Anderson and Military Rehabilitation and Compensation Commission (Compensation)
[2018] AATA 4188
•8 November 2018
Anderson and Military Rehabilitation and Compensation Commission (Compensation) [2018] AATA 4188 (8 November 2018)
Division:VETERANS' APPEALS DIVISION
File Number(s): 2016/5799
Re:Barry Anderson
APPLICANT
AndMilitary Rehabilitation and Compensation Commission
RESPONDENT
DECISION
Tribunal:Deputy President Boyle
Date:8 November 2018
Place:Perth
The Tribunal affirms the reviewable decision.
....[sgd]....................................................................
Deputy President Boyle
CATCHWORDS
COMPENSATION – whether there is a permanent impairment – whether there is non-economic loss – obstructive sleep apnoea – deviated septum – applicant suffered broken nose in the course of his defence service – whether the applicant’s obstructive sleep apnoea is contributed to, to a significant degree, by the applicant’s employment by the Commonwealth – the reviewable decision is affirmed
LEGISLATION
Military Rehabilitation and Compensation Act 2004 (Cth)
Military Rehabilitation and Compensation (Consequential and Transitional Provisions) Act 2004 (Cth) – ss 7, 7(1)(b)
Safety, Rehabilitation and Compensation Act 1988 (Cth) – ss 14, 16, 19, 24, 27
Safety, Rehabilitation and Compensation (Defence-related Claims) Act 1988 (Cth) – ss 5A(1)(a), 5A(1)(b), 5B, 14, 24, 27, 28, 141Safety, Rehabilitation and Compensation Legislation Amendment (Defence Force) Act 2017 (Cth) – ss 2, 64,
CASES
Anderson and Military Rehabilitation and Compensation Commission [2013] AATA 360
Commonwealth v Verwayen (1990) 170 CLR 394
Filsell and Comcare [2009] AATA 90
Rana and Military Rehabilitation and Compensation Commission [2008] AATA 558
Telstra Corporation Limited v Hannaford (2006) 151 FCR 253; [2006] FCAFC 87Waltons Stores (Interstate) Ltd v Maher (1988) 164 CLR 387
SECONDARY MATERIALS
Lexis Nexis, Halsbury’s Laws of Australia, (as at 28 March 2018) ‘General Nature and Principles of Estoppel’ [190-1]
REASONS FOR DECISION
Deputy President Boyle
8 November 2018
THE APPLICATION
The Applicant seeks the review of the Respondent’s decision dated 1 September 2016 (the reviewable decision) (T39) by which the Respondent affirmed the determination dated 3 June 2016 (T35) that the Applicant was not entitled to payment under s 24 (permanent impairment) or s 27 (non-economic loss) of the Safety, Rehabilitation and Compensation Act 1988 (Cth) (SRC Act) in respect of the Applicant’s accepted condition of obstructive sleep apnoea (OSA).
The application for review was made on 28 October 2016 (T2). By operation of s 64 of the Safety, Rehabilitation and Compensation Legislation Amendment (Defence Force) Act 2017 (Cth) (Amending Act), the process, including the claim for compensation and the application, are taken to have been begun under the Safety, Rehabilitation and Compensation (Defence-related Claims) Act 1988 (Cth) (DRC Act).
Pursuant to s 64 of the DRC Act the Tribunal has the power to review the reviewable decision.
BACKGROUND
The Applicant is 48 years of age. He entered the Royal Australian Navy (RAN) as an apprentice electronics technician, on 8 January 1988, aged 17. He retired from the RAN on 1 August 2011 having attained the rank of Chief Petty Officer.
On ANZAC Day 1988, while serving at HMAS Nirimba in New South Wales as a naval apprentice, the Applicant was required to attend the ANZAC Day march in Sydney as a banner bearer. At the after-march function he was struck by a fellow naval apprentice and suffered a broken nose (T13 at 37).
The Applicant says that while serving on the HMAS Melbourne in 1992 it was noted by the PO medic that he had a deviated septum (T13 at 37). He says that he started to develop symptoms of sleep apnoea around 2006.
In February 2010 the Applicant underwent a sleep study conducted by Dr Jack Philpott. Dr Philpott’s report (T4 at 21 and T5 at 23) concluded, amongst other things, that there was evidence of moderately severe OSA with mild symptoms. The OSA was confined to the supine position. Dr Philpott said that the Applicant should be encouraged to lose weight. He recommended a trial of posture modification and a trial of nasal continuous positive airway passage (CPAP) and that if the Applicant failed to tolerate CPAP, consideration should be given to the use of a mandibular advancement splint (MAS).
Following on from the sleep study the Applicant was referred to ear, nose and throat specialist Dr Chady Sader. In his report dated 25 March 2010 (T7), Dr Sader noted that the Applicant was 186 cms in height and weighed 110 kgs with a body mass index (BMI) of 32. His examination showed that the Applicant had “large tonsils with a deviated septum”. He further recorded that after discussion of the pros and cons of surgical versus conservative management, the Applicant opted for uvulopalatorpharyngoplasty (UPPP) and septoplasty. Dr Sader indicated that at the time of that surgery he would also reduce the size of the Applicant’s turbinates. At the hearing Dr Sader explained the UPPP procedure as follows (Transcript, p 62):
…it involves a tonsillectomy. It involves reshaping the pharynx so that it is less compliant. So it is firmer and more taut, and less likely to reverberate and contribute to snoring and sleep apnoea. So you increase the amount of air that is in the upper airway. And it – you increase the amount of air that travels behind the palette. So it generally moves the soft palette a little forward.
In his post-operative report dated 30 April 2010 (T8), Dr Sader reported that the Applicant “had quite a dislocated septum which I corrected and at the same time reduced the size of his turbinates” (T8, at 29).
In May 2011 the Applicant lodged with the Department of Veterans’ Affairs (DVA) a claim for acceptance of liability under the Military Rehabilitation and Compensation Act 2004 (Cth) (MRC Act) for the condition of OSA. In August 2011 a delegate of the Respondent made a determination disallowing the Applicant’s claim. That determination was affirmed by the decision of another delegate of the Respondent in August 2012. On 10 October 2012 the Applicant made an application to the tribunal for a review of that decision.
By decision of Deputy President Hotop dated 31 May 2013 in Anderson and Military Rehabilitation and Compensation Commission [2013] AATA 360, the Deputy President determined that the MRC Act did not apply to the Applicant’s claim.
On 6 August 2013 the Applicant’s claim for compensation for the conditions of deviated septum and OSA were accepted by the Respondent (T15) under the SRC Act on the basis that the Applicant suffered from those conditions as a result of a broken nose and deviated septum suffered by the Applicant on 25 April 1988 in the course of his defence service.
