Beech v Timney & Anor [2013] EWHC 2226 (Admin)

Case No 6WH01017[2013] EWHC 2226 (Admin)
IN THE HIGH COURT OF JUSTICE
QUEEN'S BENCH DIVISION
Venue MANCHESTER DISTRICT REGISTRYDate 29/07/2013
Sitting at:
35 Vernon Street
Liverpool
L2 2BX
Before
MR JUSTICE TURNER
Between
JOSEPH MICHAEL BEECHClaimantDr A P TIMNEY1 st DefendantMr A W PATERSON2 nd Defendant
Mr Bill Braithwaite QC & Dr Simon Fox (instructed by K J Commons & Co) for ClaimantMr James Rowley QC &(instructed by MPS) for DefendantsHearing Hearing dates: 17 th to 25 th June 2013
JudgmentMr Justice Turner :Introduction
[1]On 6th November 2003, the claimant, then aged 35, had a stroke as a result of which he now suffers from physical and cognitive deficits which will be permanent.[2]He contends that his stroke was caused by the negligence of the defendants. The first defendant, Dr Timney, was the claimant’s general practitioner. The second, Mr Paterson, was a consultant oral and maxillo-facial surgeon. Those representing the claimant have conceded that this is a case in which either both defendants are to blame or neither. In the event, therefore, the evidence and submissions in the case have been confined to matters material to Dr Timney’s involvement and I am not required to make any specific findings as to the role of Mr Paterson.[3]In essence, the claimant’s case is that his stroke was caused or materially contributed to by high blood pressure. It is contended that Dr Timney should have measured and recorded his high blood pressure at an early stage and that, had he done so, the claimant would then have embarked on a treatment regime which would probably have prevented the stroke.[4]Preliminary issues relating to breach of duty and causation now fall for this court to determine.

Background

[5]Prior to the events leading up to his stroke, the claimant’s medical history was, for the most part, unremarkable. He was an infrequent visitor to Dr Timney’s surgery. However, on 21 March 2003, he attended complaining that he was waking up with headaches which often recurred at teatime. Dr Timney made two records of this visit. One was in a handwritten note in the Lloyd George card format. The other was by way of an entry on a computer. At the time, the practice was graduating from the traditional method of record keeping to the more modern. Dr Timney was in the habit of using both.[6]The handwritten note relating to this visit records that Dr Timney had taken the claimant’s blood pressure which he recorded to be 110/80. This is a reading which falls within the low side of normal.[7]Dr Timney attributed the claimant’s headaches to ergonomic factors. He recommended postural exercises and proscribed Meloxicam, a drug with analgesic properties.[8]This treatment did not, however, provide a cure. In May 2003, the claimant was complaining of facial pain and “bad heads” to his dentist who referred him to Mr Paterson for a second opinion. Mr Paterson went on to remove the claimant’s left lower wisdom tooth under local anaesthetic. He did not take the claimant’s blood pressure.[9]This procedure did not alleviate the problem. Indeed, on 28 October 2003, the claimant went back to Dr Timney and presented him with an array of problems comprising: i) recurrent anxiety; ii) headache; iii) a toe infection; iv) swelling to the thigh; v) backache; vi) blood in the urine (haematuria); and vii) blood in his ejaculate (haemospermia).[10]Of these signs and symptoms, Dr Timney was most concerned about the haematuria and haemospermia and referred the claimant to a consultant urologist. He did not, on this occasion, take the claimant’s blood pressure.[11]On 6 November 2003, disaster struck. The claimant was admitted to Workington Infirmary suffering from slurred speech and weakness in his right arm and leg. He was found to have suffered a stroke in the form of a large left frontal intracerebral haemorrhage.[12]In the aftermath of this catastrophic event, tests revealed a number of potentially relevant features: i) very high blood pressure; ii) left ventricular hypertrophy; iii) a mildly dilated aortic root; iv) grade II changes to the optic fundi.

