Leemark Fire Protection Pty Ltd v Malios
[2014] VSC 654
•18 December 2014
| IN THE SUPREME COURT OF VICTORIA | Not Restricted |
AT MELBOURNE
COMMON LAW DIVISION
JUDICIAL REVIEW AND APPEALS LIST
S CI 2014 00391
| LEEMARK FIRE PROTECTION PTY LTD | Plaintiff |
| v | |
| DR JOHN MALIOS (As Convenor of the Medical Panel) & ors (according to the attached schedule) | Defendants |
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JUDGE: | WILLIAMS J |
WHERE HELD: | Melbourne |
DATE OF HEARING: | 24 September 2014 |
DATE OF JUDGMENT: | 18 December 2014 |
CASE MAY BE CITED AS: | Leemark Fire Protection Pty Ltd v Malios & Ors |
MEDIUM NEUTRAL CITATION: | [2014] VSC 654 |
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ADMINISTRATIVE LAW – Judicial review – Determination of Medical Panel – Unrelated injury or cause of impairment – Adequacy of reasons – Accident Compensation Act 1985 s 68(2), s 91(7)(c).
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APPEARANCES: | Counsel | Solicitors |
| For the Plaintiff | Mr J Noonan QC with Mr M Hooper | Thomson Geer |
| For the Fourth Defendant | Dr K Hanscombe QC with Mr P Over | Maurice Blackburn |
HER HONOUR:
The claim
The fourth defendant worker made a claim under s 98C of the Accident Compensation Act 1985 (‘the Act’) against the plaintiff, his former employer. Liability was ultimately accepted in relation to his injury of left sided pleural thickening and mild emphysema. As the extent of the worker’s resulting impairment was not agreed, a medical panel was appointed under the Act to make that assessment.
The first to third defendants were the convenor and members of the medical panel (‘the panel’) which, on 5 December 2013, determined that the worker had suffered a 20 per cent whole person impairment as a result of the accepted injury (‘the determination’). They do not appear before the Court, adopting the course sanctioned by the High Court in R v Australian Broadcasting Tribunal; Ex parte Hardiman.[1]
[1](1980) 144 CLR 13.
The employer seeks an order in the nature of certiorari quashing the determination. Essentially, it maintains that the panel erred in law either by failing to comply with its obligation under s 91(7)(c) of the Act to disregard impairment resulting from an unrelated injury or cause or by failing to give adequate reasons required by s 68(2) of the Act to show whether it had or had not complied with those statutory requirements.[2]
[2]See Wingfoot Australia Partners Pty Ltd v Kocak 303 ALR 64, 72-73 [26]-[28] (French CJ, Crennan, Bell, Gageler and Keane JJ).
The employer also asks the Court for an order in the nature of mandamus remitting the questions referred to the panel to another medical panel for determination.
The Act
The relevant sections of the Act are these:
68 Opinions
(2)The Medical Panel to whom a medical question is so referred must give a certificate as to its opinion and a written statement of reasons for that opinion.
91 Assessment of impairment
(1)In this Part, a reference to the assessment of a degree of impairment in accordance with this section is a reference to an assessment—
(a) made in accordance with—
(i)the A.M.A Guides as applicable subject to subsections (1A) and (1B); or
…
(ii) methods prescribed for the purposes of this section—
and in accordance with operational guidelines (if any) as to the use of those Guides or methods issued by the Minister; and
(b)if the Minister has approved a training course in the application of those Guides or methods, made by a medical practitioner who has successfully completed such a training course.
(1A)Despite anything to the contrary in the A.M.A Guides, an assessment under subsection (1) of the degree of impairment resulting from an injury must be made—
(a) after the injury has stabilised; and
(b)subject to subsection (7), based on the worker’s current impairment as at the date of the assessment, including any changes in the signs and symptoms following any medical or surgical treatment undergone by the worker in respect of the injury.
(7) For the purposes of section 98C— …
(c)impairments from unrelated injuries or causes are to be disregarded in making an assessment;
Background
I will set out the background to the application before coming back to the questions and the panel’s reasons for their answers.
On 13 April 2009, the worker lodged a claim under the Act for weekly payments of compensation for a bronchial condition which he identified as Chronic Obstructive Airways Disease. He referred to the fact that he was affected by asbestos exposure. On 19 May 2009, his claim was rejected.
The worker then lodged a claim for compensation under s 98C of the Act on 16 July 2010. He claimed that he was affected by impairment of respiratory function and chronic pleural fibrosis. On 1 September 2010, his s 98C claim was also was rejected.
The worker then commenced a proceeding in the County Court, claiming weekly payments of compensation, medical and like expenses. He described his injury as pleural thickening, emphysema, pleural effusion, chronic obstructive pulmonary disease (‘COPD’), reduction in lung capacity, respiratory impairment and anxiety and depression.
