Callum Joe Guest v Nottingham University Hospitals NHS Trust

In a clinical negligence claim, causation must be determined on the balance of probabilities by evaluating the whole evidential picture. Where competing medical explanations exist, the court may prefer a plausible explanation supported by clinical experience, ordinary practice and medical literature over an exceptional explanation unsupported by those sources. A laboratory result may be rejected as spurious where its magnitude and rapid change are highly improbable and there is a credible explanation for an inaccurate reading.

Where the alleged negligent mechanism is not proved to have caused the injury, the claim fails. The court may nevertheless record conditional findings on breach and causation.

The claimant suffered substantial bilateral visual impairment after complex spinal surgery. During the operation his condition deteriorated, the surgery was stopped, and he suffered a cardiac arrest while being turned from the prone to the supine position.

He alleged that the arrest resulted from hyperkalaemia caused by the treating anaesthetist’s failure to act promptly on an arterial blood gas result. The defendant admitted breach in failing to act once the result became available, but contended that the relevant potassium result after the arrest was spurious and that the arrest was caused by pulmonary embolism. The central issues were the cause of the arrest, breach and causation in relation to hyperkalaemia, and whether the arrest caused or exacerbated posterior ischaemic optic neuropathy.

1. Cause of cardiac arrest. The court found that the post-arrest potassium result of 9.5 mmol/l was spurious. The rapid rise from 6.2 mmol/l and subsequent fall were exceptional and unsupported by the experts’ clinical experience, ordinary clinical practice or the medical literature. Haemolysis provided a plausible explanation, particularly given the stressful circumstances in which the sample was taken during cardiac arrest.
2. The evidence also supported pulmonary embolism as the cause of the arrest. The arrest coincided with turning the claimant, the CTPA showed multiple pulmonary emboli, the presenting rhythm was PEA, and effective CPR could plausibly have dispersed a clot. The court therefore concluded on the balance of probabilities that the arrest was caused by pulmonary embolism rather than hyperkalaemia.
3. Because hyperkalaemia was not established as the cause, the remaining issues fell away. Had they required determination, the court would have found no breach beyond the admitted breach and would have found that treatment by calcium gluconate by 19:20 would probably have avoided a hyperkalaemic arrest.
4. The court would also have found that the posterior ischaemic optic neuropathy had probably occurred during the surgery before the arrest. It was a recognised complication of the surgery, the claimant had relevant risk factors and marked facial swelling indicating raised intraorbital pressure, whereas cardiac arrest was not a recognised risk factor. The evidence did not establish that the arrest materially exacerbated the injury.
5. The claim was dismissed.