Cox and Comcare
[2006] AATA 521
•15 June 2006
Administrative
Appeals
Tribunal
DECISION AND REASONS FOR DECISION [2006] AATA 521
ADMINISTRATIVE APPEALS TRIBUNAL )
) A2005/21
) A2005/67
GENERAL ADMINISTRATIVE DIVISION ) Re GARRY COX
Applicant
And
COMCARE
Respondent
DECISION
Tribunal Mr S. Webb, Member Date15 June 2006
PlaceCanberra
Decision The decision under review is set aside. In place thereof the Tribunal decides that Mr Cox suffered aggravations of his paraumbilical and epigastric hernias on 9 October 2003, 9 January 2004 and 24 May 2004 for which Comcare is liable.
Comcare is to pay Mr Cox’s reasonable costs in these proceedings pursuant to s 67(8) of the Act, as agreed or taxed.
..............................................
Mr S. Webb, Member
CATCHWORDS
COMPENSATION - paraumbilical and epigastric hernias – aggravation – frank injury or disease – aetiology and progression of hernias - expert evidence – inconclusive epidemiological evidence - mechanical factors of significance in employment - incarceration of tissue and enlargement of hernia – physiological changes - decision set aside
Administrative Appeals Tribunal Act 1975 s 67
Safety, Rehabilitation and Compensation Act 1988 ss 4, 14
Browne v Dunn (1893) 6 R 67
Makita (Australia) Pty Ltd v Sprowles [2001] 52 NSWLR 705
Kennedy Cleaning Services Pty Ltd v Petkoska (2000) 200 CLR 286
REASONS FOR DECISION
15 June 2006 Mr S. Webb, Member 1. These applications are for review of two Comcare decisions (that were affirmed on reconsideration) to reject claims by Garry Cox, the Applicant, for compensation in relation to paraumbilical and epigastric hernias. Mr Cox claims the hernias were caused or aggravated by certain activities he was required to carry out in performance of his duties at the National Gallery of Australia (“the Gallery”). Those activities include opening and closing a heavy door to access the ‘tunnels’ area of the Gallery, and climbing ladders, crawling in confined spaces and squeezing past obstructions when accessing the risers and platforms within the air-conditioning system of the Gallery.
factual context
2. Mr Cox commenced work at the Gallery in 1985. At the time of the claimed injuries in 2003-2004 he was employed by the Gallery in the position of Facilities Manager.
3. On 27 June 1989 Comcare accepted liability for a work-related rectus abdominus tear. Whether that injury is significant in relation to Mr Cox’s hernias is unclear. Neither Dr Barry nor Dr Stevenson were satisfied that there is any relationship between the rectus injury and the hernias under claim in these proceedings.
4. The Gallery air-conditioning system is contained within the ‘tunnels’ area. That area is accessible through two doors, one of which leads directly to the plant room and the other (the main access door) gives access to the air-conditioning system risers (several storeys high) and ducting. The risers are accessed by a system of ladders and platforms. Photographs of the access doors and the risers are at Exhibit A4. It is not in dispute that significant force is required to open and close the main access door as a result of a vacuum created by the air-conditioning return system. It is accepted and I find that the forces required are significantly greater than the applicable standard for safe manual handling. In order to open or close the door from the outside, pulling against the vacuum, a force of 64.44 kilograms is required and to open or close the door from the inside a force of 53.66 kilograms is required (see report by Mr Lehmann at AT21A).
5. In the period from mid 2002 to October 2003 Mr Cox was required to access the tunnels area, using the aforementioned door, in the course of his duties. Mr Cox estimated that he accessed the tunnels area up to 200 times during this period. He gave evidence that he accessed the tunnels area up to 30 times in some weeks. Plainly enough the precise number of times Mr Cox accessed the tunnels area using the main access door during this period, or on a weekly basis, is unknown. However, I accept that Mr Cox’s duties required him to access the tunnels at least three or four times each week and up to 30 times in some weeks.
6. On 9 October 2003 Mr Cox complained of abdominal pain. Radiological investigations were conducted on 13 October 2003 in relation to possible left ureteric colic. Dr John Connors reported, in part:
“A small fat containing midline hernia is noted just above the umbilicus.”
