Inkersell v Accident Rehabilitation and Compensation Insurance Corporation

IN THE DISTRICT COURT HELD AT WELLINGTON Decision No. 9 /2000 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 STEPHEN PATRICK INKERSELL DCA 40/98 Appellant AND ACCIDENT COMPENSATION CORPORATION Respondent JUDGMENT OF JUDGE M J BEATTIE ON THE PAPERS The issue in this appeal is whether the respondent was correct in its decision of 8 April 1997 to revoke the appellant's claim for cover and cancel entitlements pursuant to section 73(1) of the Act. Counsel for the appellant and the respondent have filed written submissions in this appeal and have requested that the Court determine the issue on the papers. The facts as I find them and which are relevant to determine this appeal are as follows: The appellant is now aged 41 years and up until June 1996 had been employed as a meat processor and slaughterman for some 19 years. 2 On 10 June 1996 the appellant's GP completed a claim for cover on behalf of the appellant giving a diagnosis of "right rotator arc tendonitis". The injury was said to have been caused through repetitive pushing into carcasses using an elastrator and from which pain has developed in the appellant's right shoulder. The appellant's claim for cover was treated as a gradual process claim and the appropriate questionnaires were forwarded to the appellant, his GP, and the employer. Following receipt of those questionnaires the matter was referred to the Corporation's Regional Medical Officer and the decision was made that the appellant's claim for cover be accepted as a gradual process injury arising out of and in the course of his employment with Canterbury Frozen Meats, that decision being notified to the appellant and his employer on 1 August 1996. The appellant continued in his employment from 10 June 1996, being the date when his injury was diagnosed, on light duties but by July 1996 his condition was such that he was certified as being fully unfit for work. He continued to receive weekly compensation until the end of the season and there matters rested until it came to the commencement of the 1997 season in March of that year. The appellant's GP had indicated that he was not fit to commence normal freezing work duties at the beginning of the 1997 season and it was at that point that the respondent sought an opinion from Dr Daniel Ching, Consultant Physician and Rheumatologist. Dr Ching examined the appellant on 17 March 1997 and provided a report dated the same day. That report stated inter alia as follows: "Examination: There was cheiroarthropathy in both hands. This is flexion deformities in his fingers such that he is unable to make a proper 'prayer sign'. He also has a reduced range of movement with both wrists. He has full range of movement with both shoulders, but has crepitus in both shoulders. His shoulders were obviously stiff. The signs in his fingers, wrists and shoulders, are characteristic of diabetic cheiroarthropathy and come on many years prior to the development of diabetes mellitus. He is overweight. He does not know if he has got diabetes. There is a mild reduction in the range of movement of his cervical spine, and he has obvious discomfort on extending his cervical spine. Neurology of his upper limbs was unremarkable other than some subjective loss of sensation to pinprick in the right deltoid muscle. Both shoulders were tender anteriorly, worse on the right side. Stressing the rotator cuff tendons in the right shoulder produced marked tenderness, and stressing the left rotator cuff tendons produced mild tenderness. No muscle wasting. With his consent I injected the right shoulder with 40 mg Kenacort and 1% lignocaine using the anterior and lateral routes. He had immediate improvement of his pain following the injection, and I have advised him this is due to the local anaesthetic. Diagnosis: Mr Inkersell has certainly got signs of diabetic cheiroarthropathy, and it is difficult to be precise as to how much his job is the cause of his rotator cuff lesion, and how much is due to natural processes. Rotator cuff lesions and adhesive capsulitis related to diabetic cheiroarthropathy are notoriously resistant to intra-articular steroid injections, and this is likely to be why Dr Fanning's two injections last winter were not of much help. However, it is worth trying again, and some patients do seem to improve with several injections. Even if his job is not the cause for his shoulder problem, it would certainly exacerbate his shoulders and cheiroarthropathy. However, further investigations might provide a clearer diagnosis. Management: Besides injecting his right shoulder, I have explained the possible diagnoses to him. I have reassured him that the pain in his cervical spine is secondary to the congenital fusion and nothing to do with his occupation. I have also 4 reassured him that the stiffness in his hands and wrists are not secondary to his job but that he has got a condition called cheiroarthropathy. It is difficult at this stage however, to know how much of his shoulder problems are related to his job. If he has got calcified tendons, then the cause of his shoulder problems has occurred naturally rather than brought on by his job." Dr Ching arranged for x-rays and certain tests to be carried out and following those tests he gave a further report