Vescio and Telstra Corporation Limited (Compensation) - [2022] AATA 1353

Vescio and Telstra Corporation Limited (Compensation) [2022] AATA 1353 (26 May 2022)
Division:GENERAL DIVISION
File Number(s): 2020/0487
Re:Norina VESCIO
APPLICANT

AndTelstra Corporation Limited
RESPONDENT

DECISION
Tribunal:The Hon. Dennis Cowdroy AO QC, Deputy President
Date:26 May 2022
Place:Sydney

The Tribunal decides that the decision under review be set aside and substituted with the decision that the respondent is liable to make payments of compensation to the applicant pursuant to sections 17 and 18 of the Safety Rehabilitation and Compensation Act 1988 (Cth).
........................................[SGD]................................
The Hon. Dennis Cowdroy AO QC, Deputy President
CATCHWORDS
COMPENSATION – asbestos-related pleural diseases – multiple comorbidities – whether deceased’s death caused by asbestos-related pleural diseases or other comorbidities – whether asbestos-related pleural diseases can be considered an injury under s 5A(a) or s 5A(b) – whether Applicant entitled to compensation under ss 17 and 18 of the Safety Rehabilitation and Compensation Act 1988 (Cth) – decision set aside and substituted.
LEGISLATION
Safety, Rehabilitation and Compensation Act 1988 (Cth) ss 4, 5, 7, 14, 17, 18.
CASES
Comcare v Starkey [2017] FCAFC 151
Military Rehabilitation and Compensation Commission v May [2016] HCA 19
Wuth v Comcare [2022] FCAFC 42
SECONDARY MATERIALS
Henry Gray FRS, Anatomy Descriptive and Surgical (Barnes & Noble Books New York, 15th ed, 1995) 954.
REASONS FOR DECISION
The Hon. Dennis Cowdroy AO QC, Deputy President
26 May 2022

Ms Norina Vescio (“the applicant”) initiated proceedings for recovery of compensation under Section 17 and 18 of the Safety, Rehabilitation and Compensation Act 1988 (“the SRC Act”) arising out of the death of her husband, the late Giovanni Vescio (“the deceased”) who died on 12 January 2019 aged 85 years. The respondent rejected such application.
By Application for Review of Decision made on 29^th of January 2020, the applicant seeks review of the decision of the respondent made on 17 December 2019, which affirmed the original decision dated 5 August 2019. Each decision found that the deceased’s death did not result from benign asbestos-related pleural disease.
As will become apparent, the principal issue in these proceedings is whether the deceased died as a result of pulmonary disease or from renal failure.
APPLICANT’S CLAIMS
The Applicant is the widow of the late Giovanni Vescio ("deceased"). The deceased was born on 14 June 1933 in Italy. The deceased was employed as a linesman by the Respondent (formerly Post Master General's Department, then Telcom Australia) from 23 August 1972 to 4 November 1992.
Throughout the deceased's employment by the Respondent as a linesman, he was exposed to and inhaled asbestos dust and fibre. The deceased's exposure to and inhalation of asbestos dust and fibre during his employment by the Respondent occurred in the manner and circumstances set out in paragraphs 4.1.1 to 4.1.21 of the Form 1 Statement of Particulars executed by the deceased on 11 December 2014 during his claim for common law damages against the Respondent in the Dust Diseases Tribunal of NSW.
As a result of the deceased's exposure to and inhalation of asbestos dust and fibre during his employment by the Respondent, from at least 2009, the deceased suffered from:
(a)Pleural plaques; and
(b)Rounded atelectasis; and
(c)Diffuse pleural thickening; and
(d)Asbestos related pleural disease.
Each of the deceased's pleural plaques, rounded atelectasis, diffuse pleural thickening and asbestos related pleural disease, constituted "injury" and "disease" within the meaning of those terms in the Safety Rehabilitation and Compensation Act 1988 ("SRC Act").
The deceased had also suffered from emphysema, chronic obstructive pulmonary disease, ischaemic heart disease, diabetes, and chronic renal disease.
In or about 2018, the deceased developed a recurrent right sided pleural effusion. Between 16 and 26 October 2018 the deceased was admitted to the Manly Hospital because of worsening breathlessness. During his admission to the Manly Hospital, the deceased's right sided pleural effusion was drained revealing that the pleural fluid was an exudate (oozing fluid).
On 13 November 2018 the deceased was admitted to Northern Beaches Hospital with worsening breathlessness and recurrent right sided pleural effusion. During his admission to Northern Beaches Hospital, the deceased's right sided pleural effusion was drained revealing that the pleural fluid was an exudate.
As at 12 November 2018 the deceased required the use of oxygen therapy and his oxygen saturation was 81-86% at rest. On 18 December 2018 the deceased was admitted to St George Private Hospital with a recurrent right sided pleural effusion. During his admission to St George Private Hospital the deceased had a pleural biopsy and pleurodesis which revealed the presence of blood clots and dense adhesions between the parietal and visceral pleura, and white thickening of the parietal pleura.
The deceased died on 12 January 2019 in respiratory failure.
Pursuant to the SRC Act, as at the date of the deceased's death, the Applicant was a
dependant of, and wholly dependent upon, the deceased.
The deceased's recurrent right sided pleural effusion was caused, and/or contributed to, to a significant degree, by his exposure to and inhalation of asbestos dust and fibre during the course of his employment by the Respondent as referred to in paragraph 5 above.
The deceased's recurrent right sided pleural effusion constituted "injury" and "disease" within the meaning of those terms in the SRC Act. The deceased's death was caused, and/or contributed to, to a significant degree, by his diffuse pleural thickening, rounded atelectasis, asbestos related pleural disease and recurrent asbestos related right sided pleural effusion.
The Applicant has not received compensation or damages in respect of the deceased's employment by the Respondent, his injury and disease. On 21 May 2019, the Applicant applied to the Respondent for compensation as a dependant of the deceased.
On 5 August 2019, the Respondent determined that the Applicant was not entitled to compensation ("Original decision").
By letter dated 9 December 2019, the Applicant requested a review of the Original decision. On 17 December 2019, the Respondent affirmed the Original decision to deny the Applicant's claim ("Review decision").
DECISION UNDER REVIEW
The decisions under review is the reviewable decision of the Respondent made on 17 December 2019, which affirmed the original decision dated 5 August 2019.
The Original decision and the Review decision determined that the Applicant was not entitled to compensation under ss 17 and 18 of the SRC Act in respect of the death of the Deceased.
ISSUES BEFORE THE TRIBUNAL
Whether the applicant is entitled to compensation pursuant to ss 14, 17 and 18 of the SRC Act, because:
(a) The deceased's death was caused by, and/or resulted from, and/or was contributed to, to a significant degree by each, and/or all of, the following injuries and diseases: diffuse pleural thickening, rounded atelectasis, asbestos related pleural disease and asbestos related right sided pleural effusion.
(b) The deceased's diffuse pleural thickening, rounded atelectasis, asbestos related pleural disease and asbestos related right sided pleural effusion were caused by, and/or were contributed to, to a significant degree, by the deceased's employment by the Respondent.
As will be apparent from the medical reports referred to hereunder, the deceased, prior to his death, suffered from emphysema, renal failure, diffuse pleural thickening and right sided pleural effusions. The expert reports provided by the applicant found that the deceased’s death resulted from his pleural thickening, rounded atelectasis and the right sided pleural effusion and that his condition deteriorated due to a surgical procedure performed at Manly Hospital in December 2019. The applicant’s medical experts claim that the cause of death was not due to renal failure nor to emphysema.
The expert report provided by the respondent assert that the cause of the deceased’s death was renal failure, or the effects of infection or pneumonia.
CHRONOLOGICAL SUMMARY OF MEDICAL HISTORY
The applicant’s medical history commences on 23 October 2003, when an x-ray revealed consolidation or scarring at the right base and in axillary segment of the right upper lobe of the lungs. A week later, a CT scan conducted at the Warringah Medical Centre revealed pleural thickening adjacent to a small rib deformity most likely due to an old fracture.
A chest x-ray report made on 15 January 2009 recorded “The pleural shadowing with the associated minor pleural calcification is probably the result of previous asbestos exposure. The round opacity at the right base posterior/medially is non-specific but may represent rounded atelectasis or possibly a neoplastic process”.
On 30 January 2009 Dr Frankel reviewed the deceased at the Peninsula Respiratory Group. He reported:
“Mr Vescio is an elderly gentleman who has bilateral pleural changes. I think that there are features to suggest pleural plaques and previous asbestos exposure with the possibility of other asbestos related pleural disease. I think that the right basal shadowing is likely all rounded atelectasis …”
Lung function tests were repeated in the following years.
On 20 June 2013 the deceased was admitted to the Emergency Department of Manly Hospital, the reason for admission stating: “respiratory – shortness of breath”. The applicant was reviewed by Dr Patrick Coleman, specialist nephrologist, and discharged.
On 8 September 2013 the deceased again presented to the Emergency Department at Manly Hospital for what was recorded as “?? Pneumonia”. The deceased was prescribed antibiotics and a chest radiograph showed no interval change from the deceased’s previous admission (bilateral pleural effusions with no consolidation).
