Allison v Accident Compensation Corporation

IN THE DISTRICT COURT HELD AT WELLINGTON Decision No. [2010] NZACC 212 IN THE MATTER of the Accident Compensation Act 2001 AND IN THE MATTER of an appeal pursuant to Section 149 of the Act BETWEEN STEWART ALLISON (Al 592/08) Appellant AND ACCIDENT COMPENSATION CORPORATION Respondent HEARD at WELLINGTON on 27 August 2010 APPEARANCES Ms K Lau, Counsel for Appellant. Mr J Roberts, Counsel for Respondent. RESERVED JUDGEMENT OF JUDGE M J BEATTIE [1] The issue in this appeal concerns the correctness of the respondent's decision of 16 June 2007, whereby it declined to grant the appellant cover for a claimed treatment injury of steroid induced osteoporosis. [2] This is an appeal where I find there are some jurisdictional and evidential difficulties relating to the claim for cover as it is now presented by Counsel for the Appellant, with major questions being firstly what is in fact the claimed personal injury, secondly, what is the alleged causative treatment in relation thereto, and thirdly, whether, this Court in its appellate capacity has jurisdiction to consider those issues having regard to the initial claim for cover and the primary decision made thereunder. [3] Before considering those matters further, it is desirable to set out the relevant facts and the medical evidence which has been presented to the Court in relation to this claim. 2 [4] The relevant background facts may be stated as follows: . As of the date of the lodging of his claim for cover, the appellant was some 14 days shy of his 50" birthday. The claim for cover lodged by the appellant on or about 29 May 2007, sought cover for a treatment injury stated as being "osteoporosis, secondary to steroid therapy for severe COAD asthma. That claim was signed off by the appellant's GP, Dr Patricia Hastilow, of Invercargill. The respondent referred the appellant's claim to Professor Timothy Maling, Registered Specialist in Internal Medicine and Clinical Pharmacology. Professor Maling reported on 12 June 2007 and advised that the claimed injury was an ordinary consequence of the particular high dose steroid treatment that the appellant had been receiving. Consequent upon Dr Maling's advice, the respondent issued its decision on 16 June 2007, advising that the appellant's claim for steroid induced osteoporosis had been declined. A copy of Professor Maling's report was provided with that decision. The appellant sought a review of that decision and for the purposes of that review, the Appellant's Counsel sought a report from Dr David Jones, Respiratory Physician, and in response thereto the respondent sought the opinion of Dr Stephen Child, Consultant Physician. A Review Hearing took place on 30 November 2008 at which that further medical evidence was introduced. . In a decision dated 10 December 2008, the Reviewer, Mr D Walker, found that the weight of the medical evidence established that the effects of the treatment on the appellant's bone mineral density were recognised as an ordinary consequence of such treatment and therefore the appellant had not suffered a treatment injury within the definition of the Act. The respondent's primary decision was therefore confirmed. 3 For the purposes of the appeal to this Court, a further medical report has been introduced on behalf of the respondent from Dr lan Holdaway, Endocrinologist. [5] It is the case that the appellant had suffered from asthma since childhood, his condition being considered particularly severe and for which he had frequently been on courses of Prednisone, a steroid, and one of the group known as Corticosteroids. [6] The appellant's history is conveniently set out in a report from Associate Professor Patrick Klemp, Rheumatologist, who saw and examined the appellant at Southland Hospital, the appellant having been referred there by his GP, Dr Hastilow. Professor Klemp's report of 11 February 2003 to Dr Hastilow stated, inter alia, as follows: History: Mr Allison has had asthma since childhood and has been on frequent courses of Prednisone over the years. His asthma was particularly bad between ages 24-32 over which period he was on Prednisone most of the time. Between October 2001 and August 2002 he was admitted with severe asthma attacks on four occasions. At present he is on several inhalers and also on cyclical Etidronate since about June last year. He tells me that he has had two 14 day courses of Etidronate and at present is on Osteo 600 one daily. He uses Paradex for pain involving mainly the cervical and thoracic spine. Mr Allison apparently stopped smoking in about December 2000. There is no family history of osteoporosis or history of drug allergies. He is otherwise well but appears to have difficulty keeping his weight up. He is on inv Examination: Very thin. No lympadenopathy. He has what appears to be nicotine stained fingers