dated 31 March 1997. That report stated inter alia: "I have informed Mr Inkersell that the x-rays of his shoulders showed gross calcification in his rotator cuff tendons, worse on the right side, but no evidence of any rotator cuff tears. There are no secondary causes for his calcific tendonitis, and I have informed him that they have just appeared spontaneously. The injections to the right shoudler have only given him a little bit of relief, approximately 10%. As I have informed him previously, injections do not appear to help calcific tendonitis that much, and some patients do need surgery at the end of the day. Understandably he wants to avoid surgery, especially as Tilcotil does give him some relief for his shoulders. He has stopped attending for further physiotherapy and is not any worse without physiotherapy to his shoulders. I have informed him that I do not think his multiple joint symptoms are brought on by his job in the freezing works, but are exacerbated by his job. I therefore do not think he is ACC's responsibility." It was as a consequence of Dr Ching's reports that the appellant's Case Manager wrote the letter of 8 April 1997 revoking cover and entitlements and relevant parts of that letter are as follows: "I refer to your claim lodged with the Corporation following the development of your right shoulder injury. The Corporation has obtained the medical report from Dr Ching dated 17 March 1997 and a follow up report dated 31 March 1997. Following receipt of these reports I referred your file to our Branch Medical Adviser for comment. Our Branch Medical Adviser has concurred with Dr Ching that you have two natural reasons for your symptoms, ie calcific tendonitis rotator cuff left and right; and cheiroarthropathy wrists/fingers. Regretfully, these conditions are not work related therefore the Corporation must revoke your claim for cover and disentitle your claim in accordance with Sections 10(2)A and Section 73(1) of the Accident Rehabilitation and Compensation Insurance Act 1992." The appellant sought a review of that decision and a review hearing took place on 14 August 1997. The appellant conducted his own case and presented a further letter from his GP, Dr Fanning, that letter stating: "For many years, Stephen has been on the elastrator and also opening up the neck of the lamb at the freezing works. Both jobs involve flexion, abduction and rotation of the right shoulders in particular, he presented on 10/6/96 with right rotator arc tendonitis, which I feel was definitely work related, caused by repetitive movements mentioned above. As mentioned in other letters from other medical professionals there are other problems and there is no dispute that they are not work related. However the major problem is that of the right shoulder which as mentioned before is work related." In his decision the Review Officer stated whilst he accepted that the GP was of the opinion that the appellant's condition was work related, that was not the opinion of 6 the specialist Dr Ching and he considered that Dr Ching's opinion outweighed that of Dr Fanning. He considered that the provisions of section 10 of the Act applied excluding entitlement and accordingly confirmed the respondent's decision that the appellant was not entitled to cover for his condition. Following the review decision the appellant instructed Mr Cadenhead as counsel and he has introduced two reports each from Professor Glass and Professor Burry for the purposes of this appeal and the respondent for its part has introduced a further report from Dr Ching. Professor Glass an Occupational Medicine Specialist provided a comprehensive 9 page report on the appellant including an examination of his work duties and how they may have impacted upon his right shoulder tendonitis. Professor Glass had the two reports from Dr Ching to refer to and his report followed his examination of the appellant on the 6" of May 1998. Professor Glass commented on the proposition propounded by Dr Ching that the appellant's calcific tendonitis was not related to his employment but was something that had occurred spontaneously. Professor Glass responded to that as follows: "The question at issue is whether or not the calcific changes caused his pain and disability or whether this was due to his preceding rotator cuff lesion and whether the calcific changes arose as a consequence of his original rotator cuff work related condition. Firstly it is clear from Mr Inkersell's history that all the doctors reports note either a work relatedness (Dr Fanning his GP, Dr Crawford and Mr Poplawski) or a work related temporality (Dr Ching), as far as his initial right shoulder complaints were concerned. It was only after the x-rays showed calcification that Dr Ching diagnosed a 'spontaneous" condition - yet Mr Inkersell's symptoms had not changed other than in severity and no one including Dr Ching can say when the calcific changes occurred other than when the x-ray showed them to be present. The rotator cuff syndrome is the most common cause of occupationally induced 7 shoulder pain. Sometimes especially in the rotator cuff tendons calcification may occur in the areas of tendon degeneration (Turner). Calcific tendonitis - degenerative changes in the rotator cuff may be present with any type of activity which requires repetitive abduction