Skip to Content, Skip to Navigation
Advertisement

Safeguard OSH Solutions - Thomson Reuters

Safeguard OSH Solutions - Thomson Reuters



Accident Compensation Cases

Archer v Accident Compensation Corporation (DC, 25/02/03)

Judgment Text

RESERVED JUDGMENT OF JUDGE M J BEATTIE 
Judge M J Beattie
[1]
The issue in this appeal relates to the decision of Catalyst Insurer Services Limited (Catalyst), the respondent's agent, of 3 January 2002 whereby it suspended entitlements to the appellant pursuant to section 116 of the Act on the grounds that the medical condition which she presented at that time was not attributable to or caused by the personal injury for which she had been granted cover in 1996. 
[2]
The background facts relevant to the determination of this appeal may be stated as follows: 
In July 1996, the appellant lodged a claim for cover and for treatment expenses for an injury described in the claim as OOS — repetitive injury involving extensor tendons left and right wrists and forearms. This injury was said to have arisen from repetitive typing. 
At the time the appellant made her claim for cover, she was aged 46 years and was employed as Office Manager by Lower Hutt Business Advisory Service. 
The duration of the appellant's employment had been from January 1996 until August 1996 when she was certified by her GP as being incapacitated. 
The respondent accepted cover by letter dated 15 August 1996 and its acceptance of cover was said to be for the injury “OOS, both wrists and forearms”
The only specialist to see the appellant at the time cover was claimed was Dr C Rajapakse, Rheumatologist, to whom the appellant was referred by her GP and who provided three reports of 19 August 1996, 20 December 1996 and 16 June 1997 respectively. 
After the appellant ceased her employment in August 1996 she remained off work until December 1996 when she commenced part-time work for one or two hours per week from home in her husband's business. 
In June 2000, the respondent referred the appellant to Dr Mark Haywood, Occupational Medicine Specialist for a case review and it was Dr Haywood's diagnosis that the appellant now suffered from chronic regional pain syndrome. He also advised that there were no objective signs of injury. 
In August 2000, the appellant was seen by Dr Graham Chiu, Rheumatologist, who advised that he found clinical evidence of bilateral carpal tunnel syndrome, some flexor tendinitis in both hands and soft tissue swelling in MCP joints consistent with an inflammatory arthritis. 
In 2001 the appellant's Case Management was transferred to Catalyst and in September 2001 Catalyst referred the medical reports that had been provided by specialists over the years to Professor Des Gorman, Head of Occupational Medicine at University of Auckland School of Medicine. Professor Gorman agreed with Dr Haywood that the appellant was displaying symptoms of a chronic pain syndrome but stated that this was a condition totally unrelated to any work place injury. 
In November 2000, Catalyst referred the appellant to Dr Keir Howard, Consultant & Specialist in Occupational Medicine & Rehabilitation. He too gave as his diagnosis that the appellant was suffering from a chronic regional pain syndrome. He advised that there was no evidence that any muscle strain or tendinitis, which may have been present in 1996, still existed and that the chronic pain syndrome was unrelated to those influences. 
It was as a consequence of the reports of Professor Gorman and Dr Howard that Catalyst advised the appellant by its letter of 3 January 2002 that it was suspending her entitlements on the basis that her condition was not attributable to the injury for which she had been granted cover. 
The appellant sought a review of that decision and for the purposes of that review she sought a report from Dr R D Wigley, Consultant in Rheumatology & Rehabilitation Medicine. Dr Wigley provided a report dated 22 March 2002 for that purpose. 
A review hearing took place on 13 May 2002. In his decision dated 7 June 2002, the Reviewer preferred the evidence of Dr Howard and Professor Gorman to the effect that there was no causative link between the current diagnosis of chronic pain syndrome and the injuries for which the appellant had been granted cover. He found that the CPS had arisen from other factors and he therefore confirmed the decision to suspend entitlements. 
[3]
The issue in this appeal calls for a consideration of the medical evidence on which Catalyst made its decision to suspend and the evidence, principally from Dr Wigley, which the appellant contends establishes that her eligibility for entitlements under the Act should continue. 
The Medical Evidence: 
(1)
Report dated 19 August 1996 from Dr C Rajapakse, Rheumatologist to appellant's GP: 
Dr Rajapakse notes the history as given to him by the appellant and which she described as pain radiating through the fingers extending through the dorsal aspect of the hand through to the forearm and then to the shoulder and neck. Dr Rajapakse, after examination of the appellant, indicated there was no evidence of carpal tunnel syndrome or deQuervain's tenosynovitis. His diagnosis was “overuse syndrome, left arm more than right, related to use of a mouse in the left hand”
(2)
Report dated 16 June 1997 from Dr C Rajapakse, to appellant's GP: 
The diagnosis was still overuse syndrome but he noted that it had recently spread to the appellant's right hand even though she was left handed and had used her left hand predominantly for mouse and keyboard work. 
