WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 2610/08

Transcription

1 WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 2610/08 BEFORE: M. Crystal : Vice-Chair B. M. Young : Member Representative of Employers J. A. Crocker : Member Representative of Workers HEARING: December 4, 2008 at London Oral hearing Post-hearing activity completed on June 4, 2009 DATE OF DECISION: August 14, 2009 NEUTRAL CITATION: 2009 ONWSIAT 1899 DECISION UNDER APPEAL: WSIB ARO decision dated April 26, 2005 APPEARANCES: For the worker: For the employer: Mr. B. Davis, Office of the Worker Adviser Did not participate Workplace Safety and Insurance Appeals Tribunal Tribunal d appel de la sécurité professionnelle et de l assurance contre les accidents du travail 505 University Avenue 7 th Floor 505, avenue University, 7 e étage Toronto ON M5G 2P2 Toronto ON M5G 2P2

2 Decision No. 2610/08 REASONS (i) Introduction [1] This appeal was heard in London, on December 4, The worker appeals the decision of Appeals Resolution Officer (ARO) N. Kissoore, dated April 26, That decision determined that the worker s estate was not entitled to survivor s benefits on the basis that his death was unrelated to his compensable asbestosis. [2] The worker s estate was represented by Mr. Brent Davis, Office of the Worker Adviser. The worker s daughter appeared and testified at the appeal hearing. The employer did not participate in the appeal. [3] After the appeal hearing was completed, the Panel referred certain questions, relating to whether the worker s compensable asbestosis contributed to his death, to a Tribunal Medical Assessor. The Assessor, Dr. Michael A. Hutcheon, respirologist, prepared a report dated March 18, 2009, addressing the Panel s questions. The Panel s questions and the content of the report will be described in greater detail below. Following an opportunity to review Dr. Hutcheon s report, Mr. Davis provided written submissions, dated May 22, (ii) The issues on appeal [4] The sole issue to be addressed in this appeal is whether the worker s estate is entitled to survivor s benefits on the basis that his death was related to his compensable asbestosis. (iii) The evidence [5] After completing the hearing for this appeal, on December 5, 2008, the Panel prepared a memorandum to Tribunal Counsel Office (TCO), to advise that it wished to obtain further medical information in relation to this appeal from a Tribunal Medical Assessor. The memo provided a brief summary of the case. It stated: The Panel completed the hearing portion of this appeal yesterday. The case concerned a worker who died on July 17, The estate is seeking survivor benefits. The employer is not participating in the appeal. According to a Discharge Summary, dated July 17, 2003, prepared by Dr. Kenneth Yoshida, specialist in internal medicine and medical oncology, the worker s Final Diagnosis prior to autopsy was respiratory failure, aspiration pneumonia, Parkinson s disease and degenerative lower motor neuron disease, asbestosis. Subsequent to his death, a diagnosis of occupational asbestosis was confirmed, and the Board granted the worker entitlement, including a non-economic loss (NEL) award, for the asbestosis. The issue to be determined in this appeal, is whether the worker s estate is entitled to survivor benefits on the basis that the worker s death was related to his compensable asbestosis. As noted, entitlement for asbestosis was allowed by the Board and is not an issue in this appeal. According to the medical information included in the case materials, in the last portion of his life, the worker suffered from dementia and a neurological condition which affected his speech and his ability to swallow food and liquid. At the appeal hearing, however, the deceased worker s daughter testified that she did not believe that her father suffered from dementia, and that he stopped talking only in the last few months of his life. The deceased worker s daughter also testified that: Even before the 1990 diagnosis of pleural plaques in the worker, the worker suffered from frequent colds, and complained frequently of feeling blocked up ;

3 Page: 2 Decision No. 2610/08 The day that the worker died, Dr. Mendoza, the worker s treating respirologist, made a comment to the family to the effect that the worker s asbestosis was taking over or that his asbestosis was a contributing factor in his death; The statement made in the January 21, 2003 report prepared by Dr. J. Muhunthan, the worker s treating neurologist, was not accurate, in that the worker did not require 24 hour supervision, as stated in the report. The worker s daughter testified that the worker was generally able to dress and wash himself, although he needed to be watched while eating, to ensure that he did not place too much food into his mouth. She agreed, however, that during the last few months of his life, the worker required more supervision. An autopsy was performed on the worker, however, the autopsy only investigated the worker s chest cavity and respiratory condition, and a diagnosis of asbestosis was confirmed. The brain and spinal cord were not part of the autopsy, and therefore the autopsy did not shed light on the worker s neurological condition. It was noted in the hearing ready certification letter, dated August 29, 2008, that MLO the Tribunal s Medical Liaison Office had reviewed the file and that MLO recommended to the Panel that an Assessor in neurology be asked to review the case materials and provide further information regarding the worker's condition. Having completed the conduct of the hearing, we have determined that further medical information about the worker s condition would be helpful, and that the case should be referred to an Assessor. We are seeking your assistance in that regard. After reviewing the case materials and hearing evidence from the deceased worker s daughter, however, the Panel has concluded that the Assessor should be a physician who has special expertise in the fields of both respirology and neurology. If an Assessor with this type of expertise cannot be obtained, the Panel may wish to have the matter reviewed by both a respirologist and a neurologist. In this case, the Panel believes that it might be more practical to have the review performed by a respirologist first, and to allow the Panel to determine whether a further review by a specialist in neurology is required. The Panel has reviewed the questions proposed in the hearing ready certification letter. We have revised and added to the questions. We would like to pose the following questions to the Assessor(s): 1. What effect did the worker s asbestosis have on his neurological or respiratory difficulties at the time of his death? 2. Please comment on the nature of this worker's neurological condition. a. What effect would the worker's neurological condition have had on his respiration? b. Are you able to estimate its impact on the worker's ventilatory function and his lung volumes? Please explain. 3. Please comment on the cause of the worker's death. Is it medically reasonable to attribute the worker's death to the consequences of his neurological illness? Is it likely that the worker s death was caused by the combined effect of his asbestosis and any neurological condition? Please explain the reasons for your opinion. 4. Is there any other medical information, which you feel would be of assistance to the Panel or Vice-Chair and parties in understanding the nature and aetiology of the worker's condition or the cause of his death? There was no evidence presented in the appeal in relation to the worker s level of exposure to asbestos, however, since entitlement for asbestosis is not in dispute and the issue under appeal is whether the worker s asbestosis significantly contributed to his death, the Panel expects that this will be determined primarily on the basis of the medical

