This is the trial of breach of duty and causation in a clinical negligence claim following spinal surgery which C underwent on 29 May 2019. The surgery was long and complex. During its course C’s condition deteriorated and a decision was made to stop the operation. It was after that decision was made, and whilst C was being turned from the prone position he had been in throughout the operation to supine that he suffered a cardiac arrest. He was successfully resuscitated but it subsequently transpired that he had at some point suffered posterior ischaemic optic neuropathy (PION), causing substantial bilateral loss of vision. [1]
PION is a recognised albeit rare complication of C’s surgery. In this case, however, he claims that it arose as a result of the cardiac arrest rather than as a complication of the surgery itself. The cardiac arrest, he claims, was due to hyperkalaemia (high serum potassium) which the treating anaesthetist negligently failed to treat. [2]
Bloods were taken regularly throughout the surgery. [5]
Some ECG changes are noted (but not particularised) on the records at 19:15. they were not typical of hyperkalaemia which she said she understood to give rise to huge peaked T waves. [13]
Between 19:20 and 19:25 all the monitors and infusions were disconnected in order to turn C supine. Once the turning had been done and the monitors were reconnected, very quickly there C went into cardiac arrest due to Pulseless Electrical Activity (PEA). CPR was started and he was given calcium gluconate, sodium bicarbonate and adrenaline. On the third round of CPR the PEA rhythm converted to Ventricular Fibrillation (VF) and the defibrillator was used successfully. The total “downtime” was some 10 minutes. End-tidal CO2 was present throughout CPR. [14]
Very shortly after C went into cardiac arrest a further blood sample was taken, the results for which were printed at 19:34. They show a rise in serum potassium to 9.5 mmol/l. The next results were printed at 19:51 and show a fall to 5.2 mmol/l. [15]
At 20:25 C underwent a pulmonary angiogram (CTPA)… this indicates bilateral pulmonary emboli within the left upper lobe, left lingula and right lower lobe. It did not show a central embolism. [18]
there were two possible causes of the cardiac arrest, namely hyperkalaemia or pulmonary embolism… if the 19:34 serum potassium level of 9.5 mmol/l was a true result, then on the balance of probabilities the arrest was due to hyperkalaemia, whereas if it was a spurious result then, on the balance of probabilities, the cause was pulmonary embolism [21]
Pulmonary embolism is a non-negligent cause of cardiac arrest. If the arrest was due to hyperkalaemia then C’s case is that prompt treatment of his raised serum potassium shown in the 18:28 result would have had the effect of averting the cardiac arrest. [22]
highly improbable that the 19:34 result was a true result. A rise of that magnitude in that time is not supported by expert clinical experience, by ordinary clinical practice, nor by any literature whatsoever. [65]
there is a plausible explanation for the spurious result, in the form of haemolysis of the sample. [66]
D has proved on the balance of probabilities that the 19:34 result was spurious [67]
the cardiac arrest was caused by pulmonary embolism rather than hyperkalaemia [68]
entirely plausible that C’s cardiac arrest was due to pulmonary embolism which was subsequently dispersed by way of external cardiac massage, unlike the theory that his serum potassium rose and fell by such large amounts in the short periods as the 19:34 result would indicate, which is wholly implausible.
It follows from my finding as to the cause of the cardiac arrest that the claim must be dismissed. [80]
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