Case No: 361/98
IN THE SUPREME COURT OF APPEAL
OF SOUTH AFRICA
REPORTABLE
In the matter of:
LEONIDAS SOUZOU MICHAEL
First Appellant
THELMA MICHAEL
Second Appellant
and
LINKSFIELD PARK CLINIC (PTY) LIMITED
First Respondent
DR HUGH M THOMAS
Second Respondent
CORAM:
Howie, Farlam JJA and Chetty AJA
Date Heard:
19 February 2001
Date Delivered:
13 March 2001
Medical negligence alleged - approach to expert evidence - whether a case for
adverse costs order against successful defendant .
J U D G M E N T

THE COURT
INTRODUCTION
[1] This is a tragic case indeed.   A boy of seventeen underwent corrective
nasal surgery and suffered cardiac arrest while under general anaesthesia.   By
the time resuscitation had restored heart 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 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 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 patient”) had sustained an injury
to his nose when taking part in sport.   He consulted a plastic and
reconstructive surgeon, Dr MS 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.
[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.
[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 DE Glaeser who was the anaesthetic sister assigned
to this particular operation.   They were both registered nurses.
[6] Included in the clinic’s emergency equipment was a resuscitation trolley
carrying, among other things, a Lohmeier 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 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 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 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 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 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 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 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 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 and diminishes the
contractility of the myocardium - the heart muscle.   Another is its propensity
to result in 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.
[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
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 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 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 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 sixty 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 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 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 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 known as
asystole, in which there is no electrical activity in the heart at all.   Because
shocking by defibrillator damages 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 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 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 Glaeser set the device
to deliver a charge of 200 joules.   When she did so she noticed that the
number of joules digitally displayed as reflecting the strength of the required
charge did not stay at 200 but started decreasing while she was busy preparing
to activate the defibrillator.   She nevertheless proceeded to cause delivery of
a shock.   The patient’s body responded but not his heart.   For some minutes
after that, CPR and adrenaline were repeated.   A second shock at 200 joules
was ordered.   The outcome was the same.   Again the number of joules on the

display fell before the shock could be given.   After renewed CPR and further
adrenaline a third shock was ordered, this time at 360 joules.   The heart
remained in arrest.   Once more the digital display decreased.  Because Sister
Glaeser and the second defendant thought that the diminishing display
indicated that the apparatus was failing to hold its charge and was therefore
defective, Sister Montgomery was sent to fetch another defibrillator.   CPR
and adrenaline were repeated.   In addition, bretylium tosylate, sodium
bicarbonate and calcium gluconate were injected into the drip-line.
[16] From the Intensive Care Unit Sister Montgomery returned in due course
with another make of defibrillator.   When programmed to deliver a charge of
360 joules, its digital display remained constant.   With the new defibrillator a
fourth and fifth shock were given.   Both elicited a body reaction and, in
addition, a heart beat.  The fourth resulted in ventricular tachycardia and the

fifth, sinus tachycardia - a fast but normal rhythm.   By the time heart action
was restored it was 10:44.   Further resuscitation was required in the Intensive
Care Unit and so the operation was not completed.   The nasal wounds were
simply closed and the patient’s nose was plugged and splinted.
[17] Prior to the cardiac arrest, and more or less contemporaneously, the
second defendant recorded certain data regarding the operation.   He used
both sides of a stereotyped form which he himself designed and which he had
had printed.   One side was referred to as his “chart”.   His recordings were
interrupted entirely by the arrest and resuscitation but later that morning he
made further entries on the reverse side of the form under the heading
“Additional notes”.   We shall refer respectively to the “chart” and to the
“additional notes”.   Later during the day he spoke to the plaintiffs and, in
expressing his regret for what had happened, said of the operation that

everything had been done correctly and that he did not know what had gone
wrong.
[18] During the afternoon the first defendant’s general manager, Dr Malkin,
spoke to Sister Glaeser.   In  recounting the morning’s events, she indicated
that in comparison with the second defibrillator the Lohmeier had seemed to
be defective.   In consequence Dr Malkin wrote to the suppliers of the
Lohmeier alleging that the resuscitation had failed because the defibrillator was
unable to maintain the required charge and expressing concern that there had
been a delay in the resuscitation.   This prompted a number of independent
tests of the apparatus concerned during the following year, the result of all of
which was that it was reported to be in working order.   It was also established
that in all defibrillators the programmed charge diminishes between the time it
is set and the delivery of a shock.   This is due to electrical resistance within

the apparatus.   Lohmeiers constitute the only make whose digital display
reflects that reduction and Sister Glaeser and the second defendant did not
know this.
[19] At 19:00 on the day of the operation the patient was examined by a
cardiologist, Dr JL Salitan, who performed an echocardiogram.   He later
reported that the patient’s heart was enlarged and its left ventricular
contractility significantly reduced.   His conclusion was that there was “marked
global myocardial dysfunction, probably acute”, possibly the result of
prolonged hypoxia.   Obviously prolonged hypoxia did occur and although it
is in dispute precisely by what mechanism the myocardial damage came to be
caused, what is not in issue is that hypoxia caused injury to the brain.   Brain
injury was sustained after the heart went into cardiac arrest and was ongoing
for as long as the resuscitation period advanced without restoration of a heart

beat.
THE ALLEGED NEGLIGENCE
[20] Of the many grounds of negligence set out in the particulars of claim (as
amended) the following summary reflects those which remain in tenable
contention at this stage.   As regards the first defendant it is alleged, in effect,
that:
1.
In respect of the Lohmeier, it failed to have a functional
defibrillator immediately available when required.
2.
Alternatively, if the Lohmeier was functional, first
defendant failed (at a time  prior to the date in question) to
inform Sister Glaeser about, and to train her in, the
workings and manner of operation of the Lohmeier,
thereby causing delay in the resuscitation process when the

Lohmeier appeared to her to be defective and to require
replacement by a substitute defibrillator.
[21] As regards the second defendant it is alleged in relation to the cardiac
arrest that:
1.
He failed to take adequate account of the effect which the
cocaine would have in conjunction with what he himself
administered and to guide Dr Fayman as to the upper dose
limits of cocaine.
2.
He failed to dilute the propranolol which was given to
combat the hypertensive crisis or to administer it in doses
of between 100 micrograms and 500 micrograms at a time.
3.
The use of propranolol in conjunction with cocaine
created the risk of sudden heart failure.

4.
He failed to recognise the risk of, or to prevent, life-
threatening bradycardia and cardiac arrest.
In relation to the resuscitation it is alleged that:
5.
He failed to ensure beforehand that a functional
defibrillator was available and that he was reasonably
acquainted with its workings.   This caused a delay in the
resuscitation process when a second defibrillator was sent
for.
6.
When the patient’s heart was in fibrillation he failed to
order defibrillation at the earliest opportunity.
Alternatively, he attempted defibrillation on an asystolic
heart thereby worsening the outcome.   In the further
alternative he failed to deliver three quick shocks in a

“stacked sequence” in accordance with certain published
algorithms approved for emergency cardiac resuscitation.
[22] We must mention for the sake of completeness that on examination by
the second defendant on the morning of the operation the patient told him that
he had managed over the preceding year to reduce his weight from 114 to 85
kilograms.   The second defendant did not enquire whether this appreciable
weight loss had possibly involved the use of any drugs harmful or potentially
harmful to the heart when used in combination with other drugs.   However,
the plaintiffs’ evidence was that the patient had not used any such substances
and no fault was attributed in the pleadings to the second defendant’s
omission to investigate this possibility.   We must therefore ignore it.
THE ISSUES FOR DECISION
[23] The first essential issue is the cause of the cardiac arrest.   The

plaintiffs’ contention is that it was propranolol and that the hypertensive  crisis
was occasioned by too light anaesthesia.   For the second defendant it is
maintained that the cause of both the hypertensive crisis and the arrest was
cocaine toxicity.   In either event the question then is whether the arrest was
foreseeable as a reasonable possibility, meaning a possibility which a
reasonable anaesthetist would foresee and guard against.   Finally, if the cause
of the arrest was cocaine toxicity and the arrest was indeed  foreseeable in that
sense, the question would then be whether the arrest was reasonably avoidable.
[24] The main subsidiary question allied to the first issue concerns the length
of time between the hypertensive crisis and the cardiac arrest and that, in turn,
depends on the credibility and reliability of the witnesses who were centrally
involved in the operating theatre at the time.   For the plaintiffs they were