of the left hand. Abdomen normal. Chest clear at prresent. Musculoskeletal examination normal. Diagnosis: Long-standing steroid dependent asthma for review regarding bone sparing treatment. A DEXA scan done in November 2001 revealed a T-score of -1.0. Radiologically there is evidence of osteoarthritis of the cervical spine (May 1999). An x- ray of the thoracic spine in October 2001 was reported as normal Management: I have given Mr Allison some information on cyclical Etidronate. I suggest that he remains on this long-term. [7] Professor Klemp referred to a DEXA scan carried out in November 2001. A report of that scan has been produced to the Court and it is noted that the reason for the scan was stated as being "long-term treatment of Prednisone use. Back and shoulder pain." The T-score, which is apparently the relevant "score" in this matter was identified as -0.1, and where the report stated that this was "Osteopenia (just)" [8] The report and advice of Professor Maling had proceeded on the basis that the appellant had developed osteoporosis from prolonged steroid treatment. He then stated: Given the above clinical context, steroid induced osteoporosis is very likely, particularly as the claimant gets older (Woolf A Curr Opin Rheumatol 2007, 19:370-5; American College of Rheumatology Recommendations. ..When the steroid daily dose is 5 mg or greater, bisphosphonate treatment is advisable. This recent recommendation (above refs.) recognises steroid induced osteoporosis management as a planned outcome of prolonged steroid treatment, in which early bone replacement treatment should always be initiated unless specifically contraindicated In the claimant's case the treatment injury of steroid induced osteoporosis may be seen as a necessary part of his steroid regimen. However, this view is retrospective in that the adverse outcome of osteoporosis is already apparent and there is therefore an assumption of inevitability. However, in the claimant's case the steroid treatment for his asthma was necessarily intermittent and osteoporosis would not necessarily have been anticipated or planned as an inevitable outcome, so that bone sparing treatment would have been delayed until his condition was confirmed as steroid dependent. Under these circumstances the claimant's treatment injury is more appropriately classified as an ordinary consequence of his steroid treatment. [9] The report of Dr David Jones, dated 30 December 2007, provided to Counsel for the Appellant for the purposes of the review, noted at the start that there is a glaring absence of any known density DEXA scan more recent than 2001. He then went on to state as follows: Although a repeat scan in 2003 is spoken about in some letters, there is no actual report of such a scan in the documents provided, and there is no description of any such scan result The diagnosis of osteoporosis requires the bone density to be lower than was stated in the 2001 study - T score of lower than -2.5. In the range of -1.0 to -2.5 the term osteopaenia is used. Therefore, unless there is a repeat scan with different measurements, the use of the term osteoporosis in Mr Allison's case is not accurate. The radiologist's comment was that even the term osteopaenia barely applied (hence his use of the word "just"). Dr Jones' conclusion from that DEXA scan and subsequent x-rays was: Borderline osteopaenia and osteoarthritis in cervical spine. Or Jones noted that the medical records showed that the Prednisone treatment was on an average 6 mg per day in the 1990's, but that in the 1980's it was even higher. He then went on to give his advice of the effect of steroids on bone as follows: The link between steroids and osteoporosis has been known for many years. In fact Cushing's disease (caused by excess endogenous steroid production) described over 60 years ago featured osteoporosis. Long term treatment with oral corticosteroids for all sorts of diseases has been known to cause decreased bone mineral density, such that long-term use of steroid is virtually expected to be deleterious to bone. 5 Dr Jones referred to a review article by van Staa et al in Osteoporosis International - Osteoporos Int (2002) 13:777-787 which concluded that 'oral corticosteroid treatment using more than 5 mg of prednisone or equivalent per day, leads to a reduction in bone mineral density and a rapid increase in the risk of fracture during the treatment period". [10] It was Dr Jones' advice that the appellant had severe obstructive lung disease due to asthma and smoking-related COPD (Chronic Obstructive Pulmonary Disease) and had received oral corticosteroid treatment of a large enough cumulative dose to affect bone density, but that the only available measurement of bone mineral density did not show osteoporosis, but the lesser entity called Osteopaenia. He advised that the steroid treatment