7. Mr Cox continued to perform his duties, including accessing the tunnels area, without further complaint until 9 January 2004.
8. On 9 January 2004 Mr Cox complained of severe abdominal pain and drove himself from work to Calvary Hospital. Dr Kaye Roberbe reported that (BT6):
“He presents with a paraumbilical hernia. It has been present possibly for the last 10 years but since October ’03 he has had 3 episodes of distention of the mass associated with severe epigastric and … pain. Today’s episode was the most severe and the hernia the most prominent…”
On examination of Mr Cox, Dr Roberbe reported:
“4cm x 3cm hard smooth exquisitely tender mass associated with tenderness penumbilically esp on LI. After morphine the mass incompletely reduced to a soft 3x2cm swelling, probably similar to its more chronic state according to the patient. The pain has resolved.”
9. Mr Cox’s oral evidence was that he was “pain free” and “100 percent cured” by 9.40am and returned to his normal duties. I note in passing that at this time and subsequently Mr Cox was working reduced hours as a result of other, unrelated, claimed injuries.
10. On 10 February 2004 Mr Cox consulted Dr Peter Barry, Surgeon, who reported (BT8):
“Mr Cox tells me that he has had the hernia for 6-7 years now, however, in the last 6 months or so he has had four attacks necessitating presentation to hospital emergency departments and sometimes requiring significant pain relief. The pain is often centered from the umbilicus radiating to the left flank and in fact he was investigated for kidney stones due to the nature of the pain. The pain has always settled spontaneously after several hours, however, it certainly sounds like a history consistent with infarction of omental or extraperitoneal fat.
…
On physical examination, there was a reducible but very tender umbilical hernia.”
On 12 February 2004 Dr Barry surgically repaired Mr Cox’s umbilical hernia (see Exhibits A9 and A10).
11. On 13 March 2004 Mr Cox returned to work and, by his own account, was pain free but developed a severe bout of influenza, which caused him to cough. On 21 March 2004 (a Sunday) Mr Cox suffered abdominal pain and attended the Calvary Hospital at 4.23pm (see Exhibit A5). He was treated with Tramal and his pain reduced after lying down for a period.
12. On 22 March 2004 Mr Cox complained of abdominal pain and nausea at work and was driven to the Calvary Hospital by a work colleague, Mr Michael Sultana. Mr Cox’s evidence was that he had a bad reaction to Tramal, which caused him to hallucinate and vomit. He presented to the hospital at 11.55am (see Exhibit A6), lay down for a period and ceased taking Tramal.
13. In the period from 22 March to 26 March 2004 Mr Cox claimed that he was largely pain free and that his nausea stopped following cessation of the Tramal medication. He was at work during this period performing his normal duties.
14. On 26 March 2004 Mr Cox complained of abdominal pain that “was not very severe” at work which he experienced during a luncheon event. He attended upon his general practitioner, Dr Yuille, who recommended he consult Dr Barry. By his own account he felt better and was pain free later that day.
15. Mr Cox remained symptom free until 24 May 2004. On that day he complained of abdominal pain at work and was taken to Calvary Hospital by Mr Sultana, where he was admitted (AT5). On 25 May 2004 Dr Barry repaired an epigastric hernia. The epigastric hernia was located “3-4cms above the previous repaired umbilical hernia”. Mr Cox was discharged from hospital on 27 May 2004.
16. Since that time Mr Cox has not experienced significant symptoms relating to his hernias and has continued with his duties at the Gallery.
17. On 12 February 2004 Mr Cox lodged a claim for compensation in relation to the paraumbilical hernia (BT7). On 2 April 2004 Comcare determined to reject his claim (BT13). That determination was reconsidered and affirmed on 3 June 2004 (BT 25).
18. On 7 June 2004 Mr Cox claimed compensation in relation to the second hernia sustained on 24 May 2004 (AT4). On 31 August 2004 Comcare determined to reject Mr Cox’s claim (AT17). That determination was reconsidered and affirmed on 7 December 2004 (AT27).
issues and law
19. The issue for determination in these proceedings is whether Mr Cox’s hernias were caused or aggravated by his employment at the Gallery.