Doctor Fayman, Doctor Rubin and Sister Glaeser.   On the opposite side the
second defendant stood alone.
[25] The other subsidiary questions are whether, irrespective of the cause of
the arrest and irrespective of the correctness of his conclusions, the second
defendant was reasonable in diagnosing too light anaesthesia as the cause of
the hypertensive crisis and in giving propranolol as the counter; whether he
was at fault in relation to either the size of the dose or the manner of its
administration; and whether it was reasonable to diagnose a propranolol over-
action as the cause of the bradycardia.
[26] The second essential issue is whether the Lohmeier was defective and,
if not, whether the ignorance of the second defendant and Sister Glaeser as to
the manner of its workings was culpable and whether their ignorance
occasioned an unreasonable delay in the resuscitative process.

[27] Allied questions (accepting that when the fourth shock was given there
must unquestionably have been fibrillation present) are whether the heart
arrested in asystole or fibrillation; when fibrillation occurred if initially there was
asystole;   whether fibrillation was immediately amenable to defibrillation and,
if not, when it first became amenable.   Finally, on the matter of delay, the
crucial enquiry is whether the fourth shock (and the fifth if required) would
have been given materially earlier had the Lohmeier been in proper working
order and had Sister Glaeser and the second defendant known that.   The
answer to that enquiry entails examination of what resuscitation measures were
in progress between the third and fourth shocks and whether the picture would
have been different in the absence of their ignorance.
[28] In support of the parties’ rival contentions regarding all these points of
dispute five expert witnesses testified.   The plaintiffs called Professor R

Koorn, Associate Professor of Clinical Anaesthesia at Columbia University,
New York and Emeritus Professor D G Moyes, former Academic Head,
Anaesthesia, at Witwatersrand University and currently Professor at the
University of Adelaide, Australia.   First defendant called Professor Pierre
Fourie, Clinical Head of the Department of Anaesthesiology at Pretoria
University.  The expert testimony on behalf of second defendant was given by
Professor AR Coetzee, Head of the Department of Anaesthesiology at
Stellenbosch University and his counterpart at the University of Cape Town,
Professor M F M James.
THE FINDINGS OF THE TRIAL COURT
[29] The trial court found that the cause of the cardiac arrest was in all
probability cocaine toxicity.   This finding was based, in essence, on the
evidence of the second defendant and Professor James and Professor
Coetzee.   Despite holding that the second defendant had given untruthful

evidence concerning the extent of the dilution and the manner of administration
of the  propranolol  and had also falsely alleged having changed the ECG leads
to try to interpret the flat line tracing, the court accepted his evidence in all
other respects.   In particular, the Judge believed his account of events
between the administration of the propranolol and the arrest.   In this regard the
second  defendant testified that within a couple of minutes of the propranolol
being given the patient’s heart rate, blood pressure and other vital signs
reverted to normal levels and remained there till shortly before the onset of
bradycardia.  On this evidence the court found that there was a so-called
period of  normality of some six or seven minutes following upon the
propranolol being administered.
[30] In coming to this conclusion the Judge relied not only on the second
defendant’s evidence but also on the evidence of Dr Rubin, preferring what
they had to say to the evidence of Dr Fayman that the whole sequence from

tachycardia to bradycardia was “very, very rapid”.   The Judge expressed that
preference notwithstanding the finding that Dr Fayman was honest, objective
and a fair observer.   The only respect in which Dr Fayman’s evidence was
preferred to that of the second defendant was in relation to what precise
procedure was being performed at the time when the hypertensive crisis arose
and whether, as alleged by the second defendant, the cocaine plugs were
removed at that stage.   As for Sister Glaeser, the court found “on the basis
of her demeanour and her testimony as a whole” that she was not reliable
concerning the speed with which the patient’s heart rate and blood pressure
changed.
[31] Following from these findings of credibility the Judge held that the
propranolol was injected into the drip line “statim” (all at once), that this
achieved the period of normality referred to and that the second defendant’s
chart and additional notes were genuine and basically correct.

[32] Although certain of the experts, including Professor Coetzee at one
stage of his evidence, considered a swift injection of one milligram of
propranolol to be unreasonable, the trial court accepted Professor Coetzee’s
later evidence, and the opinion of Professor James, to the effect that neither the
speed of administration nor the degree of dilution of a dose of one milligram
would have had any adverse effect on the patient.   These two experts were,
in the Judge’s view, independent and objective and their evidence exonerating
the second defendant in this and other respects was considered at least as
motivated, authoritative and impartial as any condemnatory evidence by the
other experts.   It was accordingly held on their evidence, and by reason also
of relevant concessions by the other experts, that the second defendant’s
respective diagnoses of too light anaesthesia,of over-action of the propranolol
and of the heart’s arrested state as asystole, were reasonable.
[33] With regard to the resuscitation, the court found that the measures taken

to combat the diagnosed asystole were appropriate and that it had been
reasonable to resort to, and persist with, defibrillation after that.   Without a
firm finding that the Lohmeier was in working order the Judge nevertheless
considered it impossible to determine when the heart become susceptible to
defibrillation and therefore held it not proved that the heart was in fact
susceptible at any time when the Lohmeier was used.   As to culpable
ignorance, it was found that the first defendant had done everything reasonable
to ensure that its staff was acquainted with the Lohmeier’s “idiosyncratic”
functioning.   No finding was made as to whether the second defendant should
have known about the reducing digital display.   In these curcumstances the
court did not consider whether further defibrillation with a properly functioning
Lohmeier would have restored the heart beat and whether such restoration
would have occurred any earlier than was in fact the case.
THE APPROACH TO THE EXPERT EVIDENCE

[34] In the course of the evidence counsel often asked the experts whether
they thought this or that conduct was reasonable or unreasonable, or even
negligent.   The learned Judge was not misled by this into abdicating his
decision-making duty.   Nor, we are sure, did counsel intend that that should
happen.   However, it is perhaps as well to re-emphasise that the question of
reasonableness and negligence is one for the court itself to determine on the
basis of the various, and often conflicting, expert opinions presented.   As a
rule that determination will not involve considerations of credibility but rather
the examination of the opinions and the analysis of their essential reasoning,
preparatory to the court’s reaching its own conclusion on the issues raised.
[35] What must be stressed in this case is that none of the experts was
asked, or purported, to express a collective or representative view of what was
or was not accepted as reasonable in South African specialist anaesthetist
practice in 1994.   Although it has often been said in South African cases that

the governing test for professional negligence is the standard of conduct of the
reasonable practitioner in the particular professional field, that criterion is not
always itself a helpful guide to finding the answer.   The present case shows
why.   Apart from the absence of evidence of what practice prevailed one is
not simply dealing here with the standard of, say, the  reasonable attorney or
advocate, where the court would be able to decide for itself what was
reasonable conduct.   How does one, then, establish the conduct and views
of the notional reasonable anaesthetist without a collective or representative
opinion?   Especially where the primary function of the experts called is to
teach, with the opportunity only for part-time practice.   In these circumstances
counsel were probably left with little option but to elicit individual views of
what the respective witnesses considered reasonable.
[36] That being so, what is required in the evaluation of such evidence is to
determine whether and to what extent their opinions advanced are founded on