4 Page: 3 Decision No. 2610/08 evidence. Accordingly, the Panel will not be releasing an interim decision in this appeal. We expect that the Assessor(s) report(s) will be based primarily upon his or her interpretation of the medical evidence included in the case materials, and we believe that the Assessor(s) would not benefit from a further summary of the medical evidence by the Panel. Please take the necessary steps, including obtaining the necessary consents from the worker s estate, to refer this matter to the appropriate Assessor(s). Please let us know if you require any further direction. Thanks for your assistance. [6] MLO identified Dr. Hutcheon as the Tribunal Medical Assessor in this case, and the Panel s memo was referred to him along with the case materials, for his review. Dr. Hutcheon subsequently provided his report on the matter, dated March 18, 2009, which is set out below. The report responded to the questions posed by the Panel. In his report, Dr. Hutcheon reproduced the questions, and they have been italicized below, for the purpose of highlighting the questions. The report stated: I have reviewed the file of [the worker] and will attempt to answer the questions that you have raised. 1) What effect did the worker's asbestosis have on his neurological or respiratory difficulties at the time of his death? There is no doubt, of course, that this worker had asbestosis. The CT scan that was carried out on 26/08/2002 demonstrates absolutely characteristic calcified pleural plaques. It also demonstrates some interstitial changes, particularly in the basal regions. In addition, the post-mortem examination showed interstitial lung disease with ferruginous bodies, once again consistent with asbestosis. I note that on a chest radiograph from December 18, 1996, significant abnormalities were documented: There are extensive old, thickened pleural plaques seen on both sides with some pleural calcification. Pulmonary function studies in 1997 were normal in terms of lung volumes and flow rates, with a slight decrease in diffusing capacity. The first chest radiograph available for review is from 12/03/2003 and this demonstrates extensive pleural disease. Lung volumes, on the other hand, are relatively well preserved. I suspect that, in the absence of further exposure to asbestos, these findings have been relatively stable through this period of time. Pulmonary function studies are available from May 24, These demonstrate an apparent decrease in vital capacity. However, I do not think that these are likely to be reliable. Accurate lung function testing requires significant effort and cooperation on the part of the patient. Examination of the flow volume curves demonstrate that some difficulties were being experienced and the technician does document poor effort. I also note the comment by Dr. M.A. Mendoza from September 25, 2002: I was not able to get him to take deep breaths for a better assessment. He also states at this time that [the worker] is not experiencing any dyspnea with usual daily routines. In the radiologic record from July 15, 2003 until the last film of July 17, 2003, there is evidence of the appearance of air space disease in the right lung that progresses to involve atelectasis and consolidation. There also seems to be the development of pleural fluid. I would conclude from this evidence that [the worker] had asbestosis with both interstitial and pleural disease that was likely stable over many years. The extensive respiratory changes occurring in July 2003 are superimposed on this process and are not caused by it. Further, [the worker s] neurologic disorder was not related to or worsened by his asbestosis. 2) Please comment on the nature of this worker's neurological condition.