The County Court referred two medical questions to a medical panel. Those questions and that first medical panel’s answers on 17 June 2011 were these:
Question 1.What is the nature of the Plaintiff’s medical condition relevant to the injuries pleaded in paragraph 5(d) of the Statement of Claim?
Answer:In the opinion of the Panel the Plaintiff suffers from the medical conditions of left sided pleural thickening and mild emphysema.
Question 2.As to each of the medical conditions identified by the Medical Panel under question 1 does the Plaintiff’s incapacity for work result from or is it materially contributed to by any of these conditions and if so which condition or conditions?
Answer:In the opinion of the Panel the Plaintiff has an incapacity for any work resulting from the medical conditions of left sided pleural thickening and mild emphysema.
After the first medical panel gave its opinion, the parties settled the County Court proceeding on about 11 October 2011. The employer agreed to accept liability under s 98C in respect of the worker’s injuries of left sided pleural thickening and mild emphysema.
It was then necessary under the Act that the worker be assessed by an independent medical examiner for an opinion as to the extent of his impairment resulting from the accepted injuries.
Dr Denis G Robertson, a consultant respiratory physician, examined the worker on 14 November 2011. He took a history from the worker and analysed the results of lung function testing and radiological investigations performed in November 2011.
Dr Robertson concluded that the worker had a whole body impairment of 15 per cent, 50 per cent of which was attributable to his smoking.
As a consequence of that opinion, the employer’s claims handling agent advised the worker on 23 November 2011 that it had decided that he had an 8 per cent whole person impairment. He was, consequently, not able to obtain any form of compensation under s 98C because he had not reached the requisite 10 per cent threshold under that provision.
The worker disputed the assessment and sought to have medical questions in the form of those in s 104(9)(a) and (b) of the Act referred to a medical panel.
The second medical panel was made up of Dr Abraham Rubinfeld, a respiratory physician, and Dr David Barton, an occupational physician. It answered the medical questions by stating its opinion that the worker’s degree of whole person impairment assessed under s 91 of the Act was 4 per cent resulting from the accepted left sided pleural thickening and mild emphysema. The second panel was also of the opinion that the worker had suffered no resulting total loss injury mentioned in the table in s 98E(1).
The second panel gave reasons for its opinion dated 21 February 2012. It had taken a history from the worker and had examined him. It had also arranged for further lung function testing on 9 February 2012.
The second panel said this in its reasons:
The Panel concluded that the worker is suffering from left sided pleural thickening and mild emphysema in part contributed to by smoking and dust exposure during his employment, relevant in part to the accepted left sided pleural thickening and mild emphysema injury and in part to the worker’s pre-existing unrelated condition (smoking). The Panel considers his medical condition has stabilised.
The second panel noted the results of 9 February 2012 lung function tests it had arranged. It referred to the requirement that it disregard any pre-existing impairment. It noted the worker’s smoking history, estimated by the previous panel as at least 30 pack years. It noted that his reduction in lung capacity was most pronounced for single-breath diffusing capacity of carbon monoxide and that this capacity was most affected by emphysema and not by the worker’s pleural disease.
The panel concluded that the effect of the worker’s past occupational dust exposure on his lung capacity would have been minimal in comparison with the effects of smoking and attributed 80 per cent of the worker’s whole person impairment for reduced lung capacity to that smoking as an unrelated injury which should be disregarded under s 91(7)(c).
The worker challenged the second medical panel decision in this Court. It was agreed that the lung function tests upon which it had relied had not been carried out in accordance with the American Medical Association’s Guides to the Evaluation of Permanent Impairment (‘the Guides’) and that the opinion should be quashed by consent. The Court ordered that the same medical questions be considered by a new panel. It was in those circumstances that the panel came to make the determination which is now challenged by the employer.
The determination
On 5 December 2013, the panel answered the medical questions in this way:
Question i)
What is the worker’s degree of permanent whole person impairment resulting from the accepted injury/s as assessed in accordance with S91 (sic) and is the impairment permanent?
Answer:
In the Panel’s opinion the worker has a 20% whole person impairment resulting from the accepted left sided pleural thickening and mild emphysema injury when assessed in accordance with Section 91 of the Act. The degree of impairment is permanent.
Question ii)
Does the worker have an accepted injury, which has resulted in a total loss injury mentioned in the table in Section 98E(1)?
Answer:
No.
The panel’s reasons
The panel stated that it had formed its opinion by reference to a history from the worker, its own examination of him and the documents and information referred to in enclosures to the reasons. Those documents included Dr Robertson’s 17 November 2011 report, the first medical panel’s 24 June 2011 opinion and reasons and various reports and test results.