logical reasoning.   That is the thrust of the decision of the House of Lords in
the medical negligence case of Bolitho v City and Hackney Health Authority
[1998] AC 232 (H.L.(E.) ).   With the relevant dicta in the speech of Lord
Browne-Wilkinson we respectfully agree.   Summarised, they are to the
following effect.
[37] The court is not bound to absolve a defendant from liability for allegedly
negligent medical treatment or diagnosis just because evidence of expert
opinion, albeit genuinely held, is that the treatment or diagnosis in issue
accorded with sound medical practice.   The court must be satisfied that such
opinion has a logical basis, in other words that the expert has considered
comparative risks and benefits and has reached “a defensible conclusion” (at
241 G - 242 B).
[38] If a body of professional opinion overlooks an obvious risk which
could have been guarded against it will not be reasonable, even if almost

universally held (at 242 H).
[39] A defendant can properly be held liable, despite the support of a body
of professional opinion sanctioning the conduct in issue, if that body of
opinion is not capable of withstanding logical analysis and is therefore not
reasonable.   However, it will very seldom be right to conclude that views
genuinely held by a competent expert are unreasonable.   The assessment of
medical risks and benefits is a matter of clinical judgment which the court
would not normally be able to make without expert evidence and it would be
wrong to decide a case by simple preference where there are conflicting views
on either side, both capable of logical support.   Only where expert opinion
cannot be logically supported at all will it fail to provide “the benchmark by
reference to which the defendant’s conduct falls to be assessed” (at 243 A-E).
[40] Finally, it must be borne in mind that expert scientific witnesses do tend
to assess likelihood in terms of scientific certainty.   Some of the witnesses in

this case had to be diverted from doing so and were invited to express the
prospects of an event’s occurrence, as far as they possibly could, in terms of
more practical assistance to the forensic assessment of probability, for
example, as a greater or lesser than fifty per cent chance and so on.   This
essential difference between the scientific and the judicial measure of proof
was aptly highlighted by the House of Lords in the Scottish case of Dingley
v The Chief Constable, Strathclyde Police, 200 SC (HL) 77 and the warning
given at 89 D-E that:
“(o)ne cannot entirely discount the risk that by immersing himself in every detail
and by looking deeply into the minds of the experts, a judge may be seduced into
a position where he applies to the expert evidence the standards which the expert
himself will apply to the question whether a particular thesis has been proved or
disproved - instead of assessing, as a judge must do, where the balance of
probabilities lies on a review of the whole of the evidence.”
THE CARDIAC ARREST
[41] We proceed now to consider the issues, commencing with the question

as to what caused the cardiac arrest.   The first matter to which attention must
be given is whether there was a period of normality, as alleged by the second
defendant, after the hypertensive crisis had been resolved and before the
bradycardia manifested itself.
[42] The second defendant’s evidence on that score, and to the further effect
that once the blood pressure and pulse rate declined to within physiologically
satisfactory limits Dr Fayman actually resumed surgery for a short while, is in
conflict with the evidence of Dr Fayman, who testified that he did not resume
surgery.  All he did was to suction up some blood and possibly make one or
two manoeuvres with his scalpel.  There were other important aspects on
which the evidence of Dr Fayman differed.   The second defendant said that
the hypertensive crisis took place shortly after 10:15, that is to say, about a
quarter of an hour after the operation commenced, at a time when Dr Fayman,
who up to that stage had been working on the right nostril, had just moved

over to the left nostril.  According to the second defendant, after the
hypertensive crisis was resolved there was a return to normality which lasted
for about eight minutes until shortly before 10:25 when the patient’s blood
pressure and pulse rate rapidly declined, culminating in the cardiac arrest.  Dr
Fayman, on the other hand, testified that having operated on the left nostril for
approximately fifteen minutes he worked on the right nostril for about ten to
twelve minutes before he noticed what he called unexpected bleeding in the
surgical field.  He stated that he commented on this to the second defendant
who replied that the blood pressure was high.  Dr Fayman said that he then
noted a tachycardia beat on the monitor.  This changed rapidly “within a very
short space of time” into a bradycardia.   At about that stage the operation was
stopped on the orders of the second defendant, the drapes were torn off the
patient and he, Dr Fayman, started a closed cardiac massage which he
continued, with interruptions for defibrillation, until the heart beat was restored.

His evidence in cross-examination revealed his difficulty in expressing in
minutes his estimate of the period from the tachycardia to the arrest but, he
emphasised, “as I recall it, under oath that is my testimony” (i.e., that there was
a short period of time, with  no return to normality between the tachycardia
and the arrest).
[43] There is no reason seriously to question Dr Fayman’s evidence,
supported as it is by his operation notes made shortly after the events in
question, as to the details of the surgery he had performed.   He testified that
the operation was routine in nature and that he had done it nearly 200 times
using the same technique.   He therefore had the knowledge and experience to
assess how long it took him to perform the surgery he had completed.  It
follows that his evidence that he had operated for about twenty-five minutes,
starting from 10:00, and that he had not just moved to the second nostril, as
the second defendant said, but had worked on it for over ten minutes, is likely

to be clearly more reliable than the second defendant’s evidence on the point.
If that is so, the hypertensive crisis probably occurred close to 10:25,some
three minutes before the cardiac arrest at 10:28, and not just after 10:15, as the
second defendant said.
[44] Dr Fayman was, on our reading of the record, by far the best of the
witnesses who testified as to the events in the theatre culminating in the arrest
and subsequent resuscitation of the patient.   He gave a basically clear and
coherent account of what happened while he readily conceded that his
estimates of the time that elapsed during what was clearly a tense and dramatic
period might differ from those of other witnesses.
[45] Dr Rubin, who was found by the trial Judge to provide support for  the
second defendant’s allegation that there was period of normality, was very
vague and unclear about what had happened.  Indeed, she stated in chief that
it was “very difficult for me to recall independently what happened in a

chronological sequence or to recall at all because it has been a long time and
I have not written anything down”.  She added, however, “when certain
situations have been described to me, I can, in certain circumstances affirm
them and certain circumstances say ‘no I do not recall that’.”  Later she stated
that what had happened was “very hazy”.
[46] She said that she had been reluctant to make a statement to the
plaintiffs’ attorneys and had initially declined to attend a meeting with them.
She gave evidence as a witness called by the plaintiffs after they subpoenaed
her.  She said that through the discussions which took place at consultations
she eventually did attend with the plaintiff’s representatives, she had recalled
certain things “more or less”.
[47] She testified that the first indication she had had that something unusual
was happening in the course of the operation was when the resuscitation trolley
was brought into the theatre.  (It is clear from the evidence that the

resuscitation trolley was brought in on the second defendant’s instructions
after Sister Glaeser had drawn up the isoprenaline for  him.   This happened
shortly after the bradycardia.)   She then busied herself in trying to do a blood
test on the patient.  When the resuscitation trolley was brought in CPR was
being performed.
[48] She said that surgery was being done “for most of the time” until the
CPR started.  She could not recall who was performing the CPR nor that a
second defibrillator was brought into the theatre during the resuscitation.
[49] She testified that she recalled that Dr Fayman had mentioned during the
operation that there seemed to be increased bleeding but she could not say
exactly how long this was before the resuscitation trolley was brought in - “if
it was half an hour, 20 minutes or 10 minutes I cannot tell you, but it was
before.”   Contrary to Dr Fayman’s evidence, she claimed that the operation
had continued after the bleed had been reported by Dr Fayman until the

resuscitation trolley was brought in.   Such continuation was a matter of
minutes not seconds, so she said,  but she could not estimate how many
minutes.
[50] When she was cross-examined by counsel for the second defendant it
was put to her that the patient went from a high tachycardia to a bradycardia
over a period of “several minutes”.  She began, “That sounds right but...”,
counsel for the second defendant then interrupting her by asking , “That is the
best you can do, it sounds right?”, to which she replied in the affirmative.
[51] The resuscitation trolley was brought in at a stage after the second
defendant had administered 25 milligrams of ephedrine to counter the decline
in the heart rate and when the blood pressure had fallen to 70 systolic  over 45
diastolic, and after he had asked for isoprenaline to be brought to him from the
recovery room.   Dr Rubin said that she had no recollection of drugs being
fetched from outside the theatre before the trolley came in.   In our view the