5 Page: 4 Decision No. 2610/08 A review of the notes from the neurologist, Dr. J. Muhunthan, reveals that [the worker] had a history of cognitive dysfunction leading back to around 2000 and I note that be had had a CT scan of his brain in He was also taking Aricept. Dr. Muhunthan documents a 6 month history of progressive difficulty with speech and a tendency to choke on his food. Further, there are changes in facial expression, slight rigidity, and a tremor in the right arm. This is contained in his letter of July 16, Further evaluation took place on January 21, 2003, and on June 13, These document bulbar muscle weakness with atrophy and fasciculation in his tongue. This is likely to be part of a progressive bulbar palsy. He also continues to have evidence of cognitive dysfunction and findings suggestive of Parkinson's disease. [The worker] clearly was experiencing classic symptoms of bulbar disease with difficulty clearing his saliva, a tendency to choke on liquids and solids, difficulty with speaking, and weight loss. I would conclude that the important neurologic problem related to his demise was progressive bulbar palsy. This by itself would not have an effect on his respiration, nor on lung volumes. However, repeated episodes of aspiration for which he was certainly at risk could cause further lung scarring or pneumonia. This has the potential to cause some decrease in lung volumes. Also, about 25 percent of patients with progressive bulbar palsy develop over time more widespread symptoms related to amyotrophic lateral sclerosis of which it forms a subset (I note with interest that [the worker s] sister died of ALS). More extensive anterior horn cell disease of ALS can be associated with a decrease in lung volumes through diaphragmatic weakness. However, on Dr. Muhunthan's examination from January 2003, he notes: There is no muscle fasciculation noted in the extremities. This would argue against an ALS-type syndrome and more for progressive bulbar palsy. 3) Please comment on the cause of the worker s death. [The worker] died of respiratory failure. This was related to the acute onset of bronchopneumonia in a patient who was having episodes of aspiration. I do not understand the comment by Dr. Gidwani from his letter of August 5, 2004: but the bronchopneumonia process certainly did not appear to be secondary to aspiration. It may well be that no food particles were seen but that does not necessarily exclude aspiration. Aspiration with pneumonia is a very common terminal event in patients with progressive bulbar paralysis. I would conclude that [the worker s] death was caused by pneumonia as a result of aspiration related to his progressive bulbar paralysis. He has a background history of asbestosis which I expect was stable and not related directly to his death. 4) Is there any other medical information which you feel would be of assistance? The file was quite complete and the radiology was also helpful. I do not feel that further information would be useful. (v) Other medical information [7] The case materials included a copy of an x-ray report, dated October 26, 1990, prepared by Dr. R. Marcinkowski, radiologist, which was apparently associated with treatment of a cracked rib. In addition to noting that the worker s rib injury had presumably healed without deformity the report went on to state that bilateral calcified pleural plaques are identified along the lateral chest walls and along the left hemidiaphragm and that this was indicative of previous occupational asbestos exposure. [8] In 1997, the worker was suffering from gastrointestinal symptoms, including abdominal pain, and the case materials included a report, dated November 6, 1997, prepared by Dr. Barry Singleton, anaesthesiologist. The report noted that the worker had fairly extensive pleural plaques suggesting old exposure to asbestosis; however it noted that on his last chest x-ray these apparently are not changing to any significant extent.

6 Page: 5 Decision No. 2610/08 [9] The worker underwent an enhanced CT scan of the brain and posterior fossa, and a report on the scan, dated January 31, 2000, was prepared by Dr. S. A. Cooper, radiologist. The report noted that the worker s CT scan was in keeping with marked diffuse cerebral atrophy. A further report on an electroencephalogram (EEG) performed on the worker on February 8, 2000, noted that the worker s clinical information indicated progressive dementia, although the report indicated that the EEG was poorly developed and showed no abnormal focal or paroxysmal features. [10] A further radiological report, dated March 12, 2002, prepared by Dr. Cooper, noted that the pleural plaques appear to be slightly more prominent on today s examination than on the previous examination, although the underlying lung parenchyma appears clear and no other significant findings were evident. [11] Dr. J. Muhunthan, neurologist, saw the worker and prepared a report, dated July 1, 2002, which noted that that the worker was diagnosed to have progressive cognitive problems suggestive of dementia about a year ago and that he had had symptoms related to cognitive dysfunction for about 2-3 years. It stated that the worker was having difficulty expressing himself through speech, and that he tended to choke on food. Breathing difficulties were also noted, and that these were being treated by Dr. M. Mendoza, respirologist. The report noted that the worker had difficulty articulating his words and that there was clinical evidence of cognitive dysfunction. [12] Dr. Mendoza provided a report dated September 25, 2002, which again referred to the presence of extensive bilateral pleural plaque formation as well as evidence of interstitial changes in the subpleural area of both lung bases. The report also stated that the family was not reporting any new symptoms or concerns, and that he was not experiencing any dyspnea (difficult or laboured respiration). The report noted that this type of condition was usually chronic and not amenable to therapeutic manipulation. A preventative approach with yearly influenza vaccines was recommended. [13] Dr. Muhunthan provided a further report, dated January 21, 2003, on the worker s neurological condition. The report stated: I saw this 69 year old male on follow up in the Neurology Clinic on December 19, He has had symptoms related to dementia for more than a year and in the past year they have noticed increased difficulty with swallowing. He tends to choke on fluid and he is managing soft diet. He does have significant cognitive dysfunction and he is managing reasonably well at home with his wife s help. He needs 24 hour supervision. His wife has to help him with dressing and bathing. He is on Aricept 10 mg daily and Paxil 20 mg at night. He is managing to take his pills. He has had a CT scan of the head two years ago when he was reported to show diffuse atrophy. No evidence of significant ischemic changes. He is mobilizing independently and his wife says he is sometimes unsteady in his legs. His symptoms seem to fluctuate from day to day. He is quite pleasant and no history suggestive of any agitation or aggression. He does have atrophy of his tongue and there is some fasciculation in the tongue. Most likely he has a neurodegenerative disorder with bulbar palsy and cognitive dysfunction. There is no muscle fasciculation noted in the extremities. His speech problem is related to the atrophy of the tongue. I have explained to their family members the progressive nature of this condition and have recommended supportive therapy. I have advised them on soft diet and also thickened fluids. I will see him on follow up in a few months but I would be happy to see him earlier if necessary. [14] The worker was seen on May 14, 2003, by Dr. Abe Reinhartz, specialist in occupational medicine, at the Occupational Health Clinics for Ontario Workers Inc. (OHCOW).