The central issues

[13]This litigation has generated a very considerable number of collateral issues upon most of which there has been a substantial amount of dispute between the experts. Whilst it would be wrong to discount these areas of controversy as being wholly immaterial to the task of determining the outcome of this litigation, it remains important not to lose sight of the central issues. They are: i) was Dr Timney’s blood pressure reading of 21 March 2003 taken and recorded with reasonable care? ii) if not, would a reading taken and recorded with such care have resulted in the initiation of treatment which would have prevented the stroke? This approach to the issue of causation should be taken impliedly to include within its scope any issues of “material contribution” under the three stage test laid down in Bailey v Ministry of Defence[2009] 1 WLR 1052 to which I will return later in this judgment.[14]These issues are crucial because, whatever other mistakes Dr Timney may or may not have made, the claimant concedes that only the controversial blood pressure reading/recording of 21 March 2003 could have been causatively relevant to the stroke.

The parties’ respective cases on the central issue of fault

[15]The claimant’s case is that the claimant’s blood pressure was probably significantly elevated at the time of his first visit to Dr Timney. The recorded measurement of 110/80 was not correct and if Dr Timney had acted with reasonable care he would have appreciated that the claimant’s blood pressure was actually in the region of 180/100 or higher.[16]The defendants’ case is that Dr Timney took and recorded the claimant’s blood pressure accurately and with reasonable care.

What could have gone wrong?

[17]Initially, the claimant advanced three distinct theories to explain how Dr Timney may have come to record a falsely low blood pressure. These included(i) a fault in the instrument used to take the reading and(ii) the improper interpretation of the “auscultatory gap”. In opening, Mr Braithwaite QC for the claimant all but abandoned these explanations. He was realistic so to do. There was no evidence that there was any likelihood that a fault had arisen in the sphygmomanometer sufficiently serious to give rise to a wildly inaccurate reading and which could otherwise have gone unnoticed. Further, it was conceded by Mr Saltissi, the claimant’s expert cardiologist, that, whereas a mistaken interpretation of the auscultatory gap might plausibly give rise to an underestimation of systolic blood pressure and/or an overestimation of diastolic blood pressure, it could not explain an error of underestimation of both at the same time.[18]This left only one residual explanation consistent with negligence. Dr Timney had measured the claimant’s blood pressure correctly at a very high level but had subsequently recorded it inaccurately at a relatively low level.[19]There can be no doubt that if this is what occurred then it represented a very serious mistake indeed. In particular, if the blood pressure as measured was 180/100 or higher then it would have been a very clear indication of a seriously elevated level upon which a generally competent general practitioner would be expected to act regardless as to whether he had subsequently noted it down accurately. It is inherently unlikely that such a bad mistake would be made. Dr Boyd, the claimant’s expert in general practice had only ever once before come across a similar (but not identical) case in which a doctor had actually omitted to take a blood pressure reading but had subsequently recorded a normal reading in the notes. In the present case it is the accuracy and not the genuineness of the entry which is in issue.[20]One basis upon which the claimant seeks to undermine the reliability of the recorded measurement is with reference to other respects in which it is suggested that Dr Timney’s acts and omissions fell short of what could have been expected of a competent practitioner. The greater the extent of his other shortcomings, the easier it is to conceive of him inaccurately recording the blood pressure reading and failing to act on a disturbingly high measurement.