trial Judge erred, with respect, in failing to apportion substantial weight to Dr
Fayman’s evidence on this crucial aspect and in according undue weight to the
evidence of Doctor Rubin.
[52] Turning to the evidence of Sister Glaeser, she testified that she had been
present when the anaesthetic was administered  to the patient and had then left
the theatre.  Some time later she was called back by Dr Rubin from the
recovery room where she was attending to patients and told that the second
defendant needed to see her immediately.  From Dr Rubin’s voice, said Sister
Glaeser, there was an air of urgency about the matter.  When she came into the
theatre she saw the second defendant standing in front of the cardiac monitor.
She could hear by the noise of the monitor that the heartbeat was fast.  When
she asked the second defendant what the problem was he answered that the
patient had a tachycardia and ordered her to get him some propranolol from
the anaesthetic trolley in the theatre.  She drew up the propranolol in a syringe

and gave it to him.   He then asked her to get him some isoprenaline.  Because
this was kept in a refrigerator she had to leave the theatre.    When she came
back with the isoprenaline the patient was receiving cardiac massage.  She
thought the second defendant was applying it but it is clear on the evidence
that it was being given by Dr Fayman.  She had just put the syringe containing
the isoprenaline on the anaesthetic apparatus when  the second defendant
called for the resuscitation trolley to be brought in.  She stayed in the theatre
from then on.
[53] Under cross-examination by counsel for the first defendant she said that
the fetching of the isoprenaline followed on the drawing up of the propranolol
with no long time delay in between.  When asked how quickly the patient went
from the tachycardia to the low bradycardia, she said it happened “very
quickly”.  In describing how she saw the period of time from the tachycardia
to the low bradycardia, she used the word “frightening”.   Explaining what she

meant, she conveyed it had happened frighteningly quickly.   Later she was
cross-examined by counsel for the second defendant on the length of the
period from the tachycardia to the bradycardia.   Her answers appear from the
following extract from the record:
“Are you able to help us in saying how long the time period was
from the tachycardia to the bradycardia and how long the time
period was from the bradycardia to the cardiac arrest? -- No.
From the tachycardia to the cardiac arrest could be ten minutes?
-- I do not know.
It could be five minutes? --I do not know.
It could be 15 minutes? -- I do not know.
You do not know.  And similarly, sister, the period from the
tachycardia to the bradycardia, if I call that the first period, and
if I call the period from the bradycardia to the cardiac arrest the

second period, can you tell me whether the first period is longer
than the second period? -- No.
Can you tell me whether they were about the same length? -- I do
not know.”
At another stage of her evidence, she said “I do not remember time”.
[54] When one interprets that last comment in the light of the earlier-quoted
answers it is apparent that her difficulty really lay in her inability, like Dr
Fayman, to recall time in terms of minutes.   Over all it seems fair to say that
if the period between tachycardia and arrest was truly very short it is not
surprising she could not recall the duration of each of its component phases.
She would not have had problems, we think, recalling the fact of such a
remarkably sudden change if indeed it occurred.   The same holds good
regarding her recall that she was summoned by Dr Rubin in order to draw up
propranolol  and that, apart from  her going out of the theatre to fetch the

isoprenaline, the second defendant requested she stay there until the arrest.
[55] Sister Glaeser’s evidence as to when she was sent for is to be compared
with the second defendant’s version on the same point.  In a report prepared
by the second defendant early in 1995 to enable his attorneys to respond to an
enquiry by the plaintiffs’ attorneys, the second defendant, in dealing with the
situation when the patient’s condition deteriorated, said the following:
“The heart rate had deteriorated sequentially 120, 110, 70, 55.  I asked
someone to call Sister Glaeser to help, and administered 15mg of Ephedrine i v
i.” [He later stated this was incorrect: in the space of a minute he gave two doses
of ephedrine, firstly 10 milligrams and thereafter, when he saw that this was not
going to be sufficient, a further 15 milligrams.]
[56] In his evidence-in-chief, by contrast, he said that it was at the time of the
tachycardia that he called for Sister Glaeser as he needed assistance and an
extra pair of hands to assist him “in drawing up things or fetching things”.  He
thereafter administered the propranolol which was drawn up, he said, into a 10
millilitre syringe.   He testified that after that the operation continued for a short

period.  Thereafter “over the following several minutes” the heart rate declined.
He administered ephedrine to counter the decline in heart rate and blood
pressure and then asked for isoprenaline to be brought from the recovery
room, which Sister Glaeser fetched.   (We shall revert to the matter of the size
of syringe in due course, as also the administration of the ephedrine.)
[57] During cross-examination by counsel for the plaintiffs the second
defendant said for the first time that he had called for Sister Glaeser at least
twice, once at the stage of the tachycardia and later when he administered the
ephedrine.  When it was put to him that he only summoned her once he said:
“I recall distinctly Sister Glaeser being called for the tachycardia ... And I recall
her being called at the point of the ephedrine, whether she was in theatre at the
time I have no specific recollection.”
[58] In our view there are no grounds to reject the evidence of Sister Glaeser,
however imprecise her recollection of temporal detail,  that she was only called
into the theatre once and that when she left it thereafter she did so on the

instructions of the second defendant and returned with the isoprenaline.  It
follows that his  assertion, not contained in his preliminary report and raised
for the first time in cross-examination, that she was sent for twice - with an
interval in between - falls to be rejected.  We find that she was called once and
that between the propranolol administration at tachycardia and the ephedrine
administration at bradycardia, there was good reason for her to remain on hand
and not return to the patients in the recovery room.   The compelling inference
is that she was on urgent standby throughout that period.   This ties in with the
period having been a short one and, more particularly, it negates a period of
normality.
[59] There is a further factor which indicates a strong preponderance of
probability in favour of a finding that there was no period of normality between
the tachycardia and the bradycardia.  The second defendant testified that when
the bradycardia took place he ascribed it to an over-action of propranolol.

Therefore he decided to solve the problem by administering isoprenaline
which, as he put it, “forms the ideal antidote to propranolol”.  It is common
cause that propranolol reaches sixty per cent of its peak effect within the first
minute of it’s administration.  The second defendant testified that it has its
peak effect approximately two minutes after injection.  One can readily
understand how he could have thought that a rapid fall from tachycardia to
bradycardia occurring over a period of about two minutes could be caused by
an over-action of the propranolol.  What one cannot understand is how he
could have ascribed to the propranolol the fall that took place from what he
called physiologically normal levels to a low bradycardia some six or seven
minutes after the propranolol was administered.  He would have known that the
propranolol had long since reached its peak.  His diagnosis of an over-action
of propranolol (whether the diagnosis was correct is a question which we shall
consider later in this judgment) indicates on the probabilities that the decline

must have taken place during the period when, to his knowledge, the
propranolol was reaching its peak or at the latest had just reached its peak.
[60] The trial Judge’s finding that there was a period of six or seven minutes
of normality after the propranolol was administered was based on several
considerations.   Firstly, he accepted the evidence of Dr Rubin and the
accuracy of two allegedly contemporaneous recordals by the second
defendant of monitor readings reflecting relative stability in the patient’s
condition shortly before the arrest.   He also accepted estimates by Professor
Coetzee of the various steps which the second defendant said he had taken
from the onset of the hypertensive crisis until the administration of the
isoprenaline.   In the light of those considerations the trial Judge rejected  the
evidence of Dr Fayman and Sister Glaeser.   He also rejected an argument,
strongly advanced by the plaintiffs’ counsel, based on the fact that the second
defendant made entries in the additional notes meaning that there was

