IN THE HIGH COURT OF SOUTH AFRICA WESTERN CAPE HIGH COURT, CAPE TOWN
Case No.: 5450/2005
In the matter between:

and

JUDGMENT: 18 May 2009

DAVIS J:

Introduction

[1] Plaintiff, a close corporation, entered into a contract of insurance with defendant in terms whereof defendant, inter alia, agreed to pay compensation to plaintiff in the event of the death of a member of its managerial staff through bodily injury caused solely by violent, accidental, external and visable means which injury, shall independently of any other cause be the sole cause of death.

[2] On 10 October 2002, Mr Dennis Compton-James ('the deceased'), who held a 35% member's interest in plaintiff was involved in a motor accident. At the time he was the chief executive officer of plaintiff. He subsequently died on the 18 May 2003, pursuant to which death, plaintiff claimed in terms of the contract of insurance.

[3] The quantum of plaintiff's claim in the amount of R 611 693.24 has been admitted and is no longer an issue in dispute. The case turned on a question of causation; that is whether the death of the deceased fell within the scope of the contract of insurance.

[4] In turn, that question is dependent upon the meaning and scope of the contract of insurance, the critical part of which is to be found in the following clause:
"Conditional upon the prior payment of premium by the insured and the receipt thereof by or on behalf of Mutual & Federal Insurance Company Limited (hereinafter called "the Company") the Company shall insure and agrees to indemnify the insured by payment or at its option by reinstatement or repair or to pay compensation in respect of the Defined Events as provided hereinafter in the Sections forming part of this Policy occurring during the Period of Insurance Limit of indemnity amount of Compensation or other amounts specified.
These General Exceptions and Conditions shall apply in all respect to the Insurance granted by this Policy except as they may be varied by any specified Exception or Condition in any Section Specification or Annexure to any Section Endorsement which are to be read together and any word or expression to which a specific meaning has been given in any part thereof shaii hear such meaning wherever it may appear.
This insurance contract is conditional upon and will come into effect only following payment of the Premium by the insured and the receipt thereof by or on behalf of the Company.
PERSONAL ACCIDENT (GROUP) SECTION DEFINED EVENTS
The events insured by this Section are as follows If any Occurrence described hereunder shall happen to the Insured person during the Period of Insurance and the insured Person shall thereby suffer any Result described hereunder the Company will pay to the Insured the Compensation specified hereunder. 	OCCURRENCE
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.

RESULTS	COMPENSATION	
A.    Death	A.    A sum equal to the number of years remuneration or the Amount state in the Schedule	

[5] In order to ascertain the exact contours of the dispute between the parties, it is now necessary to set out a brief chronology of the medical history of the deceased.

Dennis Compton-James: a history of coronary problems?
[6] On 6 December 1999, the deceased first consulted Dr Joseph Tyrell, a cardiologist. Dr Tyrell determined that the deceased suffered from high blood pressure, a cystolic murmur and had previously been on treatment to lower his blood pressure. Dr Tyrell also noted that the deceased smoked cigars, consumed alcohol and that he presented clinical features of aortic stenosis, indications of a previous myocardial infraction together with a slightly leaking mitral valve and evidence of left ventricular hyptrophy.

[7] On the 19 December 2001, the deceased again consulted Dr Tyrell. It appeared that he had developed mild claudication, a narrowing of the arterial supply to the muscles of the legs. He also suffered from moderate aortic stenosis and there was some ECG evidence of cardier disease. He was again advised to stop smoking and drinking.

[8] On the 1 July 2002 the parties renewed the contract of insurance, which was known as 'asset care'.

[9] On the 10 October 2002, the deceased was involved in a motor accident in Bothasig, Cape Town in which he sustained serious injuries. He was admitted to Milnerton Medi Clinic for trauma care and treatment. His injuries included an intratrochanteric fracture of the right femur, a comminuted supra-condylar fracture of the femur, a comminuted fracture left of the patella and an injury to the right chest and abdomen.

[10] Pursuant thereto, on the 11 October 2002, he was taken to theatre at the Medi Clinic where Dr Sander performed an operation, in terms of which he carried out an open reduction and internal fixation of the right femur fracture and an open reduction and internal fixation of the left femur and a patellectomy of the left knee.