7 Page: 6 Decision No. 2610/08 Dr. Reinhartz report of that date referred to the presence of pleural plaques, as well as pulmonary function testing that the worker had undergone previously. The report concluded by stating: Opinion: [The worker] has bilateral pleural plaques and bilateral interstitial disease, all compatible with parenchymal asbestosis. He also has a bona fide restrictive impairment. I will submit a Form 8 on his behalf for asbestosis with respiratory impairment. [15] Further radiological studies were performed on the worker s chest on May 4, The report on the studies, of that date, prepared by Dr. Cooper stated: IMPRESSION: Marked calcified pleural disease indicative of asbestos related disease. There is no evidence of air trapping or a pneumothorax related to foreign body. [16] As noted above, the worker passed away on July 17, He was seen July 15, 2003, by Dr. Kenneth Yoshida, specialist in internal medicine and medical oncology. His report, of that date, stated, in part: His family describes him as having neurologic disease for at least the past year and a half and over the past year his symptoms have been worsening. He has had difficulty ambulating for the past six months and has only been able to ambulate with assistance. He has lost his ability to speak. He then developed some swallowing difficulties and aspiration over the past month and he was admitted because of dehydration from his aspiration pneumonia. He has seen Dr. J. Muhunthan and she has told me that he has a combination disease with some Parkinson's features, some dementia and some lower motor neuron features. It appears that he had a bit of aspiration this morning and ran into difficulties. He was given Furosemide and seems to have improved. The family were unaware of any other symptoms except that he was also having trouble urinating and he has now had a catheter put in place. PAST MEDICAL HISTORY: reveals that his family are unaware of any other medical problems except for asbestosis. He has had surgery in the past but the family were not sure what it was. FAMILY HISTORY: reveals that his sister died of ALS at 50. A brother died at 42 of a brain tumour. Another brother died at 51 of a brain tumour. Another brother died at 42 of a hematologic disease. There is no other history of neurologic disease or cardiac disease in the family. SOCIAL HISTORY: reveals that he smoked a pack a week for ten years but quit 30 years ago. He used to have two or three standard drinks in a day but he has now quit for the past several months. PHYSICAL EXAMINATION: blood pressure is 130/75. Pulse is 100 and mostly regular, mostly sinus but occasionally regular. Chest: increased air entry in the right base but I do not hear any crackles but air entry seems to be decreased in both lung fields. There are definite coarse crackles in the left base. Abdomen: reveals no organomegaly or masses and his bowel sounds are normal. Neurological: he would not cooperate for neurologic examination.. His chest x-ray I think shows some interstitial changes and I think there is probably a bit of congestive heart failure. The right base shows atelectasis and I think a bit of pneumonia IMPRESSION: 1. Parkinson s disease with possibly lower motor neuron disease and dementia.

8 Page: 7 Decision No. 2610/08 2. Aspiration pneumonia 3. Mild congestive heart failure 4. Asbestosis PLAN: 1. I discussed the situation with the family. They are aware of the severity of his neurologic disease and the irreversibility of it. However at this time his wife states that she wishes that he have intubation and ventilation. I asked her if she believes this is what her husband would want and the daughter spoke to the wife and said her mother wishes that he remain a full code. Since she is the next of kin, we must comply with her wishes. 2. I have spoken to Dr. J. Muhunthan and she will once again go over with the family the severity of his neurologic disease in the situation.. [17] A Discharge Summary, dated July 17, 2003, was prepared by Dr. Yoshida. The report stated: This 70 year old gentleman had neurologic disease for years and it was progressing over the past year. He was developing an inability to swallow and he in fact was aspirating. He was becoming dehydrated and he was brought in because of inability to feed on his own. COURSE IN HOSPITAL: He had aspiration pneumonia and he then had an episode in which he went into respiratory failure and there was confirmation of sudden atelectasis of one of the lobes of his lung likely due to mucous plugging. He was transferred to the ICU and treated with Ceftriaxone and Metronidazole and initially his chest x-ray improved. He then had a consultation with Dr. Rosenblum and the family declined aggressive measures, i.e., intubation or ventilation or ostomy. He was then transferred to the palliative care unit. He then developed another episode in which he suddenly developed respiratory distress and again the chest x-ray confirmed despite the fact that his lung had re-expanded that he had a sudden atelectasis of one of the lobes of his lung again. Again the family were spoken with and it was quite clear they believed [the worker s] wishes to be to have palliative measures only. He passed away peacefully on July 17, The family requested an autopsy to confirm asbestosis. I looked at his chest x-ray, and it appeared that he in fact did have asbestos exposure. I inquired about, given that they wished to have an autopsy, having the brain and spinal cord examined to confirm the exact nature of his degenerative neurologic condition. However, [the worker s widow] did not wish to have that done because of the invasiveness of the procedure, i.e., an incision to remove the brain and spinal cord. They only wished that the autopsy be limited to the chest and lungs. They are aware that as the family requested the procedure that there may be a charge from the hospital for the autopsy, although they could submit it to the WSIB board. Consent was obtained for the autopsy as outlined above. The death certificate was signed prior to the autopsy being completed with the provisions that there may be further information relating to the cause of death available later and that an autopsy would be done. FINAL DIAGNOSIS (prior to autopsy): Respiratory failure Aspiration pneumonia Parkinson s disease and degenerative lower motor neuron disease Asbestosis [18] The autopsy was performed on the worker, on August 5, 2003, by Dr. Ram Gidwani, pathologist. His report on the autopsy, dated October 10, 2003, stated:

9 Page: 8 Decision No. 2610/08 FINAL DIAGNOSIS Autopsy examination was limited to the chest only. 1. The autopsy is requested by the Family because of history of exposure to asbestosis. 2. Extensive plaques both chest wall involving pleura and diaphragmatic area. 3. Changes of chronic obstructive pulmonary disease. 4. Bronchopneumonia. 5. Coronary artery heart disease (right, moderate). 6. History of degenerative neurological disease.? etiology (CNS [central nervous system] examination not permitted). Synopsis: This 70 year old gentleman died after a prolonged illness. During life there was a history of exposure to asbestosis with respiratory problems. The post-mortem was requested by family for compensation purposes and was limited to examination of the chest and the family had agreed to pay for the post-mortem. At autopsy there were the above mentioned findings. There were extensive plaques involving the chest wall, pleura and diaphragmatic areas. The sections of the lungs show changes of bronchopneumonia and scattered ferruginous asbestos bodies. The final cause of death was attributed to bronchopneumonia. Based on the presence of extensive plaques involving the chest wall, pleura and diaphragmatic areas, along with the presence of ferruginous bodies on microscopic examination, I believe that this case is compensatable [sic] by W.S.I.B. [19] Subsequent to the worker s death and the autopsy, Dr. Reinhartz, the OHCOW physician who had seen the worker prior to his death, provided a report, dated November 5, 2003, to the Board s Claims Adjudicator (CA). In his report, Dr. Reinhartz stated that he did not agree with the Board s view that the there was no evidence of any permanent impairment as the lung tests are within normal limits, as indicated by the Board in correspondence, dated July 22, 2003, addressed to the worker. Dr. Reinhartz referred to pulmonary function tests (PFTs) that the worker had undergone in May 2002, which indicated a decline in function when compared to PFTs done a few years earlier. The report also referred to the fact that the worker s autopsy disclosed the presence of fibrosis and ferruginous bodies consistent with asbestosis as well as the presence of the pleural plaques. The report concluded by stating that the worker had asbestosis, as well as a respiratory impairment prior to his death and that the worker s claim should be re-evaluated. [20] In further correspondence, dated May 26, 2004, from Dr. Reinhartz to the worker s widow, Dr. Reinhartz stated that he was in agreement with the W.S.I.B. that your husband did not die from his asbestos related disease. He went on to state, however, that he disagreed with the Board s view that the worker had not experienced any respiratory impairment prior to his death. Dr. Reinhartz indicated that the worker s respiratory impairment would have affected his life while he was alive but that this did not have any relationship to his cause of death. [21] Dr. David C. F. Muir, the Board s consultant in respirology, prepared an internal Board memorandum, dated May 6, 2004, on the issue of the worker s entitlement. The memo stated that although there was clear evidence of asbestos effects on the chest x-ray (pleural plaques), the terminal events were dominated by the onset of dementia and bulbar palsy. The memo stated that although the 2002 PFTs showed an apparent reduction in respiratory capacity, by this

10 Page: 9 Decision No. 2610/08 time the patient had evident bulbar palsy and [the PFTs] are unlikely to represent true abnormality of ventilatory capacity. The memo concluded by stating: SUMMARY: On the evidence available to me there are evident pleural plaques due to asbestos exposure, but no asbestos or associated impairment of pulmonary function. The terminal events were due to respiratory failure, as a result of inhalation pneumonia caused by progressive bulbar palsy. [22] A further memo prepared by Dr. Muir, dated July 2, 2004, again indicated that, although the worker s PFTs in 2002 indicated an apparent reduction in respiratory capacity, the 2002 testing cannot be accepted as a true estimate of ventilatory capacity because the patient had evident symptoms of bulbar palsy. The memo went on to state that the worker s plaques did not affect lung function and that there is no reliable objective evidence, that the patient had impaired pulmonary function as a result of asbestos exposure. [23] Dr. Gidwani prepared a report, dated August 5, 2004, addressed to Dr. Muir, which noted that, in addition to the pleural plaques which he described in the worker s autopsy report, he had failed to mention that in addition there was evidence of scattered interstitial fibrosis as well. The report stated in part: In my view the bronchopneumonia process is terminal, involving the existing lung disease which is further compromised by extensive plaques involving the chest wall, pleura and diaphragm. While it is true that this patient had a neurological problem, unfortunately we were not permitted to do that examination and, therefore, I cannot comment on that, but the bronchopneumonia process certainly did not appear to be secondary to aspiration. As you know in Sarnia, we have performed numerous autopsies on patients who have had exposure to asbestosis, both with and without malignant mesothelioma. I believe, based on the gross and microscopic findings of this case, this case is at least partially if not fully compensable because of the exposure to asbestos, as an occupational hazard in this case. [24] In a further internal Board memorandum, dated September 2, 2004, Dr. Muir maintained his earlier views that the presence of plaques were not a cause of impairment of pulmonary function, and that the 2002 PFTs did not provide an accurate indication of ventilatory capacity, because of the muscle impairment from the neurological and cerebral disorder. The memo noted that the worker s cause of death was associated with gradual deterioration over the last year, with developing inability to swallow and aspiration of food or fluids and that the final terminal event appears to have been sudden mucus plugging with atelectasis of a lobe of the lung. [25] Dr. Muir s memo, however, acknowledged the reference made by Dr. Gidwani in his August 5, 2004 report, excerpted above, to scattered interstitial fibrosis which would imply some impairment of pulmonary function. He indicated that it would be difficult to estimate the extent of the worker s impairment, but concluded that a reasonable estimate might be 15% dated two years before death. He concluded the memo, however, by noting that such impairment would not be a factor as a cause of death. [26] By correspondence, dated September 20, 2004, the worker s widow was advised that, in light of the new information from Dr. Gidwani, the Board had reconsidered its decision in relation to the worker s entitlement to benefits for asbestosis, and concluded that the worker was entitled to a non-economic loss (NEL) award for asbestosis. The correspondence indicated, however, that the denial of entitlement to survivor s benefits was being upheld by the Board