would have been a major contributor to this condition. He further stated: My understanding of the term "necessary part of treatment" applies to things like a surgical incision which has to occur to give access to the offending organ. That term would not apply. The general knowledge of steroid effects on the bone is such that a low BMD would be considered a very likely (but not inevitable) consequence of long- term steroid treatment. [11] The next report of relevance is that of Dr Stephen Child. He noted the history and had the earlier medical reports for reference. He then stated as follows: The first point of note is that the physical injury described in the claim is uncertain. The only bone density measurement from seven years ago would be consistent with ocalised osteopenia (to which he just qualifies) but there is no confirmation of a diagnosis of osteoporosis. ... There may however be further information not available to this reviewer, such as more recent bone density and/or CT/MRI of the lumbar spine region. On the information provided to me however, I cannot confirm a diagnosis of osteoporosis nor is there a specific diagnosis for his symptom of back pain for which he is receiving the invalid's benefit. ... Patients with more severe compromise in lung function were more likely to have evidence of osteoporosis and this appeared independent of the dose of inhaled corticosteroids that they had achieved. Mr Allison's possible reduced mobility from his back pain as well as with reduced weight, smoking history and vitamin D deficiency, would also all contribute to low bone mineral density. Although it is therefore impossible to make an accurate prediction, the literature would appear to suggest that >50% of patients like Mr Allison would have evidence of osteopenia or osteoporosis on bone mineral density irrespective of the use of corticosteroid therapy. . . . In summary therefore, in my opinion Mr allison's personal injury can be defined as osteopenia or symptomatic back pain. While this personal injury did occur in the context of treatment I believe that the majority of the osteopenia was caused wholly or substantially by his underling health conditions and therefore does not qualify for treatment injury claim. 6 [12] The final medical report produced for this appeal is from Dr lan Holdaway, Endocrinologist, Head of the Department of Endocrinology at Auckland Hospital. Dr Holdaway, when referring to the 2001 DEXA scan, stated: "His 2001 measurement was well above the osteoporotic range ( I score of -2.5 or less), so reference to him having osteoporosis within his file is incorrect. Additionally, in relation to his back problems, his spinal bone density in 2001 was completely normal. It should be noted that osteopenia and osteoporosis do not cause any pain or other symptoms of themselves, the only consequences being possible deformity (e.g. spinal curvature) and increased risk of low impact fracture." Dr Holdaway then commented on the corticosteroid treatment which the appellant had been receiving over the years and he stated as follows: "Because of the known effect of corticosteroid treatment on bone density PHARMAC will currently approve funded potent bisphosphonate treatment if the bone density T- score is -1.5 or lower in those taking 5 mg prednisone or more continually for >3 months. Mr Allison's lowest T score in 2001 was -1, so he would not qualify for funded potent bisphosponate treatment if this was his measurement at present. He was treated n 2002 onwards with the less potent bisphosphonate, etidronate, to provide future bone protection, which was a reasonable therapy decision at that time." After identifying that multiple factors were likely to have contributed to the mild reduction in the appellant's bone density, only one of which was steroid treatment, he did state: "...reduced bone density is common in those treated with corticosteroids, affecting many persons so treated, although to a variable extent in individual cases. Risks are greater with higher steroid doses over longer treatment periods Dr Holdaway then went on to consider the question of bone sparing treatment, that is, medication to offset the potential for reduced bone density. He stated as follows: "...If reduced bone density is anticipated as a result of a medical treatment (e.g. use of corticosteroids, hormone treatment of breast and prostate cancer etc) it is felt to be good practice to consider whether concomitant treatment to protect the bones (to spare them from deterioration in bone density) would be desirable. The decision depends on the intensity and likely duration of the risk-inducing treatment, and if possible a baseline bone density assessment should be done. If the baseline measurement is reduced or the perceived risk of osteoporosis is high, bone protection therapy is usually recommended." He then