On 8 August 2013 the Applicant completed a needs assessment form (T16) by which he sought assessment of his entitlement to permanent impairment compensation.
By determination dated 26 February 2016 (T32) the Applicant’s claim for a permanent impairment lump sum payment for “broken nose” and “deviated septum” was rejected. By a determination dated 3 June 2016 (T35) the Applicant’s claim for a permanent impairment lump sum payment for the Applicant’s OSA was rejected.
The Applicant through his lawyers requested a reconsideration of the determination of 3 June 2016 relating to the Applicant’s OSA (T38) and by the reviewable decision on 1 September 2016 that determination was affirmed (T39).
LEGISLATIVE FRAMEWORK
As noted at [2] above, the Applicant lodged this application on 28 October 2016. Under s2 of the Amending Act the DRC Act came into effect on 12 October 2017. The Amending Act, in effect, substantially duplicated the terms of the SRC Act and that duplicate Act became the DRC Act.
The Amending Act also made some amendments to the SRC Act including:
(a)amending section 4AA of the SRC Act to provide: “Neither Comcare nor the Commission has any liability under this Act in respect of an injury, loss, damage or death that relates to defence service (whenever it occurred)”. By this amendment, liability for defence-related claims was transferred to the DRC Act or the MRC Act, depending on the date of the injury; and
(b)repealing Part XI of the SRC Act, which had been the Part of the SRC Act that had contained provisions in relation to liability for defence-related claims. Part XI remains in the DRC Act.
Section 64 of the Amending Act provides:
Claims, applications, requests and other processes begun under the Safety, Rehabilitation and Compensation Act 1988
(1) This item applies if:
(a)a process begun (including by claim, application or request) under a provision of the Safety, Rehabilitation and Compensation Act 1988 before the first commencement time was not completed by that time; and
(b)immediately after the second commencement time, there is a corresponding provision in the Safety, Rehabilitation and Compensation (Defence‑related Claims) Act 1988.
(2) Without limiting its effect apart from this item, the process is also taken, after the second commencement time, to have been begun under the corresponding provision.
The first commencement and the second commencement time for the purposes of s 64 of the Amending Act is 12 October 2017. Section 62 of the Amending Act provides:
62 Definitions
In this Part:
first commencement time means the time when Part 1 of this Schedule commences.
second commencement time means the time when this Part commences.
Section 2 of the Amending Act provides the following table relating to commencement:
2 Commencement
(1) Each provision of this Act specified in column 1 of the table commences, or is taken to have commenced, in accordance with column 2 of the table. Any other statement in column 2 has effect according to its terms.
Commencement information Column 1 Column 2 Column 3 Provisions Commencement Date/Details 1. Sections 1 to 3 and anything in this Act not elsewhere covered by this table The day this Act receives the Royal Assent. 14 September 2017 2. Schedule 1, Part 1 The 28th day after this Act receives the Royal Assent. 12 October 2017 3. Schedule 1, Part 2 Immediately after the commencement of the provisions covered by table item 2. 12 October 2017 5. Schedules 2 and 3 Immediately after the commencement of the provisions covered by table item 2. 12 October 2017
As the application was commenced before 12 October 2017 and there are provisions in the DRC Act corresponding to provisions in the SRC Act, the application is taken to be made under the DRC Act.
Section 141 of the DRC Act defines defence-related claims to which the DRC Act applies as follows:
defence‑related claim means a claim under this Act made before or after the MRCA commencement date (including a claim made but not determined before that date) in respect of an injury, loss, damage or death:
(a)to which the MRCA does not apply; and
(b)that relates to defence service that occurred before the MRCA commencement date.
Section 7 of the Military Rehabilitation and Compensation (Consequential and Transitional Provisions) Act 2004 (Cth) (MRC (Transitional Provisions) Act) is as follows:
Application of the MRCA to certain injuries, diseases and deaths
(1) The MRCA applies to a person’s injury, disease or death if:
(a)the injury is sustained, the disease is contracted, or the death occurs, on or after the commencement date; and
(b)the injury, disease or death either:
(i) relates to defence service rendered by the person on or after that date; or
(ii) relates to defence service rendered by the person before, and on or after, that date.
The Applicant relies on the injury sustained to his nose in an incident on 25 April 1988 as the causal connection between his OSA and his defence service. Having regard to s 7(1)(b) of the MRC (Transitional Provisions) Act and s 141 of the DRC Act, the DRC Act applies to the determination of the Applicant’s claim and these proceedings, as the injury occurred prior to the commencement of the MRC Act on 1 July 2004. The non-applicability of the MRC Act to the Applicant’s circumstances was confirmed by the tribunal in Anderson and Military Rehabilitation and Compensation Commission [2013] AATA 360: see at [29]-[30] of that decision.
Section 14 of the DRC Act, relevantly, provides:
Compensation for injuries
(1) Subject to this Part, the Commonwealth 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 24 of the DRC Act relevantly provides:
Compensation for injuries resulting in permanent impairment
(1) Where an injury to an employee results in a permanent impairment, the Commonwealth is liable to pay compensation to the employee in respect of the injury.
(2) For the purpose of determining whether an impairment is permanent, the MRCC shall have regard to:
(a)the duration of the impairment;
(b)the likelihood of improvement in the employee’s condition;
(c)whether the employee has undertaken all reasonable rehabilitative treatment for the impairment; and
(d)any other relevant matters.
(3) Subject to this section, the amount of compensation payable to the employee is such amount, as is assessed by the MRCC under subsection (4), being an amount not exceeding the maximum amount at the date of the assessment.
(4) The amount assessed by the MRCC shall be an amount that is the same percentage of the maximum amount as the percentage determined by the MRCC under subsection (5).
(5) The MRCC shall determine the degree of permanent impairment of the employee resulting from an injury under the provisions of the approved Guide.
(6) The degree of permanent impairment shall be expressed as a percentage.
(7) Subject to section 25, if:
(a)the employee has a permanent impairment other than a hearing loss; and
(b)the MRCC determines that the degree of permanent impairment is less than 10%;
an amount of compensation is not payable to the employee under this section.
(7A) …
(8) …
(9) For the purposes of this section, the maximum amount is $80,000.
Section 27 of the DRC Act relevantly provides:
Compensation for non‑economic loss
(1) Where an injury to an employee results in a permanent impairment and compensation is payable in respect of the injury under section 24, the Commonwealth is liable to pay additional compensation in accordance with this section to the employee in respect of that injury for any non‑economic loss suffered by the employee as a result of that injury or impairment.