Further medical consultations took place throughout 2014 and 2015. On 23 November 2015 Dr Coleman referred to, in a letter to the deceased’s general practitioner Dr Monica Merey, various issues including progressive stage 4 kidney deterioration and the lung condition..
Further consultations took place between the deceased, Dr Coleman, Dr Merey and Dr Philip Lee, respiratory specialist, in 2016.
On 16 January 2017 the applicant was attended by paramedics and taken to Manly Hospital. He was discharged on 20 January 2017. A similar incident occurred when the deceased was attended by paramedics on 26 September 2017 when the deceased was admitted to Manly Hospital. On this occasion he was found to have a right sided pleural effusion. Tests did not reveal any pneumonia or infection.
A medical report made on 2 February 2018 notes that the deceased had no episodes of chronic obstructive pulmonary disease (COPD) exacerbation in the previous three months; a chest x-ray performed on 3 November 2017 revealed bilateral pleural effusion which was worse on his right side.
On 3 August 2018 the deceased was admitted to Manly Hospital suffering from “respiratory – shortness of breath” and “infective exacerbation of COPD”. Antibiotics were prescribed. On 8 August 2018 the deceased was discharged from Manly Hospital with antibiotics. By letter dated 17 August 2018, Dr Coleman wrote to Dr Merey reporting on the deceased’s condition. Dr Coleman recommended that the deceased be referred to the Community Palliative Care Team and advised that due to the deceased’s age and comorbidities, he was not a suitable candidate for renal replacement therapy.
On 16 October 2018 the deceased was again admitted to Manly Hospital with shortness of breath. Pneumonia was not detected nor was any influenza virus or other infection. The chest report of Dr Goldin reported:
“A large pleural effusion present. This has resulted in compressive volume loss in the right lung mainly in the lower lobe”
On 19 October 2018 a catheter was introduced into the right pleural cavity and 700 ml bloodstained fluid was aspirated. No infection was present. On 26 October 2018 the deceased was discharged from Manly Hospital with antibiotic medication.
On 12 November 2018 the deceased was again admitted to Manly Hospital with respiratory problems. The report recorded acute deterioration in October resulting in his hospitalisation. The report also indicated significant re-accumulation of his right sided pleural effusion. Arrangements were made for the deceased to be admitted to Northern Beaches Hospital.
On 13 November 2018 the deceased was attended by paramedics due to shortness of breath. He was admitted to Northern Beaches Hospital on that day under Dr Lee. Results from tests conducted on drained pleural fluid showed no infection. The pleural effusion was drained in the following as noted:
“A large triangular density concave to the lung parenchyma projects along the entire right lateral hemithorax. It is indistinguishable from the right hemidiaphragm. At the base of the abnormality it has a depth of 6 cm.”
It should be noted that Gray’s Anatomy describes the pleural cavity, where the effusion was found, as follows:
‘The space between these two layers is called the cavity of the pleura, but it must be borne in mind that in the healthy condition the two layers are in contact and there is no real cavity until the lung becomes collapsed and a separation of it from the wall of the chest takes place.’[1]
[1] Henry Gray FRS, Anatomy Descriptive and Surgical (Barnes & Noble Books New York, 15th ed, 1995) 954.
On the 22 November 2018 a chest x-ray was made and compared with one conducted on 17 November 2018 with the following conclusion:
“The large right-sided pleural effusion. Ill-defined opacities in both lungs. Overall appearances are unchanged”.
On the same day no infection was detected. The deceased was discharged on 28 November 2018.
On 18 December 2018 a chest x-ray reported:
“There is an increase in size of the right pleural effusion since the previous x-ray of 03. 11. 2017…”.
Dr Lee, the treating respiratory specialist, was concerned by the reaccumulation of the right sided pleural effusion and arranged for urgent referral to St George Hospital under Dr Matthew Horton, cardio thoracic surgeon. On the same day the deceased was admitted to St George Hospital and Dr Horton noted:
“… Large effusion
“Asbestosis?.Meso?”
The notes record that in the two weeks previous 700 m/l of bloodstain fluid was drained.
On 21 December 2018 Dr Matthew Horton performed surgery at St George Private Hospital. His report relevantly states:
… There were quite significant adhesions between the lung and the chest wall and there were some thick white parental pleura noted to be attached to the lung. There were also some clots within the pleural space. The line was partially mobilised away from the chest wall, although some of the adhesion was so dense that they were not able to be mobilised…
The histopathology report of Dr Juliette Byrne, pathologist states:
“The majority of the material shows features consistent with an organising haemorrhagic fibrinous effusion… The features are regarded as those of florid mesothelial proliferation. The features are insufficient for a diagnosis of malignancy.”
On 22 December 2018 a drain had been placed in the pleura. It was noted:
“There is extensive pleural thickening on both sides. There is an infiltrate present in both lungs suggesting fibrosis.”
The deceased was discharged under the care of a palliative doctor. It was noted that he had marked myoclonic jerks continuously. The evidence before this Tribunal discloses that such jerks can be related to both renal and respiratory failure. His life was regarded as being in the terminal phase and end-of-life carer support was discussed.
On 12 January 2019 the deceased died at home.
MEDICAL REPORTS
The Tribunal considered the following medical records: -
Experts for Applicant
(a) Associate Professor (AP) David H Bryant who had provided medical reports for the deceased commencing on 22 October 2014; 22 December 2014; 2 September 2015; 22 November 2019; 2 July 2020; 27 October 2020; 16 December 2020. AP Bryant’s specialty is respiratory diseases;
(b) Dr Anthony Johnson, respiratory and sleep physician who provided reports dated 12 April 2021 and 29 October 2021;
(c) Associate Professor (AP) Paul J. Champion de Crespigny, consultant physician and nephrologist who provided reports dated 9 May 2020 ;12 July 2020; 15 July 2020; 3 November 2021.
Experts for Respondent
(d) Associate Professor (AP) David K. McKenzie, respiratory and sleep physician who provided reports dated 5 December 2020; supplementary reports dated 25 August 2021 and 21 October 2021
(e) Professor Richard Fox, specialist oncologist, who provided a report dated 20 March 2021;
(f) Dr Richard Singer, consultant nephrologist who provided a report dated 10 September 2021.
During the hearing extensive oral evidence was provided as follows:
(a) 17 November 2021: concurrent evidence by AP Bryant, Dr Johnson and AP McKenzie.
(b) 17 November 2021: individual oral evidence was provided by AP de Crespigny,
(c) 18 November 2021: individual oral evidence was provided by Professor Fox, and by Dr Singer,
(d) 28 January 2022: concurrent evidence was again provided by AP Bryant, Dr Johnson, and AP McKenzie.
ASSESSMENT OF DECEASED’S MEDICAL CONDITION
Medical records establish that the deceased had been suffering from several medical diseases for several years prior to his death. Extracted hereunder are the critical extracts from the medical reports of the medical experts who provided reports and who provided testimony to the Tribunal upon their specialty. For convenience, the reports are provided in chronological order as far as possible.
Associate Professor Bryant
Report October 22, 2014
AP Bryant first examined the deceased on 21 October 2014. The deceased had diabetes mellitus which was then managed by tablets and insulin injections and was reportedly well-controlled. The deceased also had peripheral neuropathy with numbness and tingling in his feet; he smoked 15 to 20 cigarettes per day and for the previous 10 to 12 years he had gradually increased breathlessness which made it difficult to walk 15m at average pace. He also had a cough which at times produced a small amount of mucoid sputum.
Between 1972 in 1992 the deceased was employed by Telecom as a linesman. His work involving installation of fibro asbestos pits, installation of fibro-asbestos conduits and running telephone lines through the spaces. His daily work involved him in handling, cutting and rasping fibro- asbestos material on average 2 to 3 hours per day. He was also required to remove old Telecom pits which sometimes involves smashing them into small pieces using a hammer and then placing the pieces on a pile for removal. No protective gear had been provided until his final year of employment, when employees were given paper masks.
A CT scan of the thorax dated 15 January 2009 showed bilateral diffuse pleural thickening with some calcification at the base of both lungs posteriorly and anteriorly. An area of rounded atelectasis existed the base of the right lung. A high resolution CT scan dated 14^th of April 2009 showed similar changes but in addition bilateral lower zone changes of traction bronchiectasis was evident.
A CT scan dated 27 July 2009 showed similar changes as to the scan dated 21 August 2009. A CT scan dated 14 August 2003 showed similar pleural thickening as above described and in addition there were a few “tiny areas” of mediastinal lymph node calcification. No evidence of silicosis and no evidence of any marked worsening of the deceased’s diffuse pleural thickening were found in the CT scans from 2009. However scans from the year before the report was written, 2013, showed more fibrosis in lower zones than was previously present. The deceased’s pleural thickening was given a 20% chance of deteriorating in the next few years.
Report 22 December 2014:

AP Bryant refers to his previous report in which he found that the deceased had evidence of “mild chronic airflow limitation based on his spirometry (FEV1 1.5 L, 74% of predicted) together with the presence of mild emphysema on his CT scans; diffuse pleural thickening sufficiently severe to be capable of causing impairment of ventilatory function”.
Additional lung function test results dated 20 February 2009 and another dated 30 July 2009 which were provided to AP Bryant showed “evidence of quite severe airflow limitation (with an FEV1 of 48% of predicted and 51% of predicted) and a marked impairment of the diffusing capacity (35% and 40%). One of the tests done on 20/2/2009 did not show any evidence of gas trapping (residual volume 80% of predicted) whereas the test done on 30/7/2009 showed a residual volume at the upper limit of normal (114% of predicted).”
These results indicated to AP Bryant that Mr Vescio had a moderate degree of emphysema and chronic airflow limitation and that this was likely to fluctuate in intensity but was more than minimal in degree. It was therefore “likely that this was making it a significant contribution to his impaired ventilatory function”. The report continues:
“… his oxygen saturation falls after he walks for only 25 metres indicating the presence of a severe impairment of ventilatory function and, at the time I saw him, there was only a minor degree of airflow limitation detected (FEV 1 74% of predicted) suggesting that other changes in lung function are likely to be contributing to his disability and that the reduction in his diffusing capacity (due to emphysema) and a restriction of lung movement as a consequence of benign asbestos-related pleural disease are likely to be the major contributing factors”.
Report 2 September 2015:
This report states:
“In my previous reports I came to the Mr Vescio has a marked degree of diffuse pleural thickening due to benign asbestos related pleural disease and that he also has a moderate degree of COPD and of airflow limitation”.
Report 22 November 2019
In this report AP Bryant acknowledged that he had received a large bundle of documents and was now providing his medicolegal report. This report relates to the fact that AP Bryant diagnosed chronic renal failure, emphysema, and diffuse pleural thickening due to benign asbestos-related pleural disease as reported in his previous reports. He stated that the deceased was likely to have had significant asbestos exposure beginning in 1972 when he was employed by Telecom as a linesman. The report states:
“… and that, as a consequence of this, he has evidence of bilateral diffuse pleural thickening due to benign asbestos related pleural disease with changes suggesting rounded atelectasis at the base of the right lung. Dr Graham Dunn, in his report dated 13/06/2015, confirmed these views.
Based on the scans which I saw I could find no evidence of asbestosis and I note that Dr Dunn agreed with this assessment. I also note that [the deceased] is likely to have had silica dust exposure over the 21 years that he worked for Mills Brick Works and subsequently Brickworks Limited. However I could find no radiographic evidence of any silicosis and I note that Dr Dunn agreed with this assessment.
Based on the information available to me in December 2014 and noting that your clients lung function was progressively deteriorating, that his exercise distance had fallen to 25 meters I expressed the view then that your client had a severe impairment, approximately half of which was due to emphysema and half due to benign asbestos-related pleural disease and that he had at least a 40% impairment as a consequence of his benign asbestos-related pleural disease.”
As to the opinion as to the cause of the deceased’s death, AP Bryant states:
“Although all the medical conditions which affected Mr Vescio are likely to have contributed towards his demise it is my opinion that, were it not for him developing worsening asbestos-related pleural disease and an asbestos-related right-sided pleural effusion, that Mr Vescio would have survived for a longer period and that his death is attributable to benign asbestos related pleural disease.”
Report October 27, 2020
AP Bryant refers in his report to a report of AP de Crespigny, nephrologist as follows:
“Professor de Crespigny’s reports indicate that he is of the opinion that the major cause for Mr Giovanni Vescio’s physical disability was his chronic lung disease and that there was little or no contribution to his immobility and associated deconditioning from his renal disease. He believes that Mr Vescio’s cause of death is more likely than not to have been related to his respiratory disease rather than his chronic renal impairment.
The NSW Ambulance reports disclose that the ambulance was called to Mr Vescio on 16/1/2017, 26/9/2017, 3/8/2018, 16/10/2018 and 13/11/2018. On each occasion he was in respiratory distress with rapid breathing and low oxygen saturation requiring oxygen administration. These reports therefore do not cause me to change the opinions that I expressed to you regarding the likely cause of Mr Vescio’s death. As set out in my report to you dated 22 November 2019 it is my opinion that Mr Vescio had severe respiratory ailment due to (i) benign asbestos-related pleural disease causing both extensive pleural thickening plus a bloodstain pleural effusion, and (ii) moderately severe COPD. These changes were severe and resulted in him being breathless on trivial exercise in the period leading up to his death, at which time his renal impairment was not severe enough to be contributing to his disability”.
Report 16 December 2020
In this report AP Bryant states:
“I remain of the opinion that your client did have significant respiratory disease due to a combination of COPD, diffuse pleural thickening causing rounded atelectasis at the base of the right lung, together with a large right-sided pleural effusion requiring drainage.”
AP Bryant noted the deceased’s breathlessness had worsened just prior to his admission to the Northern Beaches hospital on 13 November 2018; that the deceased’s breathlessness improved after 510ml of pleural fluid was removed but the fluid quickly recurred, and 2L of pleural fluid were removed on 15 November 2018. He states:
“Because of a continuing pleural effusion, a talc pleurodesis was performed on 21st December 2018 and only a small amount of pleural fluid was evident at surgery but there was thickened pleural with adhesions. There was no evidence of any bacterial infection in the pleural fluid, and although the medical discharge summary mentions the presence of community-acquired pneumonia, I can see no documentary evidence of this diagnosis in the days after Mr Vescio was admitted to hospital and when the cause of his pleural effusion was being sought.”
AP Bryant refers to an opinion of AP McKenzie (respiratory and sleep physician) that “asbestos related pleural disease is a very uncommon cause of death”. AP Bryant disagreed with such proposition, stating :
“I agree that it is a less common cause of death than malignant mesothelioma of the pleura, but the Dust Diseases Board of NSW (Dust Diseases Care) records disclose that, between 1968 and 2005, benign asbestos-related pleural disease was deemed to have been the cause of death in 168 individuals, compared to 1812 due to mesothelioma (i.e. approximately 9% of deaths due to all asbestos-related pleural changes were due to ARPD). Similar figures were obtained in a large-scale survey published by Abos- Herrandiz et al (Canadian Respiratory Journal 2017, Volume 2017, Article ID 9015914).”
AP Bryant concluded:
“It is therefore my opinion that Mr Giovanni Vescio had multiple factors contributing to him (sic – his) impaired respiratory function but, of these, the most significant was his right-sided pleural changes and his COPD. Both of these, in my opinion, made a material contribution to his disability and death and, on the balance of probabilities, benign asbestos-related pleural disease was a substantial cause of the right-sided pleural effusion which developed over the course of 2018”.
Associate Professor McKenzie.
Report 5 December 2020
AP McKenzie in his report dated 5 December 2020, having considered the medical evidence, concluded:
“Therefore, the major cause of respiratory impairment in 2009 was COPD and pulmonary emphysema.
There was a progressive decline in pulmonary function between 2008 and 2018 with FEV 1 recorded in 2017 at 1.1 L. There was also a progressive decline in arterial oxygen saturation. Mr Vescio was largely housebound from around 2015 and this was mainly due to severe COPD and pulmonary emphysema. There was likely a contribution from his affective disorder with depression and the obstructive sleep apnoea which he was never treated appropriately. Mr Vescio’s terminal illness began in late October 2018 when he was admitted to hospital for management of a right-sided pleural effusion thought to be para pneumonic, related to pneumonia. The differential diagnosis for this effusion includes an asbestos -related pleural effusion and other inflammatory causes of an exudate.…
In my opinion, the most likely cause of death was Type II respiratory failure on the basis of underlying severe COPD and emphysema with analgesic and sedative medications acting as contributing factors. The renal failure may have contributed, but in my opinion, was not the prime cause of death. The tachypnoea and myoclonic jerks are consistent with this conclusion.
In my opinion, the recurrent pleural effusions and inflammatory pruritus did not cause the respiratory failure. Asbestos-related pleural disease is a very uncommon cause of death. It is more commonly cause of mild or mild to moderate disability. Mr Vescio had progressive respiratory failure over a period of more than three years prior to the development of a large right pleural effusion. However, the narcotic analgesics used to treat post-operative pain would have contributed to the development of Type 11 respiratory failure…”
Report 25 August 2021:
In his report dated 25 August 2021 AP McKenzie reviewed the reports of other medical experts, namely Professor Fox dated 20 March 2021 and of AP Bryant of 16 December 2020 and of Dr Johnson of 12 April 2021. He considered that the surgical procedure and subsequent analgesic and palliative treatment worsened the deceased’s pre-existing respiratory failure and hastened his death. He did not alter his view previously expressed concerning the cause of death.
AP McKenzie agreed with Professor Fox’s conclusion that the deceased death was due to a combination of his chronic obstructive pulmonary disease “with exacerbation of his renal failure”. AP McKenzie states:
“In my opinion, the COPD with its resultant respiratory failure, aggravated by analgesic and palliative medications, was a major factor. There were no blood tests reported in the terminal phase so it is not possible to confirm or exclude the extent to which renal failure may have contributed.”
In answer to AP Bryant, AP McKenzie disagreed with data relied upon by AP Bryant concerning the FEV1 was 74% predicted. AP McKenzie opined that the predicted value for a man of the deceased age and height would have been about 2.6 L. Accordingly and FEV1 value of 1.5 L would have been 58%. AP McKenzie also referred to other statistical reports which he claimed supported his opinion. He also disagreed with AP Bryant’s opinion that from 2014 the asbestos-related pleural disease was contributing to breathlessness and disability in the deceased. He maintained that the diffuse pleural thickening in 2009 was moderately extensive but not sufficient to cause any restriction of lung capacity. Further, he observed that there was nothing in the documents to suggest that any worsening of the pleural disease between 2015 and 2018 until the development of the pleural effusion in November 2018. He states that the cause of such pleural effusion has not been definitively diagnosed. He states that the deceased recurrent pleural effusion has many features which are not typical of asbestos-related pleural effusion. He concluded on the balance of probabilities that the diagnosis was an inflammatory (parapneumonic) pleural effusion following lower respiratory tract infection; that the surgical procedure and subsequent analgesic and palliative treatment worsened the deceased’s pre-existing respiratory failure and hastened his death.
Report 21 October 2021
In his report dated 21 October 2021, AP McKenzie referred to serial spirometry results which he extracted from documents provided to him. He said:
“The results show moderate airflow limitation. There was a small improvement in airway function between 2009 and 2014, and a decline between 2015 and 2017 FVC is at the low end of the normal range and is reduced because of airway closure during lung deflation (i.e., gas trapping). The latter conclusion is confirmed by results for total lung capacity in 2009 which were above predicted. There is no change in FVC between 2009 and 2015. The only measurements of pulmonary diffusing capacity were made in 2009 the showed severe impairment (about 40%)”.
Dr Anthony Johnson
Report 12 April 2021
In his report dated 12 April 2021, Dr Johnson expressed the opinion that on the material supplied to him, he considered it was likely that the deceased died from his respiratory disease.
“That is the emphysema, chronic obstructive pulmonary disease, diffuse pleural thickening, asbestos-related pleural effusion and rounded atelectasis. I consider that Mr Vescio’s extensive asbestos-related pleural disease significantly contributed to his death”.
Report 29 October 2021
In his report dated 29 October 2021, Dr Johnson considered whether kidney failure was a cause of the deceased death. Having considered the reports of associate Professor David McKenzie and of Dr Richard Singer, he observed of Dr Singer’s reports:
“He [Dr Singer] notes however, had he received dialysis to treat the kidney failure, it is unlikely to have extended his life significantly due to the severity of his respiratory disease.
For the reasons outlined in my previous report I think is more likely a benign asbestos-related pleural effusion rather than parapneumonic and in my opinion remains unchanged that the diffuse pleural thickening significantly contributed to his death.”
Professor Richard Fox, oncologist:
Report 20 March 2021
Professor Fox, medical oncologist, provided a report dated 20 March 2021. In his report he stated:
“I do not consider the pleural thickening and associated pleural effusion was causative of Mr Vescio’s death.
My reason for this is the underlying extent of his COPD and renal disease. The pleural effusion had been treated and did not appear to be an ongoing issue.
His death was a combination of his chronic obstructive pulmonary disease with an exacerbation of his renal failure.”
Associate Professor de Crespigny
Report 15 July 2020
AP de Crespigny provided a report dated 15 July 2020 in which he disagreed with the observations of Professor Fox that the renal ultrasound report dated 14 December 2017 showed atrophied kidneys. He said:
“Professor Fox’s report refers to an ultrasound showing “bilateral renal atrophy”. I do not have a copy of an imaging report that shows such a finding. Such an imaging appearance, usually an ultrasound or CT scan, would be unusual in diabetic nephropathy where often renal sizes are preserved, on occasions increased and sometimes mildly decreased. In this instance I consider the renal ultrasound report dated 14 December 2017 did not show atrophied kidneys. It should be noted Mr Vescio had mild to moderate proteinuria which was a little lower than is often seen in patients with diabetic nephropathy, but the low level may in part relate to his treatment with irbesartan. The attached Excel spreadsheet gives protein excretion levels which were mild to moderate which include a 24 hour urinary protein dated 15 February 2016 of 1.1 6G/day and 19 July 2016 of 0.8 1G/day. In my opinion, evidence for Renovascular disease has not been provided although cannot be excluded. In a diabetic with mild to moderate proteinuria and significant renal impairment, the most likely diagnosis is diabetic nephropathy.”
Having seen a report of a renal ultrasound dated 14 December 2017, AP de Crespigny stated:
“Given that Mr Vescio’s renal function had fluctuated but not significantly declined between the time of that ultrasound and final renal function tests I have reviewed from 22 December 2000, I consider his renal size would have been stable.”
Report 3 November 2021
In his report dated 3 November 2021 AP De Crespigny disagreed with Dr Singer, whose report is outlined at [79] below, that “kidney failure is the only reasonable explanation” for the myoclonic jerks exhibited by Mr Vescio a couple of days before he died; he states:
“In my opinion, there are multiple causes of myoclonic jerks; kidney failure is just one cause. Mr Vescio’s renal impairment was not severe enough to be likely to cause myoclonic jerks. He has comorbidities including respiratory disease, that can cause myoclonic jerks. Furthermore, I have not seen the result of a serum creatinine within a month of Mr Vescio’s death, which shows there was, in fact, a decline in his kidney function in the month prior to his death
…
In my opinion, there is no evidence that Mr Vescio’s renal function deteriorated in the two-year period before his death.
In my opinion, his renal function was remarkable for its apparent stability. At worst, there had been a slight decline in his renal function in the two-year period before his death. Renal function does decline with age.
With respect to pruritus and myoclonic jerks, renal function tests have not been provided that would usually be considered likely to be associated with the symptoms of pruritis and myoclonic jerks. In fact such a conclusion, in my opinion, would be unusual. Pruritis and myoclonic jerks are usually associated with more severe levels of renal impairment. In my opinion, it is more likely than not that Mr Vescio’s pruritis and myoclonic jerks did not relate to his renal impairment. It should be noted that end-stage renal failure can, and frequently is, associated with no pruritis or myoclonic jerks.
…
In my opinion Mr Vescio’s deteriorating respiratory condition, his hospitalisation for the same and the need for surgery (talc pleurodesis), may have resulted in an effect on his renal function but conversely, may have had no effect.
In my opinion, no evidence is provided that his respiratory condition, up to 22 December 2018, had a progressive effect on Mr Vescio’s renal function. In my opinion, he had relatively stable but severely impaired renal function as discussed in question 2 above. If his renal function had declined subsequent to 22 December 2018, it is more likely than not that it was consequential to his respiratory condition. Whilst progressive renal disease could develop, in the context of his comorbidities, it is more likely than not that any decline in renal function related to a worsening of his comorbidities or a complication of his comorbidities.
Dr Richard Singer, nephrologist
Report 10 September 2021
Dr Singer, consultant nephrologist, concluded in his report dated 10 September 2021:
“The condition diagnosed by me is end-stage kidney failure. On the balance of probabilities, I think this did significantly contribute to his death. I give significant weighting to the presence of uraemic (kidney failure) symptoms in the four or five months prior to his death as well as the presence of severe uraemic symptoms (myoclonic jerks) in the couple of days prior to his death. However, had he received dialysis to treat the kidney failure it is unlikely to have extended his life significantly due to the severity of his respiratory disease. I think on the balance of probabilities the kidney failure contributed approximately 50% towards the final cause of death.”
It should be noted that during the course of his oral evidence, Dr Singer did not consider that the kidney function tests were “catastrophic” as at 22 December 2018 as stated by Professor Fox (TP 152.5); he noted that there was no blood test that showed that the deceased had a deterioration of kidney function (TP 151:35); and stated that he would not have expected the deceased to die suddenly from kidney failure (TP 153.1).
THE HEARING