[11] On 25 October 2002, the deceased was transferred to the Panorama Rehabilitation Unit for after care. On 29 November 2002 it appeared that his left knee flared up and was painful. On the same day, 29 November 2002, Dr Sander carried out an arthroscopy and a wash out of turbid fluid of the left knee. Again he was taken back to the Panorama Rehabilitation Unit.

[12] On the 13 December 2002, he was discharged to his home. He walked with the aid of a walking frame and required the use of a wheelchair. While at home, it appeared that there was a wound on the left heel and toe. A nurse was required to change the dressing. He was then referred to Dr Henk Lourens, a vascular surgeon, who, on 15 January 2003, carried out a femero-popliteal bypass of the leg. He was again discharged 23 January 2003. On 27 January 2003 a process of physiotherapy commenced at the deceased home, conducted by Ms Wanda van der Merwe.

[14] After a series of test, Dr Du Toit determined that the deceased had developed a methacillen resistant stafaureus infection.    He placed the deceased on vancomissien and rifampesien, which are two powerful antibiotics.

[15] On 18 February 2003 an orthopaedic surgeon, Dr Lategan, removed hardware from the right hip because it was infected.

[16] The deceased consulted Dr Du Toit again on 7 March 2003. Dr du Toit indicated that the deceased's condition had improved. He could walk with a frame, his CRP had dropped to 40, his sodium level has improved and his blood pressure had now been controlled because he was taking norvasc.

[17] On the 14 April 2003, Dr Du Toit noted that the left knee was now sore that the right hip was improved, the CRP level had improved to 30 his haemoglobin had improved from 9.1 to 11.4, but the sodium level was still low at 114 mol per liter.

[18] According to Ms van der Merwe, physiotherapy ceased on the 15 April 2003 as no further improvement appeared to be possible. The deceased at this stage walked approximately 20 meters with a zimmer frame he attended work on a daily basis but only for a couple of hours. He determinedly continued to attend office for a few hours a day on a relatively regular basis until the 18 May 2003 when he was found dead.

The essence of the dispute

[19] Plaintiffs case therefore is that his death, on 18 May 2003, flowed from the collision of 10 October 2002 or as stated in the pleadings, the death 'resulted directly and solely from the bodily injuries sustained in the said motor vehicle accident (which) occurred independently of all other causes and was the sole cause of death.'

[20] Defendant did not dispute that the deceased died on 18 May 2003, probably of a myocardial infarction precipitated by a plaque rupture. Defendant contended however that plaintiff was obliged to prove that the injuries suffered by the deceased in the accident, independently of any other cause, was the sole cause of the deceased death in order to justify its claim in term of terms of the policy.

Plaintiff's Case

[21] The plaintiff relied, to a considerable extent on the evidence of Dr Tyrell who had been the cardiologist whom the deceased had consulted on a regular basis. Dr Tyrell postulated the cause of death as myocardial infarction caused by coronary thrombosis. He informed the court:
"So the mechanism of myocardial infarction, which is the - in the heart, is this process of plaque rupture, clot formation and so-called coronary thrombosis.   And that leads to the condition where the heart muscle is deprived of its blood supply and becomes damaged

"/ think it is highly likely that he died of myocardial infarct, precipitated by, caused by those multiple traumas that he - to which he had been exposed."

[22]   Dr Tyrell then continued:
"... its well recognised that's (sic) various natural and unnatural triggers can lead to myocardial infarction...
And then various unnatural triggers ay also provoke myocardial infarction and the way they do that is because they cause release of pro-inflammatory chemicals and they tend to make blood more likely to clot. So they increase the likelihood that these plaques, which are dormant in the coronary and other vascular circulation, may rupture ... So both by increasing the probability of plaque rupture and by increasing the tendency of blood to clot, they create an environment in which myocardial infarction is more likely to occur".
In essence, Dr Tyrell took the view that, while the deceased could hardly be described as a fit or a completely well person prior to the accident.
However at the time immediately before the collision, his peripheral vascular disease may have been chronic but it was stable. At that stage his condition in no way affected his day to day functioning. In short, according to Dr Tyrell, a stable chronic condition had been rendered lethal by the overall impact of the various insults to the deceased body which had taken place as a result of the accident and the medical treatment that the accident had so necessitated.