(2) The amount of compensation is an amount assessed by the MRCC under the formula:
($15,000 x A) + ($15,000 x B)
where:
A is the percentage finally determined by the MRCC under section 24 to be the degree of permanent impairment of the employee; and
B is the percentage determined by the MRCC under the approved Guide to be the degree of non‑economic loss suffered by the employee.
Section 28 of the DRC Act relevantly provides:
Approved Guide
(1) The MRCC may, from time to time, prepare a written document, to be called the “Guide to the Assessment of the Degree of Permanent Impairment”, setting out:
(a)criteria by reference to which the degree of the permanent impairment of an employee resulting from an injury shall be determined;
(b)criteria by reference to which the degree of non‑economic loss suffered by an employee as a result of an injury or impairment shall be determined; and
(c)methods by which the degree of permanent impairment and the degree of non‑economic loss, as determined under those criteria, shall be expressed as a percentage.
(2) The MRCC may, from time to time, by instrument in writing, vary or revoke the approved Guide.
(3) …
(3A) A Guide prepared under subsection (1), and a variation or revocation under subsection (2) of such a Guide, is a legislative instrument made by the Minister on the day on which the Guide, or variation or revocation, is approved by the Minister.
(4) Where the MRCC or the Administrative Appeals Tribunal is required to assess or re‑assess, or review the assessment or re‑assessment of, the degree of permanent impairment of an employee resulting from an injury, or the degree of non‑economic loss suffered by an employee, the provisions of the approved Guide are binding on the MRCC or the Administrative Appeals Tribunal, as the case may be, in the carrying out of that assessment, re‑assessment or review, and the assessment, re‑assessment or review shall be made under the relevant provisions of the approved Guide.
(5) The percentage of permanent impairment or non‑economic loss suffered by an employee as a result of an injury ascertained under the methods referred to in paragraph (1)(c) may be 0%.
(6) …
THE ISSUES
In its Statement of Issues, Facts and Contentions (Respondent’s SIFC) the Respondent identifies the issues as follows (R1):
2.1 The only issue for consideration by the Tribunal is whether the Applicant is entitled to compensation for permanent impairment and non-economic loss under ss 24 and 27 of the DRC Act for the OSA condition. This requires consideration of the following:
(a)Did the Applicant’s former military employment significantly contribute to the OSA condition or in the alternative does the Applicant’s former military employment continue to significantly contribute to the OSA condition? If so,
(b)Is the Applicant is [sic] entitled to compensation under ss 24 and 27 of the DRC Act in respect of the OSA condition? This requires consideration of:
(i) Whether the OSA condition is permanent, in the sense of being ‘likely to continue indefinitely’ for the purposes of s 24(2) of the DRC Act?
(ii) If so, whether the degree of WPI as a result of the OSA condition is at least 10%, by reference to the Comcare Guide to the Assessment of the Degree of Permanent Impairment, edition 2.1 (the Comcare Guide) or in the alternative by reference to the American Medical Association Guide, 5th edition (AMA Guide).
(iii) If the WPI as a result of the OSA condition is at least 10%, what the WPI assessment is and what the amounts payable under ss 24 and 27 of the DRC Act for the OSA condition is.
(Original emphasis)
In its Statement of Issues, Facts and Contentions (Applicant’s SIFC) the Applicant identifies the issues as follows (A1):
The Applicant considers that the issues for the Tribunal to determine are as follows:
1. Whether the assessment of impairment in this case should be undertaken aided or unaided; incorporating the following sub issues:
(a)When assessing impairment what is being measured?
(b)Does CPAP or a mandibular split constitute ‘rehabilitative treatment’;
(c)Does CPAP or a mandibular splint lessen the injury?
2. At what percentage is the impairment; incorporating the following sub-issues:
What is the appropriate assessment tool?
(a)Is there any discretion about what assessment tool is used?
(b)What factor or factors should influence the exercise of any such discretion?
3. Was a further medical assessment and sleep test necessary for the Respondent to reach an opinion about the Applicant’s impairment?
4. Whether the impairment arises from the compensable injury, incorporating the following sub-issue:
(a)What nexus is required between the compensable injury and the impairment?
5. Is it permissible in this case for the Respondent to disclaim the nexus between injury and impairment by disputing a compensable injury exists, incorporating the following sub-issues:
(a)Where liability for an injury is admitted can it be revisited in these proceedings?
(b)In this particular case is the Respondent estopped by its conduct from disclaiming liability for the accepted injury and/or the nexus between the impairment and the injury;
(c)Does estoppel by conduct apply in this jurisdiction?
6. Does the Applicant have to bring separate claims for his nasal resistance, hypotestosteronism, obesity, hypertension and cognitive impairment/depression, or are they assessable as sequelae and combined in his WPI, incorporating the following sub-issues:
(a)If they are not separate claims how should the Tribunal inform itself at [sic] to what impairments each attracts and whether those impairments are permanent?
(b)Was the Respondent correct to take into account the Respondent’s mechanical lower limb problems to determine his obesity was not an impairment resulting from OSA and his depression to determine his cognitive impairment was not due to OSA and his (corrected) deviated septum and broken nose to determine his increased nasal resistance was not due to OSA?
7. What is the Applicant’s permanent impairment (WPI) arising from his OSA and any assessable sequelae.
THE HEARING AND THE EVIDENCE
The application was held in Perth on the 14 and 15 August 2018. The Applicant was represented by Ms Sorgiovanni. The Applicant did not attend the first day of hearing as he had been admitted to hospital. The Applicant appeared by telephone on 15 August 2018 and gave evidence. He was cross-examined by the Respondent’s counsel. The Respondent was represented by counsel, Ms Oliver, who was instructed by Sparke Helmore Lawyers.
The Tribunal also heard evidence from the following witnesses during the hearing:
·Dr Brian Galton-Fenzi, Occupational and General Physician (in person);
·Dr Jack Philpott, Respiratory and Sleep Physician (by telephone);
·Dr Robert Delcanho, Consultant in Pain Medicine, Head, Face and Oral Pain (in person);
·Dr Chady Sader, Adult and Paediatric Otolaryngologist (by telephone); and
·Dr Michael Prichard, Sleep Physician (by telephone).
The following documents were admitted into evidence as follows:
(a)the Applicants SIFC dated 9 April 2018 (Exhibit A1);
(b)the Applicant’s Book of Documents dated 12 April 2018 (Exhibit A2);
(c)the Applicant’s report request to Dr Galton-Fezi dated 31 May 2017 (Exhibit A3);
(d)the Applicant’s report request to Dr Galton-Fenzi dated 15 May 2017 (Exhibit A4);
(e)the Respondent’s SIFC including attachments dated 25 May 2018 (Exhibit R1);
(f)the summonsed documents from Western ENT, Sleep WA and Clinical Integration Solutions (Exhibit R2); and
(g)the T-Documents from pages 1 – 174 (T1 – T40) received by the Tribunal on 28 November 2016 (Exhibit R3).
