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[2010] ZASCA 133
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Mutual & Federal Insurance Company Ltd v SMD Telecommunications CC (486/09) [2010] ZASCA 133; 2011 (1) SA 94 (SCA) ; [2011] 2 All SA 34 (SCA) (1 October 2010)
Links to summary
THE
SUPREME COURT OF APPEAL OF SOUTH AFRICA
JUDGMENT
Case no
:
486/09
In the matter between:
MUTUAL & FEDERAL INSURANCE COMPANY LTD
......................
Appellant
and
SMD TELECOMMUNICATIONS CC
..................................................
Respondent
Neutral citation:
Mutual & Federal Insurance Company
Ltd v SMD Telecommunications CC (486/09)
[2010] ZASCA 133
(1 October
2010)
Coram:
NAVSA, CLOETE, MHLANTLA, SHONGWE and TSHIQI JJA
Heard: 19 August 2010
Delivered: 1 October 2010
Summary:
Insurance contract – Occurrence Clause covering
bodily injury caused ‘solely’ and ‘independently’
of any other cause – Exception Clause excluding any
pre-existing death or infirmity.
______________________________________________________________
ORDER
______________________________________________________________
On appeal from:
Western Cape High Court (Cape Town) (Davis J
sitting as court of first instance):
The appeal is dismissed with costs.
______________________________________________________________
JUDGMENT
______________________________________________________________
TSHIQI JA (Navsa, Cloete, Mhlantla, Shongwe JJA concurring):
[1] On 1 July 2002, the appellant and the respondent concluded a
contract of insurance. The clauses relevant to the present dispute
are the Occurrence and Exception Clauses. In terms of the Occurrence
Clause, the appellant undertook to compensate the respondent
in the
event of disability or death of one of its managerial staff,
occurring as a result of ‘bodily injury caused solely
by
violent, accidental, external and visible means which injury shall
independently of any other cause be the sole cause of any
of the
results’ (which included death). The Exception Clause
specifically excluded cover for ‘any occurrence consequent
upon
any pre-existing physical defect or infirmity’.
[2] On 10 October 2002 Mr Keith Compton-James (‘the deceased’),
who held the position of Chief Executive Officer of
the respondent,
sustained orthopaedic injuries in a motor vehicle collision. On 18
May 2003, seven months later, he died. His death
was precipitated by
a plaque rupture which
caused
a myocardial infarction (a heart attack). It was not in dispute that
the deceased fell within the ambit of managerial staff
as
contemplated in the contract.
[3] Before the collision, the deceased had a history of coronary
problems. In 1999 and 2001 he was diagnosed by a cardiologist,
Dr
Tyrell, to be suffering from high blood pressure and presented with a
cystolic murmur. He had also presented clinical features
of aortic
stenosis (narrowing of the aortic valve of the heart) together with a
slightly leaking mitral valve and evidence of left
ventricular
hypertrophy (the heart muscle was thicker than normal). He was
advised to change his lifestyle and to stop smoking
and drinking. An
electrocardiogram and echogram indicated he had had a previous
myocardial infarction. On both occasions Dr Tyrell
also noted that
the deceased had developed mild claudication (a narrowing of the
arterial supply to the muscles of the legs).
[4] On the day of the collision he was admitted to the Milnerton Medi
Clinic for trauma care and treatment. On 11 October 2002,
he was
taken to theatre where a doctor carried out an open reduction and
internal fixation of the right femoral fracture and an
open reduction
and internal fixation of the distal left femur and a patellectomy of
the left knee were performed. He remained there
until 25 October 2002
when he was transferred to the Panorama Rehabilitation Unit for after
care. On 29 November 2002, it appeared
that his left knee had flared
up and was painful. His doctor carried out an arthroscopy and a wash
out of turbid fluid of the left
knee. He was taken back to the
Panorama Rehabilitation Unit.