of the arm. Prolonged working in an overhead position should also be avoided (Owen). Occupational factors which have been associated with musculoskeletal symptoms in the shoulder relate to both physical aspects of the work such as physically heavy work, working with arms, at or above shoulder height, repetitive work, lack of sufficient rest, occupations which are monotonous, time pressures and high workload (Pope et al). My Opinion Mr Inkersell worked in a physically demanding job, with time pressures, high work load, monotony above shoulder work and a repetitive nature to that work for over twenty years. After some fourteen years of this work he developed right shoulder symptoms diagnosed as of the rotator cuff type. He had to stop work and his ACC claim was accepted. A year later at x-ray, calcific changes were noted particularly in the right supraspinatas tendon (part of the rotator cuff). It is not possible to determine when these changes appeared but while a 'spontaneous" cause can be postulated a "degenerative" cause can equally be postulated particularly when it occurs in a person in their late 30's/early 40's, who has done this type of work described and who already had symptoms of a rotator cuff injury. Mr Inkersell's work was such that a work related chronic degenerative condition of the rotator cuff is the more likely diagnosis given the details presented." The appellant's counsel sought a second opinion from Professor Hugh Burry another specialist and expert in this field and Professor Burry also had the benefit of Dr Ching's reports. Professor Burry examined the appellant in August 1998 and his report dated 14 August 1998 states inter alia as follows: "I do not have any doubt that the problems that Mr Inkersell has experienced in his right shoulder are the results of two decades of extremely hard physical labour in which great strains have been placed upon the right shoulder joint while carrying out repetitive tasks demanding very strong action of the right shoulder joint, often in unfavourable postures. Deposition of calcium salts may occur in normal tissues without causing any symptoms whatsoever and are not uncommonly seen as incidental findings in asymptomatic persons. This is particularly the case in the attachments of tendons and ligaments which are the site of considerable repetitive stresses. Bony spurs may actually be created in such anatomical positions, e.g. the attachments of the plantar fascia to the os calcis in the heel without being associated with symptoms, or sometimes as the end result of an enthesopathy where persistent strain has led to inflammatory changes within the tendon attachment which subsequently resolve with bone formation. I cannot believe that the calcium salt deposition which has occurred in the tendons of Mr inkersell's right shoulder are located there merely by chance. Although as noted before, calcium salts may deposit without any known cause, such deposition is much more likely to occur in dystrophic tissue. Persistent and recurrent overload of tendons is likely to result in such dystrophic change which may or may not be accompanied by calcification. Finally, I find the notion raised by Dr Ching that Mr Inkersell has a diabetic cheiroarthropathy to be quite extraordinary. Mr Inkersell has the type of hands and arms that can be expected in a man who has carried out heavy manual tasks for 20 years as evidenced by his massive grip strength and there is no evidence whatsoever that he suffers from diabetes. The existence of a congenital fusion of C5 and Co vertebrae is likewise irrelevant. Such abnormalities have minimal, if any, effects on cervical spinal function and are not contributing any impairments in this case." Following the providing of those two reports to counsel for the respondent those reports were referred to Dr Kevin Morris, Acting Corporate Medical Advisor to the 9 Corporation, and Dr Morris has commented on the issue raised by these three specialists as follows: "The diagnosis is agreed by all to be calcific tendinitis of both shoulders with the right being more noticeably affected than the left. I would view this as constituting "personal injury". The debate here is as to what has caused this condition. The file contains reports from a currently practising rheumatologists in Timaru, Dr Ching, from an occupational physician in Christchurch, Dr Glass and a retired rheumatologist in Hammer Springs, Dr Burry. Dr Ching has expressed his view that in the absence of any evidence of secondary causes of the calcification such as a rotator cuff tear, he was of the view that the calcification had appeared spontaneously. He had also referred to the claimant's work by stating that: 'If he has got calcified tendons, then the cause of his shoulder problems has occurred naturally rather than brought on by his job." Alternative perspectives have been advanced by Dr Glass and Dr Burry. Dr Glass postulates that: "Mr Inkersell's work was such that a work related chronic degenerative condition of the rotator cuff is the more likely diagnosis given the details presented.." and also "It is not possible to determine when these changes appeared by while a 'spontaneous" cause can be postulated, a "degenerative" cause can equally be postulated particularly when it occurs in a person in their late 30's/early 10 40's, who has