ESTOPPEL
In effect, two estoppel arguments appear to be raised by the Applicant. The first is set out in paragraphs 45 and 46 of the Applicant’s SIFC as follows:
45. In the determination dated 3 June 2016 (affirmed 1 September 2016) the Respondent’s delegate said she ‘needs evidence you suffer an impairment as a result of a work related injury’ [sic] Having had the claim for injury accepted, there was no further onus on the Applicant to address causation. ‘Work related’ is not the test for the definition of ‘injury’ nor is it the test for the nexus between ‘injury’ and ‘impairment’, in any event. The nexus between the impairment and the service is that the impairment must result from the injury’. It need not be the sole or predominant cause.
46. The Respondent cannot now disclaim the nexus having admitted liability, for the reasons outlined above. Admitting liability incorporates admitting causation. There is no evidence to suggest the link between the admitted injury and the impairment has been broken.
(Footnotes omitted)
The Respondent answers that assertion in its SIFC as follows:
4.8 The Respondent disputes the Applicant’s contention that the Respondent is estopped from contending that the Applicant’s OSA condition is not an injury (including a disease) as defined by the DRC Act.
4.9 The Respondent contends that a preliminary consideration of s 24 of the DRC Act is that the Tribunal must satisfy itself that the Applicant suffers an injury (including a disease) as defined by the DRC Act. Section 24 relevantly states that:
(1) Where an injury to an employee results in a permanent impairment, Comcare is liable to pay compensation to the employee in respect of the injury [original emphasis in quote].
4.10 The Respondent relies on the following in support of this:
(a)The Tribunal will need to consider whether the Applicant’s OSA condition is an injury as defined by the DRC Act as part of the permanent impairment application and can make findings which undercut the original determination as noted by Deputy President Kendall’s recent decision of Den Hartog and Comcare [2017] AATA 1164, where DP Kendall made findings in line with the Full Court Decision of Telstra Corporation Limited v Hannaford [2006] FCAFC 87.
(b)Deputy President Forgie in Rana and Military Rehabilitation and Compensation Commission [2008] AATA 558 noted that s 25(4) of the AAT Act provides that: ‘The Tribunal has power to review any decision in respect of which application is made to it under any enactment’ and found at paragraph [110] that the Tribunal has power to review the reviewable decision and principles of res judicata or issue estoppel cannot stand in the way of the statutory provisions giving the Tribunal the power to review it.
…
4.12 The Full Federal Court held in Telstra Corporation Limited v Hannaford [2006] FCAFC 87 that the Tribunal was ‘duly empowered…to make findings of fact that effectively undercut the necessary findings of fact made in the initial or original decision of Telstra under s 14 of the SRC Act to accept liability…’ in respect of the claim for compensation.
4.13 The Respondent relies on the Full Federal Court decision in Hannaford and contends that it is open to the Tribunal to make a finding that the determination dated 6 October 2013 in which liability for the OSA condition was accepted was incorrect (T15).
The Respondent also cites [58] and [59] of the decision of Deputy President Jarvis in Filsell and Comcare [2009] AATA 90 as affirming and following the approach taken by Deputy President Forgie in Rana and Military Rehabilitation and Compensation Commission [2008] AATA 558.
The Tribunal notes the comments in paragraph 45 of the Applicant’s SIFC quoted at [33] above relating to the use of the term “work related” in the delegate’s reasons for decision, however, that point is not critical to the Applicant’s argument of an estoppel arising out of the Respondent’s previous acceptance of liability, as the Tribunal understands the argument. As the Respondent submits, the argument raised by the Applicant appears to be, in effect, the argument that was addressed by the Full Court of the Federal Court in Telstra Corporation Limited v Hannaford (2006) 151 FCR 253 (Hannaford). For the same reasons that the Full Court rejected that argument in Hannaford, the Applicant’s argument must also be rejected.
In the present case, in order to make a determination as to liability under ss 24 and 27 of the DRC Act, the Respondent (and the Tribunal standing in the shoes of the Respondent) must, amongst other things, satisfy itself, not only that there is a permanent impairment, but also that there is an injury which “results in the permanent impairment”. In order to qualify as an injury, the relevant condition, if it is an injury for the purposes of s 5A(1)(b) of the DRC Act, must be one resulting from a physical or mental injury arising out of or in the course of the Applicant’s employment, or if it is an injury under s 5A(1)(a) of the DRC Act (disease) that it is an ailment that was contributed to, to a significant degree, by the Applicant’s employment by the Commonwealth.
In Hannaford a previous acceptance of liability under s 14 of the SRC Act for Ross River Fever did not prevent a subsequent denial of liability for compensation under ss 16 and 19 of the SRC Act on the basis that the employee did not suffer from the disease for which liability had been accepted under s 14 of the SRC Act. In that case the basis on which there was a finding of no liability under ss 16 and 19 of the SRC Act was inconsistent with the previous acceptance of liability under s 14 of the SRC Act. The Full Court of the Federal Court in Hannaford held that such a finding was open to the decision-maker.
The Applicant’s argument also overlooks the fact that circumstances change. The fact that in 2013 the Respondent accepted liability on the basis that the Applicant’s then OSA was related to his employment by the Commonwealth, specifically related to the incident in 1988 in which the Applicant suffered a broken nose, does not mean that the Respondent is thereafter forever prevented from arguing that the Applicant’s OSA no longer results from that incident. The effect of the Applicant’s argument is that once an employer accepts that a medical condition is, at that point in time, the result of a work related injury, the employer is forever bound to accept that the medical condition continues to be the result of the injury irrespective of the effluxion of time and changes in circumstances. That cannot be the case. While it may be that at a particular point in time the medical condition was the result of or contributed to, to a significant degree, by a work incident, as other factors, in particular aging, take effect, that “nexus”, to use the language of the Applicant, may cease to exist. That has to be an argument open to the Respondent.
The Applicant’s first estoppel argument must fail, not only because it is contrary to the principle established by the Federal Court in Hannaford, but also because it is contrary to the reality that circumstances affecting the employee may change.
It must also fail because there is no recognised legal basis for it. Halsbury’s Laws of Australia observes that:[1]
In essence, estoppel prevents a party to litigation from relying on or asserting as true a particular proposition of fact or law, whether or not the proposition is true. There is no single principle to explain the ‘complex array of rules spanning various categories’ embraced by the term ‘estoppel’. There are the divisions between common law and equitable estoppel, between estoppel by conduct and estoppel by representation, and the distinction between present and future fact. There are titles such as promissory estoppel, proprietary estoppel and estoppel by acquiescence. Yet all of these categories and distinctions are intended to serve the same fundamental purpose, namely ‘protection against the detriment which would flow from a party’s change of position if the assumption (or expectation) that led to it were deserted’.