20. Under the Safety, Rehabilitation and Compensation Act 1988 (“the Act”) Comcare is liable to pay compensation in relation to an injury that results in incapacity for work, impairment or death (s14). ‘Injury’ is defined to mean, relevantly, a disease or a physical injury or an aggravation of a physical injury arising out of or in the course of employment (s4). ‘Disease’ is defined to mean an ailment, or the aggravation of an ailment, that was contributed to in a material degree by the employment (s4).
consideration
21. During the hearing it became apparent that Mr Cox’s reliability as a witness was in issue. In his evidence in chief Mr Cox asserted that he suffered abdominal pain after using the tunnel access door at work on 21 March 2004 and drove himself to hospital as a result. He gave detailed evidence concerning the time he commenced work and his activities at work on that day. However, under cross-examination, when it was revealed to him that 21 March 2004 was a Sunday, he conceded that he was not at work on that day.
22. I am satisfied that Mr Cox’s evidence must be treated with some caution. His recollections of events may be faulty and unreliable. For that reason I will not attach significant weight to his evidence in the absence of corroboration. In Mr Cox’s submission it would be contrary to the rule in Browne v Dunn (1893) 6 R 67 to find fault with his credibility on the basis of issues that were not put him during cross-examination. If indeed Mr Cox was denied the opportunity to explain inconsistencies in his evidence I would agree. However, Mr Cox was provided with just such an opportunity in relation to the events of 21 March 2004 and he could provide no explanation other than his recollection was faulty. It is not necessary to go further and consider other matters that were not put to Mr Cox in cross-examination.
Were Mr Cox’s paraumbilical and epigastric hernias caused by his employment?
23. Mr Cox asserts that his activities in employment caused his hernias. The Respondent asserts that Mr Cox’s hernias were either constitutional or congential in origin and were not caused by Mr Cox’s employment.
24. Mr Cox’s medical history and the evidence of Dr Barry reveal that a paraumbilical hernia was present for several years prior to 9 October 2003, from 1996 or 1997. Plainly enough that previously existing hernia could not be caused by the events on or immediately prior to or after 9 October 2003. The specific cause of Mr Cox’s paraumbilical hernia is unknown. I note in passing that Mr Cox commenced work in the facilities area of the Gallery in or about 2001, a significant period after the apparent onset of his paraumbilical hernia. It follows that Mr Cox’s paraumbilical hernia was not caused by his employment after 2001.
25. Dr Barry’s stated that an epigastric hernia was identified on 21 March 2003. He and Dr Stevenson were in agreement that that hernia was in all likelihood caused by bouts of paroxysmal coughing over preceding days. I accept that evidence and so find. It follows that Mr Cox’s epigastric hernia was not caused by his employment.
Were the hernias aggravated by Mr Cox’s employment?
26. The Respondent submits that either Mr Cox’s activities in employment did not contribute to the progress of his hernias, or if there was a contribution it was insignificant, or if there was a significant contribution it did not result in any lasting physiological change within the meaning of injury.
27. As will appear, I do not agree.
28. The evidence of Dr Barry, Mr Cox’s treating surgeon, was that:
“… the hernias would have enlarged as a result of repetitive increased abdominal pressure, and the enlargement therefore means that there’s a higher likelihood of incarceration as well.” [Transcript, PA Barry, p.13]
“I think there are occasional instances where a sudden twisting movement or a very heavy exertion or movement could suddenly lead to incarceration, which we see only very occasionally, I must say. More often than not it might be a bout of some cause of raised intra-abdominal pressure. That event then leads to a final sort of incarceration, so often it’s a repetitive and progressive issue that eventually then leads to something, so its actually very difficult to pin hernias or their complications down to a particular event.” [Transcript, PA Barry, p.15]
29. Thus on Dr Barry’s evidence, while it is possible, there is little likelihood that a single strenuous event, such as using moderate to severe force to open a heavy door, would cause the enlargement of a hernia or the increased likelihood of incarceration of tissue thereby. What is more likely is that repetitive actions that increase intra-abdominal pressure, such as repeatedly using moderate to severe force to open the main access door over a period of time, may progressively lead to the enlargement of hernia or the increased likelihood of incarceration of tissue.