The hearing took place on 17 November, 18 November 2021 and on 29 and 30 March 2022 using the Microsoft Teams platform. On the first day of the hearing, AP Bryant, Dr Johnson, AP McKenzie provided concurrent evidence. The following paragraphs contain the summary opinions of the medical experts provided to the Tribunal during the concurrent evidence.
The experts agreed that a patient could have emphysema and COPD together with asbestos related pleural disease in the form of plaques, diffuse pleural thickening and pleural effusions simultaneously.
AP Bryant concluded that it was unlikely that the degree of obstruction to the deceased’s airways changed materially between 2009 and 2017. Dr Johnson agreed but AP McKenzie stated that it was not possible to say that the deceased’s lungs had deteriorated or otherwise based upon the two measurements of lung function recorded in 2009 and 2015.
Dr Johnson agreed with AP Bryant’s opinion that the deceased’s asbestos-related pleural disease, and diffuse pleural thickening, was a substantial contributor to his death. AP McKenzie disagreed, observing that there was no change in the lung function test between 2009 and 2015, and that the deceased’s pleural disease and diffuse pleural thickening in 2015 were not sufficient to cause any restrictive component to his lung function test.
AP McKenzie opined that there was no lung impairment in 2015 but the deceased was severely disabled as a result of his COPD and emphysema. In addition AP McKenzie said that the deceased had kidney disease, diabetes and other conditions, but that there had been no major change in those conditions other than from his pleural disease. There was, he said, no indication that the deceased’s pleural disease deteriorated between 2015 and 2018. However, the respiratory physician, Dr Lee, had records which showed that up until 2018 whilst the deceased’s COPD was stable, his oxygen levels were deteriorating. AP McKenzie agreed that there were pleural effusions in 2009 and pleural thickening which were caused by asbestos. AP McKenzie acknowledged that the deceased’s COPD had deteriorated between 2015 and 2018.
AP Bryant pointed out that there was evidence from x-rays which established the deceased’s pleural thickening worsened between 2014 and 2018 on the left side and accordingly there was deterioration in the diffused pleural thickening between those dates. AP Bryant considered that it was highly likely that his lung capacity was adversely affected.
Dr Johnson considered that in 2018 the large pleural effusion developed followed by worsening of the deceased’s diffused pleural thickening related to the effusion. Dr Johnson opined that the effusion, which appeared in approximately August 2018, worsened and was caused by asbestos exposure which made the deceased’s respiratory failure much worse and led to his death. However AP McKenzie considered that in August 2018 the deceased did not have a large pleural effusion; he was admitted to Manly hospital with an infective exacerbation of his COPD and emphysema. The admission was complicated by the development of atrial fibrillation which required treatment and anticoagulant; it was complicated further by significant exacerbation of his chronic kidney disease. On discharge he was treated by his treating respiratory specialist, Dr Philip Lee. Dr Lee observed that the deceased’s oxygen saturation worsened but there was no evidence that was actually due to any form of pleural disease.
In October 2018 the deceased was readmitted with a pleural effusion to Manly Hospital with what was believed to be pneumonia complicated by parapneumonic effusion. The effusion was tapped and the deceased was treated with antibiotics and reviewed by Dr Lee on 12 November 2018 at which time he was worse; the fluid had re-accumulated and he was readmitted on 13 November when further drainage procedures were conducted and the deceased was ultimately referred for a surgical procedure on 20 December 2018.
AP McKenzie acknowledged that there had been a significant change in the deceased’s condition resulting in his visits to Manly Hospital and that after that he went into a spiral which led to his death.
AP McKenzie considered that it was his severe kidney disease, his severe lung disease, the emphysema, and the surgery which contributed to his death on 12 January 2019.
Dr McKenzie acknowledged that the pleural effusions were more probably than not caused by asbestos exposure; and that the deceased asbestos-related pleural effusions were a contributor, and a significant contributor to his death.
Dr Johnson considered that the effusion had resulted in the worsening of the deceased’s diffused pleural thickening and that caused the deceased’s death; the respiratory failure resulting from pleural thickening that subsequently caused his death. AP Bryant agreed
The records of Dr Philip Lee (treating respiratory specialist) were before the Tribunal. Dr Lee wrote to Dr Matthew Horton (cardiothoracic surgeon) on 18 December 2019 and asked him for urgent assistance with the deceased. Dr Horton provided a letter to Dr Lee reporting on the advanced stage COPD of the deceased and of the fact that he was now oxygen dependent. Dr Horton arranged for a pleurodesis but due to technical reasons, only a thoracentesis could be conducted. He reported that 500 to 700 mls of bloodstained fluid was evacuated with negative cytology and the effusion had reaccumulated. He suspected mesothelioma may have been accountable. In his operation report at St George Hospital, Dr Horton refers to the admission of the deceased on 18 December 2018 with a view to draining the effusion again on 19 December 2018. His report states:
Under general anaesthetic with a double lumen endotracheal tube in position, a right two-port thoracoscopy was performed. There were quite significant adhesions between the lung and the chest wall and there was some thick white parietal pleura noted to be attached to the lung. There were also some clots within the pleural space. The line was partially mobilised away from the chest wall, although some of the adhesions were so dense that they were not able to be mobilised. A number of pleural biopsies were taken and some further fluid was taken for cytology. A small amount of talc was instilled in the pleural space posteriorly and basally. Apically (sic) the lung appeared well and truly adherent. A single intercostal catheter was inserted. Intercostal blocks were fashioned and Mr Vescio was taken back to the ICU in a very stable condition.
AP Bryant and Dr Johnson opined that, excluding cancer, infection and pneumonia, there was no other reason (for the deceased’s lung condition) other than asbestos exposure. AP McKenzie did not agree, stating that pleural effusions were common and there were many causes; that asbestos-related pleural effusions “are distinctly uncommon, even among people who are exposed to asbestos”. AP McKenzie stated that merely because the deceased had an asbestos-related pleural effusion in the past and because he had an asbestos-related pleural thickening, did not lead to the conclusion that he cannot “get a pleural effusion due to the myriad of other potential causes. So, I would disagree that the only possibility left for this man was asbestos. That is just manifestly not true.” AP McKenzie did not agree that asbestosis was the most likely cause, stating “it is in fact uncommon for asbestos -related pleural effusion is to be recurrent”
AP Bryant stated that in his experience pleural effusions occur not uncommonly in people with diffuse pleural thickening. Whilst such effusions are often not very large they can occur and result in significant respiratory restriction.
Dr Champion de Crespigny
AP de Crespigny confirmed that the ultrasound report of the deceased’s kidneys made on 14 December 2017 did not show atrophied kidneys. He stated that the deceased’s renal function had fluctuated but had not significantly declined between the time of the ultrasound and the final renal function test on 22 December; that whilst the function was not normal, the spreadsheet recording readings showed a “remarkably stable renal function. In fact, remarkable, I mean and I really do mean remarkable. Between November 2011 and the last creatinine I was given in 2018, it was somewhat extraordinary to me that someone with renal function was that stable”.
The records showed that the deceased had severe renal impediments in 2010 on the plasma creatinine tests. It appeared that, reading from the report of Dr Singer dated 10 September 2021, that the deceased experienced renal impairment. In 2020 the deceased’s plasma creatinine was 210 MC M0. With regard to eGFR, plasma creatinine test, it was 210 which AP de Crespigny said was “Less than a third of normal renal function. It’s severe renal impairment”
AP de Crespigny referred to the fact that the deceased’s renal function was fluctuating; that there was a reversible deterioration from some factor which could have been medication related, or endocrine infection; that there are a large number of reasons why the deceased could have a transient substantial decline in renal function which was not sustained. He acknowledged that the deceased’s renal disease would affect his life expectancy.
AP de Crespigny did not regard that uremic tinge was a reliable sign and observed that the deceased’s urea was not “very high at all.” As to the symptoms of nausea, occasional vomiting and significant pruritis, AP de Crespigny acknowledged that they were “the classical symptoms of near-end-stage renal failure which really requires you start dialysis and in the very near future, but in fact, they are also symptoms you can get the ulcers and other diseases such as peptic ulcer, various medications, antibiotics or whatever”. He noted that the deceased urea was sub - 20 which indicated the need for dialysis very soon. He explained that there were many vascular diseases with which renal diseases are associated; that the deceased’s renal disease would have affected him or contributed to his death but in an indirect way. He observed that there was a substantial improvement in the deceased’s test result from 11% function to 18% function; then to 20% function in the glomerular filtration rate (eGFR) of serum creatinine which gives a reflection of overall kidney function.
Dr de Crespigny considered that the most likely cause of the deceased’s kidney disease was diabetes, i.e. diabetic kidney disease. He also considered that there were many reasons for myoclonic jerking he said of the deceased:
“He had at least two diseases that can cause it. Kidney failure with urea that wasn’t high enough to cause it and respiratory disease which – I’m not a respiratory physician, no I have his carbon dioxide levels I can’t, and whether that was. And you do see it in people with no good explanation on occasion.”
A table of results showing the date, creatinine reading, eGFR and urea was tendered. It showed that from 2016 to 8 August 2018, creatinine was increasing; but thereafter the levels fell back to the levels which existed as at 2011 and were, according to Dr de Crespigny, relatively stable.
Dr de Crespigny stated (TP 89 line 38)) that on the data which he had been given:
“I don’t have evidence that renal failure caused his death. It may have contributed and I think there’s – which is hypothesis – there is actually no proof that it even contributed because there is no suggestion he had myocardial infarct or a stroke or a major vascular event but on – again, in probability, there is a reasonable chance he had a vascular – a major vascular event. But so – respiratory disease can predispose and the respiratory people need to talk to you about that…”.
Such opinion was confirmed (TP 92 line 39).
Professor Richard Fox
Professor Fox is an oncologist and has practised extensively in cases involving mesothelioma. It should be observed that all experts agreed that there was no evidence that the deceased’s death resulted from cancer or mesothelioma, nor was cancer ever detected in the deceased.
Professor Fox stated that he had experienced many lung cancer patients most of whom were all heavy smokers; that some claim to have asbestos exposure. In addition there are patients with pleural thickening and pleural plaques namely persons who have been exposed to asbestos. He said that pleural plaques have no relationship to the subsequent asbestos development of lung cancer. Pleural plaques are an indicator of some level of exposure. Pleural plaques are not fatal unless they develop mesothelioma which does not originate in a pleural plaque.
Dr Fox has been involved in the introduction of drugs for treatment which can cause renal damage such as Cisplatin. Similarly, Methotrexate. He has been following renal function very carefully in patients who have received such drug since 1970.
Dr Fox considered that the charting of the deceased’s renal function showed a progressive fall and by 2014 to 2016 it remained at less than 20. In 2018 namely, between June July and August, it was very low, 17, 18, 15 so that it was about a quarter of normal.
Approximately a month or two before he died there are no readings available. In 2008 it was 50% of normal renal function, but the function fell to 25% in 2018: there was a serious renal episode. Dr Fox referred to a letter from Dr Coleman, nephrologist who was caring for the deceased, that the deceased had “multifactorial stage 4 chronic kidney disease for conservative case care management.”
Dr Fox opined that such statement meant that the deceased was not suitable for a renal transplant. Dr Fox also referred to the fact that Dr Coleman had explained to the deceased’s son that the deceased had between 10 and 15% of renal function and was likely to deteriorate further. Dr Coleman also noted: “His prognosis was guarded and that he may succumb to his uraemia”.
Dr Coleman’s note dated 17 August 2018 stated:
his kidney function had deteriorated in the interim and he looks all of his 85 years and has a uremic tinge.
Professor Fox considered that this history conformed to the readings in the table that had been prepared by AP de Crespigny.
In cross-examination, it was put to Professor Fox that the table of readings showed that there was an improvement in the renal function of the deceased shortly before his death is as follows:
And then, if we get down that list, really up until 22 December 2018, Professor Fox, you’ll see – there’s a bit of variation – but generally speaking, the creatinine, eGFR and the urea were better than they were when Dr Coleman gave his dire prognostication. Is that a fair thing to say?
A little better, but they’re still catastrophic.
Professor Fox said “there’s really minimal recovery though – and we don’t have the levels after 22 December 2018. There still catastrophically low.”
Further questions were put to Professor Fox to show that there was an improvement when the deceased entered Manly Hospital with respiratory problems. It was put to Professor Fox that on 22 December 2018 there was an improvement in renal function:
Significant improvement?
It’s improved, but it was still catastrophically low.
Professor Fox agreed that the deceased probably had severe kidney disease from 2008; that it became worse in 2017; improved and then there was a significant deterioration through August 2018; thereafter by November 2018 went back to 15; then 18; and 16 in December 2018 “So it’s progressive deterioration”
Such conclusion was challenged. Professor Fox agreed that the renal function dropped significantly between March 2014 and August 2018 when it fell to 11, “and then there is some improvement”:.
So it has dropped significantly over that period of time. It shows you, with an interim lung infection, how significant that decreased. And then there is some improvement, but minimal, right through – and you’re not that far away, when you get down to late December, where it 17, which is a quarter of normal kidney function?
Yes
The records show that between June and August 2018 the deceased was admitted to hospital with a chronic obstructive airways disease with infection and “ that had a fairly significant impact on his renal function.” (TP 114)
Professor Fox agreed that the deceased’s renal function on 22 December 2018 “was slightly better than it had been on 20 July 2015”
It was then put to Professor Fox that there was no evidence that after 22 December 2018 that the deceased’s death was caused or contributed to by his renal function, and that there was no scientific evidence to support such a conclusion. Professor Fox replied that there was no scientific biochemical tests and that the deceased died at home but the features appeared to be that of a uraemic death. Professor Fox said:
“The observation is that he appeared clinically – which is pretty scientific, as far as pretty well everything we do – that his death was associated with renal disease. A man like this, as he ages, is only going in one direction”
Professor Fox agreed that myoclonic jerks can be a feature of end-stage respiratory failure but is more classically described with kidney disease. Nausea is a similar symptom.
Professor Fox said that the deceased had a high level of potassium on admission in November 2018 at the Mona Vale hospital at Northern Beaches; that the deceased had hyperkalemia, namely a very high serum potassium which is close to a fatal level and could cause cardiac arrest. He was given medication. It was put to Professor Fox that the levels in December 2018 as per the table showed the potassium level was “not too bad” the following question and answer I recorded:
if you look at this table…?
Oh yes. You mean in terms of renal function?
Yes. In terms of the potassium, which is just what you’re been talking about: 4.8, HCO3 26. That doesn’t indicate that he is about to die of renal failure, at least on 22 December 2018?
At that moment in time, yes”
Professor Fox said that high levels of potassium is a “potentially very significant part of renal failure.” (TP 118)
Professor Fox provided the following evidence:
So can I just put this to you, please, Professor Fox: other than the non-specific symptoms that could have been related to renal disease and could have been related to end-stage respiratory failure, there really is no other evidence to implicate this man’s death to renal disease after 22 December 2018; do you agree that?
No, because his death is clearly one of the problems of end-stage renal failure. You’re on a sort of tight rope and the balance can flick very rapidly one way or the other. The combination of this man’s gross respiratory disease and chronic obstructive airways disease and an episode of infection or disturbance could completely throw him into renal failure, and death was a combination of his respiratory disease due to chronic obstructive airways disease and end stage renal failure.
But that’s an hypothesis?
Well, that’s actually what happens in the real world with people with multi--comorbidities, the whole process goes with a series of comorbidities, and his two major comorbidities, apart from his diabetes and other issues, where his end-stage renal failure and chronic obstructive airways disease. (TP 118)
Professor Fox considered that the deceased was “lucky to survive the episode in August”. But he agreed that there was no evidence that the deceased’s renal function deteriorated after 22 December 2018 and caused his death:
But there is no evidence at all that this man’s renal function deteriorated after 22 December 2018 and caused his death?
No, apart from that what would be clinically predicted, a man in end-stage renal failure who deteriorates in the way that he has with his chronic obstructive airways disease would be the logical cause of death. When he gets an infection like that the renal failure goes right off, so…
Professor Fox acknowledged that his expertise is not in persons who have kidney disease, however he often encounters patients with kidney disease and/or cancer as well as kidney disease “with a lot of comorbidities in aged people”. He acknowledged that AP de Crespigny was an expert in treating kidney disease and that he (Professor Fox) did not have such specialist knowledge.
Dr Richard Francis Singer