Dr Timney

[21]Dr Timney was criticised on a number of counts. The defendant’s expert in general practice conceded that some of these criticisms were valid.[22]In particular, it was common ground that early morning headaches are a “red flag” symptom with respect to the possibility of raised intracranial pressure and that a general practitioner should always inspect the optical fundi for evidence of damage. Dr Timney did not do this. His explanation was that his surgery was too light in the daytime and that he would ask patients to come back in the evening if such an examination were needed. He said that he did not use drops to dilate the pupils because this could be uncomfortable.[23]These explanations were inadequate and I am in no doubt that, even making all due allowance for the lighting conditions, Dr Timney should have made sure that he was able to perform the examinations which the complaint of early morning headaches mandated. As it happens, we know from the results of later fundoscopies that even if Dr Timney had carried out an examination it would not have sounded alarm bells so as to have given rise to a causative difference on the facts of this case.[24]Another area in which Dr Timney was subject to legitimate criticism was in respect of poor record keeping. His notes of the visit of 23 March and other visits were inadequately detailed. In particular, his record of the history of headaches presented to him in March was too concise. Another example of poor record keeping was afforded by a computer entry which purported, on its face, to relate to the claimant but actually referred to an attendance by his father.[25]In his first witness statement, Dr Timney was dealing, hypothetically, with the course of treatment he would have recommended had the claimant been diagnosed with seriously high blood pressure in March. He identified a long acting, low dose beta-blocker before referring to one Adalat 50 mg tablet per day.[26]In fact, Adalat, although used in the treatment of high blood pressure, is a calcium-channel blocker rather than a beta blocker. It is not long acting and does not come in 50mg tablets. 50 mg would probably be too high a dose to start with because of side effects including flushing and fainting.[27]In his second witness statement, Dr Timney corrected the position, at least in part, and stated in cross examination that he had spotted the mistake himself. It had not been pointed out to him by any of the defence medical experts.[28]Other criticisms of Dr Timney were more controversial. An issue arose as to whether he should have carried out a brief but focussed neurological examination of the claimant on 23 March. However, once he had missed the red flag symptom of early morning headaches, his omission thereafter to perform a neurological examination was effectively subsumed within his initial mistake. Even if he had spotted the red flag, it is by no means clear that a further neurological examination beyond that of the fundi would be mandated. Bearing in mind that the average length of a consultation with a GP lasts only a little longer than twelve minutes, a full neurological examination would have been impracticable. Care must be taken not to judge with the benefit of hindsight. It may be that some general practitioners in Dr Timney’s position might have spent two or three minutes looking for gross neurological signs, even if primarily for the purpose of reassuring the patient, but, in this case, I am not satisfied that this would be other than a counsel of perfection.[29]A further criticism relates to the failure of Dr Timney to take a second blood pressure reading on 28 October 2003. Such criticism is mitigated by the fact that there was no specific complaint of morning headache on this occasion and that the presentation had become a relatively complex one bearing in mind the spectrum of new complaints raised at the same time. Taking into account the record of the low normal blood pressure reading of 23 March, it was perhaps understandable that no further reading was taken on this attendance. Doubtless there would be some practitioners in the same position who would have taken the precaution of performing a further blood pressure test but I do not conclude that Dr Timney’s omission was such as materially to strengthen the argument of general incompetence on his part.[30]In conclusion on this issue, taking the evidence as a whole, I consider that it reveals that Dr Timney was properly criticised for(i) failing to spot the “red flag” of early morning headaches,(ii) inadequate record keeping and(iii) some initial confusion over the hypothetical prescription of Adalat.[31]The question then arises as to whether these findings, seen in the context of the scientific evidence as a whole, are such as to equip the claimant to prove, on balance, that Dr Timney negligently misrecorded and failed to act upon a very high blood pressure reading on 23 March 2003.

The scientific evidence

[32]It is necessary at this juncture to note the fact that most of the expert witnesses in this case were subjected to a considerable amount of criticism from the respective advocates concerning the way they had conducted themselves both before and during the trial. A considerable proportion of enthusiastic cross examination and submissions was taken up with the objective of discrediting their opinions on this basis. This was tactically permissible but the important medical dispute in this case is, I find, capable of resolution based on rational scientific analysis rather than the outcome of a forensic corrida. For that reason, I do not consider that it is either necessary or appropriate to embark upon a detailed consideration of these alleged shortcomings. It is true that a number of experts on both sides made mistakes such as initially offering opinions on matters outside their expertise and launching theories which they were constrained thereafter to abandon. These examples, in my view, showed that they were fallible but not incredible.[33]The claimant is inevitably substantially reliant upon the evidence of consultant cardiologist, Dr Saltissi, to the effect that the claimant’s blood pressure must have been very highly elevated on 23 March 2003. The defendant’s cardiologist was Professor Hall.[34]There were some issues upon which the cardiologists were agreed. In particular, they agreed that the claimant had been suffering from high blood pressure over a period prior to his stroke. However, the readings taken in the immediate aftermath of the stroke would be expected to have been higher than the claimant’s blood pressure would have been before the stroke. As the haemorrhage puts pressure on the brain, the body responds to the perceived priority of delivering more oxygen to the brain. This it does by raising the blood pressure still further hence the additional element of elevation. In this case, the claimant’s blood pressure remained elevated even in the long term after the stroke. This suggests that, even before the stroke, the claimant’s blood pressure had been elevated to some extent.[35]It was also agreed by the experts that high blood pressure was implicated in the occurrence of the stroke.[36]The important issue, however, is whether it can be concluded on the scientific evidence that the claimant’s blood pressure was significantly raised at the time of the 23 March attendance on Dr Timney.[37]One challenge to the process of attempting to work back from the agreed elevated blood pressure immediately before the stroke to the position at the time of the examination in March 2003 is that the claimant’s medical condition presents with a number of egregious features which necessarily make it harder to draw firm conclusions from statistical data drawn from a population falling predominantly within more familiar categories of presentation.[38]For example, it is common ground that it is unusual for a man in his mid-thirties to suffer intra cranial haemorrhage. Youth usually provides good protection against stroke. It is to be noted that the Quereshi paper of 2007 despite the involvement of a large population for study provides no single example of an intra cranial haemorrhage in the male cohort in the thirties age group.[39]Nevertheless, the claimant’s case is that certain features of his presentation make it sufficiently improbable that his blood pressure could have been normal on 23 March 2003 that the court would be justified in concluding that Dr Timney had not recorded it accurately.[40]The defendants’ case is that a low reading on this date is not scientifically inconsistent with the factors relied upon by the claimant and that these factors fall far short of providing strong evidence that the March reading was wrongly recorded.[41]The salient features upon which the claimant relies are: i) The complaints of headaches; ii) The presence of left ventricular hypertrophy; iii) A mildly dilated aortic root; iv) Blood in the sperm and urine; v) Retinopathy.[42]I propose to deal with each in turn.