(3)
Report dated 30 June 2000 from Dr Mark Haywood, Occupational Medicine Specialist to ACC: 
Dr Haywood was asked to provide a review of the appellant's case and he was provided with the various specialist and physiotherapy reports that had been obtained. Dr Haywood noted that the appellant complained of symptoms of generalised pain above the waist. This pain was stated to be in a number of different areas and was of varying degrees. Dr Haywood noted the symptoms that had been identified and described by Dr Rajapakse in 1996 and he considered that her current symptoms were the same as those that had been complained of since seeing Dr Rajapakse. He gave as his diagnosis a chronic regional pain syndrome. He identified multiple tender points but an absence of any neurological signs of such things as radiculopathy or myelopathy, no specific tendinitis, loss of range of movement of joints or specific ongoing muscular tenderness injury. He identified the appellant as having subjective symptoms of pain and illness behaviour beliefs. Dr Haywood confirmed that he did not identify any specific injury and that non-physical stressors appeared to be the most significant factors in her chronic pain. He advised that whilst the pain was real it was not causing any further injury and the injury that is present is only really one of pain perception with no objective neurological or muscular dysfunction. 
(4)
Report from Dr Graham Chiu, Rheumatologist to ACC dated 17 August 2000: 
Dr Chiu found on examination that there was clinical evidence of bilateral carpal tunnel syndrome, some flexor tendinitis in both hands with reduced grip, bilateral rotator cup signs and soft tissue swelling between both index and middle MCP joints consistent with an inflammatory arthritis. He also identified signs of hyperkeratosis over elbows and ankles consistent with a diagnosis of psoriasis (a disease of the skin). It was his assessment that the appellant had a low-grade form of psoriatic tendinitis with carpal tunnel syndrome as a cause of her symptoms. He went on to state that he found the short period of overuse in 1996 as being an unconvincing explanation for the cause of her symptoms which had persisted for over three years despite ceasing the work that was said to have caused the problem. 
(5)
Report from Dr Sue Rudge, Rheumatologist dated 9 October 2000 to appellant's GP: 
At the time of her examination in October 2000, she noted no signs of psoriasis and no obvious active synovitis in the small joints of both hands. She did however note that the appellant was tender in the upper limb muscles. 
The main focus of Dr Rudge's reports were to note and monitor the elevated ESR which had been found and she did not address other matters more particularly related to the appellant's OOS type symptoms. 
However, in a report to ACC dated 5 November 2001, Dr Rudge advised that the appellant's ESR fluctuation, in her opinion, had no bearing on her symptomatology. She also advised that there was no underlying arthritis or connective tissue problem which could be responsible for her symptoms. She stated that she agreed with both Dr Rajapakse and Dr Chiu that the appellant's ongoing symptoms were related to the original diagnosis of occupational overuse syndrome. 
(6)
Report from Professor Des Gorman, to Catalyst dated 10 September 2001: 
Professor Gorman was asked to carry out a clinical audit by file review and for which he was provided with all the medical reports that had been gathered on the appellant's condition since the lodging of her claim for cover. Professor Gorman noted a conflict between the two Rheumatologists, Dr Rudge and Dr Chiu, where the latter had found bilateral CTS and tendinitis whereas Dr Rudge had found no such discreet disorder. However, he noted that no doctor save Dr Chiu had found any signs of inflammation of a muscle joint or tendon. He noted that the consistent clinical finding had been that of muscular tenderness. Prof. Gorman adds as his diagnosis as follows: 
“Mrs Archer clearly has problems with asthma, migraine headaches and obesity. 
However, Mrs Archer's predominant health problem is that of persistent pain, which affects the upper half of her body. This pain should be analysed in terms of nociceptive physiological, non-nociceptive physiological and psychiatric components. From a nociceptive basis, Dr Chiu provided a long list of musculoskeletal disorders. He thought the predominant problem was that of psoriasis. However, no other clinicians have found such findings. Indeed, the only persistent finding has been that of muscular tenderness, which by itself does not establish a nociceptive basis for pain. The possibility of an underlying inflammatory condition nevertheless is still real here both because of Mrs Archer's history of small joint swelling and the finding of a persistently raised ESR level. 
