Brien v Accident Rehabilitation and Compensation Insurance Corporation

IN THE DISTRICT COURT HELD AT AUCKLAND Decision No. 315 /99 IN THE MATTER of the Accident Rehabilitation and Compensation Insurance Act 1992 AND IN THE MATTER of an appeal pursuant to section 91 of the Act BETWEEN PAUL BRIEN (DCA 229/97) Appellant AND ACCIDENT REHABILITATION AND COMPENSATION INSURANCE CORPORATION Respondent HEARD on the 7th day of October 1999 APPEARANCES Mr A H Hillary, advocate for appellant Mr D Tui, counsel for respondent RESERVED JUDGMENT OF JUDGE M J BEATTIE The substantive issue for determination in this appeal is whether the appellant has suffered personal injury by medical misadventure, being medical error. The determination of this issue requires the Court to consider whether or not the appellant has suffered personal injury and if so, whether that personal injury was caused by medical error. The factual background which is relevant to this appeal is as follows: The appellant is now aged 43 years. From 1974 to 1994 he was a soldier in the New Zealand Army and at the material time held the rank of Warrant Officer. In 1988 microscopic haematuria (blood in the urine) was detected during a routine medical check. At that time the appellant's blood pressure was 120/80. No further tests or follow-up action was taken consequent on this detection and the appellant continued with his normal duties as an army officer. 2 In or about May 1991 the appellant underwent a further routine medical check-up and was found to have proteinuria (a condition in which proteins, principally albumin are present in the urine) and microscopic haematuria. Proteinuria is a condition which can be a symptom of kidney disease. The appellant underwent a 24 hour urinary protein test and was found to have 0.46 g of protein in his urine. This state of affairs was detected by Dr C Nicholson, an Army Doctor, and he referred the appellant to Mr R Smart, Urologist in September 1991. Mr Smart initially reported to Dr Nicholson on 25 November 1991 when as a result of the examination that he had done and from the facts that he had been given, he stated: "It seems likely in view of the significant proteinuria which you found and the suggestion of granular casts on microscopy that this problem is due to a previous glomerulonephritis. However this assumption needs to be backed up by more adequate investigations excluding other causes of haematuria." Mr Smart duly carried out further investigations and further reported to Dr Nicholson on 19 December 1991 when he stated: 'A 24 hour urinary protein showed that he puts out 780 mg of protein/24 hours which is slightly elevated. The only abnormality is the mild proteinuria with the slight elevation in some of the anti-streptolysin titres and I think this is consistent with there having been a mild nephritis in 1988 to explain this microscopic haematuria. There is no other cause for it at present. I don't think there is any further activity with regard to this and I think it will continue to be detectable. Should there be a change in the haematuria, for example should it become macroscopic or other symptoms develop then he should be referred again." The next medical examination of the appellant was conducted in June 1992 when he was being considered for a posting with a peace-keeping force in Sinai. Again a routine urinalysis was carried out which showed both proteinuria and haematuria and a 24 hour urine test showed a urine protein of 4.2 grams. This medical examination was carried out by Dr G Q Nguyen, an Army Doctor and it was his opinion that the appellant was fit for the projected tour of duty in Sinai. That opinion was confirmed by the Director of Medical Services. Dr Nguyen did not initiate or propose any further specialist intervention. For reasons totally unrelated to the appellant's health he did not in fact go on the tour of duty to the Sinai but continued with normal duties in the army stationed at Papakura. The prospect of a posting to the Sinai again arose in April 1993 and the appellant was examined for his fitness for that service by Dr S Helagi at the RNZN Hospital, Devonport. Dr Helagi was aware of the past findings of haematuria and proteinuria and carried out tests which showed a level of proteinuria of 7.74 g. Dr Helagi noted that the appellant was at that time asymptomatic. Dr Helagi referred the appellant to Mr Roger Chambers, Urologist, in April 1993 and Mr Chambers reported to Dr Helagi on 30 April 1993. Mr Chambers noted that whilst the appellant was still very fit and active, he considered that the nephritis had taken a turn for the worse as he was now putting out 7 gm per day of albumin and his creatinine had gone up to 0.15. His blood pressure was also elevated at 160/100. Mr Chambers 3 considered that the appellant required a renal biopsy and he was referred to Dr John Collins at Auckland Hospital for that purpose Dr Collins reported to Major Murray, Assistant Director, Army Medical Services, on 15 June 1993. The renal biopsy showed that the appellant had IgA nephropathy. Dr Collins went on to state: 'Given the abnormal renal function, marked proteinuria, hypertension and the presence of histology of significant chronic renal damage, it is quite clear that Paul Brien is in a poor prognostic category and will progress over time into end stage chronic renal