[23]   Dr Tyrell was asked whether he was surprised that the deceased had died some seven months after the accident. To this question he replied:
"Not really. For example, My Lord, post-operative heart attack or myocardial infarction is a common problem in everyday practice, and my colleagues see many patients, who were sent specifically to try and assess what the risk of patients who have a myocardial infarction or heart attack after some none-cardiac surgery. One tries to assess the risk and then one of course tries to minimise the risk of this sort of thing happening, but it is a common and well recognised and feared complication of surgery. ... And then the same applies also to conditions of chronic inflammation, for example bronchiectasis, which is a chronic inflammation of the lungs, or rheumatoid arthritis which is a chronic joint conditions. So these are chronically - chronic inflammatory conditions which also increase the risk of myocardial infarction."
He then told the court:

[24] Under cross examination by Mr Dane, who appeared on behalf of the defendant, Dr Tyrell was asked in particular as to how surgery and trauma was instrumental in causing the plaque to rupture which then precipitated the myocardial infarction:

"My Lord, we can deal with this in two ways. One is the epidemiological evidence, and that is that after none-cardiac surgery the risk of myocardial infarction is increased.   Obviously it depends on what kind of surgery it is, and it depends on the patient to who you are referring. But the epidemiological evidence is that the risk of myocardial infarction is increased after surgery of various kinds. The other way to look at it, if one wants a mechanism, is to deal with this problem of the process of plaque rupture, and the mechanism is simply that some plaques are vulnerable, and some plaques are stable and what surgery tends to do and what trauma tend to do, it tends to induce and inflammatory state, and that is the body's response to trauma or to surgery. That initiates the healing process. So, for example white blood cells. Heart rate increases. Blood pressure goes up. The platelets in the blood become more active. They are more likely to initiate proteins in the blood, the levels of clotting proteins in the blood increased. The surgery and trauma induce a pro-inflammatory state and they induce a pro-coagulant state. These two combined increase the possibility of plaque rupture and thrombosis...".

[25] Plaintiff also called Mr Mower to testify on its behalf. His evidence was of limited importance. He was employed by plaintiff from 1974 as the company driver. He became friendly with the deceased before the accident. He assisted the deceased both before and after the accident with his purchasers. He testified that prior to and subsequent to the accident deceased drank between 1 and 2 glasses of wine per day and smoked at least one cigar. After the deceased was discharged from hospital, he could only move with the Zimmer frame and a wheelchair. Mr Mower took the deceased both to work and home. Although there was considerable debate about the extent to which the deceased employed a treadmill for exercise which was located at his home, (and hence was relatively active prior to the accident) Mr Mower never saw him actually use the treadmill.

[26] Ms van der Merwe, a physiotherapist visited the deceased home on 27 May 2003 at which stage he was mobilised in a wheelchair and employed the Zimmer frame. When she saw him again on 19 March 2003 his left knee was particularly stiff. On 26 March 2003 she reported that his left knee could not extend and that he complained that he was dizzy he stretched his quads. On 31 March 2003 she reported that his condition was slightly improved. The quad lag was 30 degrees. He walked in an improved fashion from the couch to the kitchen. She saw him again on 4 April 2003, on 07 April 2003, on 22 April 2003 at which stage he walked approximately 20 meters with the Zimmer frame. The quad lag was still 30 degrees. She decided that, at this stage, as there was no improvement in his condition, she should not continue and thus ceased treatment.

[27] After the plaintiff had closed its case it sought by way of an application to reopen its case in order to lead the testimony of a vascular surgeon Dr Jeffery. The basis upon which Dr Jeffery's opinion was sought was due to a suggestion from defendant that the infected heal and toe could have been the result of the natural progression of the deceased's peripheral vascular disease (PVD) and was thus unrelated to the injuries sustained in the collision. Before Dr Jeffery were called, defendant indicated that it no longer persisted with any basis of causation on the grounds of the heel and toe; that is that the injury to the heel and toe may have interrupted the chain of causation. Plaintiff however continued with its presentation of the evidence of Dr Jeffery because it contended that this was material to the general theory advanced by Dr Tyrell regarding plaque rupture. The question as to whether this part of Dr Jeffery's evidence is relevant and indeed admissible can only be determined after an examination of the evidence presented by defendant.