Dr Singer disagreed with the opinion of AP De Crespigny. Dr Singer considered that the deceased’s respiratory disease was a significant contributor to his death but he had no opinion on the cause of the respiratory disease. Dr Singer considered that the history of the deceased showed a deterioration in his renal function and that is why he considered that renal function was a significant contributor to his death. He said:
“So, I think he had pre-existing severe kidney failure and his kidney failure was not particularly stable. There was quite a lot of fluctuation over the previous three years. At the time he was discharged, his eGFR, which is the standard way of measuring overall kidney function, was reasonable. It was 17. However, it’s not necessarily accurate in anyone, but particularly in him for the reasons I outlined in my report. And when he was discharged, he seemed from the notes I read, to be in reasonable condition and in two days before his death he was referred to palliative care and that point he had severe shortness of breath based on his respiratory rate, and he had a lot of myoclonic jerks and there had been a history before that of the weight loss and significant itchiness. And so, I think his kidney function had deteriorated, and the most likely reason for the deterioration, if indeed it has and we don’t have a blood test to prove it, is some co-morbidity and the most likely one would be some complication related to his respiratory condition and the previous surgery.”
Dr Singer agreed that myoclonic jerks could be caused by respiratory failure and by renal failure; or end-stage renal failure just before death.
Dr Singer acknowledged that the oxygen saturation in the two days before he died was not measured; and that there were no renal function tests after 22 December 2018. The following evidence was given:
Right. So, the extent that you have provided an opinion that the renal disease contributed to his death, you are doing so on the basis that he had severe renal disease for a long time?
Yes
He had symptoms that one might see with renal failure but also with respiratory failure?
Except for pleuritis.
Pleuritis is itchiness, is that right?
Yes
Can I put this to you, Dr Singer, you have no renal function evidence after 22 December 2008 into draw a causal inference between the renal disease and this man’s death. What do you say to that?
It’s true that I have no renal function test?
That’s correct. However, even in the presence of a renal function test it is possible to die from kidney failure and in fact I’ve seen people die from kidney failure with the creatinine that’s lower than Mr Vescio’s. So, there is an absence of evidence of a change in his kidney function and are making some assumptions based on his history and the symptoms that he had just prior to his death as to what happened.
Dr Singer agreed that the readings did not establish that renal failure was the cause of death. He said:
… Because merely having an eGFR of 11 is not sufficient to suddenly die.
That’s right. And of course, if you had an eGFR of 17 that would apply equally?
It would, as long as you know the context that it is measured in. And I think in the context of Mr Vescio, I would agree that a eGFR of 11 or 17 by itself is a handful of readings for a short period of time is not sufficient to say he died from kidney failure.
The following question was asked:
Would you describe his kidney failure as at this date, that is, the last recorded record we have as 22^nd December 18, would you regard his kidney condition to be catastrophic?
No (TP 152)
Professor Fox also said: “Yes, I wouldn’t have expected him to suddenly die from the kidney failure”.
SUBMISSIONS
The Tribunal was provided with written submissions by each party. In addition, two full days were allocated for the hearing of oral submissions.
The submissions of the respondent asserts that but for the disease or aggravation suffered, the death of the deceased would not have occurred at a significant later time as referred to in s 7(5) of the SRC act. The respondent relies heavily upon the expert evidence of Professor Fox and refers to the slowly progressive decline in renal function as was recognised by AP de Crespigny.
The respondent also relies upon the evidence of AP McKenzie, particularly his statement to the effect that Stage 5 kidney disease causes fluid retention which can severely exacerbate the impaired respiratory function in patients with COPD and emphysema. Further reliance is placed upon AP McKenzie’s opinion that recurrent pleural effusion has many features which are not typical of asbestos-related pleural effusion and his concluded view that the deceased’s pre-existing emphysema, renal failure and anticoagulant treatment probably contributed to the severity of the effusion and blood standing.
CONSIDERATION OF THE ISSUES
Was respiratory failure the cause of the deceased’s death?
Dr Johnson provided the following opinion:
“… I am of the opinion that his asbestos related respiratory disease i.e. the diffuse pleural thickening, pleural effusion and rounded atelectasis significantly contributed to his death. This is my opinion as there was relatively extensive diffuse pleural thickening on his radiology and in my experience, this amount of diffuse pleural thickening would have significantly contributed to his respiratory impairment and failure. The asbestos related pleural effusion resulted in him having to a have pleural drain, thoracoscopy and pleurodesis which worsened his diffuse pleural thickening. Was this not to have happened, it is very likely he would have survived for a significantly longer period. Therefore, in my view Mr Vescio’s death was attributable to his benign asbestos related pleural disease.”
AP McKenzie disagreed with the joint expert opinion contained in the report dated 25 August 2021 as follows:
“Prof Fox, Prof Bryant, Dr Johnson and I agree that Mr Vescio died as result of respiratory disease and respiratory failure. Prof Bryant, Dr Johnson and I also agree that the thoracoscopic surgical procedure and post-operative issues hastened his death. Prof Bryant disagrees with the other experts on the severity of Mr Vescio’s COPD and its contribution to the cause of death. The experts disagree about the extent to which the pre-existing asbestos-related pleural disease and renal failure contributed to his death.”
AP McKenzie provided his contrary opinion as follows:
“In my opinion, the most likely cause of death was Type II respiratory failure on the basis of underlying severe COPD and emphysema with analgesic and sedative medications acting as contributing factors. The renal failure may have contributed, but in my opinion, was not the prime cause of death. The tachypnea and myoclonic jerks are consistent with this conclusion.”
Dr Johnson agreed with the view expressed by AP McKenzie earlier that whatever the position was prior to 2017 regarding the relative contributions to impairment/disability from emphysema on the one hand and asbestos related pleural thickening on the other, “something changed in this man in 2018”. Dr Johnson described the nature of this change in Mr Vescio’s health in 2018, as follows:-
“Well, I think it was a large pleural effusion and then subsequent worsening of his diffuse pleural thickening related to that effusion and also then to his drainage of it and the biopsy and the thoracoscopy, the surgical procedure. So I think he developed a large effusion around August [sic: October] which worsened things and as a result of that effusion, which I consider to be benign due to asbestos exposure, that caused worsening of his diffuse pleural thickening and then I think that made his respiratory failure much worse and led to his death.”
AP McKenzie was asked if he agreed that if one left aside the issue of the likely cause of the pleural effusion, the presence of recurrent pleural effusions, the need for surgery, the pain killers that were given to him after the surgery, were “significant contributors to this man’s death?”. He said, “I agree with all of that except for when you said the need for surgery. I think the need for surgery could be debated… I think it was a difficult question, and I am not going to criticize it.” Dr McKenzie clarified that he would not have subjected Mr Vescio to surgery in December 2018 but he confirmed that regardless of that, the recurrent pleural effusion which started in October 2018 recurred in November and recurred again in December together with the surgery and its after effects led to Mr Vescio’s death, stating, “OK. Look, they contributed…”
AP McKenzie opined that “I think the surgery was probably the final straw together with post-operative pain and pain killers and so on.”
Importantly, AP McKenzie agreed with the proposition that “The pleural effusions, the findings of Dr Horton in his operation report, the need for pain killers after the surgery were a cause of this man’s death”, stating: “I believe so, yes. And I wrote that in my report.”
AP McKenzie also agreed that if the pleural effusions were more probably than not caused by asbestos exposure then he would agree that the deceased’s asbestos related pleural effusions were a cause of his death, he responded: “A contributor to his death.” When pressed further under cross examination, AP McKenzie agreed that the asbestos related pleural effusions would have been a “significant contributor to his death”.
Dr Johnson opined:
“I believe the pleural effusion in 2018 was caused by asbestos, and I say that for a number of reasons. We know that he had asbestos exposure, the characteristics of the fluid when it was analysed were that it was an exudate which means that it was not due to his kidney or heart problems. There was no infection found in the fluid, and there was no other cause found for that fluid and the diagnosis of benign asbestos related pleural effusions is basically a diagnosis of exclusion, so there is nothing specific about that fluid when you look at it, says this is from asbestos, but if you’ve got someone who had asbestos exposure, and you’ve looked through all the other causes and ruled them out, then that’s when we say, this is a benign asbestos related effusion. And I believe in this man that was the case. The other characteristic is that it recurred, and that would not have happened if that was due to pneumonia as we have discussed before. And then that effusion has resulted in worsening of his diffuse pleural thickening and I believe that has caused his death, the respiratory failure resulting from that and then that subsequently caused his death.”
AP Bryant agreed with Dr Johnson, stating as follows:
“Yes I do. I would also add that I haven’t seen any radiographic evidence of pneumonia in this man, and therefore I would be surprised if there was sufficient pneumonia that couldn’t be seen on an x-ray but was sufficient to cause what was quite a substantial pleural effusion. I haven’t seen evidence of significant infection in this man at the time that the pleural effusion became problematic in November. He didn’t have a temperature, he didn’t have an elevated white cell count. The only evidence I have seen which might have made one think about pneumonia was that there were crackling sounds on the lower part of the right lung. However, crackling sounds are very common in areas of rounded atelectasis, which this man had at the bottom of his right lung. So its my opinion that the diagnosis of pneumonia was likely to be incorrect, and that in fact he may have an exacerbation of his COPD, but that would not have caused the pleural effusion and we have no evidence, objective evidence, that this man had pneumonia causing the pleural effusion that subsequently led to his surgery.”
Further, Professor Bryant and Dr Johnson agreed that if the deceased had pneumonia that was of such clinical significance as to have caused an effusion, they would both have expected to have some kind of radiological evidence supporting the diagnosis of pneumonia. Dr Johnson explained that he could not find any evidence of pneumonia in Mr Vescio’s case, stating:
“No, and the radiographic features of pneumonia are what we call consolidations and that’s where part of the lung is full of fluid and infection, and on x-rays and on CAT scans it has a characteristic appearance and on reviewing his x-rays and CT I did not see evidence of consolidation. You can get a bit of collapse of the lung under the effusion, so the effusion is quite large, its collapsing a bit of the lung underneath it, which I think he had, but in pneumonia there are other things we see on the x-ray, things like air bronchograms which are characteristic features you see. And I did not see that on his x-rays or scans.”
Finding: Was respiratory failure the cause of death?
Based upon the above evidence, the Tribunal accepts the evidence of AP Bryant and of Dr Johnson concludes that asbestos exposure caused an asbestos-related pleural disease, or at least can contributed to, the deceased’s death.
Did the deceased suffer infection or pneumonia?
The Tribunal refers to the above extracts from Dr Johnson’s evidence that there was no indication of pneumonia in the deceased. Further, Dr Johnson said that the recurrent nature of the effusions in 2018 were not characteristic of pneumonia.
Importantly, Dr Johnson testified that the fact that Dr Lee referred the deceased to Dr Horton for consideration of pleural surgery. Such treatment was inconsistent with Dr Lee having formed the view that Mr Vescio’s effusions were due to pneumonia. Dr Johnson said:
“No. you would not refer someone if you thought this was for recurrent pneumonia. I mean, you would know that from your scans and you would see they’ve had pneumonia and you would be treating that, so that was not the case. Your referring then because this fluids coming back, I don’t know what the cause is, they have had asbestos exposure, I am worried he might have cancer in there and he needs to know that and I need to know that as well.”
Professor Bryant agreed with Dr Johnson’s opinions. When Professor Bryant was asked to comment upon the proposition regarding Dr Lee’s actions that had been put to AP McKenzie he said:
“I would understand from the referral letter that it was the impression of the treating doctor that there was an asbestos related problem causing this man’s pleural effusion, that he didn’t attribute it to pneumonia but he attributed it to mesothelioma or a related issue.”
There is no evidence that the deceased had any infection, empyema or puss. The clinical notes of the final hospitalisation record that the deceased was discharged with a course of antibiotics. However, the pathologist report does not record any infection.
Dr Johnson was taken to the operation report of Dr Matthew Horton, cardiothoracic surgeon. Dr Johnson was asked, in the absence of any mention by Dr Horton in his operation report of infection, empyema or puss, what conclusions one was able to draw about whether there was any evidence of infection observable in the operation. He said:
“I believe that’s unlikely to be an infection, given that, yes.”
Dr Johnson agreed that if Dr Horton had found any evidence of infection or pneumonia that might be responsible for the effusions and the pleural thickening that is something that as a surgeon, he would put in the operation report. Professor Bryant agreed with Dr Johnson.
Importantly, AP McKenzie agreed that if Dr Horton had found evidence of pneumonia or infection or puss at operation, that is something that he would have almost certainly recorded in his operation report because of its importance in the future treatment of Mr Vescio, stating : “Yes, I would expect him to.”
There is no mention of pneumonia, infection or puss in Dr Horton’s operation report. A hospital record of Manly Hospital made on 8 October 2018 made a reference to “community-acquired pneumonia” however such a provisional diagnosis was found to have no factual basis. Similarly, other references to the deceased having contracted community-acquired pneumonia were never substantiated. Neither Dr Lee nor Dr Coleman were required to give evidence. In the circumstances, the conclusions drawn that they had no information to verify that the deceased was suffering from pneumonia at any critical stage.
In cross examination, AP McKenzie was cross-examined upon the absence in his report of any statements which suggested the deceased was suffering from pneumonia:
“MR TZOUGANATOS: I see, I see. In your reports, throughout the course of this case, you identified two differential diagnosis as potential causes for this man’s recurrent pleural effusions when one of them, pneumonia infection, is absent because of the absence of evidence of those. Then, you would have to reconsider your opinion and look at other causes other than asbestos, is that what you’re saying?
DR MCKENZIE: That is what I am saying.
MR TZOUGANATOS: I see. Why didn’t you put that in your reports?
DR MCKENZIE: I don’t know.”
The Tribunal accepts the evidence that the presence of fluid outside the lung was indicative that the deceased did not have pneumonia. Dr Johnson opined that, based on the CT scan of 16 October 2018, the fluid or effusion found in the deceased was only outside the lung and in the pleura. There was no evidence of fluid or “consolidation” inside the deceased’s lungs. Dr Johnson said: “It's fluid outside. Now if you've got a pneumonia or some illness in your lung, you will see fluid and other things in your lung. But a pleural effusion is referring to fluid just outside the lung.”
When he was taken to the report of radiologist of the CT scan on 16 October 2018 Dr Johnson said:
So it's not - what we're looking for in pneumonia is a term called consolidation and that is what you see in pneumonia, so you see a part of the lung, sort of, drowned in fluid and infection. And it's not mentioning that, I don't know if it goes further down to the next page.
Yes, so the doctor that reported it, in comment, that third paragraph, the major abnormality is a large right sided pleural affusion. They thought that the opacity, or the things they were seeing in the lung itself, was probably around atelectasis. So they haven't commented on consolidation or pneumonia, they haven't described seeing that.”
As to community acquired pneumonia, Dr Johnson said:
“No, I don't think it was because it was persisting and in retrospect, as we've been through - when we gave evidence last time and now, in hindsight I think it's unlikely that that effusion that he went to hospital with in November was due to pneumonia and the reasons for that are at the CT scan that we went through did not show consolidation, which is the term we use of what you see on the scan for pneumonia. The analysis of the fluid didn't show the infection but the most important thing, I think, is that the fluid didn't go away and if that fluid, when he went to hospital in October, was due to pneumonia, it should've got better with the pneumonia getting better and treated, but it didn't, and that's what caused Dr Lee to be concerned because that indicates that it likely was not parapneumonic effusion or an effusion from pneumonia. It was likely something else caused it, which is why he's doing further tests and then sends him to a surgeon, Dr Horton. If he thought that that effusion or fluid was due to pneumonia he wouldn't have done those things, you wouldn't normally send someone to a surgeon to have an operation on an effusion if you thought it was due to pneumonia”.
AP McKenzie conceded that in his report he had confused the deceased’s two admissions in 2018 and had assumed erroneously that the fluid from the effusion had not been tested. The evidence established that such fluid had been tested, and that it revealed no pathogens or infection. AP McKenzie also conceded that the deceased did not have a fever when he was admitted to hospital in 2018 with the pleural effusions, but said that people with renal failure and diabetes may not have a fever even with severe infection. However, such opinion is not contained in his reports. Neither is his later contention that there might have been some kind of different form of pneumonia where there is no consolidation or fluid in the lung (T.214.26-44). The Tribunal finds AP McKenzie’s evidence on this subject to be speculative as he had not reviewed Mr Vescio’s radiology after 2009.