The history
The worker told the panel that he had worked interstate, installing fire protection equipment between 1980 and 1986 when he moved to Victoria. He had done similar work for different employers in this state between 1986 and 2009. Throughout, he had not worn any form of protective breathing equipment as it was physically impossible to do so in the confined spaces in which he worked. He had been regularly exposed to dust including concrete dust and believed that he had been exposed to asbestos dust on several occasions.
The worker described symptoms of shortness of breath from approximately 2005, as well as a productive cough. He had kept working without seeking medical help.
In November 2005, his symptoms of shortness of breath and productive cough had increased and he had developed a wheeze. He told the panel about his 2006 pleural effusion.[3]
[3]The panel and Dr Robertson both incorrectly refer to the effusion as right-sided.
The worker had stopped work for the employer in November 2009 after a diagnosis of COPD and emphysema and after he had been certified unfit. He told the panel that he had not previously suffered from bronchitis, pneumonia or asthma or required medical attention for any chest or pulmonary condition.
Significantly, the worker gave the panel a history of smoking between 15 and 20 cigarettes a day from about the age of 14 to about 2008, when he was approximately 50 years old. He had told the panel that he had smoked 30 cigarettes a day for about five more years and that he was still smoking one to two daily when examined by the panel in July and October 2013.
The worker described his shortness of breath when active and said that he needed to stop to catch his breath. He experienced exertional wheeze from time to time and coughed frequently, producing yellow sputum. Wheezing at night occasionally disturbed his sleep and was relieved by a bronchodilator.
The panel’s tests
The panel noted previous lung function test results from testing in January 2007, February and May 2009 and November 2011. It conducted its own pulmonary function studies. As both the FVC (forced volume capacity) and FEV (forced expiration volume) were between 60 and 79 per cent of predicted, the worker’s respiratory impairment was found to be Class 2, calculated in accordance with the Guides.[4] The panel identified a low range Class 1 respiratory impairment as a result of a DLCO (or gas transfer) measurement of in excess of 60 per cent of predicted.
[4]Guides, 162, ch 5, table 8.
Material before the panel
The panel had before it relevant reports from the worker’s treating general practitioner, Dr A Chau, his treating thoracic physician, Dr Nicholas D Manolitsas, and medico-legal reports from Professor M C F Pain, a consultant thoracic physician, and Dr Jonathon Burdon, a respiratory physician. It also had reports of radiological and other investigations.
Dr Chau
9 July 2009 report
Dr Chau was a general practitioner at the Carrum Downs Medical Centre where the worker had been a patient since December 2004. Dr Chau made a report dated 9 July 2009.
Dr Chau reported the worker’s 2006 left sided pleural effusion and the pleural tap and bronchoscopy procedures he had undergone at Frankston Hospital. He noted that the worker had had follow up CT chest scans and medical review by Dr Manolitsas.
The worker had attended upon Dr Chau in February 2009 after collapsing at home feeling short of breath. Dr Chau had organised for respiratory function tests which took place on 12 February 2009 and a CT scan of the worker’s chest on 2 March 2009. The 12 February 2009 respiratory function test results were of mild restriction of spirometry without air flow obstruction and no significant change following bronchodilator. There was also ‘moderately severe impairment of gas transfer’. The 2 March 2009 CT of the worker’s chest revealed residual left pleural thickening but no effusion.
Dr Chau reported that the worker’s diagnosis was of emphysema and features of chronic obstructive pulmonary disease. His smoking history was a contributory to his respiratory condition. In Dr Chau’s opinion, the worker’s dusty working conditions and work with concrete dust was a significant contributing factor to his inability to work in his usual job. His pre-injury work would aggravate his respiratory condition. He was capable of non-physically demanding work not in a dusty environment.
Dr Manolitsas
22 July 2009 report
Dr Manolitsas reported to the worker’s solicitors on 22 July 2009. He had seen the worker in early 2007 in relation to his respiratory condition and pleural effusion and again on 30 April 2009.
On 30 April 2009, the worker told Dr Manolitsas that he was short of breath after walking about 200 metres. He was reasonably comfortable walking from room to room at home and showering and dressing. He was short of breath if hurrying his household duties and walking upstairs. He had not been able to do heavy physical work due to his worsening respiratory condition.
Dr Manolitsas referred to the worker’s February 2009 lung function tests showing mild restriction of spirometry without airflow obstruction and moderately severe gas transfer impairment. He noted that the spirometry was slightly better than it had been 2007 but the gas transfer measurement was slightly worse. Dr Manolitsas also noted that the CT scan on 2 March 2009 showed no obvious emphysematous changes, no evidence of other interstitial lung disease and some minor pleural thickening at the left lung base.
Dr Manolitsas went on to conclude:
Mr Berry is dyspnoeic with moderate exertion which appears to be due to a microscopic degree of emphysema (not evident on CT Scanning). ….
I have not found evidence of significant asbestos related lung disease. His worsening respiratory status is likely to be due primarily to ongoing smoking.