Headaches

[43]Although, it might seem counter-intuitive to the lay person, the medical relationship between headaches and high blood pressure has proven to be an elusive one.[44]A paper by Law et al (2005) presents a meta analysis from which the authors concluded:
“Our results show that blood pressure lowering drugs prevent a significant proportion of headaches…This in turn indicates that high blood pressure is a cause of headache but this conclusion is not supported by observational studies of blood pressure and headache. The uncertainty over whether high blood pressure causes headache does not, however, detract from the practical use of blood pressure tablets in preventing headaches…”
[45]There is a recognised category of hypertension (accelerated or malignant) which involves a significant rise in intracranial pressure which is uncontroversially associated with headaches. This condition is, however, rare and the experts are agreed that the claimant in this case did not suffer from it.[46]Dr Saltissi considers that the Law paper establishes a link between headaches and an elevated level of blood pressure which falls short of that which would be necessary to produce significantly raised intracranial pressure. The defendants’ experts do not accept this conclusion and rely upon the observational studies referred to in the Laws paper. Dr Saltissi also referred to the abstract of a Brazilian paper which, however, was so lacking in detail that I found it to be of no help.[47]In my view, the greatest difficulty faced by Dr Saltissi is the fact that a high proportion of the population generally suffers from headaches. Tension headaches and migraine are very common. Even if one were to accept a possible causal link between high blood pressure and headaches the prevalence of both conditions in the general population, in any event, would preclude the confident assertion that, in any given case, there was a causal link. Even though attempts at treatment of the claimant’s headaches had not succeeded by October 2003, I am not satisfied that it is possible to conclude with any degree of confidence that his headaches were related to high blood pressure.

