Accident Compensation Corporation v Robertson

Decision No. [2011] NZACC 327 IN THE DISTRICT COURT HELD AT WELLINGTON IN THE MATTER of the Accident Compensation Act 2001 AND IN THE MATTER of an appeal pursuant to Section 149 of the Act BETWEEN ACCIDENT COMPENSATION CORPORATION (ACR 619/10) Appellant AND CASSANDRA ROBERTSON Respondent HEARD at WELLINGTON on 25 October 2011 APPEARANCES Mr A D Barnett, Counsel for appellant. Ms E Wilson and Mr J Miller, Counsel for Respondent. RESERVED JUDGMENT OF JUDGE M J BEATTIE [1] This appeal arises from a review decision dated 3 September 2010, whereby the Reviewer quashed the appellant's primary decision and granted cover to the respondent for a treatment injury. [2] The appellant's primary decision was given on 9 June 2007, whereby it declined to grant cover to the respondent for a treatment injury stated as being: Delay in diagnosis of IgA nephropathy resulting in kidney damage and progression of renal disease. [3] This appeal requires a determination of two issues: firstly, whether or not as a matter of fact, there was a delay in diagnosis which amounted to a failure to diagnose the respondent's medical condition of lgA nephropathy; and secondly, whether any delay which may have been established caused a treatment injury within the meaning 2 of the Act, it being accepted that the respondent's medical condition was not a treatment injury, it being an existing underlying condition. [4] The claimed treatment injury is the more aggressive progression of the appellant's chronic kidney disease and where it is contended that that progression could have been delayed by months, or as much as two years, if there had been an earlier diagnosis and the appropriate treatment instigated. [5] It is accepted that the appellant's medical condition was such that it could not have been cured, and that it was inevitably going to reach the stage of renal failure, and the point is if that end state of renal failure could have been put off for some limited period of time by earlier instigation of treatment, has the failure to do so given rise to a treatment injury. [6] The relevant background facts may be stated as follows: As of the date of the appellant's primary decision the respondent was 33 years of age. The respondent had been under the care of her GP, Dr M Allen, since 1995, and there is evidence that she suffered from a number of conditions which required treatment and attention over the years, and as noted by one of the specialists who has later given evidence on the issue in question, the respondent had a background of medical problems, those medical problems dating back to 1992. Over that same period the appellant has given birth to six children. It is the case that in the 1990's, on more than one occasion, the respondent was identified as suffering from urinary tract infection. On two occasions, namely January and August 2002, analysis of the respondent's urine showed proteinuria, but there was no further investigation done on those respective dates. In January 2004, the respondent was identified with high blood pressure and blood tests then taken identified severe renal failure. On 20 January 2004 the respondent was referred by her GP, Dr Allen, to Professor Walker, Nephrologist, at the Department of Renal Medicine, Dunedin Hospital, where her then end stage renal failure 3 was identified and she immediately began to receive the appropriate treatment for same. In January 2007, Dr J Schollum, Nephrologist (Renal Physician) lodged a claim with ACC for a treatment injury which he described as "lack of diagnosis for ongoing kidney problem over a period of two years. Now has lgA nephropathy - GP was Dr Murray Allen." The appellant referred the matter firstly to Dr A Macdonald, Consultant Renal Physician, and he provided a report dated 14 May 2007, and it also sought a report from Dr I St George, a GP, and he provided a report dated 7 June 2007. Consequent upon those reports the appellant issued its decision declining cover on 9 June 2007. The respondent sought a review of that decision and it is the case that further medical reports were obtained for both parties for the purposes of that review. By decision dated 3 September 2010, the Reviewer, Ms K Stringleman, quashed ACC's primary decision and determined that the respondent was entitled to cover for a treatment injury, that injury being identified as a significant progression of the disease consequent upon the delay in diagnosis. For the purposes of the appeal to this Court, no further medical evidence from that which was presented at review, has been introduced. [7] The medical opinions relating to the issue of delay in diagnosis are as follows: 1 . Report from Dr A Macdonald, Consultant Renal Physician, dated 14 May 2007 Or Macdonald had been requested by ACC to provide an opinion on the issue of any delay in diagnosis. Dr Macdonald had details of all the respondent's medical attendances from 1995 onwards at the premises of her GP, Dr Allen. Relevant notes from those GP consultations were as follows: (a) 29/1/02 Urinalysis showed urinary protein 3+ and blood 3+. This was during a nurse consultation. Noted to be currently having a period. 29/1/02 Back pain 9/4/02 Stress symptoms 24/7/02 Stress symptoms (b) 16/8/02 Urinalysis showed urinary protein 3+ and blood 3+. This was during a nurse consultation. The lab report indicates that this is "a contaminated specimen, please repeat". 11. 10.02 Ocular symptoms 23/20.02 Back pain There follows a series of nursing consultations regarding weight. (c) 24/4/03 Dizziness, noted to be hypertensive @ 170/96. 