In AXO v Salisbury NHS Foundation Trust [2019] EWHC 1454 (QB)  Mrs Justice YIP considered the issue of causation in a clinical negligence case.  Liability was admitted but the claimant failed to establish causation.


The claimant child was born prematurely.  Shortly after birth he received a tenfold overdose of pancuronium bromide. It was the claimant’s case that this led to brain damage and resulted in cerebral palsy.

It was admitted that the overdose was negligently administered. However the defendant denied that the neurological injury was related to the overdose.



The judge commented that one of the doctors had gone beyond their expertise:

To some extent, I considered that Dr Newton strayed beyond his area of expertise. I fully accept that the care of a sick neonate inevitably involves a multi-disciplinary approach such that in practice the boundaries between experts in different disciplines are somewhat fluid. I acknowledge that Dr Newton’s practice over the years has required him to understand and to explain multifactorial causes of neonatal brain injury to parents and others. It is often very helpful to have the input of experts from different disciplines to provide a complete picture on causation. However, Dr Newton acknowledged that parts of his evidence were based upon “undergraduate medicine” and his management of neonates as a junior doctor but no directly relevant experience for 20 years. The weight to be given to such evidence must inevitably be limited.”


The judge considered the evidence in detail and found that a causal link had not been established.

  1. It is natural to suspect a link between the significant overdose of pancuronium and AXO’s severe neurological injury. I have the greatest of sympathy for AXO’s parents who have witnessed their son suffer an adverse outcome after a significant medical error. However, a close analysis of the evidence does not establish the necessary causal connection between the two.
  2. AXO was very sick at midnight. There were real difficulties ventilating him and I have accepted that Dr Brown feared that he might die that night. This was before the pancuronium was administered as a response to his critical condition. It is not clear whether the drop in blood pressure occurred shortly before or shortly after the overdose. AXO also received Curosurf around the same time. That drug caused his blood pressure to drop the following afternoon. In cross-examination, Professor Mitchell acknowledged the difficulty in attributing the fall to one drug rather than the other.
  3. Professor Mitchell’s explanation as to the mechanism by which an overdose of pancuronium would cause the rapid onset of hypotension did not withstand cross-examination. Having accepted that the majority of neonates would be fully paralysed by a therapeutic dose of the drug, his explanation that the overdose caused a greater loss of muscle tone cannot be maintained.
  4. Although the claimant need not prove the mechanism by which harm was done in order to establish causation, once Professor Mitchell’s theory has been discounted, all that is left is the temporal connection between the overdose and the hypotension. However, it is not possible to say more from the factual evidence than that the onset of significant hypotension was between midnight and 01.00. By itself, this is not sufficient to establish a causal link as a matter of probability, particularly in a baby who had a tendency to low blood pressure (per Dr Newton) and who suffered documented hypotension following the administration of Curosurf.
  5. I have reflected carefully on the product data from Australia and New Zealand, which describes significant hypotension as one of the symptoms of pancuronium overdose. This, coupled with the temporal connection, might suggest a causative link. However, Dr Hawdon’s unchallenged evidence was that hypotension is only a recorded side effect where anaphylaxis occurs. It is highly improbable that AXO suffered an anaphylactic reaction.
  6. I have also had regard to the pharmacology evidence. Dr Cockbill propounded no pharmacological explanation for a link between the overdose and the hypotension. Professor Ferner’s evidence (upon which he was not cross-examined) was that it is unlikely that the fall in blood pressure was caused by the pancuronium.
  7. The evidence does not establish that the hypotension recorded at 01.00 was probably caused by the overdose. Having seen the neonatologists give evidence and after cross-referencing all the other evidence in the case, I prefer the evidence of Dr Hawdon that AXO’s hypotension at 01.00 was probably part of his overall condition, flowing from his prematurity, severe RDS and the difficulty in ventilating him.
  8. Although I have found that a second insult occurred around the time of AXO’s transfer, this was not caused by his accidental extubation. Reintubation was carried out quickly and skilfully and the observations before and after the extubation show no change in blood pressure, heart rate or oxygen requirements. There had already been a significant drop in blood pressure before the transport team arrived, which led to the introduction of the second-line inotrope, dobutamine.
  9. The neurology experts agree that this episode of hypotension was causative of neurological damage. However, there is no evidential basis for a link to the earlier overdose. Dr Newton’s opinion was clearly predicated on the basis that the fall in blood pressure followed the extubation but that does not reflect the facts as I have found them. Professor Ferner’s unchallenged evidence is that the effects of the overdose could not explain this episode of low blood pressure.
  10. There is no alternative basis for finding that the overdose contributed towards a hypoxic-ischaemic episode around the time of transfer. On Professor Mitchell’s evidence, AXO was predisposed to neurological injury at this time. He suffered a further significant drop in blood pressure before the extubation. That (according to the agreed evidence of the neurologists) contributed to his PVL. Professor Mitchell’s evidence that he was unable to withstand the extubation because of the effects of the pancuronium overdose is not supported by the chronology.
  11. Overall, I find that AXO’s neurological injury is explained by his prematurity and perinatal course. Although he was born in relatively good condition, he was a vulnerable baby by reason of his prematurity and the early rupture of the membranes. He developed severe respiratory distress syndrome, leading to significant deterioration in his condition by midnight. The mechanisms underlying the development of PVL are not always clear. It is known though that babies of this gestation who develop cerebral palsy are more likely to have had significant complications such as respiratory distress syndrome.
  12. I fully recognise the importance of my decision to AXO and his parents. It may be of little comfort to them, but I have looked very closely at all the evidence before reaching my conclusions. Having done so, I find that causation is not established. I must therefore dismiss this claim.