[5] On 13 December 2002, he was discharged to his home. He walked
with the aid of a walking frame and at times required the use
of a
wheelchair. While at home, it appeared that there was a wound on the
left heel and toe. He utilised the services of a nurse
to change the
dressings. It became necessary for him to be referred to a vascular
surgeon, who, on 15 January 2003, carried out
a femero-popliteal
bypass of the leg. He was discharged on 23 January 2003. On 27
January 2003 he commenced at his home with a
process of
physiotherapy.
[6] On 30 January 2003 (more than three months later) the deceased
was readmitted to Panorama Rehabilitation Unit because it appeared
that his health condition had deteriorated. He could not get out of
bed, his speech was slurred and he looked pale and drawn. Dr
Rossouw,
a general practitioner, was consulted. On 5 February 2003, Dr Rossouw
referred him to Dr Du Toit, a physician. After setting
out the
deceased’s condition and his prescribed medication, he
commented: ‘Ek mis iets hier ek hoop jy kan help’.
In the
referral, Dr Rossouw also described the deceased’s condition as
anaemic, that he stammered, and that his C-Reactive
Protein (CRP)
which had been 226 had reduced rapidly to 195, after five days of
anti-biotic treatment. His sodium level was 120.
(CRP is found in
blood in small quantities and the normal level is less than five mg
per litre. It is an important measurement
of inflammation in the
body.) On 6 February 2003 he was readmitted at Panorama Hospital for
treatment of sepsis that developed
in relation to a plate in the
right hip by Dr Lategan.
[7] After a series of tests, Dr Du Toit determined that the deceased
had developed a methicillin resistant staphylococcal infection.
He
placed the deceased on vancomissien and rifampesien, which are two
powerful antibiotics. On 18 February 2003 an orthopaedic
surgeon, Dr
Lategan, removed the hardware from the right hip because it was
infected. The deceased consulted Dr Du Toit again on
7 March 2003. Dr
Du Toit noted that the deceased’s condition had improved. He
could walk with a frame, his CRP had dropped
to 40, his sodium level
had improved and his blood pressure was under control because he was
taking a prescription drug called
norvasc. On 14 April 2003, on a
further visit to Dr Du Toit, he noted that the left knee was sore,
that the right hip had improved,
that the CRP level had improved to
30, and that his haemoglobin had improved from 9.1 to 11.4, but the
sodium level was still low
at 114 ml per litre. On 15 April 2003, his
physiotherapist discontinued her sessions because she believed that
no further improvement
appeared to be possible. At that stage he
walked a maximum of approximately 20 metres with a zimmer frame. He
attended work on
a daily basis, but only for a few hours. He
continued to attend work on a relatively regular basis until 18 May
2003 when he was
found dead, at home.
[8] During the deceased’s lifetime, the Insurance Company paid
out an amount to the respondent in respect of temporary disablement.
Subsequent to his death, the respondent lodged a claim arising out of
the contract of insurance. The appellant repudiated the claim
and
denied that the death fell within the scope of the contract of
insurance. The respondent instituted a claim in the Western
Cape High
Court. That court (Davis J) held in favour of the respondent. This
appeal is directed, with leave of the court below,
against that
finding.
[9] Put simply, having regard to the Occurrence Clause referred to in
paragraph 1 , the dispute between the parties in the court
below and
before us can be telescoped as follows: The appellant contends that
the deceased was at high-risk before the collision,
that he had
already suffered a heart attack in the past and had maintained a
lifestyle that was not conducive to good health and
that the plaque
rupture had occurred naturally because of these factors and cannot be
said to be due to the collision as required
by the Occurrence Clause.
This, they submitted was especially so given the lapse of
approximately seven months from the time of
the collision to the time
of his death. The respondent, on the other hand, contends that the
serious injuries that were directly
due to the collision were such
that they developed complications, including infection, and that this
led to a marked deterioration
in his health and ultimately caused his
death within the terms of the Occurrence Clause.
[10] The divergence of views set out in the preceding paragraph, were
predicated on the views of the parties’ respective
experts. The
court below favoured the views of Dr Tyrell, the deceased’s
cardiologist, against the views of Dr Mabin, a cardiologist
who
testified in support of the appellants’ case.
