The radiological finding at issue
Hepatic portal venous gas (HPVG) is the presence of gas within the portal venous system of the liver, visible on plain abdominal radiographs as branching lucencies projecting over the liver periphery, and on ultrasound as echogenic bubbles tracking through the portal vessels. In neonatal intensive care, HPVG is a well-recognised radiological sign associated with a narrow range of conditions. The Crown’s lead expert, Dr Dewi Evans, interpreted the presence of HPVG in certain indicted cases as evidence consistent with deliberate introduction of air into the gastrointestinal or vascular system.
The prosecution’s argument required that HPVG in these infants could not be adequately explained by natural causes and therefore pointed to a deliberate act. That argument does not survive scrutiny once the differential diagnosis for HPVG in extreme preterm neonates is properly considered.
What NEC is and how often it occurs
Necrotising enterocolitis is an acute inflammatory bowel necrosis that predominantly affects premature infants. It is characterised by intestinal mucosal injury that can progress to full-thickness bowel-wall necrosis, perforation, peritonitis and sepsis. NEC affects 7 to 10 percent of infants born weighing less than 1,500 grams and carries a mortality of 20 to 30 percent in affected infants, rising substantially in surgical cases requiring bowel resection.
NEC is the leading cause of gastrointestinal emergency in preterm neonates and a major cause of death in neonatal intensive care units globally. Its presentation can be insidious — early features include feeding intolerance, abdominal distension, and temperature instability — or it can present with acute haemodynamic collapse. The condition is frequently diagnosed radiologically, with the classical findings being pneumatosis intestinalis (gas within the bowel wall) and HPVG.
HPVG in NEC arises because gas produced by bacterial fermentation within the necrotic bowel wall enters the mesenteric venous drainage and tracks into the portal system. The mucosal disruption caused by NEC removes the barrier that normally prevents luminal gas from entering the mesenteric veins. HPVG is therefore a direct and expected consequence of NEC in its advanced stages and is documented in neonatal radiology literature as a primary feature of the condition.
Why NEC is the differential of first choice
When HPVG is identified in a preterm infant on a neonatal intensive care unit, NEC is the differential of first choice for the following reasons. First, NEC is common in this population. Second, NEC independently and mechanistically produces HPVG through the bowel-wall disruption pathway described above. Third, the clinical context of extreme prematurity, formula feeding, infection and mucosal immaturity creates the predisposing conditions for NEC independently of any external act.
Several of the infants whose cases were the subject of criminal charges had post-mortem features consistent with NEC. Independent reviewers examining those post-mortem reports have identified histological findings — including mucosal necrosis and transmural inflammation — that are the pathological hallmarks of NEC. These findings were not the primary focus of the prosecution’s expert evidence, which emphasised the HPVG imaging finding while treating the underlying bowel pathology as less significant.
Supporters of a Criminal Cases Review Commission referral contend that the failure to adequately explore the NEC differential before the jury was a material deficiency in the defence of the relevant counts. If NEC provides a full natural-cause explanation for HPVG and for the associated bowel pathology, then the radiological finding cited by the Crown does not advance the proposition that a deliberate act occurred.
What the Crown’s mechanism required and why it doesn’t survive
For the Crown’s deliberate-air-injection theory to account for HPVG in infants without NEC, the mechanism required: air introduced from outside the body (by injection or other means) to reach the portal venous system in sufficient volume to be detectable on imaging, while the bowel wall remained intact enough not to show NEC pathology on post-mortem examination. This is mechanistically difficult to reconcile.
Gas introduced into the vascular system directly would produce air embolism, a distinct and rapidly lethal condition. Gas introduced into the gastrointestinal lumen would face the same barriers to portal entry — the intact bowel mucosa — as described in the NG-tube physiology analysis. The prosecution’s mechanism does not identify a credible route by which externally introduced air reaches the portal system while leaving the bowel mucosa sufficiently intact to exclude a NEC diagnosis.
Post-mortem gas redistribution as a further confounder
Post-mortem gas redistribution is a well-established artefact in forensic and neonatal pathology. After death, tissue decomposition and the collapse of vascular pressure gradients allow gas to migrate from the gastrointestinal tract into adjacent vascular structures. In neonates, whose tissues have low mass and decompose relatively rapidly, this redistribution can occur within hours of death.
Radiological images taken at post-mortem examination or in the hours following death therefore cannot reliably distinguish between ante-mortem gas accumulation and post-mortem redistribution. The forensic radiology literature specifically cautions against interpreting post-mortem HPVG as evidence of ante-mortem pathology without careful correlation with the clinical timeline.
In several of the indicted cases, the interval between death and post-mortem imaging or examination raises questions about whether the gas distribution observed reflected the clinical state at the time of deterioration or was substantially modified by post-mortem redistribution. The Panel’s review addresses this issue and identifies it as a significant limitation on the evidential weight that can be attached to the radiological findings cited by the prosecution.