failure. It is difficult at this stage to define the rate at which he will progress, though an evaluation of his regular creatinine levels after three or four months should enable a trend to be defined. It is possible that he will be in end stage kidney failure within a year, or it may take as long as five or six years." Currently he is quite fit and well with no symptoms. There is no specific treatment that can be utilised to reverse the primary glomerulonephritis affecting his kidneys. The most important measure that can be instituted is to maintain his blood pressure under consistently good control. ... In some patients a reduction in protein intake to a lower but safe level (provided adequate calorie intake occurs) can also have an effect on slowing down the decline in renal function." Dr Collins made a further report to Major Murray in July 1993 and advised that the tests which had been carried out since his earlier examination indicated that the rate of renal functional deterioration was quite slow. Dr Collins expected that this trend would be maintained, particularly with good blood pressure control. Dr Collins also revised his prediction of the time it would take him to enter end stage renal failure to between three to six years. He further noted that he did not expect Mr Brien would display any symptoms for at least another two years. The appellant was put on a course of medication, particularly for control of his blood pressure. In August 1993 the appellant lodged a claim for cover with the respondent in which he described his injury as: "contracted kidney infection has progressed through medical mismanagement to 30% - 40% loss of kidney function. End result 3-6 years dialysis/ transplant." The appellant's claim was referred to the Medical Misadventure Advisory Committee (MMAC) and the issue as identified by it was described as "misdiagnosis of glomerulonephritis resulting in loss of kidney function". The Committee sought reports from the various medical personnel who had treated the appellant. In addition to lodging a claim for cover it is to be noted that the appellant made a complaint to the Medical Practitioners Disciplinary Committee in which he questioned the actions of Drs Nicholson, Smart and Nguyen. The MMAC elected to defer any decision until the MPDC had completed its determinations. That Committee enquired into the actions of the three named specialists and came to the conclusion that there were no grounds for any formal enquiry into their conduct and the Chairman so advised the appellant and noted that he did not believe that any earlier firm diagnosis of his condition would have made any significant difference. 4 The MMAC further considered the claim in March 1995 and the advice of the MMAC was as follows: "The Committee is of the view that Mr Brien's lgA nephrophehy is due to the underlying kidney condition and it is not a personal injury that Mr Brien has sustained as the result of treatment by or at the direction of a registered health professional. The Committee is not convinced that any alleged delay in treatment has altered the natural progression of the disease. As there is no evidence to establish that Mr Brien has sustained a personal injury, this claim therefore does not fall within the jurisdiction of the MMAC." The MMAC proposed that the claim for cover be declined and a formal decision letter advising the appellant of that was forwarded on 16 October 1995. It should be noted that prior to coming to its final decision the MMAC sought the opinion of a specialist Nephrologist, Dr Alastair Macdonald. After reviewing the facts as they had been presented to him in the various reports to which he was referred, Dr Macdonald stated the following: '1) At the time of presentation in 1988 Mr Brien had microscopic haematuria and proteinuria. An initial follow up showed that his proteinuria had resolved. His blood pressure was normal. Given this set of circumstances the usual practice would have been to perform follow up tests. If there had been only haematuria then nephrologists are divided as to whether they would perform a kidney biopsy. Factors important in this decision would be the possible hazards of doing a kidney biopsy against the knowledge that isolated glomerular haematuria is usually a benign condition. If follow up had shown proteinuria then most nephrologists would perform kidney biopsy (1) The reason for doing a biopsy in this situation would have been for prognostic reasons. 2) With regard to the delay in making the diagnosis, this undoubtedly occurred and I do not need to comment upon this any further. Assuming that he had had a kidney biopsy in 1988 or in 1991, I will speculate as to any changes that might have been occurred as a result. a) He would have had a specific diagnosis made earlier. This would have allowed him to be advised/counselled regarding the nature of the condition. b) I believe there would have been no significant difference in the course of his disease. As to specific treatment for lgA nephropathy, there is none. Thre are important general factors which may retard deterioration in renal function such as blood pressure control. With regard to restriction of protein and the use of drugs such as Enalapril, large trails of their use in kidney failure have failed to provide a clear indication to support their use in this situation. This is said even though many nephrologists utilise both treatment modalities and can attest to the efficacy of such an approach in individual situations. This opinion is reflected in Dr Collins' correspondence c) With regard to any stabilisation of renal function that may have occurred subsequent to having had the diagnosis of lgA nephropathy made, it is difficult to attribute this to any particular intervention (eg blood pressure control/dietary protein restriction/ the use of drugs like Enalapril) in an individual. Experience shows that renal function can vary in the absence of any particular intervention. 