Defendant's case
[28] In essence, defendant's case was that there was no empirical basis to support the theory of Dr Tyrell, that surgery, trauma and inflammation precipitated rapture of the plaque resulting in the myocardial infarction seven months after the initial accident and three months after the last procedure to which the deceased had been subjected on 18 February 2003.

[29] The thrust of the evidence of Dr Neil du Toit and Dr Thomas Mabin, both of whom were called by the defendant, was to contend that neither clinical practice nor the available medical literature supported the approach adopted by Dr Tyrell.

[30] I turn first to deal with evidence of Dr du Toit. Dr du Toit who practiced as a specialist physician at the Panorama Medi Clinic until June 2008, testified that on 6 February 2003 he was approached by Dr Rossouw to assist in the treatment of the deceased's condition. Subsequent to a popliteal bypass on 15 January 2003, the deceased's condition had suddenly deteriorated. Pursuant thereto, Dr du Toit conducted numerous investigations. His emphasis indicated that the deceased presented with a low sodium, a CRP of 196, a haemoglobin count of 9.1 and a methacillen resistant staf auraeus infection cultivated from the left heal. An ECG test indicated that the deceased suffered from aortic stenosis. After the operation by Dr Lategan, in which the infected hardware had been removed from the right on 18 February 2003, some form of improvement in the deceased condition took place.

[31] When Dr du Toit saw him on 7 March 2003, the CRP had declined significantly to 40. There remained a course of treatment of three weeks of anti biotics. The sodium level had also improved. Further improvements took place when Dr du Toit saw the deceased again on 14 April 2003. The left knee at this stage appeared to be warm and therefore the issue arose to whether it had been infected. According to Dr du Toit, he did not know from the deceased of a previous myocardial infarction. He only become aware of this condition some months later. For this reason and, given reports by Dr Murray and Dr Bodenstein which had suggested severe aortic stenosis, Dr du Toit testified that, when he completed the death certificate, he had written that aortic stenosis had been the cause of death. It was only after obtaining the further information that he accepted that the deceased's death was as a result of myocardial infarction.

[32] Dr du Toit resisted Dr Tyrell's evidence that the deceased's death had been precipitated by plaque rupture which was the result of surgery trauma and inflammation. He also rejected the suggestion by Dr Tyrell that inflammation is the same in all conditions and that Dr Tyrell's conclusion was supported by the condition of rheumatoid arthritis which had been linked to acute myocardial infarction.

[33] In this connection the thrust of Dr du Toit's evidence was reflected in the following passage:

[34] A critical part of Dr du Toit evidence in dealing, with what he referred to Dr Tyrell hypothesis, was that, if this hypothesis was true, Dr du Toit would have expected the deceased to have suffered a myocardial infarction when he was at his worst condition, that is in February 2003 when his CRP was 226, when he was suffering from infection, when there was a reduced haemoglobin and a low sodium level and where he was at his least mobile. According to Dr du Toit, three months thereafter, when there were clear improvements in all of these markers, when he was mobile, albeit using the Zimmer frame, and where there was evidence of a slow recovery, it was highly unlikely that the inflammation would have precipitated a rupture of the plaque.

[35] Dr du Toit's evidence was supported by Dr van der Spuy, a specialist surgeon and orthopedic surgeon who have been head of National Trauma Research Programme from 1987 until August 2000. In essence his evidence was captured in the following passage of evidence. Having been asked to comment on the proposition that surgery and/or trauma leads to a myocardial infarction he answered:
"My Lord, I will do this as briefly as I can. In a long career in trauma surgery, I have never seen trauma and surgery, and, for that matter, inflammation, per se leading to myocardial infarction in a patient who had not been a particular ischemic heart disease risk. I cannot say that it cannot possibly occur. What I can say, is, in quite a number of thousand of operations of people not having manifest risk factors, I have not seen a myocardial infarction. The second part of my reply would be, on 3, 4, 5, I can't remember exactly but I have had postoperative deaths from myocardial infarction, but those usually occur intra-operatively. When I say post-operatively, I mean peri-operatively. They either occur during surgery, or within the first few days. I am not aware of - certainly not in my experience, I am not aware though in close colleagues, or in my unit, when I was at Groote Schuur, of a much delayed myocardial infarction arising from trauma and surgery."