noted: " ...In Mr Allison's case it was reasonable to commence treatment (etidronate) based on the 2001 hip bone density measurement. [13] Dr Holdaway noted that the bone sparing treatment for the appellant had commenced in June 2002 and that the particular treatment which had been established was that of Etidronate which came into general use in 2001. He advised that prior to Etidronaate there were no clinically effective therapies for steroid induced bone loss in 7 males. Dr Holdaway further advised that because there is just the one bone density measurement of 2001, there was no way of knowing if the appellant's bone density had changed or progressed until the introduction of etidronate in 2001. [14] I have set out the relevant passages of Dr Holdaway's report, which report ranges wider than the perceived issue in this appeal would require. My reason for so doing is that Counsel for the Appellant is now submitting that the Corporation incorrectly investigated the treatment injury and that the steroid induced osteoporosis, which is alleged, was caused as a result of the appellant's physician failing to prescribe early bone replacement therapy. In Counsel's own words, the submission is as follows: "It is argued that the failure to prescribe bone replacement therapy is the treatment njury that has caused Mr Allison's steroid induced osteoporosis." [15] It is Counsel for the Appellant's contention that bone sparing treatment should have been introduced for this appellant in the 1990's when the clinical knowledge of such treatment was known. [16] Mr Roberts, Counsel for the Respondent, submitted there was no evidence of injury before 2001, when the DEXA scan was carried out. Counsel submitted that reduced pain density was an ordinary consequence of steroid treatment and was an expected outcome. Counsel submitted that the advice of Dr Holdaway identified that earlier bone sparing treatment could not have been had and would likely not have had any effect having regard to the questionable diagnosis of osteoporosis/osteopenia. DECISION [17] As earlier noted, the Court has a concern as to how the substance of this appeal has changed from the time that the original claim for cover was lodged, and the declinature decision made. [18] Whilst it is the case that I am on record in a number of decisions indicating that where the claim for cover identifies what might be described as a generalised diagnosis such as a back strain, and where the actual injury sought to be covered may not yet have been identified at the time of the lodging of the claim, that in those cases it is open to the Court to identify precisely what the nature and extent of the covered injury suffered may be, based on the medical evidence which is presented to the Court. [19] In the present case, the personal injury claimed is that of osteoporosis said to have been caused by the long-term treatment, given under the direction of the 8 appellant's GP. of a Corticosteroid, namely Prednisone intended to treat his chronic asthma and COPD. [20] The problem is that the only clinical investigation, namely the 2001 DEXA scan, identified that the appellant did not have, as of 21 November 2001, osteoporosis, but rather, questionably, the lesser condition of osteopenia. [21] The medical dictionary identifies osteoporosis as "a reduced mass of normal bone". It states that the quality of the bone present is normal, but that the quantity is deficient. It is stated to be a feature of aging and so that osteoporosis is common in the elderly. The dictionary identifies that it is a feature of patients who have been on long-term treatment with corticosteroids. [22] Osteopenia is also, according the dictionary, the condition of reduced bone mass due to the rate of osteoid synthesis to a level insufficient to compensate normal bone lysis. It is stated that the term is used to refer to any decrease in bone mass below the normal. [23] In terms of the evidence which has been presented to the Court, I find that there is no basis for the Court to determine that this appellant has osteoporosis secondary to steroid therapy, for his severe COPD and asthma, as claimed. [24] Having found that, it is equally the case from the DEXA scan, that the appellant was, as of November 2001, exhibiting signs of minimal loss of bone mineral density (BMD) but the Court has received no evidence which would identify that such a condition can be considered a personal injury, that is, a physical injury, even though I find, on the balance of probabilities, that the appellant's condition, as identified in the DEXA scan was more likely than not in large measure brought about by his years of corticosteroid treatment for his asthma and COPD. [25] The material contained in an article provided to the Court from the American Journal and Critical Care Medicine on the impact of corticosteroid use on bone mineral density and vertebral fracture, identifies in the main that the loss of BMD bringing about osteoporosis, does give rise to a greater risk of bone fracture, the high risk being associated with vertebral or hip fracture. That same article identifies that low bone mass itself is asymptomatic and causes no morbidity. I take it from that that reduced BMD is not of itself an injury, but is a condition which can give rise to an increased likelihood of bone fracture. 