5 The use of such interventions by nephrologists is on the basis of prudence rather than on the basis of firm scientific evidence.' The appellant sought a review of the decision to decline his claim and the essence of his claim is identified by the Review Officer in his decision wherein Mr Brien submitted as follows: "... Over a period of five years, from 1988 through 1992, what should have been clear signs and symptoms of a developing renal disorder were ignored by NZ Army medical officers as well as a civilian urologist. The abundant signs and symptoms, all well-documented in my Army medical records, included the following observations: Jun 1988 - Haematuria Aug 1991 - Proteinuria and hypertension Sep 1991 - Proteinuria and haematuria Dec 1991 - Proteinuria Jun 1992 - Serum creatanine 0. 13 mmol/L Proteinuria 4.2g/24 hours Yet, with all the above indicators evident, it was not before March-April 1993 that I was aware that there was any threat to my health. The 1988 results were not followed up at all. Three years later, in 1991, the urologist Mr Robin F. Smart dismissed those ominous indicators as 'warranting little or no concern', did not attempt to make a diagnosis, and declined to take any further action unless the haematuria became macroscopic. Nor was I referred to a nephrologist. One year later, in 1992, Army medical officer Dr Nguyen similarly decided there was nothing wrong, despite all the results cited. 2. IgA nephropathy (in both kidneys) was diagnosed by renal physician Mr John F. Collins on 2 June 1993. By that time, 40% of my glomerular were already sclerosed, with interstitial fibrosis and tubular atrophy. It was quite clear I was in a poor prognostic category and will progress over time into end-stage chronic renal failure. ." For the purposes of the review further reports were received from Dr Collins and Or Macdonald and also a report from Dr Nacey, Associated Professor of Urology at the Wellington School of Medicine who had been a member of the MMAC which had considered the appellant's claim. In addition Dr Collins gave oral evidence to the Review Officer. The further reports considered by the Review Officer were as follows: 1. Report from Dr Macdonald dated 11 February 1996. This report was in fact a response to a letter that the appellant had written to the officer in charge of the MMAC as a response to Dr Macdonald's report of 10 September 1995 to the MMAC in which he has posed certain questions. This report sought to address the issues promoted by the appellant and the report in full states as follows: 'Thank you for your letter dated 5/2/96. You indicate that it might be helpful for me to comment on Mr Brien's contentions as they relate to my report. I will respond to his letter from paragraph 5 onwards. 6 What place is there for a renal biopsy in the setting of microscopic haematuria? Reference (1) Fehally et all is indeed a six year old study of attitudes regarding renal biopsy in isolated microscopic haematuria. It is interesting that over the subsequent six years since the study was published attitudes towards renal biopsy for isolated microscopic haematuria have changed to the extent that all of my colleagues in Wellington would not biopsy an individual with this problem unless there were associated hypertension, proteinuria or renal impairment. This conservative approach is echoed in a recent paper from the Christchurch group (2). It is helpful to reflect on the opinion expressed in a 1987 paper (3) that 'at present, renal biopsy in this group of patients makes no difference therapeutically or probably prognostically. It should not, therefore, be considered necessary for the routine management of asymptomatic haematuria'. Given that Mr Brien's presentation was in 1988, the paper, written in 1987, represents a contemporaneous philosophy. The rationale behind a conservative approach to renal biopsy relates to the fact that the entity of isolated haematuria (in the absence of a urological cause) is very suggestive of an underlying glomerulonephritis, which in the majority of cases, is a benign, non-progressive problem (4). It is extremely unfortunate that Mr Brien is one of the uncommon exceptions to this rule. In his submission Mr Brien makes reference to the renal biopsy as 'unequivocally .... A safe procedure' I would agree that this is true in many cases. However to ensure a balanced perspective I have provided a reference (5) which indicates why nephrologists may have reservations about performing this procedure. One is mindful of the rare catastrophic complications as stated in the first paragraph 'the removal of a kidney due to uncontrollable bleeding or death are rarely seen'. In our own unit in the last year a patient