29/4/03 BP now 124/90 15/5/03 Dizziness 21/5/03 Painful lump right jaw 13/8/03 Laceration of leg 23/12/03 Stressed at work. BP 170/108 99/1/04 Dyspnoeac at night, BP180/108. Weight 111 kg. 20/1/04 Referral for management of renal failure. He then commented as follows: On the basis of symptoms alone it would have been difficult for a GP to have made the diagnosis of an underlying serious kidney problem. In the list of medical consultations above there is little to suggest the presence of an underlying major chronic kidney disease. In the admission note of 21/1/04 there is mention of Mrs Robertson having had inuria during her pregnancies but no hypertension". This is the only reference to this occurrence in the extensive note available for perusal. The important consultations with regard to the occurrence of pointers of an underlying glomerulonephritis are summarised below. Dr Macdonald identified the three consultations referred to above as being important consultations. He then noted that a number of clinical indicators are associated with an increased likelihood of a kidney problem, and that these included the presence of hypertension, proteinuria and haematuria. In relation to hypertension, he noted that the earliest indication of this was 29/4/03, where her blood pressure was 170/96. He further noted as follows: In a young person with hypertension an assessment as to a primary cause is worthwhile because one is more likely to find an underlying primary cause for the elevated blood pressure. Although she was significantly overweight, and this could have been an issue in hypertension, nevertheless hypertension associated with obesity should be a diagnosis of exclusion in a young person. In relation to proteinuria this is, according to the medical dictionary, a condition in which proteins, principally albumin, are present in the urine. It is often a symptom of serious 5 heart or kidney disease. In relation to the proteinuria earlier identified in January 2002 and August 2002, he stated as follows: Had the importance of these findings been noted at the time then further investigation including a serum creatinine and estimation of urinary protein excretion might have indicated an underlying kidney problem. A renal biopsy might have been performed and treatment could have been commenced to try to minimise the progression of an underlying glomerulonephritis. In relation to haematuria (the condition of blood in urine) he stated as follows: She was noted to have a history of gross haematuria (and this was attributed to her period). She also had 3+ proteinuria. Ideally she should have this repeated at a time when she did not have her period. If Mrs Robertson had had persistent haematuria then this was an opportunity to have diagnosed her underlying glomerulonephritis earlier. He then summarised his advice as follows: There were three clinical problems which could have alerted a physician to the presence of a chronic kidney problem, namely proteinuria, haematuria and hypertension. From what I have previously described I think that at the time of the occurrence of these clinical indicators (2002 and 2003) it is very likely that Mrs Robertson had undetected but significant chronic renal impairment. If a chronic kidney problem had been diagnosed in 2002 or 2003, then treatment might have delayed the onset of end stage renal failure by a number of months or a small number of years. By the same token it might also have had no benefit at all. 2. Report from Dr St George, GP dated 7 July 2007. Dr St George had Dr Macdonald's report above for reference and he commented as follows: She developed renal failure from glomerulonephritis (GN) and had been attending her general practitioner frequently. Her symptoms during that time are very questionably caused by her GN, and in fact could as easily (and more likely) have been caused by other conditions. There is no way to tell whether her condition should, or indeed could, have been diagnosed earlier. The only symptoms that might have raised the possibility of GN in her doctor's mind were (1) haematuria in 2002 when she was normotensive, (blood pressure within the normal range for an individual's age and sex) was having her period, had her urine reported as contaminated, and had a history of urinary infections: in that context GN would have been highly unlikely. (2) rising blood pressure during the middle months of 2003, at a time when she was not having haematuria; she was obese, but aged only 30, and although in retrospect a relatively rapid, recent and persisting rise in blood pressure might have alerted the doctor to renal disease (as it eventually did). The suggestion is that the diagnosis was delayed. In my opinion there is no evidence for that. (1) there is no hard evidence her GN started earlier than January 2004, though in retrospect the mid-2003 sharp and persistent rise in blood pressure was probably the first sign. (2) the haematuria in 2002 was more likely related to contamination of the urine by menstrual blood, or caused by urinary tract infection. 6 3. Report from Dr J Collins, Renal Physician, to John Miller Law, dated 22 June 2009 This report was sought for the purposes of the review. He stated, inter alia, as follows: Reviewing the family general practitioner records subsequently provided, I note that the first hint of this problem was a urinalysis undertaken on 29" January 2002, showing 3+ proteinuria and 4+ haematuria. At that visit she had low back pain which was thought to be mechanical. There is no indication that further investigations such as blood tests were undertaken. Subsequently, on 16" August, 2002 she re-presented with a history of macroscopic haematuria and bilateral loin pain. A midstream urine at that time also showed a large amount of proteinuria and more than 1000 red cells per cmm. There is again no record of blood tests being undertaken. The presentation on 16" August is a very typical presentation for a person with IgA nephropathy. The presence of a large amount of proteinuria noted on two occasions in 2002 points directly and almost diagnostically towards glomerular protein leakage and thus some form of glomerulonephritis. It is thus clear that Cassandra had features consistent with glomerulonephritis documented first approximately two years prior to her admission to Dunedin Hospital. 