[11] At the outset it is necessary to consider the
use of the words ‘bodily injury’ in the Occurrence
Clause. There
is a long line of cases in which it has been recognised
that even if the loss is not felt as the immediate result of the
peril
insured against, but occurs after a succession of other causes,
the peril remains the proximate cause of the loss, as long as there
is no break in the chain of causation. One such case is
International
Shipping Co (Pty) Ltd v Bentley.
1
In that case
it was
stated:
‘
The
enquiry as to factual causation is generally conducted by applying
the so called “but-for” test, which is designed
to
determine whether a postulated cause can be identified as a
causa
sine qua non
of
the loss in question. In order to apply this test one must make a
hypothetical enquiry as to what probably would have happened
but for
the wrongful conduct of the defendant. This enquiry may involve the
mental elimination of the wrongful conduct and the
substitution of a
hypothetical course of lawful conduct and the posing of the question
as to whether upon such an hypothesis plaintiff’s
loss would
have ensued or not. If it would in any event have ensued, then the
wrongful conduct was not a cause of the plaintiff’s
loss;
aliter,
if
it would not so have ensued. If the wrongful act is shown in this way
not to be a
causa
sine qua non
of
the loss suffered, then no legal liability can arise. On the other
hand, demonstration that the wrongful act was a
causa
sine qua non
of
the loss does not necessarily result in legal liability. The second
enquiry then arises, viz whether the wrongful act is linked
sufficiently closely or directly to the loss for legal liability to
ensue or whether, as it is said, the loss is too remote. This
is
basically a juridical problem in the solution of which considerations
of policy may play a part. This is sometimes called “legal
causation”.’
[12] Returning to the question of which of the two views referred to
in paragraph 10 above should win the day, it is necessary
to consider
the evidence of Drs Tyrell and Mabin.
[13] According to Dr Tyrell, a person suffering from chronic vascular
disease has by definition widespread areas of plaque in arteries
throughout the body (atherosclerosis or, in common parlance,
hardening of the arteries). The most common arteries to be affected
by plaque are those supplying the lower limbs, heart and brain.
Coronary heart disease is a condition characterized by long periods
of chronicity and stability, and also at times by periods of
instability and acute events, such as myocardial infarction. In cases
of myocardial infarction the event is caused by rupture of plaque in
a coronary artery, which then leads to the formation of thrombus
(‘coronary thrombosis’), which in turn causes occlusion
of the artery and leads successively to myocardial ischaemia
(lack of
blood supply to the heart muscle which also implies shortage of
oxygen) and infarction, and – in some cases –
to
ventricular fibrillation and death. Dr Tyrell’s opinion was
that a major event such as the accident in which the deceased
was
seriously injured has a number of significant patho-physiological
consequences over and above the injuries which a patient
may sustain.
These include the development of pro-inflammatory and pro-thrombotic
states in the body.
[14] Dr Tyrell referred to the fact that the deceased had evidence of
persistent infection and inflammation in the months before
his death,
and to the fact that the deceased’s CRP level was significantly
above normal over a protracted period. In February
2003 the CRP level
was measured as 97mg/l, in March it was 38mg/l and in April (about
four weeks before his death) it was 30mg/l.
As I have said, the
normal CRP level is less than five mg/l. He regarded it as
significant that the deceased not only suffered
major trauma
resulting from the accident but also underwent multiple surgical
procedures and developed infection. According to
Dr Tyrell, each of
these consequences of the accident (‘triggers’), by
causing activation of pro-inflammatory and pro-thrombotic
pathways of
themselves considerably increased the risk of plaque rupture. He
stated that in a vulnerable person such as the deceased
(one more
pre-disposed to a heart attack than the average person), the
concurrence of these events greatly increased the risk of
a heart
attack.