unfortunately had to have a kidney removed for bleeding which had required 30 units of blood. It is salutary to realise that the prevalence of isolated haematuria varies from 2 - 5 % of the general population (2). If one were to biopsy all of these individuals not only would it imply a vast amount of futile activity but it would also expose large numbers of patients to an unnecessary risk. I think that Mr Brien has misinterpreted my statement regarding opinions amongst nephrologists being 'divided' (1) My reference was to the occurrence of isolated haematuria. As can be clearly seen from the data only 36% of those asked would always biopsy under these circumstances (ie slightly over 1/3) The majority (64%) would either sometimes or never biopsy under these circumstances. I myself would recommend biopsy in the presence of significant proteinuria as was the case in 1993. Mr Brien makes reference to Christchurch hospital having a more aggressive biopsy policy in isolated microscopic haematuria (6) He then tries to relate this to a better outcome as a result of early diagnosis and therefore intervention. The authors clearly state that there is higher renal survival rate of 92.6% at five years in this Christchurch study as compared with 83.7% in the New Zealand Collabarative Glomerulonephritis survey. They go on to say that the difference may be due to a more active renal biopsy policy used in Christchurch for patients presenting with isolated haematuria. This paper indicates the prognostic value of a kidney biopsy and makes no reference whatsoever to therapy delaying the onset of kidney failure. The more active biopsy policy seems to have tempered somewhat given the advice contained in an editorial by the same group of clinicians (2). If one has an aggressive policy in biopsying patients with isolated haematuria, one is bound to biopsy individuals at the more benign end of the scale. This will have the inevitable effect of appearing to improve the renal survival rate. The suggestion being that the apparent incidence of lgA nephropathy is related to the attitude of individual clinicians and their use of biopsy in patients with microscopic haematuria (1). What is the role of intervention in terms of delaying the deterioration of kidney function? There is reference to the large study by Klahr et al (7) This study was carried out on a total of 840 patients. Their statement is that 'the data are consistent with a small beneficial effect of this intervention (diet and blood pressure control) on the progression of renal disease' They go on to say in the abstract Among patients with more severe renal insufficiency, a very low protein diet, as compared to a low protein diet, did not significantly slow the progression of disease' This is the best study of the benefits of these interventions. It is premature to describe this study in terms of 'the evidence appears to be overwhelming' Although I prescribe a low protein diet for my patients when the serum creatinine level reaches approximately 200 umol/L (higher than Mr Brien's at the time of his biopsy) I base this advice on the prudence rather than on the basis of overwhelming evidence. Many nephrologists were disappointed at the results of this Klahr study because they had expected a much more positive result. Mr Brien is correct in pointing out that there appeared to be a definite benefit in those patients with a urinary protein level of 3 grams or more per day. His level of urinary protein in November 1991 was 0.78 grams per day. When he developed more severe proteinuria (7 grams per day on 15/6/93) it was appropriate not only for him to have a renal biopsy but also for him to be put on to a protein restricted diet. Finally it is instructive to see what actually happens in terms of therapy when a clinician actually biopsies a patient (8) In only 19% of patients was the treatment significantly changed. This occurred when there was significant proteinuria. This was the case when Mr Brien was eventually biopsied in 1993. In summary, 1) I do not think that he would have benefitted by having a renal biospy in 1988 in terms of availing himself of any specific therapy directed at his problem of IgA nephropathy. 2) Had he had a renal biopsy in 1988 he would have known what the specific cause of his glomerulonephritis was. 8 3) Given prevailing attitudes, most nephrologists would have recommended renal biopsy for Mr Brien when he began to show significant proteinuria. This would have been between November 1991 and June 1993. (From Mr Brien's recent submission I see that he had a creatinine level of . 13 mmol/L and a 24 hour urinary protein of 4.2 grams in 1992) 4) I do not think that the delay in making a specific diagnosis of IgA nephropathy in this case has had any major effect in terms of altering the natural progression of the disease. I trust that the information I have supplied is helpful for your purposes." 