11 Page: 10 Decision No. 2610/08 because Dr. Muir feels that even with the change of diagnosis from plaques to asbestosis, based on new information provided, that the cause of death was not a result of the asbestosis. [27] In response to a request by the worker s representative, Dr. Gidwani provided a further report, dated December 5, 2006, which addressed the question of the worker s cause of death. The report stated, in part: In response to your question in your letter in paragraph #2, the cause of death was more likely attributable to a neurological disease and as such not work related, following is the answer. The answer to that question is that since no neurological examination was allowed by the family at the time of post-mortem, no such examination was carried out and, therefore, I am not able to address that issue. However, review of the patient's medical records shows that during assessment by a neurologist, the patient had a problem with dementia and Parkinson's disease, and because of atrophy tongue and difficulty in swallowing, the patient had to be fed through a feeding tube. In these situations, there is always some aspiration of the food contents into the respiratory tract, which may result in aspiration pneumonia, which was not evident in this patient. In response to your second question, whether asbestosis was a significant factor in the cause of death; In answer to that question, the autopsy did show evidence of significant exposure to asbestosis in the form of extensive plaques, involving both chest wall, pleura and diaphragmatic areas. In addition, there was evidence of interstitial pulmonary disease and chronic obstructive pulmonary disease. While exposure to asbestosis was not a primary cause of death in this patient, I believe it was a significant factor in causing obstructive pulmonary disease and bronchopneumonia. The patient thus had two significant illnesses, one of which was neurological, and, I do not believe that this was a sole cause of death, even though we were not able to carry out neurological examination because of restriction on the autopsy provision, and, the second one resulting from exposure to asbestosis, which although not the sole cause, was a significant factor, and on this basis, as indicated by my previous report, that this case should be at least partially compensable by W.S.I.B. (v) Applicable law [28] The workplace accident which is the subject of this appeal occurred on a gradual onset basis. December 18, 1996 was established as the date of accident for the worker s claim for asbestosis. Accordingly, the worker s entitlement to benefits in this appeal is governed by the pre-1997 Act ( the Act ). (vi) Analysis [29] As noted above, in the circumstances of this appeal, the Board initially denied the worker entitlement for asbestosis, taking the view that, although there was some evidence of asbestos exposure, in the form of the pleural plaques, which had been apparent in radiological studies since at least 1990, this was not evidence of disability or impairment. Subsequently, however, after the worker s death in July 2003, new information was provided by Dr. Gidwani, the pathologist who carried out the worker s autopsy. In his report, dated August 5, 2004, Dr. Gidwani indicated that there was evidence of scattered interstitial fibrosis as well. This new information was reviewed by Dr. Muir, and the Board subsequently concluded that the worker was entitled to benefits for asbestosis. [30] Although entitlement for asbestosis was allowed, the Board maintained its view that the worker s respiratory problems associated with exposure to asbestos did not contribute