tachycardia with normal complex at 10:25, which contradict his recordal of
tachycardia shortly after 10:16 on the chart.
[61] While we agree with the trial Judge’s reasons for his conclusion
regarding the recordal of tachycardia at 10:25 and that the second defendant
may mistakenly have written tachycardia when he meant bradycardia, we
cannot agree with the Judge’s findings regarding the recordal of monitor
readings purportedly showing that the patient’s condition was relatively stable
after the hypertensive crisis.   On this aspect of the case the judgment reads as
follows:
“The medical experts commended the chart for its completeness and as a
specimen of its kind, allowing, naturally, for the dynamics of an operating theatre.
They did not attempt to impugn [the anaesthetic chart] on the ground that the
two recordals appeared curious or faked and I can see nothing concerning them
evincing that.   Expert testimony proving forgery, such as might relate to writing,
ink or other physical features of the document, was not adduced.   The second
defendant attested to an episode of stability and the regular making of these
recordals at the time.   The occurrence of such an episode was not ruled out by
any of the experts as medically not possible and the reality of the readings and
contemporaneousness of the recordals were clearly not refuted by the above

cited excerpts from the testimony of Dr Fayman and Sr Glaeser.   The second
defendant admitted that he made certain entries on [the chart] after the operation
had been completed, inter alia about the bradycardia event, and was criticised
for not having obtained confirmation from any potential witnesses of monitor
readings done after the operation.   This did not apply to these recordals, even
assuming that he  should have had the presence of mind and foresight to have had
the other readings witnessed - which in itself is not beyond question.”
[62] The Judge did not refer to his own finding that the second defendant
had lied in court on a number of aspects, most notably regarding the manner
in which the second dose of propranolol was administered.  Nor did he refer
to the fact that the second defendant clearly lied to the patient’s mother on the
day of the operation when he said that nothing untoward had happened, when
it is clear that he believed that the first defibrillator had not functioned properly
and when he believed that, culpably or not, he had given a dose of propranolol
which caused the arrest.
[63] It is also clear in our view that he was untruthful about the size of the
syringe used in administering the propranolol and also about the administration
of ephedrine.  As regards the syringe, he maintained till late in the trial that its

size was ten millilitres but when disclosure of his original report to his attorneys
was ordered by the Judge consequent upon a strenuously opposed
application, it was revealed that he initially referred to a five millilitre syringe.
Plainly, he intended his evidence to convey more dilution than in fact was the
case.   As to ephedrine, in the additional notes he recorded giving 25 millilitres
of ephedrine “stat”.   In evidence, his version was that there were two
administrations, 10 and 15 millilitres each, over the best part of a minute.   That
version was obviously contrived to  minimise the urgency of the occasion.
Having been prepared to lie to the patient’s mother just after the operation and
prepared to commit perjury at the trial, he was certainly capable of faking
entries on his chart.  Moreover, it is not clear why the Judge adverted to the
absence of expert evidence proving forgery.  The entries concerned were made
by the second defendant himself with the pen he was using during the events
in question.  We do not understand how could it be said that if the entries were

false they would have appeared “curious or faked”.   The ipse dixit of the
second defendant, regard being had to what has been said above about his
credibility on other issues, takes the case no further.  The fact that a period of
normality was medically possible does not prove that it occurred and is at best
a neutral factor.  Nor do the reasonable time estimates for the various actions
allegedly taken by the second defendant take the case much further because
he himself stated that there was a period of several minutes when the patient’s
condition was once more stable, when, as he put it, he “limited or
downgraded” his vigilance on the patient.
[64] In all the circumstances we are satisfied, on the probabilities, that the
second defendant’s evidence that there was a period of normality between the
hypertensive crisis and the onset of the bradycardia, was adequately shown by
the evidence of Dr Fayman and Sister Glaeser, in the respects already
discussed, to be unacceptable.  His evidence should not have been accepted

and we reject it.
[65] It is now appropriate, on the basis of the factual finding - which we
make - that there was no six or seven minute period of normality between the
tachycardia and the  bradycardia, but rather an interval of only about three
minutes of uninterrupted rapid decline, to consider what caused the cardiac
arrest.   At the trial counsel led prolonged and vigorous debate among the
experts on this issue and on related questions.
[66] For the plaintiffs, Professor Koorn said at one point that he could not
say whether  cocaine toxicity or propranolol was the more likely cause of the
arrest but at another stage he identified cocaine as the primary cause and
propranolol as only a possible cause.   He would have preferred a different
beta blocker but conceded that propranolol was not contra-indicated in this
case and a dose conforming to the package insert recommendation was not
really open to criticism.   He also said that despite the drugs administered by

the second defendant the arrest might have occurred in any event.   He
accepted that the diagnosis of too light anaesthesia was reasonable.
[67] Professor Moyes stated that in his view the cause of the arrest was the
propranolol and in particular the manner in which it was given, although he
conceded that cocaine toxicity was a possible cause.  He ascribed the
hypertensive crisis to too light anaesthesia and said that he would not have
countered it with any beta blocker but would have merely deepened the
anaesthesia.   Alternatively, had he used propranolol, he would have
administered a dose of 200 micrograms (one-fifth of a milligram) and waited
for three or four minutes to observe the effect.   In our view the existence of
the hypertensive crisis and the risk it posed, coupled with the possibility that
cocaine toxicity was the cause of the crisis, render both suggested courses of
crisis response illogical and unconvincing.   Later in his evidence Professor
Moyes said that what he objected to was the use of propranolol at all, not the

one milligram dose that the patient received.
[68] Professor Fourie, on behalf of the first defendant, expressed the opinion
that the hypertensive crisis was due predominantly to cocaine toxicity and to
a lesser degree to too light anaesthesia.   He nevertheless accepted the
diagnosis of the latter cause as reasonable.   As for the antidote, he had no
criticism of the use of propranolol and eventually conceded that the
administered dose was reasonable.   Concerning the cause of the arrest, his
view was that it was chiefly propranolol and to a lesser extent cocaine toxicity.
[69] The two experts who testified on behalf of the second defendant,
Professor James and Professor Coetzee, each expressed the view that the
hypertensive crisis and the cardiac arrest were both caused by cocaine
toxicity, with Professor James adding that the propranolol might possibly have
played a small role in bringing about the  arrest.   In their view it was
reasonable to have diagnosed too light anaesthesia, to have used one milligram

of propranolol as a counter and to have diagnosed propranolol over-action as
the cause of the arrest.   They also considered that without the propranolol the
arrest would have occurred in any event.
[70] In view of the conclusion to which we have come it is not necessary to
canvass the expert evidence in more detail.   A careful study of the record in
the light of counsel’s arguments has satisfied us that the evidence of Professor
Koorn, Professor Moyes and Professor Fourie must defer to the evidence of
Professor James and Professor Coetzee.
[71] As regards Professor Coetzee, we take into account that before his
eventual detailed exposition on final recall late in the trial (by which stage the
issue of a reasonable dose of propranolol had been reduced essentially to one
milligram versus half a milligram) he had earlier decried a one milligram dose
given all at once as unreasonable.   The fact remains that, subsequent to the
latter remark, evidence by Professor James and by Professor Coetzee himself,

and yet more evidence by both upon later recall, all of it exhaustively and
painstakingly investigated, established that dilution of the dose and the speed
of its administration were of no importance and that one milligram given all at
once into the drip-line would have had no greater adverse effect on the patient,
if any, than half a milligram or even a fifth.
[72] Professor James is an international authority on the management of
hypertensive crises and on the use of beta blockers to counter them.
Professor Coetzee is South Africa’s leading authority on the effects of
anaesthetics on the heart on heart injury related to anaesthesia, and on
circulatory perfusion in resuscitation.   Their respective fields of expertise
include all the crucial medical issues in the case.   Their eminence is, of course,
no guarantee of the acceptability of their evidence and although it does reflect
the extent of their knowledge and experience it is the quality of their reasoning
that we consider places their evidence on a significantly higher plane than that

of the other experts.   Having weighed their evidence and the arguments of
counsel, we conclude that their opinions as to cocaine toxicity, as to the
diagnoses by the second respondent and his responses to them, and as to his
management of the resuscitation, are persuasive and authoritative and, above
all, logically reasoned and supported by leading medical literature and by
personal research findings and operational experience.   Those considerations
prevail despite, in the case of Professor Coetzee, his original mistaken
impression that an excessive dose of cocaine had been used, and despite the
appearance - and it may well be no more than the appearance - of a subjective
tendency to fasten on to points even of insubstantial worth just because they
could possibly assist the second defendant.   No such criticism, or any
criticism of moment can in our view be levelled at Professor James’s evidence.
[73] Counsel for the second defendant submitted that on the acceptable
expert evidence cardiac arrest was caused by cocaine toxicity and not by

