Michael and Another v Linksfield Park Clinic (Pty) Ltd and Another

• Jurisdiction: South Africa
• Judge: Howie JA, Farlam JA and Chetty AJA
• Judgment Date: 13 March 2001
• Citation: 2001 (3) SA 1188 (SCA)
• Docket Number: 361/98
• Hearing Date: 19 February 2001
• Counsel: G Bizos SC (with L J Morison) for the appellants. B W Burman SC and N G D Maritz SC for the respondents.
• Court: Supreme Court of Appeal

The court: C

Introduction

[1] This is a tragic case indeed. A boy of 17 underwent corrective nasal surgery and suffered cardiac arrest while under general anaesthesia. By the time resuscitation had restored heart D function he had sustained major brain damage as a result of cerebral anoxia. He has been left in a permanent vegetative state.

[2] His parents sued for damages in the High Court at Johannesburg. The private company owning the clinic where the operation was performed was cited as the first defendant and the anaesthetist E as the second defendant. Negligence was alleged on the latter's part in relation to the cardiac arrest and joint negligence was alleged in respect of the resuscitation process. By agreement between the parties the trial Judge (Schabort J) was asked to determine only the question of liability. Having found that none of the alleged negligence F had been proved, the learned Judge dismissed the claim but granted leave for this appeal. For convenience we shall refer to the parties by their trial designations.

The facts not in issue

[3] The following facts are now common cause or no longer realistically disputable. The plaintiffs' son, Minas ('the G patient'), had sustained an injury to his nose when taking part in sport. He consulted a plastic and reconstructive surgeon, Dr M S Fayman, who recommended a rhinoplasty. The object was to remove a hump on the dorsal aspect of the nose and to correct a deviated septum. H

[4] The operation was arranged for 10:00 on 7 December 1994 at the first defendant's clinic. Dr Fayman was assisted by Dr Grace Rubin and the second defendant, a specialist in anaesthesiology, was the anaesthetist. All three doctors were in private practice. I

[5] Among the first defendant's employees involved in the events of that morning were Sister S Montgomery, the sister in general charge of anaesthetics and recovery, and Sister D E Glaeser who was the anaesthetic sister assigned to this particular operation. They were both registered nurses. J

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[6] Included in the clinic's emergency equipment was a resuscitation trolley carrying, among other things, a Lohmeier A defibrillator. A defibrillator is a portable electronic apparatus designed to restore normal rhythm to a fibrillating heart by way of electric shocks applied to the chest wall. It was among Sister Glaeser's duties to see to it beforehand that this defibrillator was in working order and to use it when called upon by the second B defendant to do so. As anaesthetist, he was in overall charge of all necessary resuscitation measures.

[7] At about 9:40 the pre-operative process started. The initial stages included the insertion into the patient's left hand of an intravenous tube connected to an AFC 123 drip-line and the attachment to his person of leads from items of equipment reflecting, inter C alia, blood pressure, heart rate and electrocardiographic (ECG) tracings of heart rhythm.

[8] Anaesthetic induction commenced at about 9:45 employing a combination of inhalants and intravenous drugs. Among the drugs administered intravenously was one milligram of propranolol hydrochloride (propranolol) which was given to prevent an untoward D increase in heart rate during the operation. Propranolol in medical parlance is a beta blocker. It lowers excessive heart rates by blocking the beta adrenergic receptors in the heart which govern heart rate stimulation. It is manufactured in tablet form and also in one milligram (one millilitre) ampoules for intravenous administration. In E South Africa it is sold, inter alia, under the trade name 'Inderal'. The package insert published in November 1993 by the South African distributors of Inderal stated that intravenous administration was for the emergency treatment of cardiac dysrhythmias especially including supra-ventricular tachydysrhythmias. The recommended dose was one milligram injected over one minute which could be repeated at F two-minute intervals until a response was observed or to a maximum, in the case of anaesthetised patients, of five milligrams.

[9] At roughly 9:50, with the patient now fully generally anaesthetised, Dr Fayman injected a local anaesthetic (lignocaine and G adrenaline) into the nose and inserted at the back of each nostril a plug of ribbon gauze soaked in a cocaine solution. The use of cocaine had a two-fold purpose. It is a local anaesthetic and a vasoconstrictor. The blood vessels of the nasal lining bleed very readily and it was necessary to constrict them to ensure a clear field for the surgeon. Cocaine is widely used for this purpose in ear, nose H and throat surgery. The mass of cocaine in the solution was approximately 150 milligrams (being 1,76 milligrams per kilogram of the patient's weight, which was eighty-five kilograms). The limits of a safe dose are from 1,5 milligrams to 2 milligrams per kilogram. Because not all of the solution was in contact with the inner nasal surfaces I only about eighty per cent of the cocaine would have been absorbed.