12 Page: 11 Decision No. 2610/08 significantly to the worker s death. The Board expressed the view that the worker s bronchopneumonia, which was the apparent immediate cause of death, was associated with his neurological condition. [31] The view that the worker s asbestosis did not contribute to his death was expressed by several physicians: In his memo, dated September 2, 2004, which indicated that the worker should be entitled to benefits for asbestosis, Dr. Muir indicated that this would not be a factor in his death. In his report, dated May 26, 2004, Dr. Reinhartz, who was supportive of entitlement to benefits for asbestosis, even before the new information was provided by Dr. Gidwani, stated that although pleural disease resulting from asbestos exposure would have resulted in some breathing difficulties for the worker while he was alive, this did not have any relationship to his cause of death. In his report, dated March 18, 2009, Dr. Hutcheon, the Tribunal s Medical Assessor in this appeal stated that [the worker s] death was caused by pneumonia as a result of aspiration related to his progressive bulbar paralysis and that the worker s history of asbestosis appeared to be stable and not related directly to his death. [32] We have also taken into account the statement made by Dr. Gidwani, in his report dated December 5, 2006, that although the worker s asbestosis was not the sole cause, it was nevertheless a significant factor contributing to the death. [33] We have reviewed the submissions provided by the worker s representative in correspondence dated May 22, [34] In his submissions, Mr. Davis noted that the main points of testimony provided by the worker s daughter at the hearing had been set out in the Panel s instructing memo to TCO, and that these points explain[ed] why the Estate has taken this position [that the worker s asbestosis contributed to his cause of death]. [35] In this regard, the testimony provided by the worker s daughter indicated that Dr. Mendoza had expressed the view that the worker s asbestosis contributed to his death. We note that the report on file from Dr. Mendoza, dated September 25, 2002, refers to the worker s plaque formations, but did not indicate that the condition was likely to cause death. It noted that the worker s physical examination appeared to be unchanged. There is no other documentary evidence provided by Dr. Mendoza supporting the view that the worker s asbestos related condition contributed to his death. In our view, it is likely that had Dr. Mendoza held the view that the worker s asbestosis contributed to his death, this would have been included in a medical report. We have considered the information provided by Drs. Hutcheon and Muir, both of whom are senior respirologists, which supports the view that the worker s death was not significantly related to asbestosis. In light of this information, in our view, even if prior to the worker s death, Dr. Mendoza told the worker s family that asbestosis contributed to the death, we are not able to attribute significant weight to such evidence. [36] We also note that at the hearing, the worker s daughter expressed the view that, prior to the last few months of the worker s life, the worker s neurological condition was not so severe, in that he did not require constant supervision, and was able to dress and wash himself. We note that the testimony provided by the worker s daughter in this regard is inconsistent with the information provided by Dr. Muhunthan in her reports. In particular, Dr. Muhunthan s report

13 Page: 12 Decision No. 2610/08 dated July 16, 2002 indicated that the worker had been diagnosed with progressive cognitive problems suggestive of dementia for about one year, and that he had symptoms related to cognitive dysfunction for about two to three years. Dr. Muhunthan s report dated January 21, 2003 also stated that the worker needed 24 hour supervision. We have no basis to conclude that the information provided in Dr. Muhunthan s report s was inaccurate, and to the extent that the information provided by Dr. Muhunthan is not consistent with the testimony provided by the worker s daughter, we believe that greater weight should be given to the medical documentation. [37] A point that is raised in the submissions relates to the statement made by Dr. Gidwani in his report dated August 5, 2004 that the bronchopneumonia process certainly did not appear to be secondary to aspiration. Dr. Gidwani made a similar comment in his report dated December 5, 2006 when he noted that although the worker had problems with dementia, Parkinson s disease, and difficulty in swallowing due to atrophy of the tongue, aspiration pneumonia was not evident in the worker. This was the case, notwithstanding the statement by Dr. Gidwani that in these situations there is always some aspiration of the food contents into the respiratory tract. It appears to be implicit in Mr. Davis s submission that if the worker s bronchopneumonia was not caused by aspiration, as Dr. Gidwani indicated, it is probable that that the worker s asbestosis played a more significant role in his cause of death. [38] We note that Dr. Hutcheon called into question the observation made by Dr. Gidwani, that aspiration did not play a role in the worker s bronchopneumonia. Dr. Hutcheon noted, in his response to question 3 that he did not understand this comment made by Dr. Gidwani. Dr. Hutcheon stated that it may well be that no food particles were seen [at the autopsy] but that does not necessarily exclude aspiration and that aspiration with pneumonia is a very common terminal event in patients with progressive bulbar paralysis. Notwithstanding Dr. Gidwani s statements, Dr. Hutcheon maintained his view that [the worker s] death was caused by pneumonia as a result of aspiration related to his progressive bulbar paralysis. [39] We have also taken into account the Discharge Summary provided by Dr. Yoshida which indicated that the worker s course in hospital included aspiration pneumonia which led to an episode of respiratory failure and atelectasis due to mucous plugging. We also note that Dr. Yoshida referred to the worker s aspiration pneumonia in his report dated July 15, 2003, two days prior to the worker s death. [40] In light of this medical information provided by Drs. Hutcheon and Yoshida, we conclude that it is probable that the worker s bronchopneumonia was related to aspiration, notwithstanding the fact that Dr. Gidwani did not observe evidence of aspiration at the time of the autopsy. Having concluded that the worker s pneumonia was related to aspiration, it follows that this was closely related to the bulbar palsy, which in our view represents the consensus medical view as to the cause of death. [41] We note that Dr. Yoshida s Discharge Summary, dated July 17, 2003, included a number of conditions in his FINAL DIAGNOSIS (prior to autopsy), and that Asbestosis was one of the conditions listed under this heading. We do not interpret that document to mean that asbestosis was a contributing cause of the worker s death. Rather, we interpret it to mean that, at the time of the worker s death, the worker was properly diagnosed with asbestosis. We interpret the document to mean that the worker had asbestosis at the time of his death, but we are not able to interpret the document to mean that that condition was a contributing cause of the worker s death.