Left ventricular hypertrophy

[48]Left ventricular hypertrophy (“LVH”) is a thickening of the muscle of the left ventricle of the heart. Although there was some initial issue on the point, it is now common ground that such thickening was observable in the claimant’s case from the results of ECG tests carried out after the stroke.[49]LVH is commonly associated with high blood pressure. The heart works harder to pump the blood at higher pressure and the muscle is thereby built up. This finding is, therefore, consistent with the suggestion that the claimant had been suffering from high blood pressure before his stroke for a sufficient length of time to cause such changes. The question remains, however, whether, the LVH reveals anything about the claimant’s blood pressure in March 2003.[50]Clearly, it would be unethical to conduct an experiment to determine the progress of LVH involving a control group of untreated individuals. Accordingly, the debate between the experts in this case has been based on indirect evidence. This has covered the following areas: i) The timing of the regression of LVH after treatment was initiated; ii) Studies of the timing of onset of LVH in those cases where the heart is working harder as a result of exercise rather than high blood pressure; iii) Animal studies.[51]Regrettably, I have found the arguments on these topics to be more interesting than informative. The following observations can be made concerning the weight which can be given to each of the areas identified above: i) There is no direct evidence of the relationship, if any, between the rate of regression of LVH and the period of time over which it originally developed. Such a link may seem intuitively correct but this falls short of providing evidence sufficiently robust to offer assistance in determining the issue in this case; ii) It is not clear whether the LVH caused by exercise can be compared directly with that caused by high blood pressure. It may be that, in the case of the latter, there is a higher proportion of fibrotic scarring as opposed to muscle growth which could distort the usefulness of the findings; iii) Animal studies on dogs and mice may indicate that, in certain conditions, LVH can develop relatively rapidly in these species but caution must be exercised in extrapolating results from animals to humans. Furthermore, the animals in the tests are not naturally hypertensive. They are either bred to have high blood pressure or have their circulation artificially blocked. Comparisons are, therefore, by no means straightforward.[52]In a joint report dated 4 April 2013, the respective cardiologists stated:
“Both experts agreed that in this matter opinion can only be based on informed guess work together with indirect scientific evidence e.g. that on LVH regression because specific and direct evidence does not exist.”
[53]Against this background, I am unable to conclude that the evidence relating to LVH tells me anything about the likelihood that the claimant had raised blood pressure on the occasion of his visit to Dr Timney in March 2003.

The mildly dilated aortic root

[54]In a letter dated 10 May 2004, Alan Jennison, Senior Chief Cardiac Physiologist at West Cumberland Hospital reported on the claimant to Dr Roberts of the Young Disabled Unit stating that the “echo shows that the patient has a mildly dilated aortic root”. His findings had been discussed at the weekly clinical cardiology meeting.[55]Unfortunately, the echo report upon which this observation is based was lost and no-one involved in this litigation has ever seen it.[56]On behalf of the claimant, Dr Saltissi relied upon this finding as support for his conclusion that the claimant was suffering from seriously elevated blood pressure on the occasion of the March visit to Dr Timney. There was no dispute in this case that aortic root dilation is a well recognised sign in severe hypertension.[57]Ultimately, however, as with the evidence relating to LVH, the challenge facing Dr Saltissi was to make out a case for concluding that the relevant signs after the stroke equip the court to work backwards to the date of the March visit. This he attempted to do by making assumptions based on his own clinical experience as to what “mildly dilated” might mean in terms of the likely measurement of the extent of the dilation. He went on to draw comparisons with rates of development of aortic aneurysms (involving localised dilation) in a paper by Woo and others.[58]Professor Hall, on behalf of the defendants, contended that that there was no scientific way of performing a reliable back calculation of the claimant’s blood pressure in March from the evidence available relating to the aortic root.[59]Once again, I come to the conclusion that Dr Saltissi’s approach provides more of a tribute to his ingenuity than a sure foundation for his conclusions. The degree of speculation involved in assigning a specific range of measurements to a very concise description of the lost results of an echocardiograph is simply too great to sustain the weight of his analysis thereafter.

Blood in the sperm and urine

[60]The alleged link between blood in the ejaculate or urine and high blood pressure is a controversial one. Dr Saltissi relied, in particular, upon a study by Close and others of 1991 as tending to establish a link between haemospermia and severe hypertension.[61]Professor MacGregor was very dismissive of this paper. He gave evidence that in the 200 or so cases of malignant hypertension he had seen in his career none had been noted to be associated with haemospermia. He pointed out that the Close paper had appeared in a post graduate journal and that despite the passage of over twenty years since its publication there had been no follow up studies to confirm or deny the validity of its conclusions.[62]As it happens, it is not necessary for me to reach any firm conclusion on the quality of the Close paper because, even if taken entirely at face value, it provides me with no satisfactory evidence relating to the crucial issue of what the claimant’s blood pressure was likely to have been on the occasion of the March visit.