31 August 2009 report
Dr Manolitsas was asked specific questions by the worker’s solicitors which he answered in a 31 August 2009 report. He stated that the worker had moderate impairment of gas transfer and was moderately dyspnoeic with exertion. He repeated his description of the effects of the worker’s shortness of breath noted in his previous report.
Dr Manolitsas considered the worker incapable of continuing with or returning to heavy work, including his previous work in fire protection. He had moderate chronic obstructive airways disease but his condition was not terminal. His respiratory status might slowly decline over a period of years. Dr Manolitsas thought that he was unlikely to improve.
24 November 2010 report
Dr Manolitsas reported again on 24 November 2010 to the worker’s solicitors. He had not seen the worker since April 2009 and repeated the diagnosis of moderately severe emphysema at a microscopic level not evident on CT scanning. He noted the absence of evidence of any other significant interstitial lung disease. He went on to say that although the worker did not have obvious airflow obstruction on spirometry, emphysema due to past smoking seemed to be the most likely cause.
Dr Manolitsas then concluded as follows:
In [the worker’s] work in the construction industry particularly in fire protection, I understand that he may have been exposed to significant amounts of concrete dust and asbestos dust as well as possibly other fumes. Although cigarette smoking is likely to be the major factor in the aetiology of his emphysema, it is certainly possible that exposure to fumes and dust as noted could have aggravated his condition. It is difficult to determine to what extent this could be the case.
Professor Pain
15 May 2009 report
On 15 May 2009, in a report to the WorkCover insurer, Professor Pain had concluded that although the nature of the worker’s condition overall was somewhat unclear, he had a permanent pulmonary process producing lung restriction and airflow obstruction. He had chronic pleural thickening which was a benign reaction to past asbestos exposure and was restricting his lung function and his employment potential. That condition might progress.
Professor Pain considered that the worker’s possible significant exposure to asbestos and other noxious dusts or fibres made it difficult to deny that his condition was a consequence of his past employment.
He was also of the view that the worker’s smoking habits might be playing some part in causing his mild airflow obstruction.
21 July 2010
Professor Pain reported to the insurer again on 21 July 2010. He made some further comments as a supplementary report. Professor Pain thought it was clear from the 13 November 2006 CT report that the worker’s condition was well established by that time with the presence of a large pleural effusion. As a result, he concluded that the worker’s employment with the employer after 5 September 2007 was not a factor in the causation of his illness because he had had no asbestos exposure in that employment.
Concrete dust exposure might have played some aggravating role in the worker’s mild airflow obstruction but it would not explain the pleural pathology. That pleural abnormality was most probably only asbestos-related.
Dr Burdon
27 January 2010 report
Dr Jonathon Burdon provided four reports to the employer’s solicitors. On 27 January 2010, he reported on his examination of the worker on 21 January 2010. Dr Burdon diagnosed the worker’s condition as chronic airways disease, predominantly of the emphysematous type.
Dr Burdon recorded the worker’s symptoms of shortness of breath, intermittent chest pain and tightness and cough and intermittent sputum production. He based his diagnosis on the worker’s history, his own physical examination, the X-ray reports covering the period from 16 November 2006 to 25 November 2009 and the lung function tests reported by Dr Manolitsas on 22 July 2009.
Dr Burdon considered the worker’s bronchodilator and steroid treatment appropriate as it was aimed at reducing his symptoms of breathlessness. He concluded as follows:
In my opinion, Mr Berry is not fit to return to work because of the severity of his breathlessness and lung disease. A diffusing capacity of 41% of predicted indicates significant pulmonary disease which in Mr Berry’s case is, in my opinion, is (sic) emphysema. Emphysema is a condition which does not recover. Whilst Mr Berry continues to smoke it will be progressive and even after he stops smoking he will continue to be breathless on mild exertion.
3 March 2010 report
When asked to provide a supplementary report commenting on whether the worker’s exposure to dust in the context of his employment as a sprinkler fitter from 1986 to 2009, Dr Burdon said this:
As detailed in my report to Cbus of 27th January, 2010, Mr Berry had, in my opinion, significant exposure to dust in the workplace. Mr Berry suffers from chronic airways disease, predominantly of the emphysematous type but he also had a cough indicating that it is likely that he also suffers from a mild degree of chronic bronchitis. Mr Berry has been a cigarette smoker and exposed to dust in the workplace and it would be impossible to deny that his exposure to dust in the workplace did not make some contribution to his chronic bronchitis, although it would be difficult to determine to what extent.
12 October 2010 report
Dr Burdon provided a third report to the employer’s solicitors, which the parties agree should be regarded as being dated 12 October 2010. He had been with a number of documents including the 2010 reports from Dr Manolitsas and Professor Pain.