9 [26] Another aspect of the claim which has been introduced at the appeal stage is the alleged failure of the treating professional to have earlier instituted bone sparing treatment so as to neutralise any prospective BMD from corticosteroid treatment. [27] The evidence of Dr Holdaway is that the bone sparing treatment which was introduced by way of the medication Etidronate in June 2002 was done at a time when it was considered reasonable to commence that treatment based on the 2001 hip bone density measurement. Dr Holdaway further indicated that there was no way of knowing if this appellant's bone density had changed or progressed until the introduction of Etidronate in New Zealand in 2001. It is the case that the introduction of Etidronate in 2001 was probably the first opportunity for such medication to be given as a treatment for cortisteroid users. [28] In the appellant's claim for cover which was considered in the first instance by the Corporation through the advice of Professor Maling, the treatment injury was claimed to have been osteoporosis said to have been caused by the long-term use of Prednisone as treatment for the appellant's asthma and COPD. [29] There was no claim that the alleged osteoporosis had been caused by a failure to treat by way of bone sparing medication such as Eitidronate. This latter issue has only been raised at the appeal stage and does of course give rise to a different aspect of treatment within Section 33 of the Act, as it is no longer contended to be a personal injury which occurred as a consequence of the giving of treatment, but rather of a failure to provide treatment or to provide suitable treatment in a timely manner. [30] Whilst Dr Holdaway has dealt with this aspect in some detail, and he has expressed an opinion which would be contrary to any claim for cover under this meaning of treatment being established, the matter has not been considered by the respondent at first instance. It certainly cannot be criticised for not doing so, as that issue was never on the table and did not come into the picture until Counsel for the Appellant filed submissions in December 2009 which raised the issue for the first time and which led to the obtaining of Dr Holdaway's opinion in May 2010. [31] I have hitherto not considered the actual basis upon which the respondent declined cover, namely that the corticosteroid treatment so provided by the health professional would cause a loss of bone mineral density, but that this was a known and accepted consequence of the treatment for the appellant's medical conditions with Prednisone. 10 [32] In the present case it must be found as a fact on the uncontradicted medical evidence, or at least the best evidence on which this Court can rely, that the appellant does not have steroid induced osteoporosis. Therefore the situation of whether or not osteoporosis was or was not a necessary part or ordinary consequence of the corticosteroid treatment that the appellant was receiving for his asthma and COPD, does not arise. [33] In summary, therefore, I find as follows: [i] The appellant does not suffer from the medical condition of osteoporosis and therefore there can be no claim for cover by him for this medical condition. [ii] If it be contended that the appellant has suffered a treatment injury, namely osteopenia, by reason of a health professional failing to provide treatment by way of bone sparing medication such as Etidronate, then it is the case that such claim has not been the subject of a primary decision by the Corporation and is therefore not an issue which is within the jurisdiction of this Court within the confines of this present appeal. [iii] The Court does accept it has jurisdiction to consider whether the appellant has suffered a treatment injury for the medical condition of osteopenia and for which there may be entitlement to cover under s.32 of the Act, but that it finds there is no basis for such grant of cover as, firstly there is no evidence that the appellant's BMD, as identified on the DEXA scan, constitutes a physical injury within the meaning of the Act, and secondly, in any event, the evidence establishes that the likelihood of reduced BMD is an ordinary consequence of corticosteroid treatment. [34] For the foregoing reasons, therefore, this appeal is dismissed. DATED this 22nd day of November 2010 M J Beattie District Court Judge