[15] Dr Tyrell concluded that trauma, surgery, infection and
inflammation are well-known and potent triggers for plaque rupture,
and thus heart attack – and that it is beyond doubt that these
triggers were directly attributable to the accident because
they
rendered the chronic stable condition of the deceased to become
acute, unstable and lethal. He stated that although the death
of the
deceased occurred some seven months after the motor vehicle accident,
he regarded the above multiple occurrences as various
triggers of his
cause of death. He found it significant that as recently as four
weeks before the deceased’s death there
were still signs of a
systemic inflammatory state (as shown by persistently high CRP
levels) and concluded that it was probable
that this condition
persisted up to the time of death. Dr Tyrell accordingly held the
opinion that the deceased’s death was
a late or delayed
consequence of the accident and that the deceased would not have died
in May 2003 if it had not been for the
motor vehicle accident.
[16] Dr Mabin’s opinion, on the other hand, was that the
pre-existing health complications of the deceased put him at a high
risk of an ischaemic heart attack at any time. In support of this he
referred to the fact that the deceased was already suffering
from
established atherosclerotic vascular disease at the time of the
accident. Further factors, so he stated, were the fact that
in
October 2002 his disease had already manifested as a previous heart
attack and the fact that the deceased also had disease of
the
arteries in his legs. Dr Mabin stated that the fact that the deceased
died seven months after the accident at a time when he
was improving
as indicated by his clinical state and reduction in his CRP level,
also indicates that the CRP and inflammation reaction
were unlikely
to be directly responsible for his death. He regarded it as an
important factor that the deceased survived in February
when his
condition of inflammation was acute, but died four months later when
it was described as chronic rather than acute –
thus showing
signs of improvement. Dr Mabin stated that the release of
pro-inflammatory chemicals that make the blood more likely
to clot,
occurred in the acute phase after surgery and/or trauma, either
during the event or a day or two thereafter – hence
his opinion
that death was more likely to have occurred during February, during
the acute phase and around the period of the last
surgical
intervention. He concluded that the timing of death showed that the
deceased was most likely to have died from pre-existing
ischaemic
heart disease, and not from the consequences of the accident.
According to him the deceased had sufficient evidence of
serious
pre-existing cardiac disease to have resulted in the deceased dying
at any time, irrespective of the accident – and
that it cannot
therefore be said that the deceased would not have died but for the
accident.
[17] The approach that is helpful in resolving the
divergence between Dr Tyrell and Dr Mabin is the approach adopted in
Michael & another v Linksfield Park
Clinic (Pty) Ltd & another
2
where the court held:
‘
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…’ (para 34).
‘
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
[1997] UKHL 46
;
[1998]
AC 232
(HL (E)). With the relevant
dicta
in
the speech of Lord Browne-Wilkinson we respectfully agree.
Summarised, they are to the following effect…’
‘
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
241G – 242B).
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 242H).’ (para 36-38).
‘…
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 89D-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”.’
(para 40
F-H).
[18] Before I review the evidence and consider the
probabilities in the present enquiry, it is helpful to consider the
decision
of this court in
Concord
Insurance Co Ltd v Oelofsen NO.
3
In that case the executrix in a deceased estate
instituted action for payment under a personal accident policy issued
by Concord.
The policy had an Occurrence Clause which provided that
Concord would provide cover if during the period of insurance the
insured
sustained
‘
bodily
injury which independently of any other cause results in the death’
of the insured. The Occurrence
Clause is similar to the one in issue except that the parties in
Concord
did
not incorporate ‘sole cause’ in their policy. Nothing
turns on this omission because there is no difference between
‘independently of any other cause’ and ‘be the sole
cause’. The use of both terms in the clause is tautologous.
The
deceased was subsequently involved in a motor vehicle accident from
which he emerged apparently unscathed. Within a few hours
after the
accident, he suffered a heart attack. He was rushed to hospital where
he was treated, but ventricular fibrillation developed
and he died
later the same evening. The deceased had been suffering from a
coronary disease known as triple artery atherosclerosis
for a period
of about two years before the accident and his condition was such
that he might have experienced a heart attack at
any time.