propranolol.   In particular he relied on five factors, derived from the evidence
of Professor James and Professor Coetzee, which may be summarised as
follows:
(1)
A dose of one milligram of propranolol given could not on its
own have caused the arrest   Nothing in the abundant literature
available on the drug revealed that this size of dose had ever had
such a result and Professor Coetzee, who has used propranolol
very frequently in heart surgery, said that in his experience any
connection between propranolol and the arrest could be ruled
out.   In addition, the package insert recommended precisely this
quantity and not as a maximum dose but an initial one.
(2)
The presence of bizarre and broad QRS complexes just before
the arrest is part of the classic picture of cocaine toxicity whereas
such complexes will not be caused by a beta-blocker such as

propranolol.
(3)
The ephedrine and isoprenaline would completely have countered
both the initial dose of propranolol given on induction and the
second dose given during the hypertensive crisis.   If the
propranolol had caused the arrest not only the ephedrine and
isoprenaline but also the adrenaline would have restored a heart
rhythm within the first few minutes after the arrest.  The only
explanation for the fact that the heart did not start again was the
fact that the local anaesthetic effect of cocaine on the heart had
not yet worn off.
(4)
The fact that crepitations were noted in the patient’s lungs by the
second defendant before the arrest (as stated by him in his initial
report mentioned above) is consistent with cocaine toxicity.
(5)
Dr Salitan’s echocardiogram established that the heart muscle still

showed a material injury eight hours after the arrest and that it had
an ejection fraction of 24% while that of normal persons of the
same age as the patient is above 65%.   This was consistent with
cocaine toxicity and inconsistent with an arrest caused by
propranolol because after a propranolol-induced arrest the heart
muscle would have recovered to at least 90% capacity within four
hours after the arrest.
[74] As far as factor (4), is concerned, (the presence of crepitations before
the arrest), we are not prepared to find that the second defendant’s
uncorroborated statement that there were such crepitations  can, in view of the
findings made earlier regarding his credibility, be safely accepted.  It is true that
lung oedema, for which crepitations are a diagnostic sign, was noted by Dr
Salitan when he examined the patient on the evening of the incident but it is
clear that lung oedema would be present in all cardiac failure, however caused,

and this factor accordingly does not in our view lend support to a finding that
the patient’s cardiac arrest was caused by cocaine toxicity.
[75] Counsel for the plaintiffs contended that a finding that there was a short
period of rapid decline after the hypertensive crisis should lead to the further
finding, as the natural and most compelling inference, that propranolol was in
fact the cause of the arrest.   The second defendant had falsely alleged a period
of normality in order to put “a safe distance” between the propranolol he had
administered and the arrest because he believed that the propranolol was the
cause of the arrest.  His lies regarding the manner in which the propranolol was
diluted and the use of a 10 millilitre syringe were also explicable on the basis
that he thought that the manner in which the propranolol was administered
(which Professor Moyes described as “a somewhat cavalier fashion”) had also
contributed to the arrest.
[76] In our view the second defendant’s lies regarding a period of normality

and the manner in which the propranolol was administered do indicate that he
believed at the time that the propranolol had caused the arrest.  It does not
follow, however, that his belief was correct although due weight must be given,
to the fact that, as the anaesthetist, he was in a good position to appreciate
what was happening at the time and to diagnose accordingly.  We have given
careful consideration to this point but cannot see how it can overcome the
cumulative weight of the other four factors relied on by the  second
defendant’s counsel.
[77] It is clear from the evidence of all the experts and the literature to which
they referred that although cocaine is a drug which, as Professor Moyes put
it, can “produce almost anything in the heart”, even in comparatively small
doses, instances of cocaine toxicity under general anaesthetic are indeed very
rare.  On the other hand there is nothing to show that one milligram of
propranolol, even if administered all at once into a drip-line, can cause  cardiac

arrest in a patient such as the plaintiff’s son who was young, strong and
healthy.   Moreover, according to Professor James, propranolol had for long
been the antidote to cocaine toxicity.   He also eliminated the first dose of
propranolol from the reckoning, pointing to the fact that its effect had clearly
been insufficient to prevent the hypertensive crisis.
[78] Although Professor James and Professor Coetzee were of the view that
the second defendant’s diagnosis of too light anaesthesia as the cause of the
hypertensive crisis was reasonable in the circumstances they were both of the
view, with the benefit of hindsight, that the true cause of the crisis was cocaine
toxicity .  We agree.  It will be recalled that according to Dr Fayman, whose
evidence on the point we prefer to that of the second defendant, he had
already worked for ten to twelve minutes on the second nostril before he noted
unexpected bleeding.  On the probabilities the anaesthesia, which had been
constantly maintained in flow and strength up to that stage, and was adequate

to counter the stimulus of all the rasping which had already been carried out,
would not suddenly have become too light.   This points to the only other
possible cause of the hypertension, namely, cocaine, and in all probability its
toxicity continued to be operative until into the resuscitation period.  The
classic picture of cocaine  toxicity leading to cardiac arrest includes ventricular
arrhythmia.   The latter would have been pre-eminently the warning sign of
cocaine toxicity but it was prevented, and so  removed, by the effects of
propranolol.   If, as we find probable, cocaine toxicity was already operative
at the time of the hypertensive crisis then a rapid decline of heart rate and
blood pressure thereafter was to be expected.  It follows that the fact that the
arrest was the culmination of a rapid decline from the time the propranolol was
administered does not assist the plaintiffs to overcome the cumulative effect
of the factors to which we have referred.
[79] It remains  to consider whether the arrest was not caused by cocaine

toxicity and propranolol working in combination.  Professor James, it will be
recalled, was of the opinion that cocaine toxicity was the most probable cause
of the events and propranolol only possibly played a role.  We can find no
basis for differing from that view.   Cocaine toxicity could on its own have
caused the arrest while propranolol on its own could not.  There is no expert
evidence which directly or inferentially renders it probable that a combination
of cocaine toxicity and propranolol caused the arrest.   In the circumstances
we have come to the conclusion that the cardiac arrest suffered by the patient
was, on the probabilities, caused by cocaine toxicity alone.
[80] The next question to be considered is whether the second defendant
was negligent in allowing Dr Fayman to use cocaine or in managing the case
as he did when he knew that cocaine had been used.
[81] The first point to make is that the quantity of cocaine used in the solution
in which the nasal plugs were soaked, viewed as a dose, was within the limits

of what was widely regarded as safe.  It is also regarded as acceptable for
cocaine to be used, as it was in the present case, by a plastic surgeon doing a
rhinoplasty.   Dr Fayman had used it a great many times with no adverse
results.   Professor Moyes, who originally stated that the quantity concerned
was excessive, later conceded, after re-reading the literature, that  it was not.
Cocaine toxicity - a very rare result, on the evidence, and even more so given
the quantity of cocaine actually absorbed - was therefore not at any stage
reasonably foreseeable in the sense explained earlier in this judgment.
Secondly, all the experts agreed that the second defendant’s  diagnosis of too
light anaesthesia as the cause of the hypertensive crisis was reasonable.   We
are satisfied, in addition, that there is no basis for finding that his decision to
treat it by the administration of one milligram of propranolol, in the manner
indicated in the package insert, can be regarded as negligent.
[82] Even if he should have diagnosed the cause of the bradycardia as