(Footnotes omitted)
[1] Lexis Nexis, Halsbury’s Laws of Australia, (as at 28 March 2018) ‘General Nature and Principles of Estoppel’ [190-1].
While, as Halsbury’s Laws of Australia notes, there is no single principle behind the array of categories covered by the concept of estoppel, there does have to be some legal or equitable basis for the claim. As the above cited passage identifies, there are estoppels described as common law or equitable estoppels, estoppel by conduct, proprietary estoppel and estoppel by acquiescence that arise in relevant circumstances. However, in all of those cases there is a legal or equitable principle that is triggered by relevant circumstances. They all have at their core the protection of a party against another party resiling from a previously stated position, upon which that party has relied, to its detriment (Waltons Stores (Interstate) Ltd v Maher (1988) 164 CLR 387; Commonwealth v Verwayen (1990) 170 CLR 394).
In the present case the Applicant does not point to any position taken by him, or to any action or inaction on his part, as a result of the Respondent’s previous acceptance of liability, and therefore the connection between the Applicant’s OSA (at that time) and his employment by the Commonwealth, which would give rise to an estoppel preventing the Respondent from now denying that connection. The Applicant makes the bald assertion that “[t]he Respondent cannot now disclaim the nexus having admitted liability, for the reasons outlined above” (R1, paragraph 46) without setting out any relevant facts or legal principles which would support that assertion.
The second estoppel argument raised by the Applicant is set out in paragraphs 48 and 49 of the Applicant’s SIFC as follows:
48. The Respondent is estopped by their conduct in offering to accept the Applicant’s SRCA claim, if the Applicant brought the claim pursuant to SRCA, which he did, on the strength of the Respondent’s advice that it would be accepted. This was not an obvious choice because the assault was in April 1988, predating SRCA and the onset of OSA symptoms was 2006, post-dating SRCA. As a result, the Applicant did not appeal application no 2012/4520 which claimed cover under MRCA. In the alternative the Applicant should be permitted to bring that appeal out of time with the Respondent’s consent.
49. We accept that res judicata and issue estoppel do not apply in this jurisdiction based on previous decisions of this tribunal, but the case law does not preclude estoppel by conduct.
(Footnotes omitted)
At the hearing the Tribunal requested counsel for the Applicant to explain the Applicant’s second estoppel argument. The following exchange took place (Transcript, pp 9-11):
DEPUTY PRESIDENT: Yes. I’m just a little interested in the estoppel argument. How do you say that arises? Arising out of - following Hotop DP, decision?
MS SORGIOVANNI: Certainly. There’s a few different types of estoppel, as you would appreciate. There’s res judicata, there’s estoppel arising on a decision in relation to the ultimate facts found in that decision and the decision itself. But there are a couple of other types of estoppel that we say the case law that has been canvassed in this jurisdiction doesn’t cover, and those are Anshun estoppel and estoppel by conduct. And Anshun estoppel and estoppel by conduct are arguably species of the same thing. But essentially, where a representation is made to somebody, that person acts on that representation; they act on that representation to their detriment and they forego doing something that they would otherwise have done or some other form of detriment.
Then the person who made the representation seeks to withdraw that representation causing detriment, effectively, to materialise. We say that there’s that aspect to it, the estoppel by conduct aspect, in that Mr Anderson made a claim under SRCA instead of progressing with his appeal under the MRCA Act. And secondly, that under the MRCA Act there were the, if you like, deemed causation under the statements of principles which don’t apply under the SRCA Act, which now the respondent wants to raise in these proceedings. And then, there’s Anshun estoppel, which Anshun estoppel as I understand it, relates more to what ought to have been raised in proceedings before a court, or in the course of a decision-making process.
And of course, DVA is - their delegates perform an administrative, but also a judicial function when they make a decision and also, do a reconsideration of decisions. And in this case, they made a decision in August to accept his claim, as you rightly point out, after he’d already had the surgery. And in fact, the lawyers made a representation to our firm that if he makes this claim it will be accepted. And on that basis, he went ahead and simply made an SRCA claim. We say, that from an Anshun estoppel point of view, if it was something that DVA was going to rely upon to decline his claim, it would have been appropriate to raise that at a much earlier stage than now. Presumably, at the time when they were considering liability and that would have enabled Mr Anderson to make a much earlier decision about whether he continued down that path.
…
DEPUTY PRESIDENT:…The action that the applicant took in reliance on the representation was, as I understand it, the argument is not to - was it not to appeal the decision of Hotop DP?
MS SORGIOVANNI: Yes, that is the decision that he took.
DEPUTY PRESIDENT: In which case, would the applicant, in order to get up on that argument, have to establish, I suppose, substance to the consideration in that - would you not have to establish that there was a prospect that the appeal would be successful?
MS SORGIOVANNI: I think you’d have to establish that there was a prospect; I don’t think you’d have to establish that it would have been successful.
Paragraph 48 of the Applicant’s SIFC quoted at [44] above cites the Applicant’s lawyer’s letter dated 21 June 2013 and the Respondent’s lawyer’s response dated 10 July 2013 as constituting the agreement that the Respondent would accept the Applicant’s claim under the SRC Act following Deputy President Hotop’s decision that the claim could not be brought under the MRC Act. The wording of that correspondence is important. Relevantly, the Applicant’s lawyer’s letter (A2 at 161) states:
…in open court counsel for the Respondent indicated this claim would be accepted if made under the SRCA legislation…
If the claim is subsequently denied he will appeal and it may be the case that he ultimately has to appeal both decisions. Can you confirm that if the SRCA claim is declined that the Respondent will not object to an application for leave to appeal the current decision out of time?
The Respondent’s lawyers responded in the following terms (A2 at 162):
· Any claim for acceptance of liability under the SRC Act lodged by the applicant regarding the applicant’s condition “obstructive sleep apnoea” the subject of AAT application 2012/4520 would be accepted.
· There is no reason why an appeal, if any, of the decision [2013] AATA 360 would not be sought within the usual required timeframe.
· Whether there is a claim for liability pending under the SRC Act (or any other Act) has no bearing on the issues for consideration in an appeal of the current decision.
· You have indicated that in your view there are “good grounds of appeal”, which is a matter for discussion with your client, including if and when that appeal is sought.
There are a number of things in this exchange worth noting. The first is that insofar as the Applicant now seeks to argue an estoppel against the Respondent denying liability, the Respondent did in fact accept liability shortly after the exchange. The claim under the SRC Act (which by operation of subsequent changes to the legislation became a claim under the DRC Act) was accepted by the Respondent on 6 August 2013 (T15).