[19] The medical experts in
Concord
were agreed that the
immediate cause of the fibrillation was myocardial ischaemia due to a
constriction in the area where the arteries
had already been narrowed
by sclerosis; they differed on the probable cause of the
constriction. Concord’s witness, Dr Baskind,
was of the view
that it had occurred naturally in the progression of the disease and
was unrelated to the accident. The executrix,
on behalf of the
estate, called a Professor Simson who testified that the constriction
was probably caused by a biological process
whereby, due to the shock
of the accident, the sympathetic nervous system released chemical
substances into the blood. The High
Court preferred Professor
Simson’s view. On his evidence it was held ‘
that
the ischaemia of the heart was caused by the stress of the collision
coupled with the pre-existing disease which together resulted
in a
vasoconstriction with the resultant chain of events described above’.
[20] In
Concord,
this court in considering the question of
causation in connection with the cover clause, found it significant
that the insurance
contract did not contain an Exception Clause
specifically excluding pre-existing infirmities. The court reasoned
as follows:
‘
In the
context of the cover clause it may similarly be said that the bodily
injury constituted the proximate cause of death but
in view of the
words “independently of any other cause” this is plainly
not enough. If the insured’s pre-existing
condition was a
contributory “cause” within the
intended
meaning
of this word, Concord must be absolved…’ (at 673 G-H).
‘
What
must accordingly be decided in the present case is whether the
parties, by referring in the cover clause to “any other
cause”
of an insured’s death or disablement, intended to include his
infirmity.
That they
could not possibly have attached a meaning to the word “cause”
which would embrace every conceivable
sine
qua non
is
clear. Mr
Trengrove
conceded
that such a construction would make a mockery of the agreement. The
enquiry must accordingly proceed on the basis that
the word was used
in a restricted sense. But there is no express indication of the
extend of the contemplated limitation nor can
its ambit be gauged by
way of implication from the other terms. Why then should we favour an
interpretation which would specifically
include the insured’s
infirmity? To this question Mr
Trengrove
supplied
no answer. Not a word is said in the policy about the insured’s
state of health either at the time of his application
for insurance
nor at any time thereafter and one is left with the firm impression
that it is something which simply did not concern
the parties.
Because it obviously affects the risk, an insured’s state of
health is commonly known to be of decisive importance
to any life
insurer. Indeed one can almost describe it as standard practice for
insurers to insert a provision in a life policy
whereby the
application for insurance, containing the applicant’s answers
to searching questions regarding his medical history
and the state of
his health, is incorporated in the policy. Moreover, it is not
unusual for accident policies to contain specific
provisions
excluding liability for the insured’s death or disablement
arising from or traceable to any physical defect or
infirmity
existing prior to the accident. (Such a provision appeared for
example in the policy before the Court in
Jason
v Batten (1930)
Ltd
[1969]
1 L1 LR 281 (QB) – a case on which Mr
Trengrove
relied
but which is clearly distinguishable – and in a number of other
cases.) Bearing this in mind, the significance of the
absence from
the present policy of any reference whatsoever to the insured’s
state of health is patent. It is difficult to
accept, to say the
least, that the parties meant to express in the simple words
“independently of any other cause”
an intention similar
in effect to the one evinced by the elaborate provisions in the
policies in cases like
Jason
v Batten.’
4
(at 674 B-H).
[21] The essence of the distinction the court was
referring to in the terms of the contracts in
Concord
and
Jason
v Batten
is that, in the latter case,
the policy contained an Exception Clause that
specifically excluded the pre-existing health condition of the
insured. If the intention
of the parties is to exclude pre-existing
infirmities, this should be unequivocally stated in the insurance
contract. The Exception
Clause in
Jason
v Batten
did so. It
provided
that
‘
No
benefit shall be payable under this [p]olicy in respect of [d]eath,
[i]njury or [d]isablement directly or indirectly caused by
or arising
or resulting from or traceable to –
…………………
(iii)
(a) ………………
(b) Any physical defect or
infirmity which existed prior to an accident’.
[22] In
Jason v
Batten
the court was impressed by the
fact that Mr Jason had not suffered from the thrombosis despite his
matrimonial problems and the
stressful life he was leading. Because
of these factors, the court found in favour of Mr Jason, despite the
Exception Clause. The
court stated at page 288:
‘…
and
if there is not a casual connection with the accident it is a very
remarkable coincidence that the thrombosis should have occurred
just
when it did. But I also find it established that he would have had a
thrombosis quite soon even if the accident had not occurred.