In response to questions put, Dr Burdon described the nature and cause of emphysema, chronic obstructive airways disease and a pleural effusion, relevantly as follows:
Emphysema is a pathological diagnosis. It is a condition associated with loss of lung tissue most commonly due to tobacco smoking. Other causes included hereditary alpha-1-antitrypsin deficiency; ageing may also result in minimal degree of emphysema and exposure to dusts and pollution are also recognised as potential cause of emphysema.
Chronic obstructive airways disease (COPD) is a generic term used to describe a number of conditions associated with long term airflow limitation. These include emphysema, chronic bronchitis, bronchiectasis, chronic irreversible asthma, chronic bronchiolitis, and cystic fibrosis. Emphysema and chronic bronchitis are commonly caused in our community by tobacco smoking but other causes of emphysema have been outlined above…
Pleural effusions are collections of fluid in the pleural space, that is, in the potential space between the lung and the inside of the chest wall. The causes of pleural effusion are many. Common causes include lung cancer, pleural mesothelioma, pneumonia, pleurisy and other infections including tuberculosis and some immunological conditions. Benign effusions are also seen in persons with significant asbestos exposure.
Dr Burdon stated that the common symptom of patients with pure emphysema was breathlessness and that patients with COPD experienced breathlessness, cough and sputum production associated with chest tightness and occasional chest pain.
Dr Burdon repeated his conclusion that the worker suffered from mild to moderate COPD predominantly of the emphysematous type. He referred again to the lung function test results and, in particular, the worker’s diffusing capacity result of 41 per cent of the predicted capacity and the absence of interstitial lung disease accounting for that result in someone exposed to asbestos or who has only an occasional cough and no chronic bronchitis.
Dr Burdon considered that the worker’s emphysema and chronic obstructive airways disease was aggravated, accelerated or exacerbated by tobacco use. The associated symptoms of increased breathlessness and cough, reduced exercise capacity and increased chest tightness or discomfort generally become more severe, the more a person smoked. If the worker were to stop smoking, his breathlessness would be unlikely to improve as his significantly reduced diffusing capacity indicated that he predominately suffered from emphysema.
Dr Burdon agreed with Professor Pain’s view that the pleural effusion of 2006 was probably related to asbestos exposure. Pleural reactions to asbestos inhalation were either the development of a pleural effusion relating to an inflammatory process and localised pleural scarring or plaques or more generalised diffused pleural thickening.
Dr Burdon said that significant exposure to asbestos containing dust would be necessary to aggravate a pleural reaction to past asbestos inhalation. Inhalation of silica does not cause emphysema but might contribute to the development of chronic bronchitis, if inhaled over a long period of time.
5 October 2011 report
Dr Burdon finally reported on 5 October 2011 to the employer’s solicitors. In that report, he agreed that the worker suffered from left sided pleural thickening and mild emphysema which incapacitated him for any work. He confirmed that the worker’s then current changes in his respiratory function indicated evidence of an airflow obstruction with reduced gas transfer attributable to the diagnosis of emphysema.
Dr Robertson
17 November 2011 report
Dr Robertson, the consultant respiratory physician who had been asked to assess the worker’s impairment after his injury had been accepted expressed his opinion in a report dated 17 November 2011. He had taken into account lung function tests dated 14 November 2011.
There, he said:
Analysis of findings
Accepting the x-ray reports of pleural thickening at the base of the left lung I regard this as being consistent with benign asbestos-related pleural disease. Lung function tests done in September last year and on the day of examination showed no evidence of lung restriction. The latter two tests do show mild airway obstruction and on the day of examination there was improvement after bronchodilator. His airway obstruction is attributable to his smoking and to exposure to dusts in the course of his work. Airway obstruction continues to affect him so he does have a medical condition relevant to the alleged injury.
The pleural thickening and the airway obstruction are not likely to resolve and the airway obstruction will continue to need treatment. … As he is not now exposed to dust performing his daily living activities they are not expected to cause further harm but continuing to smoke would do so.
The pleural thickening is consistent with past asbestos exposure in the course of his work and dust exposure whilst employed has probably contributed to his airway obstruction. The results of lung function tests are plausible and are considered to relate to the impairment being evaluated.
His condition is considered to have stabilised.
Impairment evaluation:
Using the results of lung function tests done on the day of examination the most normal figure for the most abnormal measurement was the forced expired volume in one second after bronchodilator which was 67% of predicted normal. From table 8 on page 162 of the AMA Guides his respiratory impairment is in class 2 at 15% of the whole person.
Apportion:
It is likely that his smoking has contributed more to his airway obstruction than his dust exposure during his employment. However those two factors operated concurrently and it is not possible to apportion the effects of either. However my clinical opinion is that at least 50% of the impairment would be due to his smoking
The first medical panel’s 17 June 2011 reasons
The first medical panel referred in its reasons to a 28 April 2011 CT scan of the worker’s chest. The CT scan demonstrated ‘some left basal pleural thickening, consistent with some pleural fibrosis or an area of pleural plaque formation, though it was a little more extensive than is normally seen with simple plaque formation.’
