What this page relies on
The medical account below is taken from the case entries for Baby 15 (trial Child O) and Baby 16 (trial Child P) in the International Expert Panel — Summary Report (February 2025). Where this page states a clinical fact or a causal conclusion, it is because the Panel states it. Nothing here is inferred beyond that report.
The clinical context
The triplets were delivered by Caesarean section at the Countess of Chester Hospital, a district general hospital, in June 2016. They were preterm, not term: both O and P were born at 33+2 weeks. Baby O was the second triplet and weighed 2.02kg; Baby P was the first triplet and weighed 2.066kg. Both had mild respiratory distress and were placed on CPAP.
One detail of the delivery matters more than any other for what followed. The Panel records that the triplets were extracted at Caesarean section very quickly — a minute apart. Extremely rapid delivery is, in the Panel’s words, a well-recognised cause of birth injury. The referral and pathway questions raised by a triplet delivery at a district general hospital are considered separately in the triplets-to-singletons referral-pathway analysis hosted on this site.
Baby O (Panel: Baby 15) — the sequence
Baby O’s haemoglobin on the day of birth was 168g/l. On day 2 he was moved to Optiflow and started on small feeds. At 36 hours he had a rising heart and respiratory rate, temperature instability and mild abdominal distension. He did not pass meconium until 32 hours of age; the Panel notes meconium is usually passed within the first 24 hours.
By the next morning his abdomen was more distended, with visible loops of bowel, and he was uncomfortable after a feed. That afternoon he vomited undigested milk and had a high blood lactate (5.4), high carbon dioxide (7.09), high bilirubin (156) and acidosis (pH 7.2). He was given fluids and antibiotics. At 1440h he suffered a profound desaturation with a low heart rate, looked mottled, and his abdomen was very distended. He was intubated and ventilated at high pressures (28/5). A small purpuric discolouration was transiently seen on his right chest during the resuscitation.
At 1551h he desaturated again and was reintubated, receiving cardiac massage, adrenaline (eight doses), bicarbonate (three doses) and saline infusions. Ventilation pressures were raised to 32/6 in 100% oxygen, dopamine was started, and a needle aspiration of the abdomen was performed. An intraosseous line was inserted because of poor circulation. At 1743h his blood gas showed marked acidosis (pH 7.014, base excess −17) and a haemoglobin level that had nearly halved, to 86g/l. No heart rate was heard. Resuscitation was stopped at 1747h. Post-mortem showed a ruptured subcapsular haematoma of the liver.
What the Panel concluded about Baby O
The Panel concluded that Baby O died from a subcapsular liver haematoma caused by traumatic delivery, resulting in haemorrhage into the peritoneal cavity and profound shock — and that this was not recognised before death. The mechanism it describes runs as follows.
- A birth injury, not an inflicted one. A subcapsular liver haematoma is the result of traction or shear forces applied to the thin, fragile liver capsule through the hepatic ligaments. In Baby O this was, on the Panel’s reading, highly likely the result of the extremely rapid delivery.
- A slow bleed, then a rupture. Bleeding into a subcapsular haematoma is characteristically slow at first, because it is contained by the pressure of the enveloping liver capsule; the early clinical signs are insidious and difficult to recognise. The slow deterioration is then followed by acute collapse when the capsule ruptures and free blood is released into the peritoneal cavity. That is what the near halving of the haemoglobin, from 168g/l to 86g/l, records.
- High-pressure ventilation made it worse. High ventilation pressures decreased venous return to the heart and contributed to liver congestion.
- The blind needle aspiration may have added injury. The Panel considers that the blind insertion of a needle into the abdomen during resuscitation may have penetrated the right lobe of the liver, causing the further injury the pathologist noted as parenchymal haematoma and laceration.
- The warning signs were missed. The significance of the rising heart rate and falling pH before the terminal collapse were not recognised.
On the prosecution mechanisms specifically, the Panel is direct. Blunt direct trauma to the right abdomen or chest is implausible, because it is very difficult to generate the kind of forces required to produce the observed injuries in a liver protected by the lower chest wall. The gaseous distension of the intestinal tract was likely due to air swallowing and insufflation during non-invasive respiratory support — not air pushed down a nasogastric tube. And the later suggestion that air was injected into his circulation is, in the Panel’s single word, conjecture.