[37] The third key witness, who testified on behalf of the defendant, was Dr Mabin. Dr Mabin testified that, with the deceased's profile, he had a 50% chance of surviving for five years; that is with his medical profile, only 50% of patients presenting with such symptoms would be alive after a five year period.

[38] Differing from Dr Tyrell, he distinguished various types of inflammation and differentiated between systemic inflammation and arterial inflammation.   Thus he informed the court:
"The inflammatory process in rheumatoid arthritis is a completely different inflammatory process to what was dealt with in this particular patient."
In short, Dr Mabin contended that there was no medical basis by which to use the condition of rheumatoid arthritis to justify a conclusion that the deceased's myocardial infarction had been increased and the fact that he succumbed seven months later, was not a major obstacle to accepting Dr Tyrell's explanation. Mr Gamble then asked Dr Mabin:
"But on the one hand you've got that, you've got surgery or trauma, and on the other - and the other end of the spectrum, of the continuum, you have rheumatoid arthritis, chronic condition. Why is there no room for something in between, such as we have in the present case?"
Dr Mabin replied:

"/ find it very difficult to believe that temporal relationship existed, such a far distance temporarily, from that last surgical event. I think the man was at high risk of having a myocardial infarction at any time".

[39] Dr Mabin's evidence concentrated, in part, on an analysis of a series of articles which had been handed up into evidence in an attempt to support or debunk the hypothesis of Dr Tyrell. Much was made of this literature by both counsel. Dr Mabin's attitude to the available academic literature was as follows:

"/ think it's an attractive hypothesis but there is no data to support it."
Amplifying upon this statement, he said:
"If it accepted the myocardial infarction was the result of plaque rupture, my contention is that there is no hard, scientific evidence that the plaque rupture would be precipitated this late after an incident, in a man who is, if anything, getting better."
In his view:

Evaluation
[40] In order to evaluate the evidence, it is necessary to examine the legal basis of plaintiff's claim. To recapitulate: the occurrence required to trigger an obligation on the part of the defendant to pay was '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 result'. The contract provided for a series of exceptions which included the following:

[41]   The occurrence clause included two critical components:
1.	Bodily injury caused solely by violent accidental external and visible means;
2.	That bodily injury was 'the sole cause of death' and occurred 'independently of any other cause'

[42] It did not appear to be disputed that the deceased had sustained 'bodily injury' which was 'caused by violent accidental external and visible means having sustained extensive and serious injuries in the motor vehicle accident which occurred on 10 October 2002. Neither was there a dispute that the bodily injuries were caused solely by the accident.

[43] The key question for determination was whether the death of the deceased on 18 May 2003 was not only causally linked to these injuries but, independently of any other cause was the sole cause of his death. The complication in this case it that the deceased suffered from PVD at the time of the accident as the factual matrix as set out earlier in this judgment has made abundantly clear.

[44] Mr Gamble conceded wisely that the deceased was more pre-disposed to a myocardial infarction than an ordinary healthy person by virtue of his PVD as well as his general life style, as emerged from the evidence of Mr Mower.

[46]   The claim was based on a following policy clause:
"If during any period of insurance an insured person sustains bodily injury which, independently of any other cause, results in the death, or permanent disablement of the insured person, the company will pay to the insured person or his estate the compensation state below."
The trial court found in favour of the insured and the matter proceeded on appeal. The insurer contended that there was no bodily injury as envisaged in the policy. This argument was rejected. The question then arose as to the causation in relation to the provision in the insurance policy, which I have already cited.

[47]   Hefer JA (as he then was) said the following, in a passage which given its significance to the present dispute, requires citing in full:
"In the context of the cover clause it may similariy 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.

"However, it seems to me quite clear that the claim must fail for other reasons. The bodily injury was not "independently of all other causes the exclusive ... cause of the disablement". There were two concurrent causes, the pre-existing arterial disease and the formation of the clot. These two causes were independent of each other, and the thrombosis would not have occurred on June 21, 1965, unless both had operated. If there were any doubt about this, it would be removed by the words of the later provision. It seems to me plain that the disablement was ... directly or indirectly caused by or arising or resulting from or traceable to-

[50] Given a distinction which is evident in the policy between a provision for cover and the exemption clause, it would appear that the intention of the parties was to cater for a pre-existing physical defect or infirmity by way of an exception; or as Hefer JA put in Concord:
"an insured's ill health at the time of the accident was not intended to constitute another 'cause'."
Furthermore, had defendant called for a medical examination of the deceased under the policy, it would then have been able to take further steps, such as the insertion of an additional clause to restrict the cover afforded under the policy.