done this type of work described and who already had symptoms of a rotator cuff injury." Dr Burry notes: "Although as noted before, calcium salts may deposit without any known cause, such deposition is much more likely to occur in dystrophic tissue. Persistent and recurrent overload of tendons is likely to result in such dystrophic change which may or may not be accompanied by calcification." Thus all three specialists acknowledge that that the calcific tendinitis can occur without known cause. This fact is also noted in the three references that I have attached from current standard texts in surgery, medicine and occupational medicine. There are two questions to ask when considering the question of causation. Firstly could A cause B? Secondly, in this case, did it? Certainly in the situation discussed above, damage to the rotator cuff of the shoulder could cause a calcific tendinitis. The question then is whether it did in this case. Dr Ching, having found no rotator cuff tears on ultrasound examination was inclined to the view that the calcification appeared spontaneously as he states in his letter of 31/3/97. It is of interest to note that there is on file a copy of an operation note on the right shoulder dated 16/10/97. This surgery was done some 7 months after seeing Dr Ching. The note states: "There are areas of calcification well down beyond the supraspinatus attachment of uncertain significance. " 11 This surgery appears to have been done primarily because an impingement problem, which the surgeon describes as being the result of work, he does at the freezing works. The surgeon has confirmed the uncertainty regarding the calcific tendinitis. Taking all the views expressed on this file into account, I am not persuaded that on the balance of probabilities, that the calcific tendinitis has been caused by this man's work." The opinion of Dr Morris was then referred to Dr Burry for comment and his comment is as follows: "Thank you for inviting me to comment on the report provided to the ACC by Dr Kevin Morris. Unfortunately Dr Morris has no specialist training in rheumatic disorders and particularly the nature and pathogenesis of soft tissue injury. He is therefore not in a position to have a personal opinion on such a matter although, presumably, he may well wish to express an opinion regarding the credibility of specialists who have interviewed and examined a claimant and arrived at different conclusions. Dr Morris appears to have misunderstood what are the issues that need to be taken into account in deciding whether Mr Inkersell's problems are related to his work or not. Focusing on the question of calcific tendonitis, in the vast majority of cases where calcification of a tendon is noted radiologically and is considered to be related to the presence of pain and dysfunction in the joint, the calcification is likely to be the result of the attrition of the tendon and, although there may be accompanying inflammatory changes which will be associated with pain, it is important to look at what caused the tendon to be damaged leading to the 12 deposition of calcium salts. In other words the calcification should be seen as an epiphenomenon rather than the basic pathology. The presence or absence of rotator cuff tears is also something of a "red herring" as studies have shown that small tears of the rotator cuff can be demonstrated in a high proportion of persons in middle life many of whom have never suffered from disabling shoulder pain. The presence or absence of a rotator cuff tear is best demonstrated by injecting radio opaque dye into the subacromial bursa and seeing whether it makes its way into the joint cavity (or vice versa) because without a deficiency in the rotator cuff there is no normal anatomical connection between the subacromial and the joint cavity. Ultrasound imaging is a very inexact way of looking for a rotator cuff tear. As a separate issue, I have to say that I feel somewhat disturbed by Dr Morris' pejorative statement in his letter in which he draws attention to the fact that I have not only retired but have retired to the country, the obvious inference being that my opinion is no longer to be respected. I continue to be extremely interested in the nature and pathology of soft tissue injury, apart from other rheumatic disorders, and having published a number of papers on the nature of soft tissue injury and tendon pathology, feel confident that I know as much about the subject as Dr Ching and probably a great deal more. " Professor Glass was also asked to comment on the observations made by Dr Morris and he stated as follows: "The issue is one of causation in which Dr Morris takes the view that the calcific tendinitis is spontaneous. In his brief report he acknowledges that "certainly in the situation discussed above damage to the rotator cuff of the shoulder could cause a calcific tendnitis". The question is did it? To answer this question one must look at Mr Inkersell's work history and at the fact that the x-ray showed more marked calcific changes on the right. In my earlier report I detailed Mr Inkersell's 13 work history, noting the excessive right handed nature of work related static loading. There is thus a clear work history which provides an explanation. Calcific tendinitis generally occurs in the 50's or 60's occasionally in