Dr
Gibson thought “he could have gone for five years without a
thrombosis”, but considering all the evidence, both
about Mr
Jason’s temperament and the kind of life he led, I think that
this is an outside figure and I find as a fact that
at the date of
the accident his expectation (using that word in the sense in which
it is used in the phrase “expectation
of life”) was of a
coronary in three years’ time.’
[23]
Jason v Batten
is distinguishable from
Concord
because the agreement in
Concord
did not contain an Exception Clause. Because of
the similarity of the present case to
Jason
v Batten
one would reasonably expect we
would follow the reasoning in that case. The problem for the
appellant, however, is that it did not
plead the Exception Clause and
no reliance can therefore be placed on its terms. Having failed to
place reliance on the Exception
Clause before or during the trial,
the appellant is not able to do so now nor can it seek an amendment
on appeal. This is so because
if the clause had been pleaded, the
onus would have been on the insurer
5
,
during the trial, to prove that the respondent’s occurrence
fell within the terms of the exception and the respondent would
not
be prejudiced because it would have had an opportunity of rebutting
this evidence. It will be recalled that during the deceased’s
lifetime, the appellant paid out a sum in respect of disability
without any reliance on the non-disclosure of the previous myocardial
infarction.
[24] The enquiry in this matter is two-fold. First, the insured would
have to prove on a balance of probabilities that the injury
sustained
in the accident was the proximate cause of the deceased’s death
and that his pre-existing condition was not a contributory
‘cause’
within the intended meaning of this word. The insured is greatly
assisted in this task by the decision of this
court in
Concord
which construed a policy for practical purposes identical to the
present as not including a pre-existing condition. Once the causal
nexus between the accident and the death has been established, the
onus would then shift to the insurer to show on a balance of
probabilities that the proximate cause of the accident was excluded
by the Exception Clause. In this matter it will not be necessary
to
engage in the second enquiry, because of the failure to place
reliance on the Exception Clause.
[25] Both Dr Tyrell and Dr Mabin agreed that the mechanism of death
and the cause lay within the domain of cardiology. Both of
them did
not dispute that the deceased’s health before the accident was
stable. Their dispute was in respect of the temporal
relationship
between the injury and the plaque rupture, which was effectively
linked to what appeared to be the deceased’s
improving medical
status. According to Dr Mabin the risk of a triggering of a heart
attack was in the early phases of acute trauma,
surgery and infection
but it diminished with time; whilst Dr Tyrell’s view was that
the risk persisted and was present even
at the chronic phase. Dr
Tyrell made reference to medical journals to support his hypothesis.
Dr Mabin noted these and could not
criticise nor disagree with them.
He agreed that he participated in the content of the journals as an
editor. His reluctance to
embrace Dr Tyrell’s opinion and the
proposals contained in the journals was based on the fact that there
was no clinical
proof to support the hypothesis. His evidence on the
issue proceeded as follows:
‘
Ja,
look, I don’t think any of us dispute the pathogenesis of
arterial inflammation, plaque rupture etcetera. The question
is what
the triggers are, and its association with generalised systemic
infection. I think we accept that, in the early phases
of acute
trauma, surgery, infection, there is a risk, and there is a risk of
triggering a heart attack. But not beyond that. I
think it diminishes
with time, but not beyond what would be a few days. So in a chronic
inflammatory state, [it] would imply a
long, protracted inflammatory
state, and I don’t think it is well recognised.’
On being asked to comment directly on Dr Tyrell’s hypothesis,
he stated
:
‘
I
think had it happened in the acute immediate period, then I would
accept that it’s an attractive hypothesis, but not months
after
the event, and certainly not at the time that he was improving. I
just find it difficult to accept the relationship between
the two.’