4. Letter from Dr St George dated 29 July 2009 to ACC Dr St George was asked to comment on Dr Collins' report. He noted the relevance of the comments of Dr Collins relating to the 16" August 2002 with respect to haematuria, and he stated as follows: I agree that in retrospect the presentation on 16 August may have been glomerulonephritis. I reiterate my previously stated view, however: it could as easily have been a urine specimen contaminated by menstrual blood, as reported at the time, and the "loin pain" could have been the lumbar musculoskeletal pain she soon afterwards presented. She was at that time normotensiv It is a great pity the follow-up urine was not done, as that would have determined the diagnosis one way or the other. 5. Report from Dr Macdonald dated 17 June 2010 to ACC. This was a report from Dr Macdonald after further background material had been obtained from the respondent and which went back into the early 1990's, in relation to the identification of proteinuria, and he stated as follows: The presence of significant levels of proteinuria would have changed the prevailing conservative attitude to performing a renal biopsy. Although I did not find any 24 hour urine protein quantification, had one known about the presence of 3-4+ proteinuria, then most nephrologists would have suggested a renal biopsy. The underlyng reason for such an approach being that the level of proteinuria is a marker for a more serious underlying glomerular disorder. (1) Had a renal biopsy been performed then it would have been possible to have diagnosed the nature of the underlying glomerular disease in Mrs Robertson's 7 6. Report from Dr St George dated 23 June 2010 to ACC. Dr St George was asked to comment on the reports of Dr Macdonald and Dr Collins, and his comment on whether the respondent ought to have been earlier referred to a renal physician was as follows: That referral depended on what was presented, what could have been discovered by examination and investigation, and on reaching a diagnosis; in this case the questions around variable urinary protein and blood did raise the question of renal disease to the extent that renal imaging was ordered four times. The renal imaging he refers to was identified in the additional background information that was provided and showed that renal ultrasounds were carried out on four occasions between July 1992 and June 1999. His final comment was as follows: There can be no certainty that Ms Robertson even had IgA nephropathy before mid 2003, and although now, afterwards, and in hindsight, that does seem probable, there were other logical explanations at the time I maintain my opinion that the general practice management of Ms Robertson was reasonable and appropriate in the circumstances and without that wisdom of hindsight, that there is no certainty that the nephropathy existed before mid 2003 and thus that there was any failure to diagnose earlier. [8] The second aspect of this appeal relates to the medical opinion as to what might have been the consequence of treatment, if indeed there had been an earlier diagnosis. 1. Report from Dr Macdonald of 14 May 2007. There were possibilities to have made the diagnosis earlier. Had the diagnosis been made earlier then there is the possibility that the onset of chronic renal failure could have been delayed. Given that at the time of diagnosis of the problem the kidneys were small and echogenic on ultrasound and that on renal biopsy there was significant interstitial fibrosis and tubular atrophy, these findings indicate that the underlying disease of progressive kidney failure due to IgA nephropathy was not of recent onset. This means that any intervention to try to improve the renal outcomes would have been at a relatively late stage in the chronology of the disease and hence was unlikely to make a major difference to the ultimate outcome it is not very likely that there would have been a great difference in the ultimate outcome of developing chronic kidney failure. t would appear that it was only in the last few months of her illness that she had symptoms that could have been diagnosed as possibly being renal in origin. As noted previously it is much easier to make this diagnosis with the benefit of hindsight. 2. Report of Dr Collins dated 22 June 2009. It is not possible to accurately define the extent to which the delay in diagnosis has made a difference in Ms Robertson's outcome. Standard therapy for IgA nephropathy is the use of antihypertensive therapy, particularly those agents that reduce proteinuria such as ACE inhibitors and angiotensin receptor blockers. There is well established evidence in 8 the literature that good control of blood pressure in proteinuric patients will have a significant effect to delay progression of chronic kidney disease. I would have expected that assuming good therapy was able to be achieved along these lines, the time taken for Cassandra Robertson to reach end state renal failure and require dialysis would have been substantially lengthened, possibly by a few years. ... It is important to emphasise that the underlying glomerulonephritis would have been well established by the time the proteinuria first became apparent and that therapy with antihypertensive treatment does not cure that problem, but can delay the progression of renal damage. 