the 40's (Klippel and Dieppe: Practical Rheumatology 1995 Dee, Hurst, Gruber Kottmeier: Principles of Orthopaedic Practice 1997). Mr Inkersell's occurred in the 30's - there is a reason for this and this is his strenuous physical work. Professor Burry has dealt with why calcific changes are likely to have occurred, and emphasises the point that it is an epiphenomenom. In summary therefore work as a causative factor is established, the condition has also occurred earlier than would be expected. Given the evidence of work and age of occurrence it is my opinion that his condition is occupational in origin and not spontaneous." Counsel for the respondent then referred all those reports to Dr Ching for his further comment and Dr Ching's report of 5 March 1999 refers to three major rheumatology text books as those text books deal with the condition of calcific tendonitis and he thereafter states as follows: "It is therefore clear from these 3 major rheumatology texts that calcific tendonitis is recognised as degenerative process, and furthermore, it occurs more often in patients with sedentary occupations. I am not aware of any report showing evidence that calific tendonitis can be caused by an occupation or has any association with any occupation. Therefore, my opinion remains that Mr Inkersell's calcific tenonitis has occurred as a result of natural events, and not caused by his occupation, although there is no doubt that his occupation would exacerbate the symptoms of calcific tendonitis. I note in Prof. Glass's report that he stated that "rotator cuff syndrome is the most common cause of occupational induced shoulder pain. Sometimes, especially in rotator cuff tendons, calcification may occur in areas of tendon 14 degeneration (Turner)". He is not specific as to the reference by Turner, as to whether this is a paper or an opinion from Dr Turner, an occupational physician." Dr Ching then refers to specific passages from the text book of rheumatology and then goes on to state: "My opinion therefore remains that rotator cuff tendonitis/impingement syndrome is a degenerative condition, and the mechanic impingement depends on the shape and slow of the acromion, whether the patient has developed spurs, and whether there is osteoarthritis in the acromio-clavicular joint, resulting in osteophyte formation which would impinge on the underlying rotator cuff tendons. This syndrome is work related in that patients who have this condition and do manual work, especially working at shoulder height or above, would exacerbate their symptoms of rotator cuff tendonitis/impingement syndrome. However, the underlying cause of this condition is degenerative in nature and age-related, rather than it being caused by the patient's occupation. Cheiroarthropathy, refers to thickening of the tendons and subcutaneous tissues in the fingers and wrists, leading to flexion deformities of the fingers and a reduced range of movement in the wrists. If the patient has Diabetes Mellitus, then he has diabetic cheiroarthropathy rather than cheiroarthropathy. This is similar to patients having a skin rash called Necrobiosis Lipoidica, but if these patients also have Diabetes Millitus, then they have Necrobiosis Lipoidica Diabeticorum. Diabetic cheiroarthropathy is also associated with peri-arthritis of the shoulders, and calcific tendonitis in the shoulders (ref. Rheumatology, 2" edition, 1998: p. 8.23.5; and Textbook of Rheumatology, 5" edition, 1997: p. 486). The 'positive prayer sign' seen in diabetic hand syndrome, or cheiroarthropathy, can be impossible to distinguish clinically from flexion deformities and thickened hands seen in manual labourers. I think it.would be amiss for a rheumatologist, if seeing a patient with calcific tendonitis, shoulder problems, reduced range of movement in the wrists, and flexion deformities of the fingers resulting in a 15 positive prayer sign, not to consider the possibility of diabetic cheiroarthropathy and check the patient out for diabetes mellitus, and to just assume that the clinical features seen in Mr Inkersell's hands are all due to his manual labour." In terms of the expert evidence it seems that the final word was that provided by Professor Burry in a further report to counsel for the appellant dated 18 June wherein Professor Burry comments on the critique and opinion of Dr Ching. Professor Burry states as follows: "I have read with interest the comments of Dr Ching and the content of his annexures, much of which I have read previously. The material related to calcific tendinitis is largely irrelevant as it is known that this condition can occur for a variety of reasons and its main significance in this case is that it is known to occur where there is tendon degeneration. My own studies have been concerned mainly with the Achilles tendon but the anatomy and physiology of the Achilles tendon is analogous to that of the rotator cuff tendons. I am inclined to support the opinion of Uhthoff that the primary stimulation to deposition of calcium is hypoxia which is known to lead to tendon degeneration. I am attaching copies of two papers that I have contributed on this topic which I believe are pertinent (refs 1,2). Although hypoxia may be the result of reduction in blood flow associated with the ageing process, in a young to middle aged person the most