Dr Johnson agreed with Professor Bryant’s view that it was improbable that Mr Vescio had pneumonia.
In his oral evidence, AP McKenzie said:
“Sorry, if it was an asbestos-related pleural effusion I would have expected to see a lot of mesothelial cells in the fluid. So mesothelial cells are these cells from the pleura. My recollection is, and I don't have that pathology report in front of me right now, but my recollection is that there were mainly white cells, red blood cells and very few, if any, mesothelial cells.” [TP 66]
AP McKenzie’s recollection was erroneous. The pathologist Dr Juliette Byrne found mesothelial cells and recorded her observations as follows:
“The features are regarded as those of florid mesothelial proliferation."
When this was put to Dr McKenzie, he appeared uncertain about which pathology report he was referring to, and appeared not to have noticed nor read Dr Byrne’s report of 21 December 2018 following the surgery conducted by Dr Horton as a result of Mr Vescio’s recurrent effusions.
Professor Bryant and Dr Johnson were asked for their views on whether Mr Vescio had pneumonia in October 2018 as the cause of his recurrent effusions. Dr Johnson said:
“I think I've been through this previously but on reviewing the records of that admission and the files, I think it's unlikely that he had pneumonia for the reasons I've said. I don't think the CT showed consolidation. He didn't get better with antibiotics, the fluid recurred and then stayed for some time, and that's not consistent with a parapneumonic effusion. So I think looking at the material I have that it was unlikely that it was a parapneumonic effusion.”
Professor McKenzie ultimately agreed that there was no evidence of consolidation (fluid collection that might signify infection/pneumonia) on the deceased’s CT scans. He also testified that that “…the literature reports indicate that about 50 per cent of asbestos-related pleural effusions are blood stained”. The deceased’s recurrent pleural effusions were in fact heavily blood stained.
Finding of pneumonia or infection causing death
The Tribunal finds that at the date of the deceased’s final discharge from hospital and thereafter, there is no evidence that the deceased was suffering from pneumonia nor from any lung infection.
Was the Deceased’s Death Attributable to Renal Failure
AP de Crespigny stated in his report of 9 May 2020:
“The disability is attributed to his respiratory disease and in my opinion, I would not consider his disability relates to his renal disease at that time on the basis of his renal function. The reason for that summation is there is no evidence provided to support that his renal function was significantly worse than it was in 2016 at which time his creatinine was documented as being 290 μmol/L. Although I have not documented in the attached flowsheet, his haemoglobin at all times was not profoundly low and it would not have explained his lethargy. Significant anaemia is often associated with chronic renal impairment; however, in my opinion, Mr Vescio’s haemoglobin was not reduced to a degree that it would be expected to cause symptoms.”
AP de Crespigny stated that there were multiple causes of myoclonic jerks which were evident in the deceased’s condition. AP de Crespigny said, “kidney failure is just one cause.” He did not consider that the myoclonic jerks were a result of any kidney failure. He also observed:
In my opinion, he had relatively stable but severely impaired renal function as discussed in question 2 above. If his renal function had declined subsequent to 22 December 2018, it is more likely than not that it was consequential to his respiratory condition. Whilst progressive renal disease could have developed, in the context of his comorbidities, it is more likely than not that any decline in renal function related to a worsening of his comorbidities or a complication of his comorbidities.
AP de Crespigny was asked to comment upon Dr Coleman’s letter dated 17 August 2018 relating to the deceased’s renal condition, and responded:
“So, there was a significant deterioration, it was a reversible deterioration from some factor, which could have been medication related, he could have had an endocrine infection, he could have gone on new anti-hypertensive that effects kidney functions. For various reasons, I actually don’t think that’s true, but there are a large number of reasons why he could have had that transient substantial decline in renal function which was not sustained. You also asked me and again I am very aware (indistinct) and not volunteer information. You did sort of imply that you wanted me to comment on his cause of death in the long term as a result of all this and what his kidneys might add to it…”
As to the use of dialysis, AP de Crespigny said:
“We normally – you don’t start people on dialysis for creatinine. You start it for urea or potassium or acidosis which I won’t bore you with that unless you want me to but its irrelevant to him because they weren’t bad. So he was going to start dialysis – you’d start him on dialysis with urea somewhere between 30 and 45. Typically I’d actually be starting between 35 and 40. He was no-where near that.”
The deceased’s renal function in fact continued to improve including on the last available tests that were performed on 22 December 2018. In respect of these tests, Professor De Crespigny explained that “… the blood tests don’t reflect it and they don’t reflect the man whose about to start dialysis.”
On the basis of the renal test results, Professor De Crespigny disagreed that the deceased had end stage kidney failure. He explained “I haven’t got any tests so – I don’t – I have no tests that shows to me that he has got end stage renal failure. He’s got severe renal impairment.”
Professor De Crespigny was asked the following question:-“If you took out of the equation his respiratory illness which we know was substantial, if you took that out of the equation do you see renal failure causing his death alone?” He answered:
“On the data I have been given, I don’t have evidence that renal failure caused his death. It may have contributed and I think there’s – which is hypothesis – there is actually no proof that it even contributed because there is no suggestion he had a myocardial infarct or a stroke or a major vascular event …”
As to the life expectancy of the deceased as at 22 December 2018 from a purely renal function perspective AP de Crespigny said:
“If he was sitting in front of me I would say I’d find your kidney function quite extraordinary (indistinct) to a patient today – it has not declined in many years which I would have never predicted if I’d seen you 10 years ago but at the moment its not going off and you’re really – except that you’re older, you are in no worse situation than you were about 10 years ago … so if he was on dialysis I can give you figures and he is going to be better than these figures so I would therefore tell you that he’s got – because he’s on dialysis, he’s got 3.1 years, so half of 6.2. Then I am going to half 3.1 again because he has got diabetes. So I am down to 1.55 years because he is on dialysis. Then I will say to you, he is not on dialysis. In fact – so he’s got to be substantially better than that. What do I mean by substantially better? I guess somewhere between 1.55 and 3.1. But ask 10 nephrologists and they’ll give you a different answer but I don’t believe anyone will tell you less than 1.55 years.”
Dr Singer made assumptions based upon the history and symptoms of the deceased prior to his death. When the EGFR reading was 11, Dr Singer would not ascribe renal failure as a cause of death had the deceased died at that time. Ultimately, Dr Singer agreed that there was no evidence that severe kidney failure caused the deceased’s death.
Dr Singer disagreed with Professor Fox’s opinion that the results of the renal function test for the deceased on 22 December 2018 was “catastrophic” and agreed that he would not have expected the deceased to die suddenly from kidney failure.
As to life expectancy, Dr Singer confirmed that from the point in time when a person was commenced on dialysis due to kidney disease “… the median survival for an 85 year old starting dialysis in Australia is just over 2 years ignoring any co-morbidities.”
Renal function results
During the hearing, a table was produced of the renal function readings containing data of creatinine, eGFR, urea, potassium and protein of the deceased. The readings in table commenced on 23 July 2008 and continued until 22^nd of December 2018. In summary, the nadir of the deceased’s kidney function occurred on 8 August 2018 (creatinine 394) but had improved thereafter. On 26^th of October 2018 the creatinine reading was 324; 13 November 2018 such reading was 248. The readings fluctuated that as at 22 December 2018 the reading for creatinine was 275. The table recorded readings which are more favourable than those taken in 2015.
Finding relating to renal failure
The Tribunal considers that the opinion of AP de Crespigny is to be accepted. Significantly, the respondent’s nephrologist, Dr Singer, agreed that he would not have expected the deceased to die suddenly from renal disease, stating (TP are 148.29 – 34):
“… because merely having an EGFR of 11 is not sufficient to suddenly die”.
And later:
I would agree that an EGFR of 11 or 17 by itself is a handful of readings for short period of time is not sufficient to say that he died from kidney failure” (TP 148:35 – 39)
As already referred to, Dr Singer did not consider that the readings as contained in the table were “catastrophic”. Such term was used by Professor Fox to describe the deceased’s renal condition. However, since Professor Fox’s expertise is that of an oncologist, and not a nephrologist, the Tribunal prefers the evidence of the nephrologist experts that renal failure was not the cause of the deceased’s death. Insofar as AP McKenzie provided evidence, in relation to renal failure, the Tribunal prefers the evidence of the qualified nephrologists.
The Tribunal raised for consideration with AP De Crespigny the possibility that the deceased’s death resulted from renal failure (TP 92.25). AP De Crespigny responded:
That arose because of Dr Singer’s opinion that the end stage kidney failure as he says did significantly contribute to his death.