I agree with Dr Haywood that there is strong evidence for a non-nociceptive physiologic disorder of central nervous system pain modulation (chronic pain syndrome). This is the best explanation for Mrs Archer's allodynia. I also note that she has a condition (migraine), which is commonly co-inherited with such pain disorders. I also agree with Dr Haywood that Mrs Archer's chronic pain syndrome does not meet the research classification criteria for fibromyalgia. It is also clear that it does not satisfy the criteria currently used to sub-classify a pain syndrome as post-traumatic (and hence compensible). The reasons for stating the latter are that first, Mrs Archer's work process and work place would have been a low risk for any musculoskeletal injury, and secondly and more importantly, that at no time has any physician found physical signs indicative of such an injury. ”
(7)
Report from Dr Keir Howard, dated 23 November 2001 to Catalyst: 
Dr Howard was asked to provide his diagnosis of the appellant's current health condition, whether there was any evidence of a discreet physical injury responsible for her symptomatology and whether there was any causal link between any initial injury and her current condition. 
Dr Howard stated that he was in broad agreement with the specialists who had considered that the appellant was suffering from a chronic regional pain syndrome predominantly affecting the right upper limb, shoulder and neck regions. He was also in agreement with Dr Chiu in that there was a strong possibility of early carpal tunnel syndrome affecting the right wrist. Dr Howard went on to state as follows: 
“There is little evidence for a discreet physical injury responsible for Mrs Archer's symptoms. I do not consider that carpal tunnel syndrome may be classified as ‘injury’ although it is possible that it may arise as a result of certain forms of work activity, but in Mrs Archer's case I do not see these as being responsible for the development of this particular condition. In my opinion Mrs Archer had some generalised muscle strain and possible mild tendinitis at some stage around 1996 relating to her work, but there is no suggestion now that these specific conditions still exist. I would judge therefore, that the development of her pain syndrome, while possibly triggered by these initial muscle strains, has been maintained largely by stressful factors in her wok and life situation from that time. I am not convinced therefore that there is a specific causal link between Mrs Archer's work and the development of her current symptoms. 
Following from my previous comments, I remain unconvinced that there is a sufficient causal link between any initial injury and Mrs Archer's current limitations in capacity to work. I view these limitations as predominantly the result of her pain syndrome. 
In my judgement any underlying muscle strains or tendinitis have in fact recovered in the intervening period since 1996. Her condition, therefore other than the carpal tunnel syndrome, is a pain syndrome that while possibly related in onset to the original muscle strains, is now being maintained by other factors. ”
(8)
Report from Dr R D Wigley, Consultant in Rheumatology dated 22 March 2002 to appellant's counsel: 
Dr Wigley was provided with all medical reports including that of Dr Keir Howard for the purposes of his report. 
Dr Wigley went in to details of the appellant's work place situation and endeavoured to reconstruct the matters which he considered were causative of her condition and in that regard he had reference to certain photographs provided by the appellant. Dr Wigley gave as his conclusions as follows: 
“My opinion is that she has indisputable evidence of injury due to excessive work in two jobs at once with unsatisfactory work stations and unacceptable work loads leading to general pain and pressure pain sensitivity above the waist. She has clear evidence of median nerve injury proximal to the wrist, rotator cuff injury and probable medial epicondylitis. These constitute clear evidence of injury. 
The work tasks and the environment in which they were carried out, carried a high risk of the development of such symptoms and injury. The environment was also conducive to this. She had very little time for any other activities. These symptoms have been sustained and further aggravated by continuing to work at unsatisfactory workstations. Her interest in needlework would not have contributed significantly. 
There is evidence from the medical literature that a high use of keyboards at abnormal postures combined with filing and photocopying type of work could lead to the type of problems that she has. There is also evidence that highly repetitive work in awkward postures contributes to carpal tunnel symptoms. The postural abnormality in her case was the pressure on the wrist proximal to the tunnel and excessive loading of the shoulders having to reach too far forward. This only recently recognised syndrome is described in the New Zealand Medical Journal (encl. 6). A formal report including a further four cases is in preparation for publication. She also had to repeatedly reach high for filing and copying. 
It seems that the underlying pain mechanism for the more widespread pain is over-sensitivity of the sensory nervous system triggered by repeated painful stimuli (nociception). This comes from muscles left switched on so that they cut off their own blood supply and become ischaemic with the release of various pain stimulating substances. The sensory cells undergo demonstrable changes. This is not a primary psychological problem though the pain causes secondary upset with the uncertainty of employment and so on. Thus the non-physical stress arises out of her work and from her symptoms so cannot reasonably be regarded as causative though compounding her problems. This mechanism explain why more generalised pain and tenderness is a common accompaniment of any overuse problem. 