2. Report from Dr Collins dated 13 March 1996: "I last reviewed Mr Brien on 7.2.96. At that visit his blood pressure control was excellent, with a sitting blood pressure of 120/70, and standing 110 systolic. His most recent investigations showed a 24 hour urine protein of 0.5g, significantly reduced from the high levels noted at his initial presentation, and indeed, subsequently. His serum creatinine level was 0.28mmol/L with a urea of 17.2mmol/L. These indicate significant further renal functional deterioration since 1993 ... remains difficult to predict when Mr Brien will enter end stage renal failure and I hope that measures instituted to control blood pressure and to reduce protein excretion will help to slow down the rate of progression. There is evidence from the medical literature, that such measures can be effective in delaying the rate of renal functional deterioration. As previously, Mr Brien has no symptoms related to his renal dysfunction and indeed I would not expect him to have symptoms until his renal function is substantially worse. Once he does begin to develop symptoms related to renal failure, he will be reaching the point where he requires renal replacement therapy in the form of dialysis or transplantation. ... Usual nephrological management in the context of the presence of lgA nephropathy where hypertension is present, would be to maintain the blood pressure to within the normal range. There is more recent data showing that in patients with significant proteinuria, more than 3g/24 hours who have mild to moderate renal dysfunction, that blood pressure control does slow down the rate of renal functional progression. This is reasonably well controlled data and indeed the results are not surprising. Mr Brien was not in that category in 1991, but clearly had entered the category by the time of first referral in early 1993. If appropriate monitoring had occurred subsequent to 1991, it is possible that renal functional deterioration and the development of more marked proteinuria would have been detected earlier, prompting a more vigorous approach to blood pressure control. I would expect that if his condition had deteriorated, for example by early 1992 to a stage where this approach to therapy was indicated, then commencement of therapy at that time may have slowed down the rate of renal functional deterioration, thus delaying a requirement for dialysis treatment." 3. Professor Nacey: "I have read the additional material you sent which includes the letters from Dr Collins and the article 'Treatment of lgA Nephropathy'. The key issue in this case is whether Mr Brien's prognosis has been adversely affected by any perceived delay in diagnosis of his lgA nephropathy. 9 I believe the Committees original decision that there is no evidence of personal injury has been further supported by the additional material. Dr Collins in his letter of 13 March 1996 to ACC now clearly states that in 1991 'there is no convincing evidence that any specific therapy would have altered his prognosis'. Mr Brien was seen by Dr Collins in 1993. Dr Collins has stated that during the period 1991 - 1992 if any deterioration in Mr Brien's condition had been detected then 'commencement of therapy at that time may have slowed down the rate of renal functional deterioration'. This is supposition and there is no statistically valid evidence to support this statement. I think the article provided by Dr Collins sums it up pretty well: 'At present, it is unclear if any therapy alters the course of progressive lgA nephropathy.' From the additional information I think the Committee should adhere to its original decision that cover be declined." 4. Addendum by Dr Collins to his report of 13 March 1996, the addendum dated 3 January 1997: "I don't believe any reasonable clinician would find fault with Mr Brien's management up to his assessment in June 1992. It is however difficult to understand why the army did not refer him back for further specialist investigation once the results of the blood and urine tests became available in June 1992. The blood pressure (140/85) at that assessment was at a level which at that time would not have prompted a more vigorous attempt at blood pressure control. A year later in June, 1993 he was however frankly hypertensive with a blood pressure of 170-180/100, which had clearly developed at some point in the interim. Earlier specialist referral in June 1992 would have resulted in a renal biopsy, with a definitive diagnosis being reached. Given the degree of proteinuria and early renal dysfunction, an earlier follow-up and more frequent review would have been arranged. It is of course speculation as to whether or not this would ultimately have resulted in any difference in his outcome as measured by delay in progression of renal disease." Dr Collins gave evidence at the review hearing and confirmed his earlier advice that in his opinion by the time the tests taken by Dr Nguyen in July 1992 were known there was sufficient evidence at that point to justify referring the appellant for a renal biopsy. He went on to state that there was not the data or the literature at that time which stated that there was a therapy which would have made a difference to the condition that was subsequently diagnosed. Dr Collins said that the condition itself would not have been altered in any way. In answer to questions from the appellant's advocate, Dr Collins stated that the current practice in Auckland was not to biopsy people with isolated microscopic haematuria and at the time when the appellant presented in 1988 and 1991 his criteria for doing a biopsy would not have been fulfilled. Dr Collins went on to advise that the appellant was reacting well to the treatment he was receiving and that it was not possible to predict