It is worth being precise about what the Panel does not say, because this page previously said it. The Panel does not attribute Baby O’s liver injury to cardiopulmonary resuscitation. Its causal explanation is the traumatic delivery. The only resuscitation-related injury it identifies is the possible additional damage from the blind needle aspiration of the abdomen — an addition to an injury that was already there, and already bleeding, before anyone laid a hand on him.
Baby P (Panel: Baby 16) — the sequence
Baby P was on CPAP for mild respiratory distress. At 16 hours of age he was changed to nasal cannula, and three and a half hours later he developed apnoea. His abdomen was full and mildly distended, but soft, non-tender and with active bowel sounds; there was mild erythema at the base of the umbilicus. Antibiotics were started.
The next day he suddenly desaturated with a low heart rate. He was intubated and ventilated at high pressures (26/6, rate 60/min) on 26% oxygen, and given adrenaline. A chest x-ray showed a moderately large right pneumothorax. An hour later he desaturated again with a low heart rate; capnography showed the endotracheal tube had become dislodged, and a new tube was inserted. The pneumothorax was needled about three hours after the first deterioration, and a chest tube was inserted a further two and a half hours after that. He had persistent metabolic acidosis despite bicarbonate infusion. An hour and a half later he suffered a cardiorespiratory arrest and died.
What the Panel concluded about Baby P
The Panel reached two conclusions. First, that Baby P died from a pneumothorax that was suboptimally managed. Second, that there was no evidence of air injection into the stomach or into the intravenous line.
- The abdominal distension was the CPAP. The initial gaseous distension of the abdomen was caused by CPAP, not by injection of air into the nasogastric tube. The Panel notes it is unclear whether the nasogastric tube was open to drainage.
- The pneumothorax needed no sinister explanation. Pneumothorax can occur in preterm infants with mild respiratory distress syndrome, especially with CPAP or other respiratory support — or even without any lung disease or respiratory support at all. The Panel adds that it is unclear whether the pneumothorax preceded or followed the resuscitation.
- Recognition and treatment were delayed. The Panel describes the care after the collapse on 24 June as mismanaged, with unacceptable delays in the recognition and treatment of the pneumothorax. That delay led to persistent metabolic acidosis, because the pneumothorax continued to cause poor circulation and poor gas exchange. The medical records do not show that a cold light test was performed.
- The treatment given was itself harmful. He was treated with high-pressure ventilation and adrenaline despite having no lung disease and requiring only 26% oxygen. The Panel calls both harmful: high ventilation pressures impede venous return to the heart, worsening circulatory failure, and adrenaline punishes the heart by overworking it unnecessarily.
- No air embolism. There were no signs of air embolism at the final collapse.
The prosecution theories, and how they moved
The Panel report records what was alleged in each case, and both allegations changed shape. On Baby O it was initially alleged that he received inflicted blunt trauma to the abdomen, causing the purpuric discolouration and the ruptured subcapsular haematoma of the liver, and that air was injected into the nasogastric tube to cause the gaseous distension of the intestines. The accusation was later changed to deliberate injection of air into his circulation.
On Baby P it was alleged that air was injected into his stomach by nasogastric tube, causing gastric distension and splinting of the diaphragm, leading to collapse. That allegation was also later changed — to air injected into his intravenous line to cause air embolism, collapse and death. The Panel found no evidence for either version. The wider problem with the air-embolism mechanism as it was run across the indictment is set out in our air embolism line by line analysis.
The third triplet
Baby Q, the third triplet, survived; the jury did not return a verdict on the count concerning him. This page confines itself to Babies O and P, because those are the two cases the Panel entries reproduced above address. Baby Q is covered on his own case page.
Why this unified review matters
The O and P counts are among the most serious on the indictment — two murders in rapid succession, in brothers from the same delivery. The Panel does not find a single shared mechanism behind them. It finds two different causes of death in two different babies: in Baby O, an unrecognised birth injury that bled slowly and then ruptured; in Baby P, a pneumothorax that was recognised late and then treated in a way the Panel says worsened the circulatory failure. On the Panel’s account, neither death requires a perpetrator. Whether that is enough to unsettle the convictions is a CCRC question.
Correction
An earlier version of this page described the triplets as term, and attributed Baby O’s liver injury to prolonged, vigorous resuscitation. Both statements were wrong and are not supported by the Panel report. The triplets were born at 33+2 weeks, and the Panel attributes the liver haematoma to traumatic delivery. The page was corrected on 14 July 2026.
Source
- International Expert Panel — Summary Report (February 2025), entries for Baby 15 (trial Child O) and Baby 16 (trial Child P). Read the report (PDF).