3. Report from Dr Macdonald dated 17 June 2010. The recognition of the significance of haematuria and proteinuria earlier in the course of Mrs Robertson's disease could have allowed her to have been advised and treated medically. This might have delayed the onset of chronic kidney disease. (1) Whether she would have developed end stage renal failure in spite of treatment is unknown. On the balance of probabilities it is likely that her disease process would have been slowed down. [9] In his submissions to the Court Mr Barnett submitted that it is not every case that a delayed diagnosis will qualify as treatment within the meaning of section 33(1)(d). He submitted that there must be an element of failure that imports a measure of deficiency or oversight, even though that can be less than a negligent failure that would have been the necessary requirement for medical error. [10] In furtherance of his submission, he referred to the fact that the respondent was at all material times under treatment of a GP only and a renal physician was not involved until January 2004. On that basis, Counsel submitted that the opinion of Dr St George was relevant, he being a highly respected General Practitioner, and it was his opinion that there was no delay in diagnosis by Dr Allen. [11] Finally, Counsel submitted that the evidence of Dr Macdonald was largely that of a specialist commenting with hindsight, and that even he acknowledged that a significant number of cases in New Zealand went undiagnosed until the end stage condition was reached. [12] In relation to the second issue, namely whether a treatment injury had in fact arisen, Counsel submitted that section 32(2)(a) applied, and that a treatment injury did not include a personal injury that was wholly or substantially caused by a person's underlying health condition. [13] Counsel submitted that in the case of this respondent the lgA nephropathy was the underlying health condition, it had not been caused by any treatment, and whilst an earlier diagnosis may have delayed progression of that condition, end stage renal 9 failure was an inevitable consequence, and that the substantial cause of that renal failure was the respondent's underlying health condition. [14] Ms Wilson, Counsel for the Respondent, submitted that a failure to diagnose does constitute a situation of treatment within the meaning of the Act, and she contended that it was simply a question of fact and that error on the part of the treating GP is not a consideration. Counsel submitted that the opinions of Dr Macdonald and Dr Collins identified that the appellant's history did give rise to identifying that earlier action should have been taken. [15] In relation to the second issue, Counsel submitted that if it is accepted that a delay in treatment caused the disease condition to progress significantly more quickly than would have been the case had it been under treatment earlier, she contended that the injury of that early arising end stage renal failure cannot considered to be wholly or substantially caused by the underlying disease condition. It was Counsel's submission that the personal injury in this case was the earlier onset of end stage renal failure and the requirement for dialysis as a consequence thereof. DECISION [16] In this case, the respondent sought cover under the Act for a treatment injury of end stage renal failure, that situation arising as a consequence of a failure to diagnose her medical condition and provide treatment in a timely manner. In terms of the relevant statutory provisions, section 32 of the Act advises that a treatment injury is a personal injury suffered by a person and caused by treatment. [17] Under section 33 the meaning of treatment includes: . .. (b) a diagnosis of a person's medical condition; (d) a failure to provide treatment in a timely manner; Also highly relevant in this current case is the provision of section 32(2)(a) which states that a treatment injury does not include a personal injury that is wholly or substantially caused by a person's underlying health condition. [18] In the present case it was asserted by the respondent that the earlier failure to diagnose her IgA nephropathy until end stage renal failure had occurred, was a failure to diagnose at an earlier time and to provide treatment in a timely manner that would have delayed the onset of end stage renal failure. 10 [19] Dealing first with the question of whether there was a failure to diagnose at an earlier point in time than did in fact occur, the Court has received opinions from two specialists in the relevant field, namely renal physicians, and it has also received an opinion from a general practitioner who has looked at the matter from the standpoint of a general practitioner, who was the medical person whose treatment has been alleged, as involving a failure to diagnose the medical condition of IgA nephropathy in 2002 or early 2003. [20] At review, in her decision, the Reviewer accepted the evidence of Dr Macdonald and Dr Collins, that is the two specialists, that on balance there had been a delay, and that there were clinical indicators at least as early as 2002 and 2003 which could have led to a referral or further investigation of the appellant's condition. [21] As earlier noted, it was Mr Barnett's submission that this issue of failure to earlier diagnose must be looked at through the lens of a general practitioner, rather than a renal physician. However, looking at the matter objectively, I consider that the question of diagnosis