Guest v Nottingham University Hospitals NHS Trust: cardiac arrest caused by pulmonary embolism, not negligent anaesthetic management

The claimant, Callum Joe Guest, underwent the second stage of a two-part surgical procedure to address scoliosis and associated chest wall deformity at Nottingham University Hospitals NHS Trust on 29 May 2019. During the operation he suffered a cardiac arrest and was successfully resuscitated, but subsequently developed posterior ischaemic optic neuropathy (PION), causing substantial bilateral loss of vision.

The claimant's case was that the cardiac arrest resulted from hyperkalaemia — an elevated serum potassium level — which the treating consultant anaesthetist, Dr Leong, negligently failed to treat. The Trust denied that the cardiac arrest was caused by hyperkalaemia, maintaining it was caused by pulmonary embolism, a non-negligent complication.

The potassium results and the central dispute

Arterial blood gas results taken throughout the surgery showed a gradual rise in serum potassium. The 18:28 result showed a level of 6.2 mmol/l, a level all experts agreed warranted treatment. The Trust admitted a breach of duty in failing to act on that result by 19:20 at the latest, though disputed whether earlier treatment would have averted the arrest.

The pivotal issue turned on a blood sample taken at 19:34 — during the cardiac arrest itself — which showed a serum potassium level of 9.5 mmol/l. A further sample taken at 19:51 showed a fall to 5.2 mmol/l. The claimant relied on this result as evidence of severe hyperkalaemia; the defendant contended it was spurious due to haemolysis.

Her Honour Judge Claire Evans found that the 19:34 result was, on the balance of probabilities, spurious. The rise from 6.2 to 9.5 mmol/l in approximately an hour, followed by a fall of 4.3 mmol/l in under twenty minutes, was described as having no support in expert clinical experience or in any published literature. The defendant's anaesthetic expert, Dr McCrirrick, gave evidence that such a precipitous rise was "almost inconceivable" and that if such fluctuations could occur during major surgery, anaesthetists would need to measure potassium every fifteen to twenty minutes — which is not clinical practice. Haemolysis, which commonly produces falsely elevated potassium readings, was found to be a plausible explanation: the sample was taken in the highly pressurised circumstances of an active cardiac arrest, where arterial pressure would have been reduced and the usual ease of drawing from an arterial line compromised.

Pulmonary embolism as the cause

Satisfied that the 19:34 result was unreliable, the judge considered the pulmonary embolism evidence. The computed tomography pulmonary angiogram (CTPA) performed post-arrest demonstrated bilateral pulmonary emboli across multiple areas of the lung. The cardiac arrest occurred as the claimant was turned from prone to supine — a movement consistent with dislodging a clot — and presented as pulseless electrical activity (PEA), the typical rhythm for a pulmonary embolism arrest. Expert evidence supported the proposition that external cardiac massage can disperse clot material, accounting for the absence of a central embolism on the post-arrest CTPA. On the balance of probabilities, the cardiac arrest was caused by pulmonary embolism.

The claim was accordingly dismissed.

Observations on the remaining issues

The judge set out findings that would have followed had hyperkalaemia been established. She would have found no breach beyond that admitted; that treatment by 19:20 would on the balance of probabilities have averted the arrest; that the PION had most likely already occurred before the cardiac arrest, given the significant facial swelling indicating raised intraorbital pressure during surgery; and that the evidence that the cardiac arrest exacerbated the severity of the PION was too speculative to found a finding of causation.

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