the progress of the disease and that he could not tell if or when end stage renal 10 failure would be reached. He said the disease had a particularly wide spectrum of outcome from the extreme of rapid deterioration to renal failure within the period of a year to the other extreme where a person never develops renal failure. He stated it was not possible to predict which course would be that of the appellant. He said to predict an outcome would be speculating. In his decision the Review Officer considers that it was common ground that a delay in diagnosis did occur and that this is mentioned by both Dr Macdonald and Dr Collins. He went on to find that there was insufficient evidence to support a finding of any negligence, but the issue was resolved against the appellant on the basis that there was no causative link between any act of a treating professional and the appellant's condition, it being as a consequence of disease. He found that the evidence fell well short of establishing that the appellant had suffered personal injury. Submissions Mr Hillary, advocate for the appellant, submitted that the appellant has suffered personal injury by medical misadventure being medical error, that personal injury being the prospect of the appellant suffering end stage renal failure at an earlier stage of his life than would be the case had his condition been diagnosed earlier and treatment for its containment commenced earlier. He further submitted that it was the case that the appellant would at all times be suffering a severer kidney dysfunction than would have been the case had treatment been undertaken from the time that he was seen by Dr Nguyen in June 1992. Following on from that submission Mr Hillary submitted that the treatment that should have been commenced for the appellant was principally that of control of his blood pressure and secondly measures to limit the amount of protein excreted into his bloodstream by monitoring the amount of protein intake into his body. Mr Hillary accepted that the appellant's condition was irreversible but that nevertheless its progress could have been slowed and that there was a treatment time that has been irretrievably lost. Mr Hillary submitted that the rate of deterioration between June 1992 and June 1993 was significant in that the 24 hour protein/urine test in June 1992 showed 4.2 grams per day whereas that figure had jumped to 7.74 grams by March 1993. Mr Hillary contended that it was Dr Nguyen who was in error in June 1992 by not being alerted to that 24 hour urine/protein figure and referring the appellant to a specialist Urologist or Nephrologist for further consideration rather than simply determining that he was fit for his intended overseas duty. He submitted that the initial tagging of the file by Mr Smart ought to have alerted him to the possibility of kidney disease. Mr Tui, counsel for the respondent, submitted that the primary issue must be whether there has been any personal injury. It was his submission that the medical evidence establishes that the appellant's condition is a disease and was not caused by any delay in diagnosis or treatment. Counsel further submitted that at the present time the appellant does not suffer any symptoms of renal failure and that the only possible injury that could be said to be suffered would be end stage renal failure, that is when the appellant's kidneys collapse, but that stage has not been reached and may never be reached in his lifetime. 11 Counsel submits that it is pure speculation that any earlier intervention would have has any impact on the progress of his condition. Counsel further submitted that no negligence of any treating health professional had been found by the MMAC nor the MPDC. He submitted that at the time that the appellant was seen by Dr Nguyen his blood pressure was normal and all other physical aspects of his health were normal and that in any event there is no evidence to suggest that any earlier action, such as a biopsy would have made any difference to the appellant's condition. Counsel submitted that there was no evidence from any medical peer that any perceived delay as to treatment was negligent or involved a departure from acceptable professional standards. Decision The first issue to be determined is whether the appellant has suffered an adverse consequence which constitutes a personal injury, within the meaning ascribed to those words under the Act, as a result of the delay in the diagnosis of his disease. Section 8(2)(c) provides for cover under the Act for personal injury which is medical misadventure as defined in s.5 of the Act. "Medical misadventure" is defined in s.5 as meaning "personal injury resulting from medical error or medical mishap". In this case we are concerned only with medical error and this is defined in the Act as: "the failure of a registered health professional to observe a standard of care and skill reasonably to be expected in the circumstances. It is not medical error solely because desired results are not achieved or because subsequent events show that different decisions might have produced better results." Thus, as might be expected, the appellant must establish that he has suffered personal injury by medical misadventure, in this case medical error. Personal injury is itself defined as meaning physical injury. Thus in the context of