The panel’s conclusions
Applying the Guides, the panel concluded that the worker suffered from a Class 2 respiratory impairment, resulting in a 20 per cent whole person impairment which the panel attributed entirely to the accepted injury of pleural thickening. The panel found a low range of Class 1 respiratory impairment and a resulting 0 per cent whole person impairment from the worker’s mild emphysema.
The panel reviewed the radiological and other investigative material before it, including the report of the CT scan of the worker’s chest on 28 April 2011.
The panel found no other identifiable medical condition or impairment resulting from the left sided pleural thickening.
The panel stated that it had considered the Court’s judgments in Alcoa Holdings Ltd v Lowthian and de Haas[5] and Chua v Lowthian[6] when evaluating the extent to which there was ‘impairment from an unrelated injury or cause … playing a part in the worker’s current impairment. It noted that, when assessing any such unrelated impairment, it required an evidentiary basis on which it could be positively satisfied of an unrelated impairment to be disregarded.
[5][2011] VSC 245.
[6][2011] VSC 468.
The panel went on to refer to the worker’s account that prior to the injury the designated date of which was 23 February 2009, he had not been incapacitated by any respiratory symptoms or sought medical treatment of investigations for a chest or respiratory condition. The panel then referred to reports of a 4 November 2005 chest X-ray and a 14 November 2005 CT scan of the worker’s chest which had shown no evidence of pleural plaque formation but had referred to ‘Scattered emphysematous bullae’.
Having described the situation before the accepted injury by reference to those matters, the panel went on to state the following conclusions:
The Panel therefore considered there was no evidence of functional impairment due to any prior injury or cause, and therefore there is no impairment due to unrelated injury or cause playing a part in the worker’s current level of impairment to be disregarded pursuant to Section 91(7)(c) of the Act (emphasis added).
The panel continued, confirming its previous findings as to the worker’s impairment resulting from the accepted injury, in this way:
The Panel therefore concluded that the worker has a 20% whole person impairment resulting from the accepted Left sided pleural thickening and mild emphysema, with a designated date of injury of 23 February 2009, when assessed in accordance with Section 91 of the Act. The degree of impairment is permanent (emphasis added).
The panel then noted:
(a) Dr Burdon’s 3 March 2010 opinion that:
[The worker] suffers from chronic airways disease predominantly of the emphysematous type, but he also has a cough indicating that it is likely that he also suffers from a mild degree of bronchitis;
and
(b) Dr Manolitsas’ 22 July 2009 statement that:
I have not found evidence of significant asbestosis related lung disease. His worsening respiratory status is likely to be due primarily to ongoing smoking.
The panel then stated its own conclusions about the worker’s smoking. It found that he had smoked between 30 and 35 pack years on the basis of the history he had given. It noted that his solicitors had included in their submission to it the worker’s own estimate of approximately 20 pack years.
The panel noted Dr Robertson’s 17 November 2011 report of his opinion that :
Using the results of lung function tests done on the day of the examination the most normal figure for the most abnormal measurement was the forced expiration volume in one second after bronchodilator which was 67% of predicted normal. From Table 8 on page 162 of the AMA guides his respiratory impairment is in Class 2 at 15% of the whole person.
Without reference to Dr Robertson’s view that at least 50 per cent of the worker’s impairment would result from his smoking, the panel then repeated its own assessment of 20 per cent whole person impairment. It stated that its assessment was based on its collective experience and expertise, its examinations on 1 July 2013 and 7 October 2013 and lung function testing on 7 October 2013.
Submissions
The employers submits that the panel failed to properly apply s 91(7)(c) of the Act by failing to disregard both the worker’s smoking and prior interstate employment as unrelated injuries or causes of the assessed impairment.
Counsel cite Lingenberg v Gallichio,[7]where Nettle and Neave JJA explained what is meant by the requirement to disregard:
The word ‘disregard’ is used in s 91(7)(c) of the Act in the sense of excluding so much of an impairment assessment as is due to unrelated injuries and causes.[8]
[7][2013] VSCA 143.
[8]Ibid [14].
They also refer to Alcoa Holdings Ltd v Lowthian and de Haas, where J Forrest J described the approach the panel should take to impairment from unrelated injury or cause (whether pre-existing or not) under s 91(7)(c), saying:
In engaging in its statutory task the Panel must do the best it can to evaluate the extent to which impairment from the unrelated injury or cause is playing a part in the worker’s current impairment. If the evidence enables it to determine the extent of the present impairment and that of the pre-existing impairment, then it must make allowance for the pre-existing impairment. [9]
[9][2011] VSC 245, [73].