Under cross examination, Dr Mabin again conceded that he found the
hypothesis of Dr Tyrell attractive and stated:
‘
It
lends itself to logical thought in terms of pathogenesis, and I don’t
think any of us disagree with the pathogenesis. What
we disagree
with, is how protracted those acute factors are in the chronic stage.
And I’ve just been unable to find a causal
factor relating to
chronic inflammation and acute myocardial infarction.’
On being questioned further, Dr Mabin appeared to embrace Dr Tyrell’s
opinion and was even constrained to concede that it
may be more than
just hypothesis. This he did in the following responses to counsel:
“
As far
as acute events are concerned, is it generally accepted now that
acute events may lead to plaque rupture?
---You mean acute trauma?
Yes…(intervention)…And
surgery?
Trauma or surgery---It can
increase the likelihood of plaque rupture.
Is that more than just
hypothesis?---I think that’s again epidemiological, and it’s
well known and well established
in medicine that in the acute phase
or major surgery, the likelihood of an acute myocardial infarction in
a patient at risk is
increased.
So that’s more than just
hypothesis---That is.’
[26] Dr Mabin was also constrained to concede that the deceased had a
further protracted difficult time after his initial surgery.
Although
he seemed reluctant to agree that the other incidences of surgery or
trauma could be termed insults to the deceased’s
body he was
constrained to concede this when they were tabulated. The importance
of this concession is that according to Dr Tyrell,
it was the
cumulative effect of these insults arising out of the progressive
series of surgical interventions which caused the
trauma that
triggered the rupture. Dr Mabin accepted that Dr Tyrell’s
hypothesis is logical, but lacks medical data to prove
it. He stated:
‘…
I’ve
analysed what’s happened and I’ve looked for medical data
to support what might have happened and the sequence
of events and I
must say I was in some way almost disappointed not to be able to find
the corroborative evidence that we are looking
for---It’s a
logical hypothesis.’
[27]
Clearly Dr Mabin
was stating that the only reason why he was reluctant to agree with
Dr Tyrell was because of the absence of corroborative
empirical
evidence to support what he himself regarded as a logical hypothesis.
On the probabilities, it can be safely concluded
that the opinion of
Dr Tyrell is logical, was attractive to a fellow cardiologist and is
supported by journal articles and studies
on closely related areas of
cardiology. His opinion in line with
Michael
v Linksfield
was in my view correctly
accepted by the court a quo.
[28] The respondent has therefore proved that the accident was the
proximate cause of the deceased’s death. It not being
open to
the appellant to raise the Exception Clause, the appeal must fail.
[29] The remaining issue is the costs order made
by the court a quo pertaining to a postponement on 30 October 2007,
after the appellant
had abandoned its special plea, and its objection
to the respondent’s intention to amend the particulars of claim
so as to
annex the correct pages of the contract of insurance. The
court exercised a narrow discretion in awarding attorney and client
costs
against the appellant and there is no submission that this
discretion was not exercised judicially. The appellant must
accordingly
fail on this aspect as well.
6
[30] The appeal is dismissed with costs.
______________________
Z L L Tshiqi
Judge of Appeal
APPEARANCES
APPELLANT: W R E DUMINY SC
Instructed by Mellows & De Swardt
Cape Town;
Symington & De Kok, Bloemfontein.
RESPONDENT: D F IRISH SC
Instructed by Otto Krause Inc,
Cape Town; Honey & Partners, Bloemfontein.
1
1990
(1) SA 680
(A) at 700F-I
2
2001
(3) SA 1188
(SCA) para 34; para 36-38; para 40.
3
1992
(4) SA 669
(A).
4
At
p 673 G-H; 674 B-H.
5
Agiakatsikas
NO v Rotterdam Insurance Co Ltd
1959 (4) SA 726
(C); See also
Rabinowitz & another NNO v Ned-Equity Insurance Co Ltd &
another
1980 (1) SA 403
(W);
Aegis Assuransie BPK v Van der
Merwe
2001 (1) SA 1274
(T).
6
Naylor
& another v Jansen
2007 (1) SA 16
(SCA)
at 23F-24D and authorities referred to in footnotes 15 to 23.