30. Dr Stevenson, consultant physician, gave evidence that a major increase in intra-abdominal pressure may “advance or precipitate hernia” (Exhibit R1, 2 May 2006 report, p2) but a single event would be unlikely to cause paraumbilical or epigastric hernias.
31. Thus it appears that Dr Barry and Dr Stevenson are in agreement that repetition of activities that result in moderate to severe increases of intra-abdominal pressure may cause paraumbilical and epigastric hernias to progress. Both doctors agreed that the forces required to open and close the main access door would raise intra-abdominal pressure moderately or severely. I comprehend their evidence to be that a hernia may progress by enlargement, or by an increased likelihood of the infarction or incarceration of tissue, and increased symptoms of pain and discomfort. I accept that evidence and so find.
32. Considering the facts of Mr Cox’s case, I am reasonably satisfied and find that Mr Cox used the main access door repeatedly over a period of many months prior to the onset of abdominal pain on 9 October 2003. The force required to open and close the access door was substantial and would have resulted in a moderate to severe increase in intra-abdominal pressure. In all likelihood the repeated increase in his intra-abdominal pressure caused his hernias to progress.
33. I note in passing that Mr Cox complained of pain spreading through his left flank without swelling on 9 October 2003. Subsequent episodes (mentioned above) involved specifically located pain at the site of the hernia and swelling. Dr Barry’s evidence that he would expect pain to be easily located with the tip of a finger in the case of incarcerated tissue but pain that resulted from tearing, such as may occur in the opening or enlargement of hernia, would not be so readily located. The pain of which Mr Cox complained on 9 October 2003 is more consistent with the enlargement of his hernia rather than the incarceration of tissue.
34. Thus, it is more probable than not that Mr Cox’s repetitive use of the main access door aggravated and enlarged his previously existing paraumbilical hernia on 9 October 2003, as a result of which there was an increased likelihood that tissue would be incarcerated following repeated increases in intra-abdominal pressure thereafter. That, I am satisfied, is what occurred on 9 January 2004.
35. I am reasonably satisfied that Mr Cox’s epigastric hernia (diagnosed on 21 March 2004 after bouts of paroxysmal coughing) was aggravated on 22 March 2004 as a result of Mr Cox retching and vomiting after taking Tramal. However, such aggravation is not compensable under the Act.
36. It is not clear whether the abdominal pain of which Mr Cox complained on 26 March 2004 during a luncheon event was related to his epigastric hernia, and even less clear what the cause of those symptoms may have been. The evidence is that Mr Cox consulted his general practitioner but did not require further treatment, but was referred to Dr Barry. There is no evidence of any lesion or physiological change in Mr Cox’s epigastric hernia. On that basis alone I am not persuaded that Mr Cox’s epigastric hernia was aggravated on 26 March 2004.
37. Nevertheless, I accept and find that Mr Cox’s repeated use of the main access door, and the resultant repeated increase in intra-abdominal pressure, in the period from 22 March to 24 May 2004 was a significant factor in the aggravation of his epigastric hernia on 24 May 2004. Mr Cox was hospitalised as a result of that aggravation and his epigastric hernia was repaired on 26 May 2004 by Dr Barry. It is possible that other activities outside work may also have caused his epigastric hernia to progress, as contended by the Respondent. However, the evidence concerning Mr Cox’s use of the main access door is consistent with that activity being a significant and proximate cause of increased intra-abdominal pressure during this period that cannot simply be ignored. The fact is his intra-abdominal pressure was repeatedly increased by his use of the main access door during this period. The medical consensus is that repeatedly raised intra-abdominal pressure may cause a hernia to progress or enlarge with the increased likelihood of infarction or incarceration of tissue. By that process Mr Cox’s epigastric hernia was aggravated by his employment on 24 May 2004. I so find.
38. Dr Stevenson reported that Mr Cox’s hernias were not caused by his employment. His opinion is based on a review of the medical literature that revealed only a small association between occupation and inguinal hernias. However, Dr Stevenson did not set out in his reports details of the precise methodology he adopted when reviewing the medical literature (the results of his researches are set out at the appendix to his report dated 30 November 2005). Dr Stevenson gave oral evidence about his use of the PubMed internet database and the search criteria he used. I note, with respect, that Dr Stevenson is a Consultant Physician and not an epidemiologist. I am not persuaded that the conclusions drawn from Dr Stevenson’s research have a sound epidemiological basis.