It was common ground that s 91(1) of the Act required the panel to assess impairment from the accepted injury, but not that from an unrelated injury or cause, in accordance with the Guides. This meant that the panel was required to apply ‘the methodologies, processes and criteria set out in the Guides for the relevant condition, body part or system.’[10]
[10]HJ Heinz Company Australia Ltd v Kotzman [2009] VSC 311, [45] (Kyrou J).
Counsel for the employer note that the panel is required to apportion the contribution of concurrent causes to the impairment[11] and that ‘apportionment’ is defined in the glossary to the Guides as follows:
2.Apportionment: This is an estimate of the degree to which each of the various occupational or non-occupational factors may have caused or contributed to a particular impairment. For each alleged factor, two criteria must be met:
a.The alleged factor could have caused or contributed to the impairment, which is a medical determination … .
b.In the case in question, the factor did cause or contribute to the impairment, which usually is a non-medical determination. The physician’s analysis and explanation of causation is sufficient.
[11]Citing Alcoa Holdings v Lowthian and de Haas [2011] VSC 245, [74] (J Forrest J).
The employer argues that the panel did not properly assess the contribution of smoking to the worker’s impairment, in the way in which Dr Robertson and, indeed, the second panel had done. The panel had inappropriately focused upon the question whether the worker had previously been incapacitated by any respiratory symptoms and equated prior injury or cause and unrelated injury or cause. The reasons show that it did not ask itself whether the worker’s smoking was also a cause of the impairment it had assessed.
Both parties cited the Guides’ summary of the effects of tobacco use in Chapter 5 dealing with the respiratory system:
Tobacco Use
The most common cause of self-inflicted respiratory impairment is cigarette smoking. While there is variable individual susceptibility to the adverse effects of cigarette smoke, a discernible dose-response relationship is known. The examining physician should standardise data collection regarding dose … .
Multiplying the number of years of smoking by the number of packs smoked per day produces the standard measure, pack-years of cigarette smoking. This information can be used in assessing the impact of personal habits on respiratory impairment and may aid in the apportionment of respiratory abnormality among various deleterious factors. Cigarette smoking is the most significant causative factor in the development of chronic bronchitis, emphysema, and lung cancer.[12]
[12]Guides, 155.
The employer also relies upon what the Guides said about the consequences of pleural thickening:
Pleural thickening usually is not associated with respiratory impairment. However, in an unusual case of diffuse massive thickening, respiratory movement may be impeded and a restrictive abnormality may result.[13]
[13]Ibid 158.
The employer refers to the 28 April 2011 CT scan results which the panel mentioned and argues that there was no evidence of any unusual diffuse massive thickening in this case. Counsel maintain that the panel should have considered whether, absent such thickening, there might have been another contributing cause of the worker’s impairment.
The worker responds to the employer’s challenge by maintaining that the panel did comply with s 91(7)(c). Counsel argue that the employer seeks to upset findings of fact which do not suit it.[14] Those finding of fact are as to the extent of the impairment resulting from the worker’s pleural thickening and mild emphysema suffered as a consequence of the accepted injury.
[14]Citing S v Crimes Compensation Tribunal (1998) 1 VR 83.
Essentially, the worker argues that it is apparent from the reasons that the panel has ignored the effect of any unrelated smoking when making the determination about the extent of his impairment resulting from the accepted injury. The worker says that the panel has plainly adverted to his smoking history and taken it into account. It must be taken to have known of the effects of tobacco use summarised in the Guides and have taken them into account. In addition, the Guides state that smoking is the most significant causative factor in conditions which include emphysema but not pleural thickening, indicating that it is not a significant cause of that condition.
The worker maintains that the panel took an evidence-based approach by considering the X-ray and CT scan results from November 2005 investigations which showed no prior pleural plaque formation and some scattered signs of emphysema.
Counsel for the worker contend that the earlier panel and the doctors to whom the employer refers all concluded that the main cause of the worker’s impairment was emphysema, and not pleural thickening, and that smoking was the main cause of the emphysema. The panel had come to a different conclusion that the respiratory impairment resulted from pleural thickening. This conclusion resulted from the panel members applying their clinical expertise to the material and their own clinical findings. The employer’s complaint arose from its dissatisfaction with the result, which did not constitute legal error.
In so far as the worker relies on the Guides to argue that smoking could not be a cause of pleural thickening, counsel for the employer reply that the Guides do not expressly or implicitly make any statement to that effect.
Discussion and conclusions
Breach of s 91(7)(c)
In my view, there was evidence before the panel of respiratory impairment from the unrelated injuries or causes of the worker’s continuing smoking and prior exposure to asbestos in previous employment. The panel was obliged by s 91(7)(c) of the Act to disregard those parts of the worker’s impairment resulting from any unrelated employment or smoking. It failed to do so and erred in law.