is not a question which must be looked at from the point of view of a general practitioner alone, as I consider it to be the situation that if there is sufficient evidence of an unknown medical condition causing significant problems, then it befalls the GP who is aware of those problems to then refer the patient to specialists for further investigation. [22] In the present case, based on the advice of Dr Collins and Dr Macdonald, I consider that there was sufficient information in the hands of the GP for him to be in a position where he ought to have referred the respondent on for specialist investigation. Whilst it must be accepted that the GP himself would not have the necessary speciality to identify potential lgA nephropathy, nevertheless I consider that some step ought to have been taken back in 2002 when there was evidence of hypertension and proteinuria, and it was of significance and ought to have given some indication that there may be an underlying kidney problem. [23] Having therefore determined that the respondent's circumstances did involve the question of treatment within the meaning of section 33(1)(b) and (d), it now requires the Court to consider whether the respondent suffered a treatment injury caused by that treatment. As earlier noted the personal injury sought to be covered was end stage renal failure, being a condition with which the respondent was afflicted as of January 2004. 11 [24] The significant statutory requirement in this case is whether the injury being claimed was caused by treatment. Having identified that the treatment in question was the failure to have an earlier diagnosis, it then falls to be considered whether that failure caused a personal injury which is a treatment injury. [25] The evidence from the specialist renal physicians is to the same effect, namely that whilst earlier treatment may have delayed the onset of end stage renal failure, it would not have prevented it, and indeed there is a real question-mark as to whether end stage renal failure would have been delayed; but even if it was delayed the evidence is clear that the outcome of end stage renal failure was the inevitable end result of the medical condition of IgA nephropathy. [26] In terms of the relevant statutory provision, namely section 32(2)(a), I find as a fact that the medical condition suffered by the respondent was that of IgA nephropathy and that this was the respondent's underlying health condition and not attributable to any treatment within the meaning of the Act, and that the condition of end stage renal failure is the inevitable consequence of that underlying health condition and it is not a condition which could have been prevented by any earlier treatment. [27] I find it therefore to be the case that because earlier diagnosis and dialysis treatment may have only slowed down the end consequence of end stage renal failure, it does not bring about a new injury, that is a treatment injury, but rather there is simply the possible acceleration of the inevitable. [28] In those circumstances I find that the respondent's medical condition of end stage renal failure was wholly or substantially caused by her underlying condition of IgA nephropathy, and as such, her medical condition is excluded from being a treatment injury by reason of section 32(2)(a). [29] Accordingly, therefore, I find that even though, on the balance of probabilities, there was treatment within the meaning of the Act in the failure of an earlier diagnosis, it is the case that that treatment has not caused a treatment injury within the meaning of section 32 of the Act. (30] In the present case I find that the medical advice to the effect that the inevitable outcome of the respondent's medical condition would be end stage renal failure, and that no treatment could prevent or resolve that condition, puts this case in a different category from other cases where delay in diagnosis was found to have caused a more severe injury than would have been the case if there had been the opportunity of earlier treatment. 12 [31] In that regard I refer to the decision of His Honour Judge Barber in Grogan (Decision 202/09) where His Honour considered that the delay in treatment led to a significantly greater tumour growth than would have been the case. Further, I consider the comments made by His Honour Judge Ongley in the case of Lewes (Decision 221/06) where at paragraph [20] His Honour stated as follows: The conceptual problem in such an appeal is whether to regard each increment of progression of a disease as an element of damage or injury. I respectfully agree with the approach taken by Judge Beattie in the cases of Estate of Veysey and Luke (above) o the effect that an injury occurs when the disease progresses beyond the stage at which treatment would have been effective. When a disease changes from a curable condition to an incurable condition there is without doubt an injury. There may also be an injury when a disease progresses to a stage at which treatment could have significantly less effect against the progress of the disease. Such a degree of change must depend on the evidence and circumstances of each case. [32] As I have found, in the present case earlier treatment would not have affected the inevitable consequence of the progress of the disease to end stage renal failure. [33] For the foregoing reasons, therefore, I find that the Reviewer was wrong to determine that the respondent had suffered a treatment injury in the circumstances of her case, and accordingly I quash the Review Decision, and the appellant's primary decision of 9 June 2007 to decline cover is hereby reinstated. DATED this 9day of November 2011 M J Beattie District Court Judge