39. Dr Stevenson reported:
“I have both before my original report and since done a computer search of PubMed and other medical databases available to me to seek any literature supporting causal association between occupation and epigastric and para-umbilical hernia. I attempted several times without success. There are no publications supporting such a link.”
What is to be made of this conclusion? Dr Barry observed “…just because there is an absence of research, it doesn’t mean that there’s an absence of causation, it just means that no one’s really researched it…” (Transcript, PA Barry, p.6). That may be true. On the basis of Dr Stevenson’s evidence I am unable to determine whether research has been undertaken into any association between environmental factors, occupation and paraumbilical and epigastric hernias in adults. All that can be said is that if there is relevant research then the methodology Dr Stevenson employed did not lead him to it. To that extent, being mindful of the principles enunciated by Heydon JA in Makita (Australia) Pty Ltd v Sprowles [2001] 52 NSWLR 705 at 729-745, I attach little weight to these aspects of Dr Stevenson’s evidence.
40. I note, however, Dr Stevenson’s evidence on the subject of causal factors of hernias (Exhibit R1, 2 May 2006 report, p2):
“In fact if one looks at the one form of hernia, inguinal and femoral, which appears on anecdotal evidence to have most association with occupation, the evidence there which I have quoted and which is confirmed in the rest of the literature is fairly tenuous. This has led to reasonable Statements of Principles and guidelines which I have quoted in the appendix to my previous report. There needs to be a strenuous event and some reasonable temporal association.
I agree with Dr Barry that elevated intraabdominal pressure, if major, may advance or precipitate hernia. However, such elevations of intraabdominal pressure are common over a lifetime…
In general the associations between work-related forcible events are fairly tenuous overall but intermittently possible in the area of inguinal hernia. In other hernias where there is a preponderance of constitutional defect, e.g. umbilical, para-umbilical and epigastric, the association is rarely raised and the argument for work-relatedness is even more tenuous. I must still regard [Mr Cox’s] problems as mostly constitutional.”
In his oral evidence Dr Stevenson agreed that if the factors of the Statement of Principles to which he referred in his report dated 30 November 2005 (Exhibit R1) are satisfied, then the argument for work-related paraumbilical or epigastric hernia would be strengthened. On the facts I have found in this case, those stress and temporal factors are satisfied and it is established as a matter of probability that Mr Cox’s employment played a significant role in the aggravation of his paraumbilical and epigastric hernias. There is nothing in Dr Stevenson’s evidence that compels me to conclude differently. It is immaterial that intra-abdominal pressure may be raised by many common activities over a lifetime. What is material is that a specific action in the workplace raised Mr Cox’s intra-abdominal pressure repeatedly over a period of months and ultimately caused symptoms within a matter of hours that were consistent with an aggravation of his existing hernias.
Are the aggravations of Mr Cox’s hernias injuries simpliciter?
41. For symptoms to be characterised as an injury simpliciter there must have been some ascertainable lesion or a dramatic physiological change, or a disturbance of the normal physiological state, that is distinct from any underlying disease pathology (Kennedy Cleaning Services Pty Ltd v Petkoska (2000) 200 CLR 286 at 300-301).
42. I accept Dr Barry’s opinion that Mr Cox’s symptoms on 9 October 2003, 9 January 2004 and 24 May 2004 were consistent with the infarction or incarceration of omental or extraperitoneal fat at the site of the existing paraumbilical hernia. That is consistent with a physiological change either in the occlusion of blood flow to distended tissue (infarction) or the extrusion of tissue through the hernial opening (incarceration). Furthermore, I have found that Mr Cox’s previously existing paraumbilical hernia was enlarged on 9 October 2003 as a result of repeated significant increases in intra-abdominal pressure over an extended period of 12 to 18 months prior to the onset of painful symptomatology. Such enlargement is also consistent with an injury simpliciter.