[51] There is no suggestion in this case that the dispute was predicated on non disclosure. Therefore, the battle ground between the parties was based on the following narrow issue: Notwithstanding any medical history or precondition, absent the accident, would the insured then have taken place in the manner in which it did.

[52] Within this context, it is possible to return to the expert evidence which was critical to the resolution of the dispute. There was considerable debate about the three levels of evidence employed by medical science, levels A, B, C (sometimes referred to as 1, 2 and 3) Level A evidence is essentially scientific proof that a well held hypothesis is correct. According to Dr Tyrell, level C evidence includes case reports, expert opinions, committee reports and non randomised cohort studies used as a guide for treatment and prevention without being able to be used to prognosticate patient outcomes.

[53] There was a considerable debate between the experts as to whether there was a viable prospect of being able to present level A evidence in this case, owing to the non availability of a sufficiently large sample group. Dr Tyrell testified that such a study would require the assessment of persons with PVD were then subject to the type of multiple insults that the deceased endured. Dr Tyrell further testified that, in his view, level C evidence would be more congruent with proof on a balance of probabilities, as opposed to level A evidence which arguably equated to proof beyond a reasonable doubt.

[54] By contrast, Mr Dane submitted that Dr TyrelPs hypothesis, unsupported by the academic literature or other expert evidence was no more than a possibility rather than a probability. Mr Dane therefore submitted that a far more probable explanation was that the deceased's death was precipitated by a rupture of the plaque as a result of his severe vascular disease. Dr Mabin's uncontested evidence was that within five years of the finding of PVD at the second visit which the deceased made to Dr Tyrell, he had a mortality rate of 50%; that is within five years of this finding, there was a 50% chance of him being dead.

[55] Mr Dane submitted that, on the totality of the evidence, that probability had materialised. As the deceased had a silent myocardial infarction prior to 1999 and further, having due regard to Dr Tyrell's evidence that plaque can rupture and embolise continually this was the probable explanation of what happened on 18 May 2003.   The deceased was in a far more precarious situation when he consulted Dr du Toit on 6 February 2003 then when Dr Lategan last saw him on 16 April 2003. It was at this time that his indicators were at their worst. On 18 February 2003 he been taken to theater where the infected hardware in his right hip had been removed. At this point, he was far more ill that at the time immediately leading up to his death. Had the accident been the cause of death, it was to have been expected that he would have died at that stage. But he did not die the nor did he have a heart attack during this perilous period which, on the basis of Dr Mabin and Dr du Toit's evidence, would have been far more likely. Therefore, no explanation had been preferred within the context of plaintiff's version as to why the myocardial infarction suffered by the deceased could be ascribed to the trauma resulting from the surgery and subsequent inflammation when this had occurred some three months prior to his death and his indicators had suggested an improvement during this period. In summary defendant contended thus: If Dr Tyrell' hypothesis had merit, it is far more probable that it would have happened earlier or within the acute phase on 18 February 2003 than on 18 May 2003. According to Mr Dane, everything pointed to the myocardial infarction on 18 May 2003 not being related at all to the surgery, trauma and inflammation.

Expert Testimony: its application

"It is true that open debate is an essential part of both legal and scientific analyses. Yet there are important differences between the quest for truth in the courtroom and the quest for truth I the laboratory. Scientific conclusions are subject to perpetual revision. Law, on the other hand, must resolve disputes finally and quickly. The scientific project is advanced by broad and wide-ranging consideration of a multitude of hypotheses, for those that are incorrect will eventually be shown to be so, and that in itself is an advance.    Conjectures that are probably wrong are of little use, however, in the project of reaching a quick, final, and binding legal judgment - often of great consequence - about a particular set of events in the past. We recognise that in practice, a gatekeeping role for the judge, no matter how flexible, inevitably on occasion will prevent the jury from learning of authentic insights and innovations. That, nevertheless, is the balance that is struck by Rules of Evidence designed not for the exhaustive search for cosmic understanding but for the particularised resolution of legal disputes"

[58] However at footnote 13 to Justice Blackmun's judgment, the following appears:
"This is not to say that judicial interpretation, as opposed to adjudicative factfinding, does not share basic characteristics of the scientific endeavor: 'The work of a judge is in one case enduring and in another ephemeral... In the endless process of testing and retesting, there is a constant rejection of the dross and a constant retention of whatever is pure and sound and fine.' B Cardozo, the Nature of the Judicial Process 178- 179 (1921)."