Secondly, what the Applicant’s lawyer’s letter of 21 June 2013 sought was not some unending, unconditional acceptance of all liability for any claim made under the SRC Act in the future, but rather was whether, if the SRC Act claim was rejected, the Respondent would “not object to an application for leave to appeal the current decision out of time”. Far from seeking (and being given) some undertaking that all liability would be accepted under the SRC Act, the Applicant’s lawyer’s letter, by its terms, accepted that the claim under the SRC Act may be rejected. The whole point of the Applicant’s lawyer’s letter was to address that possibility. This fact almost seems to be conceded by the somewhat curious (in these proceedings) submission in paragraph 48 of the Applicant’s SIFC that “[i]n the alternative the Applicant should be permitted to bring that appeal out of time with the Respondent’s consent”. This is not an application to appeal the decision in the previous AAT matter 2012/4520 and that submission is irrelevant to any issue to be considered in the present proceedings.
As far as the Tribunal can determine, the Respondent’s SIFC did not address this second estoppel argument. In its closing submissions the Respondent addressed the second estoppel argument as follows:
29. In so far as the applicant might seek to argue that he would have sought to appeal the decision of the Tribunal which affirmed the rejection of his claim under the MRCA, the respondent notes that any appeal was unlikely to be successful given the clear legislative provisions. In the earlier Tribunal proceedings, the applicant did not accept the respondent’s position that the MRCA had no application in his case, and he had elected to proceed with his claim under the MRCA. The Tribunal found the MRCA did not apply as the injury occurred prior to 1 July 2004, and dismissed the application for review (Re Anderson and Military Rehabilitation and Compensation Commission [2013] AATA 360 at [29]-[30]). If the applicant considered that decision was wrong, he could have appealed the decision. By making a claim under the SRCA the applicant was not required to forego his appeal rights in relation to the Tribunal’s decision. Rather the applicant made his own decision not to exercise his appeal rights in relation to the earlier decision.
30. In so far as the applicant might seek to argue that he has suffered detriment by virtue of the transfer of his claim from the SRCA to the DRCA, the respondent observes that the claim was transferred by operation of law, not as the result of any act on the part of the respondent. But more significantly, the respondent observes that when the DRCA was enacted it was enacted as a complete duplication of the SRCA. The enactment of the DRCA therefore did not result in any change to the applicant’s rights, in so far as any rights might have accrued under the SRCA. In the circumstances, there is no need for resort to be had to section 7 of the Acts Interpretation Act 1901 (Cth).
(Original emphasis)
The Tribunal agrees with the Respondent’s argument. Primarily, however, the Tribunal finds that there is simply no factual or legal basis for the second estoppel argument. The correspondence and the conduct of the Respondent relied on by the Applicant cannot give rise to any estoppel by which the Respondent would be prevented for denying liability for the claims the subject of these proceedings.
For the reasons set out above the Tribunal rejects the Applicant’s estoppel arguments.
THE MEDICAL EVIDENCE
On 23 February 2010, the Applicant undertook a sleep study (T4). The Tribunal refers to [7] above.
The Applicant was then seen by Dr Chady Sader who operated on the Applicant in April 2010. The Tribunal refers to [8] and [9] above.
On 22 June 2010, the Applicant undertook a further sleep study which concluded that the Applicant suffers from “severe obstructive sleep apnoea” (T10 at 31). The Applicant’s weight was recorded as 113kg with a BMI of 32 (T11 at 32). The Applicant’s apnea-hypopnea index (AHI) was recorded as 36.8 (T11 at 33).
The Applicant was referred by Dr Alastair Currie of HMAS Stirling Medical Centre to Dr Robert Delcanho, Clinical Associate Professor, University of Western Australia, dental sleep medicine specialist. In or around July 2010 the Applicant was fitted with the mandibular advancement splint (MAS) by Dr Delcanho (R2 at page 5, report of Dr Delcanho dated 29 July 2010).
On 11 October 2010, the Applicant undertook a further sleep study, with the MAS in situ. The Applicant’s AHI was 2.3, showing a “marked improvement” (R2 at page 17, sleep study report of 11 October 2010). The sleep study report also noted:
Obstructive sleep apnoea was well controlled except during REM supine sleep. There was evidence of infrequent snoring.…
The data was technically acceptable. Sleep efficiency was normal. Sleep latency was normal and REM latency was short.
The Applicant was again seen by Dr Delcanho on 18 November 2010 who, in his report of that date (R2 at page 18), said that:
I was very pleased to hear that he recently had a repeat sleep study, with the mandibular advancement splint in situ, which documented very little OSA. At a subjective level, Barry feels much more refreshed in the morning and his wife is very happy that he is no longer snoring. Barry advised that he is tolerating the treatment very well and really has not suffered any problems with his jaw or dental occlusion.
On 18 March 2011, a Medical Employment Classification Review (MECR) (A2 at 97 and 98) was undertaken. It was relevantly reported that the Applicant:
…has been diagnosed with sleep apnoea which has shown excellent control following surgery and the fitting of a mandibular advancement splint.
…
… was fitted with a MAS in January 2010 and tolerated the device well. A repeat sleep study on 11/10/10 showed a marked improvement in his apnoea with an AHI of 2.3. He describes feeling much more refreshed in the morning and appears to have stopped snoring.
On 9 January 2014, Dr Philpott examined the Applicant and by a report of that date (T17) reported that:
… He then went on to have a mandibular advancement splint made up; a follow-up sleep study in June 2010 showed good control of his sleep apnoea. …If he does not use the mandibular advancement splint apparently the apnoea persists. With the MAS in situ he reports an Epworth of 7/24 but if he does not use the MAS he reports an Epworth of 19/24. He describes his sleep as generally restful and refreshing with the mandibular advancement splint in situ. His sleep is quite restless if he does not use the guard…
He has a history of severe sleep apnoea and depression. He also describes a hearing impairment… He is an ex-smoker having given up in 1992 and drinks 50g of alcohol per week.
On examination he was obese with a BMI of 33…
On 21 January 2014, the Applicant underwent a further sleep study with the MAS in situ (T18). The Applicant’s weight was recorded as 116kg with a BMI of 34.3. The Applicant’s AHI was recorded as 6.8 (T18 at 60).
On 11 May 2015, Dr Philpott completed a permanent impairment questionnaire and reported that the Applicant’s “nasal obstruction” was “corrected following surgery [in] April 2010” and the condition is not permanent (T17 at 58). In relation to the OSA condition Dr Philpott reported “obstructive sleep apnoea – severe 2010 following surgery. Currently controlled with MAS” (T17 at 58).