43. The medical evidence is plain enough that hernias may exist for long periods at a sub-clinical level, but they progress over time with some inevitability against a background of actions in daily life that increase intra-abdominal pressure. The processes by which a sub-clinical hernia may be rendered painfully symptomatic as a result of enlargement or the incarceration or infarction of tissue are multifactorial and may include disease processes as well as more dramatic events resulting in ascertainable lesions or changes in normal physiology.
44. The contributing factors of significance in Mr Cox’s case that rise from the general background of possible factors are his repeated use of the main access door and paroxysmal coughing and retching. In both cases, balancing probabilities as opposed to mere possibilities, I am reasonably satisfied that these processes caused a sufficiently severe increase in intra-abdominal pressure to result in significant changes in Mr Cox’s physiology consistent with a frank injury. However, only one of those processes, opening the main access door, is related to Mr Cox’s employment and is, therefore, within the meaning of ‘injury’ under the Act.
were the aggravations temporary?
45. In Comcare’s submission if the incarceration of tissue is an injury in the form of an aggravation, then the aggravation ceases when the incarcerated tissue is released and returned to its usual state. That may be true if there is no evidence of any other physiological change having occurred.
46. Dr Barry gave evidence, which I accept, that Mr Cox’s paraumbilical hernia was probably enlarged by repeated increases in intra-abdominal pressure as a result of his activities in employment, whereby the hernia was rendered painfully symptomatic with an increased likelihood of incarcerating tissue. Thus, in that case, the frank injury Mr Cox suffered in aggravation of his existing hernia was not resolved by returning the incarcerated tissue to its previous state. The injury included the physical enlargement of the hernia as well as the incarceration of tissue. The injury was resolved by surgery on 12 February 2004.
47. Mr Cox’s epigastric hernia was precipitated by paroxysmal coughing prior to 21 March 2004 outside the context of his employment. Mr Cox had one episode of abdominal pain on 26 March 2004, but it is not clear whether this was the result of or gave rise to any physiological change. Mr Cox complained of swelling on that day. Swelling may be the result of a number of physiological processes, but no evidence was adduced on this point.
48. However, the episode on 24 May 2004 clearly resulted in the incarceration of tissue. Mr Cox’s evidence was that “in casualty they injected me and pushed the protrusion back…they successfully pushed it back in” and thereafter he was pain free until a few hours later when the swelling returned and pain increased while he was lying down in the hospital. He said that he asked the nurses to push it back in again but the problem was not resolved until he underwent surgical repair by Dr Barry the next day. The Calvary Hospital records (AT21D folios 55-62) reveal that Mr Cox presented with an incarcerated hernia at approximately 9.30am on 24 May 2004 and was given morphine. At 10.30am the hernia was reduced under 100mg of Fentanyl and 3mg Midozolam. At 18.09pm the records state “pain just the same… no obvious mass palpable …tender++”. On 25 May 2004 Dr Barry reported the presence of incarcerated extra-peritoneal tissue at surgery.
49. On that evidence it is apparent that the symptoms Mr Cox experienced on 24 May 2004 were not resolved merely by returning the incarcerated tissue through the hernia. That process provided some relief and Mr Cox’s symptoms were reduced. Mr Cox’s work-related symptoms were not resolved until completion of the surgical repair by Dr Barry on 25 May 2004.
50. It follows that the surgical procedures Dr Barry carried out on 12 February 2004 and 25 May 2004 were required treatment for the frank injuries he experienced on 9 October 2003, 9 January 2004 and 24 May 2004. I so find.
decision
51. The decision under review is set aside. In place thereof the Tribunal decides that Mr Cox suffered aggravations of his paraumbilical and epigastric hernias on 9 October 2003, 9 January 2004 and 24 May 2004 for which Comcare is liable.
52. As the matter is resolved in a manner favourable to Mr Cox, I order that Comcare is to pay his reasonable costs in these proceedings pursuant to s 67(8) of the Act.
I certify that the 52 preceding paragraphs are a true copy of the reasons for the decision herein of Mr S. Webb, Member
Signed: .....Peter Strauch............................................................
AssociateDate of Hearing 25-26 May 2006
Date of Decision 15 June 2006
Counsel for the Applicant David Richards
Solicitor for the Applicant Pamela Coward & Assoc
Counsel for the Respondent Lorraine Walker
Solicitor for the Respondent Dibbs Abbott Stillman
1
0