cocaine toxicity, cardiac arrest was then virtually inevitable and there was
nothing he could have done, on all the evidence, to prevent the arrest in the
minimal time available.  Therefore, in our view his failure to make that
diagnosis, even if it had been negligent, was not causally linked to the arrest.
[83] It remains to point out that even had the evidence justified the conclusion
that the arrest was due to propranolol, either alone or in part, it is seriously
open to question whether the arrest would have been foreseeable as a
reasonable possibility in the legally relevant sense but it is, in the result,
unnecessary to pursue that enquiry.
THE RESUSCITATION PROCESS
[84] The only submission for the plaintiffs that the Lohmeier was defective
essentially depends on the inference, as the most plausible one which can on
all the evidence be drawn, that a heart beat would have been restored had the
Lohmeier delivered the required charge when any of the first three shocks was

administered.   In this connection counsel for the plaintiffs also sought to place
reliance on the evidence of Sister Glaeser and the second defendant that the
reaction of the patient’s body was “sluggish” whereas when the second
defibrillator was used the body’s response was unmistakably sharper.   The
difficulty facing the plaintiffs on the question of the body reaction is the
evidence of Dr Fayman.    As already stated, we find his account of events in
the theatre the most reliable of all.   It was his evidence that the bodily response
to all the shocks was the same.   Bearing in mind that he was required, with the
delivery of each shock, to cease applying CPR and to stand back and await
developments  he would have been well positioned to observe, as well as
concerned, to note the patient’s reaction, so as to know whether it was going
to be necessary for him immediately to resume the cardiac massage.  Sister
Glaeser said she would not contradict Dr Fayman’s evidence on this point and
there is the additional consideration that the second defendant had the motive

to blame the Lohmeier and Sister Glaeser, to judge from evidence which it is
unnecessary to recount, had the motive to be partisan towards the second
defendant.   We therefore cannot accept the evidence of these two witnesses
in preference to Dr Fayman on the matter of the patient’s reaction to the
shocks with the Lohmeier.
[85] Reverting to the inference to be drawn from the failure of those three
shocks to restore cardiac activity, it is essential to  the plaintiffs’ case that the
heart was at all relevant times not only in fibrillation but in fibrillation amenable
to defibrillation.
[86] The evidence is that the ECG tracing of a flat line was present from just
before cardiac arrest until the heart beat was restored - that is to say, when a
tracing could in fact be seen in the intervals between bouts of CPR.   The
expert evidence is unanimous that from a flat line one cannot deduce whether
the heart’s state is asystole or fine fibrillation.   According to Professor James,

what fibrillation there was in this case was only ever fine because coarse
fibrillation is easily discernible on the monitor and there was no sign of that.
Fine fibrillation, on the weight of all the expert evidence, has poor prospects
of conversion because it is not always amenable to successful defibrillation.
What does, perhaps, tend to favour the plaintiffs is the consideration (also on
the weight of the medical evidence) that if cocaine toxicity alone caused the
cardiac arrest, the state of the heart when that occurred would probably have
been fibrillation, not asystole.   Consequently, if the ECG tracing remained the
same after that, all the indications are that the heart was in fine fibrillation
throughout the period that resuscitation was in progress.   The difficulty,
however, as the trial court found, is that one does not know when this
fibrillation became amenable.   In this regard we are left with very little more
than speculation.   Although Professor James did say at one stage in his
evidence that he would “guess on the probabilities” that there was reversible

fibrillation present on at least one occasion when the Lohmeier was used, he
later conceded, as we think he had to, that the success of the fourth shock is
the only real evidence of the existence of amenable fibrillation.   Although it is
possible that the ongoing CPR and adrenaline were having a progressively
stronger influence in rendering unamenable fibrillation amenable, that possibility
is counterbalanced by the recognised fact that if fibrillation is present the best
chances of defibrillation are earlier rather than later.
[87] The only other significant factor is the administration of bretylium
tosylate (“bretylium”) at some time between the third and fourth shocks.   The
second defendant testified that this drug acts in a manner analogous to injected
adrenaline, namely, to enhance the output of the body’s own adrenaline.   It has
some advantage, he said, in cases where one has not got a defibrillator that is
working and the patient is in fibrillation.   Professor James supported that
evidence, saying that bretylium is used to treat what is called intractable

fibrillation, in other words fibrillation which resists conversion despite repeated
defibrillation attempts.   It is a drug that tends to stabilise the heart rhythm and
to improve the chance of successful defibrillation.   Although Professor James
added that he could not say that bretylium actually made a difference in this
case, in our view there exists, on the evidence, a realistic possibility, not
overcome by any stronger possibility favouring the plaintiffs, that it was
bretylium that converted a stubbornly resistant fibrillation to a state amenable
to reversal and that successful defibrillation would not have been possible
earlier even with a functional defibrillator.
[88] It follows that it has not been proved that the Lohmeier was defective in
the respect contended for.
[89] We come, then, to the alternative argument advanced for the plaintiffs
concerning the Lohmeier, namely, that Sister Glaeser and the second
defendant’s culpable ignorance concerning its features and operation led to an

unreasonable delay in the resuscitation.
[90] We are satisfied that the learned Judge was not entitled to find that
enough had been done by first defendant to train its staff in the use of the
Lohmeier.   Sister Glaeser did not claim to have forgotten what she had once
known or been told about the Lohmeier.   She was clearly always ignorant of
the fact that the reducing digital display was a feature which in no way impeded
the efficacy of the apparatus.   The inescapable inference is that she had not
been properly instructed.  Clearly it was the first defendant’s responsibility to
see to it that she was.
[91] The second defendant, as the anaesthetist, was the person in charge of
the resuscitation efforts.   He was similarly ignorant.   Bearing in mind that a
defibrillator is specifically intended for use in an emergency life-saving situation
it is plainly a reasonable requirement that the anaesthetist must know how it
works.   Had Sister Glaeser been so burdened with other tasks that she had

become unavailable to operate the Lohmeier it could very well have been the
second defendant’s unavoidable duty to do so himself.   We find, therefore,
that the alleged ignorance was proved and that both defendants were negligent
in this regard.
[92] The enquiry is then whether any delay in the resuscitation process
resulted from such negligence.  This involves comparing what was done
between the third and fourth shocks with what, as far as the evidence can
show, would have been done had Sister Glaeser and the second defendant not
been culpably ignorant and had the Lohmeier not been discarded but used to
deliver the fourth and fifth shocks.
[93] An answer favourable to the plaintiffs is only possible if in the latter
scenario the fourth shock would have been not only a material degree earlier
but successful.   (One assumes that if a fifth shock had in that postulated
situation been necessary it would have followed very soon after the fourth , as

was the actual position.)
[94] In contending for undue delay, the plaintiffs’ counsel placed great
emphasis on the estimate given by the second defendant in an early report to
Professor Coetzee that it would have taken three to five minutes to fetch and
instal the second defibrillator, which time lapse would not have occurred had
the Lohmeier been known to be functional.   While it is open to the plaintiffs
to seek to rely on his estimate as being like an admission against interest (and
therefore probably true), it was only ever an estimate and it must be weighed
with the other relevant estimates, all of them made in later recollection of events
of great urgency which occurred when there was no incentive for anyone to
take specific note of time.   The evidence of Dr Fayman was that fetching the
second defibrillator took only about two minutes and Sister Montgomery - who
fetched it - made an estimate of forty-five seconds.   Sister Glaeser’s evidence
was that there was no delay in the defibrillation because she administered the

third shock while the replacement defibrillator was being fetched.   In his own
evidence, the second defendant said that took about three minutes.   He went
on to say that while it was being fetched he was busy with all those things
which had engaged his attention during the intervals between the first three
shocks and that when the next defibrillation was required the second
defibrillator was already available.
[95] Under cross-examination he said he treated as for asystole for four
minutes and indicated that the intervals between the first three shocks were each
three or four minutes, “of that order”.   Allowing for the time it would have
taken to cease massage, prepare and deliver each of the first three shocks and
wait for the ECG screen to clear to see the results, it is probable that when the
outcome of the third shock was apparent on the screen, the resuscitation
period would already have been eleven to thirteen minutes old.   One knows
that the outcome of the fourth shock was electrically monitored in the sixteenth