In my opinion her work initiated musculo-skeletal injuries and these have been sustained by continuing work at unsatisfactory workstations. I have found no evidence to support the theory that she has a continuing pain syndrome independent of her occupation. In her case I do not consider that proposition to be plausible. ”
(9)
Letter from Dr Keir Howard dated 30 July 2002 to Catalyst: 
Dr Howard was asked to comment on Dr Wigley's report and he stated the difference between his views and those of Dr Wigley were as follows: 
“The difference between my own views (and those of other physicians) and Dr Wigley is essentially one of interpretation of the clinical findings and especially about the development of chronic pain syndrome and their continuation. Dr Wigley appears to understand such conditions as arising from underlying pathology and being maintained by work and other physical factors. He places little emphasis on the psychological factors that give rise to the development of such syndromes and that maintain them long after objective pathology has largely subsided. 
It was my view that while an initial occupational origin for the musculoskeletal problems was likely, the present situation was that other factors were now responsible for the continuance of the pain syndrome. I have set out these views in my initial report. Dr Wigley however takes a diametrically opposed view and considers that the ongoing pains are work related and are part of an overuse problem. I do not doubt that physical factors play an important role in the development of pain syndromes, but the way that they develop and progress is much more a response to psychological factors and such condition invariably respond to psychological modes of treatment, such a cognitive behavioural therapy, more than they do to physical methods. ”
(10)
Report from Dr R D Wigley dated 7 October 2002 to appellant's counsel: 
In response to Dr Howard he stated as follows: 
“He suggests that his views are diametrically opposed to mine. I do not think this is so. I do accept that psychological and social effects can be important in some cases but I do not accept that all pain syndromes are due to psycho-social causes. One has to assess whether or not there is any supporting evidence in the individual case. All factors have to be weighed up for each individual. There is no evidence that median nerve injuries (CTS or DES) are of psychosocial origin. 
I did address psycho-social problems in my report but my comment was brief as I found little that could be considered causative. Causative stresses must precede the symptoms. Psycho-social disturbance that results from symptoms and the resulting adversary situation cannot be causal. I did find evidence of continuing physical causation. ”
Dr Wigley reaffirmed his diagnosis as being median nerve injury, or as he described it, “desk edge syndrome”. He considered that this condition was causally related to the appellant's 1996 gradual process injury. 
(11)
Report from Dr Peter Dodwell, Occupational Medicine Specialist dated 19 November 2002 to respondent's counsel: 
Dr Dodwell was asked to report generally and also to give specific attention to Dr Wigley's diagnosis of desk edge syndrome. 
Dr Dodwell noted that this particular syndrome had been coined by Dr Wigley but that Dr Dodwell's research into medical literature found no reference to any such syndrome. The main points made by Dr Dodwell were as follows: 
The concept which Dr Wigley proposes must be considered just a theory which remains to be tested by reputable peer reviewed published research. 
From his description Dr Wigley is describing a variation of median neuropathy (disorder function of the median nerve). 
Without nerve conduction studies it becomes impossible to say whether there is involvement of the nerve in the carpal tunnel in addition to this higher level. 
More scientifically acceptable diagnosis is that of median neuropathy but there is doubt as to whether this constitutes a physical injury and would require objective testing such as nerve conduction studies as its first step. 
Dr Wigley's examination findings cannot be applied retrospectively to the situation of 1996. A diagnosis of OOS can relate to 20 — 30 medical conditions none of which were specified in the case of the appellant in 1996. 
Dr Rajapakse specifically stated in August 1996 that there was no evidence of carpal tunnel syndrome. 
Any suggestion that any form of median neuropathy existed in the appellant in 1996 is therefore rejected. 
Decision 
[4]
The issue raised by this appeal requires the Court to consider the medical evidence that pertained at the time that the appellant sought and was granted cover in 1996 and then to consider that evidence in the light of the medical evidence that was obtained at or about the time that Catalyst determined to suspend entitlements. 
[5]
The difficulty in this case is that the medical evidence of 1996 was far from clear. This cannot be said to be any fault of the appellant. Her claim represents one of a number which this Court has been called upon to consider where the respondent has accepted cover for what is identified as a gradual process injury when there has been no proper identification of a specific physical injury in that claim for cover. Instead the respondent has accepted the description of “OOS” or its predecessor “RSI” as constituting an acceptable diagnosis of a physical injury when such is clearly not the case and this Court is on record on many occasions as stating so. 