important factor is likely to be increased tension which is known to prejudice blood flow. Activities which lead to prolonged tension in the tendons of the rotator cuff, such as the heavy manual handling tasks carried out by Mr Inkersell can lead to decreased blood flow. This is more likely to occur where there is significant impingement of the tendons of the rotator cuff against the immediately adjacent tissues i.e. the subacromial bursa and the structures that make up the acromial arch. The descriptions of Codman and Neer appear to me to be accurate and their explanation plausible. Dr Ching has said in the penultimate paragraph of his report, page 3, "However the underlying cause of this condition is degenerative in nature and 16 age related rather than it being caused by the patient's occupation. " By this statement he appears to be assuming that Mr Inkersell has developed a degeneration in his tendon because of old age, but Mr Inkersell was an energetic physically active person in his early forties when the condition first troubled him and I find it very difficult to believe that he would not have developed the problem but for the nature of the work that he was carrying out. I believe that the use of the word "degenerative" is rather misleading because one tends to think of degeneration as merely a manifestation of age, or some form of physical abuse, whereas one of the commoner causes of degeneration of tissue is insufficiency of blood flow causing hypoxia. A common example of the result of degeneration of a tendon is the sudden and unexpected rupture of an Achilles tendon in a highly trained athlete who could hardly be seen as a degenerate old person. I see no reason to suppose that Mr Inkersell was predisposed genetically or anatomically to develop any form of rotator cuff syndrome but even if we were so predisposed the onset of his disabling symptoms leading eventually to surgical correction was surely associated with the nature of the work that he was carrying out. " SUBMISSIONS Mr Cadenhead, counsel for the appellant, noted that it was the Corporation's decision to revoke the appellant's cover and disentitle him by virtue of the provisions of section 73 of the Act. He further notes that the appellant's claim had been accepted by the respondent as a claim under section 7, and that the respondent must thereby be taken to have accepted that the appellant's claim met the tests required in section 7 of the Act. He therefore submits that the question now for determination is a matter of causation, that is whether the appellant's ongoing incapacity is by reason of the personal injury for which he was granted cover or otherwise. Counsel submitted that the Occupational Physician is the paramount specialist to provide opinion evidence concerning questions of causation. Counsel refers to the reports of Professor Glass and Professor Burry, both experts in this field and who are 17 both in agreement that the appellant's condition, as presently diagnosed, is one that has been caused by certain particular characteristics of his employment. Counsel submitted that Dr Ching is not an Occupational Physician and therefore it is not surprising that his knowledge and his association of gradual process injuries is not wide, either academically or in particular, clinically. Counsel finally submitted that the weight of medical evidence supports the appellant's contention and he notes that the condition for which the appellant was afforded cover was a gradual process injury made up of numerous micro traumas, a process which can be described as degenerative in nature. Ms Scott, counsel for the respondent, identified the issue to be determined as whether the appellant's shoulder injury has been caused by his employment. Counsel submits that the Corporation's decision letter was such that cover was revoked, that is that the appellant could not meet the tests required in section 7 and that therefore the issue for this Court is whether or not the appellant has suffered a gradual process work injury in terms of section 7 of the Act. It is from that stand point that the appellant submits that the onus of proof is on the appellant to establish that his condition is as a result of personal injury caused by gradual process. Counsel submits that significant weight should be placed on Dr Ching's reports and she identifies the distinction which he makes that whilst it may be accepted that the appellant's occupation gives to rise to symptoms of the injury, it does not follow that the employment is the cause of the injury. Counsel submits that there is a distinction to be drawn between the symptoms and injury. Counsel submits that having regard to the evidence the appellant cannot satisfy the test required to be satisfied in section 7(1)(a) of the Act. DECISION 18 The substantive issue which I have identified in this appeal raises certain procedural questions, the principal one of which was adverted to by Mr Cadenhead in his submissions but not directly addressed by Ms Rice in her reply. If the Court were to deal with the matter as Ms Rice would submit, it would involve this Court in this appeal making a determination as to whether this appellant is entitled to cover under the Act pursuant to the provision 7. That is that the Court is concerned with the primary question of cover. For Mr