this appeal it needs to be shown that the appellant has suffered a physical injury and that this physical injury was caused by the medical error of a treating health professional. An obvious example of this would be the unnecessary amputation of a limb caused by a negligent misdiagnosis. The question is, can this appellant come within the rationale that that obvious example identifies. The uncontestable fact is that this appellant suffers from a disease known and identified as IgA Nephropathy. It is a disease of the kidneys which can have as its ultimate consequence a total failure of the kidneys and the need for the body to function by way of a dialysis machine. It is also a medical fact that this disease cannot be cured. It can be treated and its progress retarded. According to some medical journals its progress can be halted and not every instance of the condition progresses to end stage renal failure. The appellant was diagnosed as suffering from IgA nephropathy following a renal biopsy carried out in May 1993. He was referred to a renal physician, Dr John Collins. In his first report Mr Collins advised that it was not possible to define the rate at which his kidneys would fail and he noted that at that stage the appellant was asymptomatic. He further noted that the most important measure that could be instituted was to maintain blood pressure under consistently good control. To that end Dr Collins commenced him on daily medication for blood pressure. Dr Collins also talked about 12 possible dietary modification if it be found that the appellant's current protein intake was greater than desirable. It is to be noted that Dr Collins' opinion as to the progression of the disease, as expressed in his reports of 15 June 1993 and 19 July 1993, have altered considerably after the passage of three years when he reported in March 1996. Dr Collins last examined the appellant in February 1996 and he noted that his blood pressure control was excellent and that he now had a 24 hour urine protein of 0.5 grams - significantly reduced from the high levels noticed at his initial presentation. Dr Collins had previously advised in May 1995 that the appellant's renal status was stable at present and it was difficult to predict its future course. It was his view however, and a view he has maintained throughout, that the appellant's condition is one where at some point in the future he will suffer end stage renal failure requiring dialysis. It is noted that Dr Collins found it difficult to understand why the army (Dr Nguyen) did not refer the appellant for further specialist investigation once the results of the blood and urine tests became available in June 1992. He did however note that at that time the appellant's blood pressure was normal. Dr Collins went on to state that earlier specialist referral in June 1992 would have resulted in a renal biopsy with a definitive diagnosis being reached. He then stated however that it was speculation as to whether or not earlier follow-up would ultimately have resulted in any difference in his outcome as measured by delay in progression of renal disease. In addition to the opinion of Dr Collins there is the opinion of Dr Alastair Macdonald who indicated that even though it was only speculation to determine what might have been the situation had there been an earlier kidney biopsy, he advised that there would have been no significant difference in the course of the disease. Similarly he considered that it was difficult to attribute any stabilisation of renal function that may have occurred subsequent to diagnosis to any particular intervention. He said that the use of interventions by nephrologists is on the basis of prudence rather than on the basis of firm scientific evidence. As part of the appellant's submissions he produced various extracts from articles relating to IgA nephropathy and its treatment and it seems to be accepted by the authors of those various articles that there is some evidence that dietary regulation and control of blood pressure did show benefits in certain tests but in the principal text relied on by the appellant, namely that of Rose & Appel they state: "At present it is unclear if any therapy alters the course of progressive lgA nephropathy. It should be noted however that a long term study would be required to show benefit of treatment in this disorder in which the rate of progression is typically very slow." They went on to state that it was difficult to make definitive recommendations on the therapy of IgA nephropathy but that there was general agreement that hypertension should be treated early, preferentially with an ACE inhibitor. It is to be noted that at the time when the appellant contends Dr Nguyen ought to have taken action to refer him on to a specialist the appellant's blood pressure was normal. There is no evidence as to what his blood pressure was in the intervening nine months to March 1993 when it was found to be high. It is therefore speculation to determine 13 when that blood pressure did elevate. It is however a fact that it was taken in hand and reduced to normal, described as excellent, by 1996. The Court has heard no evidence as to what effect some indeterminate period of possible elevated blood pressure has had on the progress of the disease. In the foregoing I have endeavoured to set out the salient facts