minute but whether that shock was actually given late in the fifteenth minute one
cannot know.   All one can say, therefore, is that the interval between the third
and fourth shocks extended for a period of between three and five minutes.
Given the in-built uncertainties and the incidence of the onus, it is not possible
to find that this interval was actually longer than each interval between the earlier
shocks.   It was never suggested that the latter intervals (three or four minutes
each) were unduly long.   On the evidence of the plaintiffs’ witnesses and that
of the second defendant, the substitute defibrillator was fetched and installed
in less time than that or, at best for the  plaintiffs, not longer than that.
[96] What is also clear is that in those earlier intervals repeated applications
of CPR and adrenaline were essential to try to maintain blood flow to the
patient’s brain.   The same would probably have occurred prior to the fourth
shock had it been given with the Lohmeier .   However, the question whether
in that event the  second defendant would also have administered bretylium,

the question as to how long bretylium would have taken to render the heart
amenable and the question whether bretylium would have been given any earlier
than it was in fact, remain unresolved.
[97] In addition, there is the real possibility that if the Lohmeier had been
thought to be fully functional second defendant would not have considered
resorting to bretylium.   It was partly because he thought the Lohmeier was not
working properly that he decided to give bretylium at all.   Had he not
administered it, the chance that it was bretylium that brought about an amenable
fibrillation could never have arisen.   In that event it cannot be said that an
earlier fourth shock than was actually the case would have restored a heart beat.
In our view, therefore, it was not shown on a balance of probabilities that
Sister Glaeser and the second defendant’s culpable ignorance caused delay in
the resuscitation process.
[98] We do not overlook in this connection the letter written by Dr Malkin to

Protea Medical Services in which he complained about the Lohmeier and
referred to a delay in the resuscitation.   In his evidence, however, he explained
that he based the contents of the letter on what Sister Glaeser reported to him
on the day of the operation.   He testified that she did not allege a delay and it
was his inference from what she said about the functioning of the apparatus
that there had been a delay.   Much as the letter has the appearance of an
admission it cannot possibly have the effect of an admission once, as is clear
from the evidence, his inference was based not on personal knowledge or
anyone else’s allegation to him or any other possible factual foundation.   That
conclusion finally disposes of the case against the first defendant.
[99] It remains to consider the allegation that the second defendant negligently
managed the resuscitation by not defibrillating earlier than he did and, in
particular, by not administering three quick shocks in what was referred to in
the evidence as a “stacked sequence”.

[100] As to earlier defibrillation, our finding that it was reasonable in the
circumstances for the second defendant to conclude that the cardiac arrest was
due to propranolol over-action necessarily means that he was justified in
inferring that the heart was in asystole.   The expert evidence is clear that that
would have been the nature of the arrest had propranolol caused it.   In
addition, the flat line ECG tracing strengthened that inference.   Consequently
it was reasonable to resuscitate as for asystole for as long as he did.   To
defibrillate when that was his diagnosis would have been wrong.   Each
defibrillation causes some damage to the heart and defibrillation would have
rendered an asystolic heart less likely to be susceptible to the effects of CPR
and adrenaline.
[101] After some four minutes second defendant decided to defibrillate.   He
made that decision not because he diagnosed fibrillation but because the
alternative was to accept the patient as dead.   Indeed, there never was any

indication, but for the fact that the fourth shock elicited a heart beat, that
fibrillation was in fact existent.   He therefore decided to take the chance that
there was not asystole but fibrillation present.
[102] The evidence of Professor Moyes, in reliance upon the algorithms
mentioned above, implies that the patient should then have been given three
quick “stacked” shocks or nothing at all.   This seems to us to be illogical.   In
the first place the administration of three consecutive shocks without any
interval for attempts by way of CPR and adrenaline to maintain circulation to
the brain would, as Professor James cogently reasoned, have been dangerous.
It would have left the brain without any meaningful circulation for the best part
of a minute.   And if it was asystole after all, three quick shocks would virtually
have eliminated any recovery.  Secondly, a decision to leave the patient for
dead without even trying defibrillation could have had no reasonable basis
whatever.   These considerations reinforce the contention of Professor James

that the algorithms are predominantly guidelines for rescue services and that the
anaesthetist in the theatre is generally better placed to decide what to do if the
patient suffers a cardiac arrest.
[103] Having embarked on the defibrillation route, it was necessary after each
unsuccessful shock to maintain circulation and to take some time in order to
administer CPR and adrenaline and to let these measures have effect before
trying the next defibrillation.   It follows that up to the time of the third shock
fault has not been proved as regards the second defendant’s management of
the resuscitation.
[104] As far as events after that are concerned, what has been said earlier in
relation to the question of culpable ignorance and delay applies with equal force
here.   To repeat, it has not been shown that without the second defendant’s
culpable ignorance in respect of the Lohmeier, the patient’s heart beat would
have been restored any sooner than it was.   The case against the second

defendant was therefore not proved.
THE ORDER AND COSTS
[105] Much as the plaintiffs deserve the sympathy of all for the awful fate that
has befallen their son and the profound grief this must have caused them we
conclude that the trial Judge was right to dismiss the claim.   It follows that the
appeal cannot succeed.
[106] On the matter of costs it remains to say that although the Judge said that
he deplored the second defendant’s untruthfulness in the few respects in which
he was found by the trial court to have lied, his dishonesty on our findings went
far beyond that.   He deviously contrived a false and misleading operation
record,  he colluded with Sister Glaeser and Sister Montgomery to obtain first
defendant’s documentation concerning the Lohmeier and he knowingly gave
evidence that was false in very numerous respects in an endeavour to eliminate
propranolol as the cause of the cardiac arrest and impede a proper investigation

into that event.   There is no place for such conduct in an honourable
profession.
[107] Although the second defendant’s counsel declared during the cross-
examination of his client by the plaintiffs’ counsel (on 19 May 1997, roughly
half-way through the trial) that the defence based on cocaine toxicity depended
in no way on there having been a period of normality, investigation of that issue
took up a considerable amount of court time and the trial Judge devoted a
substantial degree of attention to it before accepting (wrongly in our respectful
view) the second defendant’s evidence on the point.   There can be little doubt
that had the second defendant not advanced this false version and not given
false evidence in the other respects mentioned above, and had he accepted at
the stage of the Rule 37 discussions (if not earlier) that the time from the
hypertensive crisis to arrest was as alleged by the plaintiffs and found by this
Court, the length of the trial and the scope of the appeal would have been

materially reduced.
[108] Counsel for the plaintiffs did not, either when requesting leave to appeal
or in their heads of argument in this Court, seek a special order for costs
against the second defendant and only referred to the matter in reply in answer
to a question from the Bench.   We think that this is an appropriate case to
consider whether such an order should be made as a mark of this Court’s
disapproval of the second defendant’s dishonesty, and also by reason of the
extent to which the duration of the proceedings was increased.   The second
defendant has not been heard on the matter of a special order and he must be
afforded the opportunity to deal with it.   It is also necessary to invite further
submissions from the second defendant as to whether this judgment ought to
be referred to the Health Professions Council.
[109] The order we make is as follows:
1.
The appeal is dismissed as regards the issue of liability.

2.
By reason of the terms of paragraph 3 below all questions of
costs, both of trial and appeal, will stand over for later
determination.
3.
The second respondent is called upon to file written submissions
on the question as to what costs order should be made by reason
of the considerations discussed in this judgment and why an order
should not be made referring the judgment to the Health
Professions Council for such action as it may consider
appropriate.
4.
The other parties are at liberty also to file written submissions on
the costs question raised in paragraph 3 above in so far as they
have an interest in such question.
5.
Submissions drawn pursuant to this order must, after mutual
exchange of respective drafts between the parties (if applicable),

be filed with the Registrar of this Court within two (2) weeks of
the date of this order.
_________________________
CT HOWIE
JUDGE OF APPEAL
_________________________
I G FARLAM
JUDGE OF APPEAL
_________________________
D CHETTY
ACTING JUDGE OF APPEAL