Retinopathy

[63]On 6 November 2003, a fundoscopy performed in the Accident and Emergency Department was found to be normal qualified by an entry reading “?? Silver wiring”. Silver wiring is the visible thickening of the retinal blood vessel walls with narrowing of their lumen. The question marks indicate, at least, a lack of confidence in the accuracy of the observation.[64]In a subsequent hospital note of 2 December 2003, it is recorded: “Fundoscopy Grade II hypertensive changes. Goes against suggestion uncontrolled HT”.[65]Dr Saltissi formed the view that Grade II changes were consistent with prolonged, significant hypertension. In response, Professor McGregor asserted that Grade II changes are a very poor indicator of very high blood pressure. In support of his stance, he referred to the paper of Dimmitt and others published in the Lancet in 1989. Dr Sharma, the defendants’ neurologist, gave evidence to the effect that it is often difficult to differentiate between Grades I and II retinopathy and that in casualty they are often “lumped together” as mild.[66]The literature relating to the relationship between retinopathy and hypertension offers little or no direct assistance on the central issue of conclusions to be drawn as to chronicity of high blood pressure and the appearance of mild changes. Again, I must conclude that this feature does not provide helpful evidence on the central question as to the level of the claimant’s blood pressure on the occasion of his March visit to Dr Timney.

What is the explanation for the low reading of 23 March 2003?

[67]I accept the evidence of Dr Sharma that single blood pressure readings are of little predictive value in the consideration of the possibility of chronically high blood pressure. Repeated readings are needed. The low normal reading on 23 March 2003, if accurate, would militate against background severely raised blood pressure but would not be inconsistent with moderately raised chronic hypertension.[68]Dr Sharma indicated that the commonest cause of haemorrhagic strokes in people in his unit under the age of 40 was arteriovenous malformation (“AVM”). AVM is an anatomical abnormality at the site of connection between arteries and veins. AVMs can be relatively small. Importantly, they may be vulnerable to rupture even in conditions of moderate and short term hypertension. Rupture causes brain haemorrhage.[69]Dr Bone, on behalf of the claimant, pointed out that the cerebral angiogram results of 6 November 2003 demonstrate the existence of no AVMs. He also rejected the idea of the occurrence of an AVM in the area of haemorrhage in this case around the caudate nucleus which is located within the basal ganglia.[70]In response, Dr Sharma stated that evidence of AVMs could be obliterated by the damage caused by the haemorrhage consequent upon the rupture. It appears that those treating the claimant did not err on the side of safety and assumed that there had been no AVM in the first place. Of particular importance, however, was the fact that the central issue between these experts was resolved by Dr Sharma’s discovery of literature that provided objective support for his clinical experience of AVMs located around the caudate nucleus. Although late in the day, the court was provided with the abstract of a paper by Sasiki and others of 1998 which make specific reference to AVMs in the caudate nucleus. This was consistent with Dr Sharma’s earlier estimate that he encountered about two cases of AVMs in this location each year at his unit.[71]Both Dr Sharma and Dr Bone have been criticised for the paths which their respective analyses took but, ultimately, it is the conclusions of Dr Sharma which are the most consistent with the scientific literature and these conclusions I accept.

Conclusion on the central issue

[72]On the balance of probabilities I am satisfied that Dr Timney took and recorded the claimant’s blood pressure accurately on 23 March 2003. In summary, this finding is based, in particular, on the following: i) It is inherently unlikely that an experienced GP could be so careless as to fail to respond to a blood pressure reading of about 180/100 and record it as being so significantly lower than this; ii) The evidence revealed that, in some respects, Dr Timney fell short of the standard to be expected of the reasonably competent GP but these examples were not so egregious as to cast doubt on his ability correctly to take and record a blood pressure measurement; iii) The clinical findings relied upon by Dr Saltissi to support his conclusion that the claimant’s blood pressure was in the region of 180/100 in March 2003 were inadequately founded in the evidence of the relevant scientific literature. In particular, even where an association between the clinical finding and high blood pressure was clearly established (as, for example, with LVH) there was little or no evidence to assist in determining for how long blood pressure would have to have been elevated and to what levels to give rise to such a finding; iv) The evidence of Dr Sharma that the direct cause of the stroke was an AVM was ultimately compelling and was consistent with a level of blood pressure which, although elevated, was not severely so. A single low normal reading in March 2003 was not inconsistent with this picture.

