosis was not systematically developed as an alternative.
What the Panel says
The Panel concludes Child A died from thrombosis — in a pregnancy complicated by maternal anti-phospholipid syndrome, with a recent non-occluding liver thrombus found at post-mortem and catheters left unperfused for up to four hours — and that Child B collapsed from thrombotic emboli originating in a kinked, non-heparinised central catheter, potentially aggravated by the same maternal anti-phospholipid syndrome (D-dimer 6219, platelets 103). It found no evidence of air embolism in either.
What independent experts add
- Central venous catheters are a recognised independent risk factor for neonatal thrombosis, especially in extremely preterm infants — and the Panel's Child B finding turns on the line itself: kinked, and not heparinised.
- Maternal antiphospholipid syndrome is a shared exposure: it affects both twins of the same pregnancy, which is why two sequential collapses need not have a common human cause.
- Sarah Hawkins's long-form analyses on this site identify the APS dimension in specific cases.
- Acute thromboembolic events in neonates can present with skin mottling that has been misread by less paediatrically-experienced observers as suggestive of air embolism.
- No post-mortem imaging suitable for detecting intravascular thrombosis was systematically obtained across the indicted cases.