1.	The process of arriving at some propositional hypothesis about a set or group of events which can be tested.
2.	The known or potential rate of error associated with using the particular scientific techniques adopted in (1).
3.	Peer review and publication; that is whether the theory or technique has been subjected to peer review and publication; and
4.	General acceptance, that is a measurement of the extent to which the experts' methods produce information that qualifies the scientific knowledge's recognized within the relevant scientific community.

[62] In any event, this court is required to adopt a legal approach to the question of causation in its evaluation of the evidence. A decision in favour of plaintiff can hardly be construed as establishing a scientific precedent. Viewed legally, it is significant that Dr Tyrell was insistent that there was no reason to adopt the view, absent the events of October 2002, that the deceased would have died in May 2003. For this conclusion he was by far the best placed expert. Although it is correct that the deceased's indicators improved during the period after February 2003, there was no suggestion that the deceased was a healthy man or had recovered to any extent to that level of health which he enjoyed prior to October 2002.

[63] In my view therefore, the evidence read as a whole justifies the conclusion that it was more probable that the thrombosis occurred because of the repeated insults to the deceased body, flowing from the accident, the body's natural responses thereto and the trauma associated with all the medical treatment which flowed directly from the accident as opposed to a natural progression of his PVD. The only defendant expert who was qualified to provide clear testimony on behalf of the defendant and the particular medical condition of the deceased (and then only after the accident) was Dr du Toit. He had the benefit of consulting the deceased. Dr du Toit was certainly a less impressive witness than Dr Tyrell. He was aggressive, he was far less thoughtful in attempting to assist the court than was Dr Tyrell. As his expert 'summary' was no more than a summation of correspondence to defendant's legal team, his expert evidence in court often shifted to the exigencies of the moment rather than being an amplification of the report. Furthermore, in his letter to defendant's attorney on 16 November 2004 there appears to be some significant ambivalence about the key issue of causation. The relevant passage reads thus:
"Ek moet by vorige opinie bly. In die lig van Mnr Keith Compton-James se vorige kardinale geskeidenis hou ek by my besluit oor die finale oorsaak van dood soos gestel in sy doodsertifikaat. Hy is waarskynlik dood as gevolg van 'n kardinale incident. Ek kan nie se dat die motor voertuig ongeiuk, die enigste oorsaak van sy dood is nie. Alhoewel die motor ongieuk groot inpak op sy aigemene gesondheid gehad het, met verskeie operasies en herhaaide infeksies.
Sy sieklike sterfte egter, byna 7 maande na die motor ongeiuk, is steeds van kardinale oorsaak." 
Under cross examination he did not appear to be very convincing as to the explanation of the contents of this letter. He argued that the referred sentence in the letter could be explained by his use of a negative in the relevant passage yet he was forced to concede the following:
"At the end of the day you are quoted as saying here that the motor
accident had a considerable impact upon his overall health.
That is true."

Costs
[64] On 30 October 2007, the matter was postponed for trial after defendant abandoned its special plea, and its objection to plaintiff's intention to amend the particulars of claim aimed at annexing the correct pages of the applicable contract of insurance. In terms of the agreed order of that date the wasted costs of the postponement including all costs postponed from the filing and withdrawal of defendant special pleas stood over for later determination.

[65] It is clear that these costs should be awarded to plaintiff. In this connection, I agree with Mr Gamble that the approach adopted by defendant was unnecessarily vexatious and accordingly, the award of these wasted costs should be on the attorney and client scale.

[67]   For these reasons therefore, the following order is made:
1.	Defendant is ordered to pay the agreed sum of R 611 693 .24 together with VAT.
2.          Interest on this sum shall commence on 1 June 2003 at the prescribed rate determined in terms of Act 55 of 1975; 
3.      Defendant is ordered to pay plaintiffs costs, including the costs of the postponement of 30 October 2007 at an attorney and client scale and the cost of trial including the qualifying expenses of Dr Tyrell.