There is no complaint about the panel’s assessment of the severity of the worker’s impairment under Chapter 5 of the Guides and its classification of that impairment. The employer objects however to the panel attributing his whole person impairment to left sided pleural thickening caused by workplace dust exposure, without making a determination of the contribution to that impairment made by his continuing smoking and or the continuing effects of relevant exposure in his earlier employment and disregarding that contribution.
The panel showed that it had failed to make the necessary determination by restricting itself to a determination as to the effects of prior, as opposed to concurrent, injury. It also failed to comply with its obligations by not taking into account any effects of unrelated injury which might have revealed themselves after the November 2005 investigations cited by the panel.
There was evidence which the panel accepted as to both the worker’s asbestos exposure in past unrelated employment and as to his past and continuing smoking. The panel had evidence too of the expert opinions from Dr Robertson and others, to which I have already referred, to the effect that the worker’s respiratory impairment was attributable to both the unrelated previous employment and to his past and continuing smoking.
Professor Pain, for example, had thought it difficult to deny that the worker’s permanent chronic pleural process was a consequence of his past employment where he had possibly had significant exposure to asbestos and other noxious dust or fibres. He considered that such a condition might progress. Professor Pain had also expressed the view that the worker’s smoking might also be causing some part in his airflow obstruction.
Dr Burdon agreed with Professor Pain that the worker’s pleural effusion of 2006 was probably related to past asbestos exposure. Dr Burdon also thought that the worker’s emphysema and COPD was aggravated, accelerated or exacerbated by tobacco use. The symptoms associated with such conditions generally became more severe with continued smoking.
The Guides, too, described the significant effects of tobacco use in causing respiratory impairment. I note that I am not persuaded by the worker’s argument that the Guides state by implication that smoking could not cause pleural thickening. I am not persuaded that the Guides provided an exhaustive list of conditions induced by smoking.
It follows that I am not persuaded by the worker’s argument that the employer in this case simply seeks to challenge a factual determination that the worker’s pleural thickening was the sole contributor to his whole person impairment.
The reasons show that the panel looked at the situation in about 2005 to determine whether there was an unrelated prior injury or cause contributing to the worker’s current impairment. The reasons state that the panel moved from a determination that in about 2005 there had been no symptoms or objective signs of impairment from a prior injury or cause, other than some emphysematous bullae, to its conclusion that no unrelated injury or cause had resulted in the current impairment. I note in this regard that the panel had previously stated that it had assessed the impairment resulting from emphysema in accordance with Table 8 of Chapter 5 of the Guides. Having had regard to the DLCO (or gas transfer) test result, it had attributed 0 per cent of the worker’s 20 per cent whole person impairment to his emphysema.
The panel erred in law and that error is apparent in the reasons and therefore on the face of the record.
Breach of s 68(2)
If I am wrong to conclude that the reasons demonstrate that the panel erred by failing to disregard impairment from an unrelated injury or cause, then, in my view, the panel would have erred in law by failing to provide reasons which sufficiently demonstrated its path of reasoning to show whether or not such an error occurred, as required by s 68(2) of the Act.
The panel was a ‘tribunal’ whose reasons for decision formed part of its decision and were incorporated in the record under s 10 of the Administrative Law Act 1978.[15] It would make an error of law on the face of the record if it failed to comply with the statutory obligation to give a written statement of its reasons for its opinion under s 68(2) of the Act.
[15]Wingfoot Australia Partners Pty Ltd v Kocak (2013) 303 ALR 64, 72-73 [27] (French CJ, Crennan, Bell, Gageler and Keane JJ).
In Wingfoot Australia Partners Pty Ltd v Kocak, French CJ, Crennan, Bell, Gageler and Keane JJ described the nature of a medical panel’s obligation to give reasons as follows:
The statement of reasons must explain the actual path of reasoning by which the Medical Panel in fact arrived at the opinion the Medical Panel in fact formed on the medical question referred to it. The statement of reasons must explain that actual path of reasoning in sufficient detail to enable a court to see whether the opinion does or does not involve any error of law.[16]
[16]Ibid 79 [53].
The conclusion that the panel has failed to comply with s 91(7)(c) is based upon my construction of the reasons. If the reasons do not indicate that the panel did not comply with its statutory obligation, the panel would, in any event, have breached s 68(2) of the Act because the reasons do not give enough detail to show, on the other hand, that it did comply. That is why I would conclude that there would be insufficient detail to show whether or not the panel had made an error of law.
The determination should be quashed and the questions referred to a different panel for determination in accordance with law.
SCHEDULE OF PARTIES
S CI 2014 00391
BETWEEN
| LEEMARK FIRE PROTECTION PTY LTD | Plaintiff |
| - and - | |
| DR JOHN MALIOS | First Defendant |
| DR ANTHONY GALLICHIO | Second Defendant |
| ASSOCIATE PROFESSOR PETER HOLMES | Third Defendant |
| KIM BERRY | Fourth Defendant |
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