Cadenhead's part, it is his submission that the Court must be concerned with considering whether the appellant has continuing entitlements under the Act pursuant to the cover previously granted to him in August 1996 or whether the appellant no longer continues to have an entitlement because he can no longer establish a causal nexus between his present condition, and the needs arising therefrom, and the personal injury for which he was granted cover. This state of affairs is brought about by the manner in which the respondent has treated this claim from the time it received the reports of Dr Ching which casts doubt on the appellant's claim for cover. The respondent's decision of 8 April 1997 to revoke the appellant's claim for cover was done so purportedly pursuant to the provisions of section 73(1) of the Act and relying on the exclusionary provisions of section 10(2)(a). The respondent did not purport to review or revise its earlier decision of 1 August 1996 pursuant to section 67A of the Act which gives it power so to do and I find that whilst it might be expedient to deal with the matter as if the respondent was invoking section 67A, I to do so would be stretching matters too far as one would assume that if the respondent had intended to deal with the matter under section 67A it would have said so. In those circumstances therefore, I find that this appeal must proceed on the basis that the appellant had cover granted to him for personal injury by gradual process arising out of and in the course of his employment and that from that stand point the matter must then proceed to a consideration of whether the appellant is entitled to continue to receive any particular treatment, service or compensation etc., or whether the 19 respondent has established on the balance of probabilities that the evidence is such that no such continuing entitlement exists. It is for this reason therefore that I rule as a preliminary point that the onus of proof is upon the respondent as it must be when the respondent is seeking to exercise powers under section 73 of the Act. The respondent, by its acceptance of the appellant's claim for cover, has accepted that the appellant has satisfied the onus which is upon a claimant to establish a right to cover. It is now for the respondent to establish on the balance of probabilities that the appellant no longer continues to have any particular entitlements pursuant to that right of cover and, in the context of this appeal, the respondent must establish that the personal injury in respect of which continuing claims for entitlements are being made is not the injury for which cover was granted. In other words the respondent must establish on balance that the appellant's present condition is not causally connected with the personal injury for which he was granted cover. That situation is quite different from the scenario that counsel for the respondent asserts, namely that the appellant cannot establish an entitlement to cover for the injury which he displays. Looking at the matter from the point of view of whether the respondent has in its possession medical evidence which can satisfy it that the appellant is no longer entitled to continue to receive benefits under the Act in respect of the injury that he presently displays, I find that the evidence cannot so satisfy and on the basis of the evidence as it has been presented to this Court the appellant has continuing entitlements under the Act in respect thereof. Despite the assertions of Dr Ching, I find that the expert opinions of Professor Glass and Professor Burry must hold sway. Each of them has looked at the appellant's injury as they have diagnosed it, and specifically related its origins to certain of the particular work tasks that the appellant has undertaken in the course of his employment as a freezing worker over the 19 years or so that he was carrying out such tasks. 20 Both Professor Burry and Professor Glass have discounted the contention asserted by Dr Ching that calcific tendonitis cannot be caused, or in the appellant's case was not caused, by tasks related to his employment but had occurred naturally. Professors Glass and Burry have looked at the injury from an occupational medicine perspective, have looked at the mechanical aspect of the work tasks and have related those directly to the particular shoulder injury that has been diagnosed. In the light of the clear and reasoned expositions of Professors Glass and Burry as to how calcifications can occur as an incident of tendonitis, brought about by the nature of the particular work activity which has caused it, I find that on this occasion they override the textbook theory and generalisation of Dr Ching. As I have previously ruled, the onus of proof is upon the respondent to establish the basis for its primary decision of 1 August 1996 and I find on the facts that it has not discharged that onus and therefore its decision to revoke cover and entitlements to the appellant was wrong and is itself hereby revoked. This appeal being successful, the appellant is entitled to costs which I fix at $800 together with the disbursements incurred by the appellant in obtaining the reports from Professor Burry and Professor Glass. th DATED at WELLINGTON this 28 day of January 2000 death M J Beattic District Court Judge ACA 40.98Inkersell.doc(gm)