[10] Cocaine, either in overdose or in patient over-reaction, has cardio-toxic effects which can lead to cardiac arrest. One of these is its local anaesthetic effect, which impairs electrical conduction within the heart J

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and diminishes the contractility of the myocardium - the heart muscle. Another is its propensity to result in A coronary vasospasm which leads to myocardial ischemia. Cocaine toxicity exhibits a well-known pattern of heart reaction, first hypertension and tachycardia, then ventricular arrhythmias, then falling blood pressure and heart rate, then ventricular fibrillation and finally cardiac arrest. B

[11] At 10:00 the operation began. The kind of operation in question usually took Dr Fayman about one hour and involved, after an incision in each nostril to enable lifting the soft tissue off the ridge of the nose, operating first in one nostril and then in the other. The surgery encompassed lowering the bony ridge to the desired degree by rasping it from both sides and then trimming the C cartilaginous portion of the nose with a scalpel. Dr Fayman completed the rasping process on the left side and went on to operate on the right.

[12] Between 10:15 and 10:28, while surgery was in progress, bleeding in the nose suddenly occurred in the right nostril which obscured the surgical field and brought the operation to a stop. With D the bleeding there was a dramatic and alarming increase in the patient's heart rate and blood pressure. In the evidence this high level of heart rate (tachycardia) and high blood pressure (hypertension) was called 'the hypertensive crisis' and the tachycardia itself was identified as a supra-ventricular E tachydysrhythmia. The second defendant diagnosed too light anaesthesia as the cause of the crisis. This did not mean inadequate anaesthesia. The difference is that adequate anaesthesia can during surgery become too light by reason, not of reduction in anaesthetic, but of excessive surgical stimulus. He deepened the degree of anaesthesia, and to bring down the heart rate and blood pressure, which F presented the risk of cerebral haemorrhage, he injected a further one milligram of propranolol into the drip-line. The heart rate and blood pressure came down as intended but thereafter they continued to decline. At below 60 beats per minute the heart rate became what is called bradycardia. Early in the bradycardia the ECG monitor displayed features of a normal tracing, including the characteristic peak and G lows referred to as the QRS complex. This complex then soon broadened, indicating a symptomatic bradycardia. At about this time the second defendant instructed Dr Fayman to undertake cardio-pulmonary resuscitation (CPR) by way of external heart massage. (Unless after this there is specific reference to the first dose of propranolol we H shall only speak of the later one.)

[13] The second defendant considered that there had been an over-action by the propranolol and to counter it he started administering, in conjunction with the CPR, a sequence of different drugs (ephedrine, isoprenaline and adrenaline) to try to raise the heart rate and blood pressure by removing the beta blockade. All these I measures failed and the patient's heart went into cardiac arrest at 10:28.

[14] Shortly before the arrest the second defendant noted that the ECG tracing had become a flat line. In other words there was no discernible wave. This led him to conclude that the patient's heart was in a state J

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known as asystole, in which there is no electrical activity in the heart at all. Because shocking by defibrillator damages A an asystolic heart he considered he was confined in his resuscitation efforts to CPR and drug therapy, those being the only measures by which rhythm can be restored if the heart is in that state. When, after about four minutes, these efforts failed to yield any apparent result, the second defendant's options were to leave the patient for dead or B to employ the defibrillator in the hope that if the heart was not in asystole but in ventricular fibrillation a heart beat could be restored by defibrillation. A fibrillating heart is one in which there are electrical impulses but no rhythm and no output. Its energy goes into rapid, random, unco-ordinated contractions, all in complete disorder. What defibrillation does is to shock a fibrillating heart into C momentary asystole and afford it the opportunity for a normal beat to resume spontaneously. (As ventricular fibrillation is the only form of fibrillation which need be mentioned we shall, from now on simply refer to fibrillation.)

[15] The Lohmeier defibrillator ('the Lohmeier') was therefore brought into action. On the second defendant's instructions Sister D Glaeser set the device to deliver a charge of 200 joules. When she did so...