On 12 January 2016, on the referral of Dr Michael Prichard, consultant respiratory physician, the Applicant underwent a further sleep study which was conducted without the MAS. The Applicant’s weight was recorded as 118kg with a BMI of 34.3 (T33 at 146). The Applicant’s AHI was 46 (T33 at 141; see also T33 at 146).
On 22 January 2016, the Applicant was examined by Dr Prichard, who, at the request of the DVA, produced a report dated 17 March 2016 (T33). In response to questions posed by the DVA, Dr Prichard commented as follows (T33, 144):
The client has had liability for a broken nose with deviated septum accepted under the SRCA. In order to correctly calculate the compensation payable to the client, it is necessary to apportion the current degree of total impairment between the original condition and the subsequent condition.
What are the relative contributions of (A) broken nose with deviated septum to (B) obstructive sleep apnoea symptoms, signs and limitations described above?
(A) Broken nose with deviated nasal septum probably contributes “about one quarter” to obstructive sleep apnoea.
(B) Obstructive sleep apnoea is multifactorial in origin. Likely causation includes obesity with a history of progressive weight gain over the past 20 years, upper airway inflammation (rhinosinusitis), craniofacial structure and sleeping position all contribute to the development of OSA. OSA is generally regarded to be a progressive disorder, increasing in severity throughout life, probably due to upper airway oedema or trauma secondary to snoring or declining pharyngeal muscle function. Increased nasal resistance contributes to worsening of OSA to some extent, however the relationship between high nasal resistance and OSA is unpredictable.
On 3 February 2016, the Applicant was examined by Professor T C McManus, consultant otolarayngologist. His report dated 16 February 2016 recorded that clinical examination showed the Applicant’s nasal septum was straight and was not interfering with his nasal airflow (T31 at 130). CT scans conducted on 6 February 2016 confirmed there was no fracture of the Applicant’s nose (T31, 131).
On 16 May 2017 the Applicant was assessed at the request of the Applicant’s lawyers by Dr Galton-Fenzi, occupational and environmental physician, who produced reports dated 16 May 2017 (A2 at 135). In response to the question:
Advise whether, in my opinion, Mr Anderson’s work either caused an injury or caused a recurrence, aggravation or acceleration of a pre-existing disease that such recurrence, aggravation or acceleration was contributed to by work to a significant degree. Give my reasons (A2 at 139).
Dr Galton-Fenzi advised:
In relation to the “injury” where Mr Anderson suffered a fracture to his nose during an assault when in military service in 1989 [sic], resulting [sic] a deviated septum leading to some level of nasal airway flow limitation on the left side, together with obstruction of sinuses on the left also.
Mr Anderson claims that “obstructive sleep apnoea” was subsequently diagnosed.
The evidence suggest that the deviated nasal septum will have had a less than significant effect on the progressively developing condition of “OSA”, which is considered to largely be constitutional - given his excess weight, the natural anatomy of his upper airway, his then smoking habit, and his propensity for sleeping on his back. (A2 at 139 -140)
On 1 June 2016, Dr Prichard produced a supplementary report. Amongst other things, Dr Prichard reported (T34 at 149) that:
He had proven moderate obstructive sleep apnoea/hypopnoea, increasing to severe obstructive sleep apnoea/hypopnoea in 2010 following ENT surgery, responding well (both symptomatically and objectively) to MAS therapy over the past 5-6 years.
With the device in place, he has less sleep disturbance, less morning tiredness and daytime sleepiness and he has not noticed any loss of effectiveness of the device over time. He is less than 100% compliant with MAS therapy, perhaps due to documented bruxism (with secondary mild TMJ dysfunction) and psychological factors.
His general impairment at present relates to a combination of factors including residual OSAH, increased nasal resistance, obesity and perhaps mechanical problems with his lower limbs…. He is likely to benefit from weight loss and improved physical condition.
Applying Table 13-4 of the AMA Guide (T34 at 150), Dr Prichard assessed the Applicant as having a 9% whole person impairment (WPI) in relation to his sleep. Dr Prichard considered that with weight loss, the Applicant’s eventual WPI would be 5% using Table 13-4 of the AMA Guide.
Dr Galton-Fenzi prepared a further report dated 3 July 2017. This report primarily dealt with the issue of the assessment of the Applicant’s impairment, not the cause of the Applicant’s OSA. In that report Dr Galton-Fenzi (A2 at 141) advises that:
You state that liability was accepted for his claim of broken nose, deviated septum and OSA, indicating that my opinion about cause or contribution of his work is not required.
(Original emphasis)
At page 3 (A2 at 143) of his report dated 3 July 2017 Dr Galton-Fenzi responds to the request to assess the Applicant’s OSA impairment pursuant to the AMA Guide (Epworth Test) aided by the MAS and unaided by the MAS. He assesses the former (aided) at 1% - 9% (Class 1) and the latter (unaided) at 10% - 29% (Class 2). Using section 2.4 of the Permanent Impairment Guide (PIG) he assesses the impairment aided by the MAS at a score of 5 equating to 45% WPI and unaided by the MAS at a score of 7 equating to 55% WPI under Table 2.4.
He was also asked to comment on the impairment (if any) relating to the broken nose and deviated septum. In relation to the broken nose, he responded to the effect that following the surgery there was no impairment resulting in a 0% assessed impairment. He observes that “[t]he fracture has united and resolved” (A2 at 143). In relation to the deviated nasal septum, he refers to the report of Professor McManus dated 16 February 2016 (see [65] above) and assesses the Applicant’s impairment at 0%.
Dr Galton-Fenzi gave evidence at the hearing. In examination-in-chief (Transcript, p 24) he explained OSA as follows:
MS SORGIOVANNI: …So anatomically what happens to the body when someone has developed OSA?
DR GALTON-FENZI: It's a progressive onset. Anatomically it's the deposition of adipose tissue, we might call that fat, and a weakening of the muscles around the epiglottis or upper airway region such that when you're in certain positions or of a certain body habitus it becomes blocked when you're sleeping because of the laxity of the musculature surrounding the airway.
MS SORGIOVANNI: What, in your experience, leads to the lax musculature of the airway?
DR GALTON-FENZI: It's constitutional, so with time everybody develops it, but there are certain contributors to that development which we now know quite well, and generally it's in males; generally it is excess weight; generally it is some other medical conditions, which might be diabetes, but it's largely a progressive onset constitutionally, in our experience.
Later in his evidence-in-chief Dr Galton-Fenzi said (Transcript, p 26):
MS SORGIOVANNI: Does the length of the period of nasal resistance have any relevance to the development of laxity in the muscles of the throat?
DR GALTON-FENZI: Not that I'm aware of.