[6]
The Accident Compensation Legislation, particularly that which has been in force since 1992, requires that as a pre requisite for cover there be a physical injury and it was therefore certainly less than an acceptable practice for the respondent to accept a diagnosis of OOS syndrome as being sufficient. 
[7]
Both the appellant's GP and Dr Rajapakse have used the term overuse syndrome as constituting the diagnosis and the only particularising from that generality was the statement made by Dr Kelly in the claim for cover when he described the condition as involving extensor tendons left and right wrists and forearms. 
[8]
This Court is not here considering whether the appellant should or should not have been granted cover as there has been no decision by the respondent seeking to revoke cover. Therefore the Court must accept as its starting point that there was a physical injury and the best evidence that can be established is that the appellant was suffering some form of tendinitis in her wrists, said to have arisen as a consequence of repetitive use of the mouse with her left hand. 
[9]
If that be the injury for which cover was granted, and I find that it is the only injury to which medical evidence points, then it is necessary to consider whether that condition is still present or causative of the condition that the appellant presented at the time the respondent made its decision to suspend entitlements, namely January 2002. 
[10]
The Court has received a considerable body of medical evidence and included in that evidence are the opinions of four Occupation Medicine Specialists, namely, Dr Haywood, Dr Howard, Dr Dodwell and Professor Gorman. Each of these specialists have identified the appellant as suffering from a chronic pain syndrome where there are multiple trigger points of pain but without any identifiable physical injury as being the basis therefore. 
[11]
The extent of the pain is identified as being over multiple points in the upper part of the appellant's body and it is simply a pain syndrome where the appellant is said to have subjective symptoms of pain and an altered pain perception. I find that the explanation made by Prof. Gorman and which I have reproduced above, which is in line with the views of Dr Haywood, would indicate that it has arisen from influences quite unrelated to any supposed work place injury. 
[12]
All the occupational medicine specialists are in agreement that the appellant is not evidencing any discreet physical injury or that there was any condition or injury in 1996 which could have been the cause of her pain syndrome which has developed well after she ceased her employment in August 1996. 
[13]
Whilst Dr Wigley has supposedly identified carpal tunnel syndrome and other median nerve type conditions, these clearly have arisen after the appellant ceased work and certainly cannot be attributable to any work place factor. It must be remembered that Dr Rajapakse identified no CTS or other tendon type injury when he examined the appellant at the time of her ceasing work and on two further occasions in the ensuing 8 months. 
[14]
I find that the evidence of Dr Wigley is not convincing, particularly as he is now advancing a new theory of injury, namely desk edge syndrome, and which he is seeking to retrospectively recreate as being the appellant's injury at the time she ceased employment. As noted by Dr Howard and Dr Dodwell, Dr Wigley has endeavoured to recreate the 1996 situation from what may have been told to him by the appellant and that source is highly questionable and I find that it does not meet the standard necessary when prior specialist investigation has not revealed symptoms which Dr Wigley now says would have been present. The fact of the matter is that I find that Dr Wigley is in effect talking about the present rather than the past and drawing somewhat of a long bow to establish some causative link. 
[15]
I am satisfied from the medical evidence that the appellant's condition of a chronic pain syndrome, the feature of which is that there is no evidence of any discreet injury or of it being linked to any discreet injury, means that it is not a condition which is compensible under the Act. The specialists have indicated that such a condition can arise from a multitude of influences and it seems that many of these influences have arisen since the appellant ceased her employment. If Dr Wigley's diagnosis of CTS is to be accepted then this is clearly an indication of the arising of a condition subsequent to the injury for which cover was granted and which per se is not compensible. 
[16]
The evidence is that the appellant has only done minute amounts of work at home since she ceased her employment, one or two hours a week, and this Court has been presented with no evidence which would indicate how such activity may have been causative of any of the many conditions which the appellant now presents, some of which have been described by Dr Wigley. 
[17]
In the final analysis the legal position is that a person is only entitled to continue to receive entitlements under the Act if she or he can establish that the reason for the need for the entitlement is attributable to the personal injury for which he / she was granted cover. In the case of this appellant the major entitlements would have been those of treatment expenses and abated weekly compensation. The latter being required to be directly related to an incapacitating condition arising from the injury for which cover was granted. 
[18]
In the present case, whilst the appellant may well establish that her chronic pain syndrome is incapacitating, I find that there is no evidence which can establish it as being linked to the wrist injury for which she was granted cover in 1996. 
[19]
For the foregoing reasons therefore the respondent's decision to suspend entitlements was correct. This appeal is therefore dismissed. 

From Accident Compensation Cases

Table of Contents