Causation in the event that treatment had been initiated

[73]My finding that Dr Timney correctly took and recorded that claimant’s blood pressure on 23 March is determinative of the outcome of this case. However, a significant amount of evidence was called on the issue as to whether, even if Dr Timney had negligently failed to act on a reading of about 180/100, the treatment which would have followed would have made any difference. This issue is now hypothetical but, out of deference to the time and effort which both sides have invested in the matter, I will set out my findings as it if it were not.[74]Dr Timney’s evidence as to what he is likely to have done if he had found raised blood pressure in 2003 was unchallenged and the GP experts agreed that this would have represented a reasonable standard of care in 2003. In summary, the institution of treatment is likely to have taken time and to have begun in a modest way. Once a patient is prescribed drugs to combat hypertension there is no going back. With a younger patient, in particular, there is a natural and justifiable reticence to embark upon a course of treatment the effect of which would be to commit the recipient to a lifelong regime.[75]In approaching the issue of treatment, Dr Saltissi wrongly applied the BHS Guidelines of 2004 rather than those of 1999. I reject his evidence as to the likely path of treatment.[76]Fortunately, there is a considerable amount of evidence in the scientific literature comparing the outcomes for patients receiving blood pressure treatment and those not.[77]A PROGRESS study published in the Lancet in 2001 charted the progress of stroke victims over a period of four years. The population was of 6,105 individuals who were randomly assigned active treatment or placebo.[78]The results were represented in both graph and tabular form. They demonstrated(i) that there was little or no difference in the incidence of a second stroke between the treated and the control group in the first six months or so and(ii) that with respect to no category of stroke had the effect of treatment achieved an improvement of greater than 50% in the chances of avoiding a second event over a period of four years.[79]A similar study is reported in the New England Journal of Medicine in 2000 based on the treatment of 9,297 high risk patients. It differs from the PROGRESS study in that it did not involve a population of those who had already suffered a stroke. Again, however, the graphical representation of the results shows no discernible difference between the treated and the control population over the first few months.[80]A paper by Woo and others published in Stroke in 2004 estimates that one in four haemorrhagic strokes would be prevented if all hypertensive subjects were to receive treatment.[81]Looking at the scientific evidence as a whole, a relatively consistent picture emerges. Treatment for high blood pressure tends to make no difference to the risk of any given patient suffering a stroke until at least some months have passed. Thereafter, the effect grows more markedly beneficial but the level of reduction of risk does not generally approach fifty percent until three to five years have elapsed.[82]The claimant’s stroke was an indivisible injury. The scientific literature demonstrates that, in any given case, the chances of making any difference to the risk of a stroke after a treatment regime in place for no more than a few months are negligible. In these circumstances, I conclude that the evidence shows that claimant would have suffered his stroke even if Dr Timney had embarked on a course of reasonable treatment in March 2003. Accordingly, the case fall squarely within the parameters of the decision of the House of Lords in Gregg v Scott [2005] AC 176. The claimant’s case on causation is further weakened by my finding that he was suffering from an AVM rather than being the victim of long term severe hypertension.[83]In Bailey v Ministry of Defence [2009] 1 WLR 1052, Waller LJ held:
“46 In my view one cannot draw a distinction between medical negligence cases and others. I would summarise the position in relation to cumulative cause cases as follows. If the evidence demonstrates on a balance of probabilities that the injury would have occurred as a result of the non-tortious cause or causes in any event, the claimant will have failed to establish that the tortious cause contributed. Hotson exemplifies such a situation. If the evidence demonstrates that ‘but for’ the contribution of the tortious cause the injury would probably not have occurred, the claimant will (obviously) have discharged the burden. In a case where medical science cannot establish the probability that ‘but for’ an act of negligence the injury would not have happened but can establish that the contribution of the negligent cause was more than negligible, the ‘but for’ test is modified, and the claimant will succeed.”
[84]In this case, the claimant falls at the first hurdle and the modified “but for” test is simply not engaged and the issue of material contribution does not arise.

Conclusion

[85]What happened to Joseph Beech on 6 November 2003 was a personal catastrophe for him and a tragedy for his family. His life and their lives were changed forever. In these circumstances, it is impossible not to feel the utmost sympathy for his plight and to empathise with the emotional impact it has had upon his relatives and close friends.[86]Sadly, however, in this case, it is not possible to mitigate the consequences of this disaster with an award of damages. The evidence simply did not demonstrate that a causative act of negligence lay behind the terrible brain haemorrhage he suffered nearly ten years ago. This claim must, therefore, be dismissed.