14 Page: 13 Decision No. 2610/08 [42] We have carefully considered the report provided by Dr. Gidwani, dated December 5, This report represents the strongest evidence in support of a finding that the worker s exposure to asbestosis was a significant factor contributing to the worker s cause of death. As noted above, in that document, Dr. Gidwani stated, While exposure to asbestosis was not a primary cause of death in this patient, I believe it was a significant factor in causing obstructive pulmonary disease and bronchopneumonia. Dr. Gidwani also stated in that report that he did not believe that the worker s neurological illness was the sole cause of his death and that exposure to asbestos was a significant factor related to his death. In light of the total body of evidence before us, however, we are not able to conclude that the estate is entitled to survivor s benefits, on the basis of Dr. Gidwani s 2006 report. [43] In his submissions, Mr. Davis has provided four enumerated reasons for the Panel to give weight to the reports provided by Dr. Gidwani. In this regard, the submission stated: 1) Dr. Gidwani conducted the autopsy and has clearly indicated that there was no evidence of aspiration on examination of the lungs. 2) Asbestosis can and does lead to bronchopneumonia 3) None of the medical reports opposing Asbestosis as a significant contributing factor had the benefit of examining the lungs first hand 4) If aspirational pneumonia was the cause of death, one would expect that to have been evident at the autopsy. [44] We have already addressed the first and fourth points above, noting that the question of whether bronchopneumonia related to aspiration was a contributing cause of death, is a point of contention in this appeal. We have referred to the fact that Dr. Hutcheon indicated that he did not understand Dr. Gidwani s comments in this regard, and that, the fact that although food particles may not have been seen upon autopsy, that does not necessarily exclude aspiration. It is clear that Dr. Hutcheon, a highly qualified respirologist, was well aware of the pathologist s comments on the matter, but that Dr. Hutcheon nevertheless concluded that [the worker s] death was caused by pneumonia as a result of aspiration related to his progressive bulbar paralysis. [45] As for the statement in the worker s submissions that Asbestosis can and does lead to bronchopneumonia, the relevant question in this appeal is not whether asbestosis can and does lead to bronchopneumonia, in the general sense, but rather whether, in this case, the worker s asbestosis contributed significantly to the bronchopneumonia, which was the immediate cause of death. The medical information provided by Drs. Reinhartz, Muir and Hutcheon supports the view that the worker s asbestosis was not a significant factor contributing to the worker s death. In particular, we rely on Dr. Hutcheon s statement that the worker s asbestosis was stable, was not directly related to his death, and that the worker s neurologic disorder, which Dr. Hutcheon identified as the cause of death, was not worsened by the asbestosis. [46] We have also taken into account the submission that, as the pathologist who conducted the autopsy, Dr. Gidwani, was best positioned to determine the worker s cause of death, and that he had the benefit of examining the lungs first hand. Although we acknowledge that Dr. Gidwani, as the examining pathologist, was in a unique position to consider the worker s case, we are not able to give weight to his view that the worker s asbestosis was a significant factor contributing to his death. [47] As stated above, we are not able to accept Dr. Gidwani s view that the worker s bronchopneumonia was unrelated to aspiration. This view is contrary to the expert view

15 Page: 14 Decision No. 2610/08 provided by Dr. Hutcheon, who was aware of Dr. Gidwani s view on this question. We also note that Dr. Yoshida provided the diagnosis of aspirational pneumonia in his report dated July 15, 2003, two days prior to the worker s death. In our view, Dr. Yoshida was at least as well positioned as Dr. Gidwani, and perhaps better positioned than him, to provide a view on whether aspirational pneumonia was an appropriate diagnosis, given that Dr. Yoshida examined the worker while he remained alive, but just prior to his death. Given that, for these reasons, we do not attribute weight to Dr. Gidwani s view that the worker s death was unrelated to factors associated with aspiration, since this is a central point in Dr. Gidwani s analysis, we attribute less weight to Dr. Gidwani s overall opinion relating to the worker s cause of death. [48] We agree with Mr. Davis submission that the assessment of evidence should not be a numbers game, in which one merely counts the number of medical opinions for or against a proposition, automatically accepting the view supported by the greater number of opinions. Rather, the persuasiveness of each opinion must be considered separately in assessing the overall body of evidence. Nevertheless, where an issue has been considered by more than one health care professional, where a consensus view emerges, the existence of such a consensus must be considered by the decision-makers. In this case, we conclude that aspirational bronchopneumonia was the probable cause of the worker s death, the worker s neurological condition of bulbar paralysis was probably a significant factor contributing to the worker s death, and that the worker s asbestosis, although ultimately accepted by the Board as a compensable condition, was not a significant factor contributing to his death. Having reviewed all of the medical information available to us, we believe that these conclusions represent the consensus medical view. We have reached this view notwithstanding that it is apparently inconsistent with the opinion expressed by Dr. Gidwani. [49] As we have noted, the conclusion that the worker s asbestosis was not a significant factor contributing to his death is supported by Drs. Reinhartz, Muir and Hutcheon. In assessing the information provided by these physicians, as well as that provided by Dr. Gidwani, we have also taken into account the very high qualifications that Drs. Muir and Hutcheon have as experts in the field of respirology. We have also taken into account the fact that there was no persuasive evidence to indicate that the worker s asbestosis was becoming progressively worse, noting Dr. Hutcheon s view that the worker s asbestosis was likely stable over many years, and that the asbestosis did not worsen the worker s neurological condition. [50] For these reasons, we conclude that the worker s compensable asbestosis did not contribute significantly to the worker s cause of death. Accordingly, the worker s estate is not entitled to survivor s benefits.