which are relevant for the determination of the question of personal injury. There was no act of commission by any treating health professional that rendered physical harm to the appellant. The only physical harm that is contended by the appellant is an earlier than would otherwise be expected end stage renal failure, that is the physical injury to the kidneys. This Court has had no evidence as to any act of omission in not initiating an earlier specialist referral as affecting the progress of the disease. Even speculation by experts cannot assist. In short I find that there is no evidence that this appellant has suffered personal injury by any act or omission from a treating health professional, leaving aside the question of whether any act or omission would be regarded as being medical error. The disease is marching inexorably on, but at a speed when it is impossible to predict it will reach end stage renal failure. The period of inaction complained of is nine months that is June 1992 to March 1993 and, as I have found, there is no evidence that any physical injury occurred to this appellant in that period, save for him having an increased creatinine level and an increased proteinuria. Both of which were controlled and reduced by subsequent medication. There is no evidence that those increases are themselves physical injury and certainly that was not propounded by the appellant as being the manifestation of the physical injury. For the foregoing reasons therefore I find that this appellant cannot be considered for cover under the Act as he has not suffered a physical injury. He is suffering from a disease and a disease only. In the event that the finding should be proved wrong, I propose to consider the issue of medical error. The question of whether or not a treating health professional has committed a medical error is a question of law and requires this Court to make a finding, based on the evidence tendered to it, whether the acts or omissions of that health professional amount to a failure to observe a standard of care and skill reasonably to be expected of that person in the circumstances. Having said that it is a question of law, this Court requires to receive evidence, particularly expert evidence, of what might be considered to be expected of a health professional in the particular circumstances which are in question. The allegation in this case is that Dr Nguyen ought to have referred the appellant on to a specialist for further investigation at the time of his physical check-up in June 1992 when he found the appellant's proteinuria level was 4.2 grams. The Medical Misadventure Advisory Committee considered this question after receiving a lengthy explanation from Dr Nguyen and it came to the view that no medical error could be established. The Medical Practitioners Disciplinary Committee also considered the issue and it noted that apart from the raised urinary protein level, the indications were that the appellant was fit and that he had normal creatinine clearance and blood pressure which suggested there was no strong need to take the matter further. It noted that with the benefit of hindsight perhaps Dr Nguyen should have initiated referral but it did not consider that to be a breach of his professional duties having regard to the other positive findings that there present. 14 Dr Collins did observe that it was difficult to understand why the army did not refer the appellant back for further specialist investigation once the results of the blood and urine tests became available, yet he too noted that the appellant had normal blood pressure at the time so that there was no need for blood pressure control. On the other side of the coin there is the fact that Dr Smart, Urologist, had been involved at an earlier stage and had noted certain irregularities but his report had simply advised that should there be a change in the haematuria, for example should it become macroscopic, that is able to be seen with the naked eye, or other symptoms develop, then he should be referred again. The report of Dr Nguyen to the MPDC and MMAC indicates that he was aware that it was only microscopic and further that the appellant was persistent and anxious to be graded fit for overseas duty. With that being the relevant evidence, and there being no expert evidence adduced on behalf of the appellant which would show that the omission to refer on by Dr Nguyen was a falling below the professional standard expected, then it is not the position of this Court to express an opinion, its function being confined to making a ruling of law based on the evidence, that is based on the opinion evidence of experts which the Court can weigh up and make a finding of what is to be expected, compare that to the actions taken, and then make the ruling of law. Accordingly then I find that there is no evidence upon which this Court could find that there was medical error on the part of Dr Nguyen in his failing to refer the appellant on for specialist investigation at the time of his physical examination in June 1992. For the foregoing reasons therefore I find that the appellant's claim for cover must fail as he can neither establish personal injury, nor medical misadventure. This appeal is therefore dismissed. DATED at AUCKLAND this (1+ day of November 1999 M J Beattie District Court Judge DCA229-97.doc(J9)