Do you say that on the evidence you have that any renal problems he had did not cause his death?
I can’t say that they didn’t cause it. I can say I haven’t got scientific data to support that they caused it but for example, if he wasn’t drinking, he could have had a very high potassium and had – his heart could have stopped because he had gone into kidney failure. He had a high potassium and he wasn’t dialysed. All he could have had an extremely high urea and there are complications relating to your heart from that.
But absent those facts – because we just don’t know what the position was, – is there any evidence that renal failure caused his death?
No
Is there any evidence that renal failure contributed to his death?
Not with respect to him. On a population basis, yes, but with respect to him there is no evidence that it contributed.
The evidence also establishes from these experts that the deceased could have been expected to live for approximately two years after commencing dialysis. The deceased had not been placed on dialysis. Whilst there is evidence establishing that the deceased’s kidney function was impaired, he may have been able to continue without dialysis for an extended period and even then, he would have had a life expectancy of two years. The deceased was able to continue without dialysis. It was wholly speculative as to the time of his requiring such treatment.
Cause of Death
The Tribunal, having eliminated other possible causes of death, accepts the evidence of AP Bryant, and Dr Anthony Johnson, that the deceased’s death resulted from a number of comorbidities, which included as significant contributors the diffuse pleural thickening, rounded atelectasis and recurrent pleural effusions resulting from the deceased’s exposure to asbestos.
The Tribunal was assisted by the expert evidence of AP McKenzie, but prefers the evidence provided by AP Bryant and Dr Johnson. This is because of a number of disadvantages that AP McKenzie had in considering the deceased’s position compared to the other experts, including: he had not viewed any recent scans of the deceased; that his factual assumptions in certain important respects were not established; whilst he considered that there was a real possibility of infection or pneumonia as a factor which caused the deceased respiratory distress, the facts show that there was never any medical evidence to support such a theory. The Tribunal acknowledges that AP McKenzie was also disadvantaged because the deceased had never been treated by AP McKenzie, whereas AP Bryant had the benefit of examining and treating the deceased for many years.
LEGAL PRINCIPLES
The applicant’s claim is brought pursuant to the provisions of ss 14, 17 and 18 of the SRC act which relevantly states:
Compensation for injuries
(1) Subject to this Part, Comcare is liable to pay compensation in accordance with this Act in respect of an injury suffered by an employee if the injury results in death, incapacity for work, or impairment.
Section 17(4) provides a right to recover compensation for dependents, and s 18 relates to compensation for funeral expenses.
The definition of “injury” is contained in s 5A and relevantly define such term as including:
(a) a disease suffered by an employee; or
(b) an injury (other than a disease) suffered by an employee, that is a physical or mental injury arising out of, or in the course of, the employees employment; or
(c) an aggravation of a physical or mental injury (other than a disease) suffered by an employee (whether or not that injury arose out of, or in the course of, the employee’s employment), that is an aggravation that arose out of, or in the course of, that employment;…
Section 7 contains provisions relating to diseases. Relevantly, subsection (5) provides:
The death of an employee shall be taken, for the purposes of this Act, to have resulted from a disease or an aggravation of a disease, if, but for that disease or aggravation, as the case may be, the death of the employee would have occurred at a significantly later time.
The approach to be taken in applying the provisions of ss 4(1), 5 and 5A of the SRC act has been stated in Military Rehabilitation and Compensation Commission v May [2016] HCA 19, especially at [49] – [52]. In summary in determining whether the employee is suffering from a “disease” or an “injury (other than a disease)”, there must be a consideration of the following:
i.Does the evidence amount to something that can be described as an “ailment”, being a physical or mental ailment, disordered defect or morbid condition?
ii.If so, was that state contributed to a material degree by the employee’s employment?
iii.If there is not a “disease” within paragraph (a) of the definition of “injury”, the Tribunal must determine whether there is an “injury (other than a disease)” within paragraph (b);
iv.Does the evidence demonstrate the existence of a physical or mental injury?.
The respondent submits that the evidence, at best, establishes that the applicant suffered from a “disease”. The applicant submits to the contrary, namely that the evidence establishes that an “injury” was sustained by the deceased.
In Comcare v Starkey [2017] FCAFC 151, the Full Court considered the circumstances in which an employee had suffered asbestosis. The Full Court said, inter alia, at [27]:
The injuries to Mr Starkey resulting in his death for the purposes of s17 of the SRC act were the inhalation and retention of asbestos fibres. It is not in dispute that 80% of Mr Starkey’s injuries were received while he was working for the Commonwealth.
Their Honours continued:
As Professor Breslin further explained, “all periods of exposure contribute to the development of asbestosis and this occurs not so much because of an interaction between the separately inhaled fibres but rather because of separate reactions dealing with each fibre contravening reactive oxygen species which added together may produce asbestosis…
Whilst the deceased did not suffer from asbestosis, the evidence has established that he suffered pleural thickening leading to his consequential death as a result of his exposure to asbestos. The Tribunal accepts the applicant’s submissions that this constituted “an injury in the primary sense”: see Wuth v Comcare [2022] FCAFC 42 at [106] where Wheelahan J said (referring to the observations of Gageler J in May):
I do not consider that Gageler J described an “injury” in materially different terms at [75] in stating –
An injury, it has long been repeatedly explained, is some definite or distinct “physiological change” or “physiological disturbance” for the worse which, if not “sudden” is it least “identifiable”.
At [76], Gageler J distinguished an “injury” involving a definite or distinct physiological change in the above sense from “any alteration from the functioning of a healthy mind or body”.
The evidence establishes that the deceased was exposed to asbestos fibres which resulted in a physiological change to his body. Accordingly, adopting the reasoning above, and of the Full Court in Starkey, the Tribunal finds that the deceased suffered “an injury (other than a disease)” as defined in s 5A of the SRC act.
It should also be observed, as a separate matter, that even AP McKenzie acknowledged, that the ultimate surgery of draining the deceased’s pleural fluid was a contributor to his death and in this sense, the surgery itself could have resulted in the finding that an “injury” was sustained by the deceased.
Irrespective of the finding that the deceased suffered an “injury (other than a disease)” the Tribunal considers that the circumstances of the deceased’s condition was such that the definition of “disease” was also satisfied. However, it is unnecessary to make any final finding in view of the fact that the Tribunal is satisfied that an “injury (other than a disease)” was sustained by the deceased. It follows that the reliance by the Respondent upon s 7(5) of the SRC act becomes otiose.
Nonetheless, the Tribunal considers it prudent to record that even if the deceased’s injury were to be considered as an injury arising from a disease in the sense of s 5A(a) of the SRC Act, s 7(5) of the act would be satisfied. There is evidence from the medical experts, in particular the nephrologists AP de Crespigny and Dr Singer, that the deceased could have expected between one and a half and two more years of life after beginning such dialysis, which he had not yet been placed on. In view of this evidence, the Tribunal considers that the deceased’s death would have occurred at a significantly later time were it not for the asbestos related lung deficiencies.
CONCLUSION
In view of the above findings, the Tribunal finds that the deceased suffered an injury (other than a disease) within the meaning of s 5A(b) of the SRC Act. The deceased’s employment with the Respondent caused or contributed to, to a significant degree, such injury. The Tribunal finds that the deceased’s death resulted from his many comorbidities, substantially contributed to by asbestos-related pleural disease in the form of diffuse pleural thickening, rounded atelectasis and asbestos-related recurrent pleural effusions.
DECISION
The Tribunal decides that the decision under review be set aside and substituted with the decision that the respondent is liable to make payments of compensation to the applicant pursuant to sections 17 and 18 of the Safety Rehabilitation and Compensation Act 1988 (Cth).

I certify that the preceding 198 (one hundred and ninety-eight) paragraphs are a true copy of the reasons for the decision herein of The Hon. Dennis Cowdroy AO QC, Deputy President

.................................[SGD].......................................
Associate
Dated: 26 May 2022

Date(s) of hearing:

17 & 18 November 2021, 28 January 2022, and 28 & 29 March 2022

Counsel for the Applicant:

Mr S Tzouganatos

Solicitors for the Applicant:

Ms A Zervos, Turner Freeman Lawyers

Counsel for the Respondent:

Mr J Wallace

Solicitors for the Respondent:

Ms E O'Connor, Sparke Helmore

Date(s) of hearing:	17 & 18 November 2021, 28 January 2022, and 28 & 29 March 2022
Counsel for the Applicant:	Mr S Tzouganatos
Solicitors for the Applicant:	Ms A Zervos, Turner Freeman Lawyers
Counsel for the Respondent:	Mr J Wallace
Solicitors for the Respondent:	Ms E O'Connor, Sparke Helmore