LN v Blackpool Teaching Hospitals NHS Foundation Trust

In a clinical negligence claim involving neonatal hypoxic-ischaemic encephalopathy, the court assessed causation on the balance of probabilities by considering the whole body of expert and clinical evidence. Therapeutic cooling could explain relatively mild development and an unremarkable MRI scan, but could not itself positively establish that HIE had occurred. The claimant proved that HIE resulted from the admitted negligent administration of oxytocin. However, he failed to prove that HIE caused his later developmental difficulties, microcephaly or visual impairment. Retinal dystrophy was genetic, and microcephaly was more probably genetic than attributable to birth asphyxia. A pneumothorax caused by resuscitation was not shown to be a consequence of the negligence.

The claimant, a child suing by his litigation friend, claimed damages for injuries allegedly caused by the negligent management of his mother’s labour and delivery. The defendant admitted breach of duty in administering Syntocinon but denied that the breach caused the claimant’s injuries.

The trial concerned whether the claimant suffered HIE, whether uterine hyperstimulation caused or contributed to it, and whether HIE caused his developmental delay and other difficulties. The court also considered the significance of the CTG trace, cord-gas readings, neonatal presentation, MRI findings, possible seizure activity, genetic retinal dystrophy, microcephaly and pneumothorax.

1. HIE. On the balance of probabilities, the claimant suffered HIE. The neonatal observations, very low Apgar scores, need for resuscitation, recorded encephalopathy and later developmental features outweighed the competing evidence, including the possibility of perinatal stroke and the absence of clear MRI evidence. The court rejected the stroke explanation as the more probable cause.
2. Uterine hyperstimulation and causation. The admitted negligent administration of Syntocinon caused uterine hyperstimulation. Chronic hypoxia from hyperstimulation probably contributed to the claimant’s poor condition at birth, although the terminal acute hypoxia caused by cord compression played the greater part in the final acidosis. The medical evidence did not permit the court to quantify the respective contributions. The relatively normal venous cord pH strongly indicated that chronic hypoxia had not caused significant acidosis, but did not exclude an additive effect which reduced the claimant’s reserves before the terminal event.
3. Therapeutic cooling. Cooling could explain why the claimant had relatively mild long-term clinical findings and no clear MRI evidence of HIE. It could neutralise the absence of radiological evidence, but could not provide positive support for the proposition that HIE had occurred. Reliance on cooling therefore required caution, since it risked presupposing the condition under investigation.
4. Later condition. The claimant’s retinal dystrophy was genetic. The more probable explanation for his microcephaly was an unidentified genetic syndrome also causing the retinal dystrophy. The claimant failed to prove that HIE caused or materially contributed to his continuing developmental, communication, motor or visual difficulties. The evidence left that possibility open but was insufficient to satisfy the burden of proof.
5. Pneumothorax. The pneumothorax was caused by resuscitation. The claimant did not establish that it would have been avoided but for the breach of duty.

The claimant therefore proved HIE caused by the admitted breach, but proved no recoverable consequence beyond the immediate depression of his condition at birth.

not stated in the judgment.