In cross-examination the following evidence was given (Transcript, pp 28-32):
MS OLIVER: Doctor, you've said that sleep apnoea is constitutional or largely constitutional in its causes, is that right?
DR GALTON-FENZI: Yes.
MS OLIVER: So most of the causes are normal anatomy of a person?
DR GALTON-FENZI: Yes.
MS OLIVER: So the blockages that occur in the throat are caused by weak muscles in the upper airway?
DR GALTON-FENZI: Generally, yes.
…
MS OLIVER: Yes. Now, on the subject of fat deposition, so being overweight will increase a person's likelihood?
DR GALTON-FENZI: Absolutely. Yes.
…
MS OLIVER: Yes. Now, you've also talked about the fact this condition will get worse as a person ages, or could get worse as they age?
DR GALTON-FENZI: Generally it is known to be the case, because of laxity of muscles, which is normal.
…
MS OLIVER: Your conclusion here, if I understand correctly, is that in Mr Anderson's case, because of his other constitutional factors, the broken nose or deviated septum, would have had less than significant effect on him developing sleep apnoea, is that correct?
DR GALTON-FENZI: I'd have to say that.
MS OLIVER: So in all likelihood, even if he hadn't broken his nose, he would have developed sleep apnoea, do you believe?
DR GALTON-FENZI: Yes. Could I amplify that, if I may?
…
DR GALTON-FENZI: ... , but one would assume that that swelling would have reduced to a suitable degree that he was now clearly mouth breathing and the trajectory of normal OSA in an overweight individual, let's say … would become - that would now cut in at some period, if you get my understanding - you're understanding that?
MS OLIVER: Yes. And that's because of the build-up of the fat deposits?
DR GALTON-FENZI: Yes.
MS OLIVER:… and the weakening of the muscles?
DR GALTON-FENZI: Yes. Yes.
MS OLIVER: with age, in any event?
DR GALTON-FENZI: And other medical conditions if they were there.
…
MS OLIVER: And the conclusion of the nasal resistance study is that there's normal nasal flow?
DR GALTON-FENZI: Correct.
…
MS OLIVER: So that report, that would support a conclusion, wouldn't it, that post the correction of the deviated septum, there was no longer any impairment of nasal flow from?
DR GALTON-FENZI: As per this report, yes.
MS OLIVER: Yes. So the surgical correction, it would be fair to conclude the surgical correction has fixed any nasal resistance arising from the deviated septum?
DR GALTON-FENZI: Yes.
MS OLIVER: But despite that correction, there's no change in Mr Anderson's sleep apnoea, is that correct?
DR GALTON-FENZI: That's my understanding, from the measures of the sleep studies being done.
MS OLIVER: Yes. Would that suggest, then, that the broken nose and the deviated septum wasn't significantly contributing to his sleep apnoea condition?
DR GALTON-FENZI: That would be my contention.
…
MS OLIVER: So after - so if it had, prior to the surgery … had some impact on his sleep apnoea, would you agree that after that surgery was completed, it was no longer having any - was no longer contributing to the sleep apnoea condition that Mr Anderson was suffering?
DR GALTON-FENZI: Yes, because we've got normal nasal flow. Yes. If that's the question you're asking, yes.
In re-examination the following exchange occurred (Transcript, pp 34-35):
MS SORGIOVANNI: … If the trauma led to the deviated septum being such that it did, I guess, cause a blockage and therefore increased nasal resistance over a prolonged period of time,…say, from 1988 through to 2010, is that a relevant factor in relation to the OSA, or not?
DR GALTON-FENZI: I'd have to say no.
…
MS SORGIOVANNI: But it's possible over that period of time - would the period of time be significant in terms of how traumatised the glottis becomes as a result of mouth breathing? If you do it for longer does it get worse?
DR GALTON-FENZI: No, is the answer.
MS SORGIOVANNI: Could you elaborate on that?
DR GALTON-FENZI: I wouldn't see that deviated septum as being a traumatising capacity for the glottis.
…
MS SORGIOVANNI: But the glottis does become weak through mouth breathing more often?
DR GALTON-FENZI: No, you couldn't say that. It was purely a constitutional issue. So the glottis is a separate entity to a nasal septum.
Dr Philpott gave evidence at the hearing. In relation to the causes of OSA, his evidence was (Transcript, pp 43-44):
MS SORGIOVANNI: What is your understanding of the things that contribute to contraction of sleep apnoea, setting aside weight?
DR PHILPOTT: There’s four factors that we need to take into account when somebody is predisposed to upper airway obstruction. One is obviously the anatomy, so if he’s got problems with his nose, which he did. If he has got a narrow airway because he is carrying extra fat around the base of his tongue and his soft palate around the outer part of his neck, that would constrict his throat. The next factor is upper airway muscles. So as you go to sleep the muscles in your throat will relax, so you don’t develop sleep - you don’t have sleep apnoea or snoring when you’re awake. So the muscles lose tone as you go to sleep, so you start to snore. Those muscles are under a significant load because the airway is narrowing, and as that negative pressure in the throat causes the airway to narrow further and eventually to block off or block off partially or completely, those muscles have to respond to that narrowing tube to maintain airway (indistinct). But they turn on to try and keep the airway open in response to a negative pressure load. So the airway is being sucked and the muscles are trying to act to keep it open. So the stress of those muscles and the activity of those muscles is important. So the anatomy is number 1. The muscle strength and function is number 2. The third thing is arousability, how arousable the patient is. So you can have people that will have an apnoea or hypopnoea, it’s very short lived, it’s usually around about ten to 15 seconds and they arouse, because their arousal threshold is quite low. So before they have a time for the upper airway muscles to kick in and actually naturally relieve the airway and keep the airway open, they arouse. So that fragments their sleep. So arousability or arousal index, as it’s referred, is another factor that is important in terms of assessing the severity of your sleep apnoea and how likely you are going to be impaired by it. The fourth thing is a concept called loop gain. Loop gain is the controller gain, so it’s the gain in the master controller which exists in your (indistinct). So it’s the drive, really, to up airway muscles and lower muscles, and how they interact with those other four factors in terms of keeping the airway (indistinct).
…
MS SORGIOVANNI: I see. You mentioned that he had had a nose - well, a nose and later after surgery I guess the soft palate, was it removed entirely or just modified?
DR PHILPOTT: Well, his nose was fixed by the surgeons. In fact, we measured his nasal resistance pre and post-surgery, so we saw that he had very severe impairment of nasal flow before, on the first study we did on him in February of 2010. The second study we did when he had severe sleep apnoea, in fact, his nasal resistance at that time was better. So the nose was fixed by the surgeon, but unfortunately the sleep apnoea became a bit worse. Now, the nose is important, because obviously that can interfere with the effectiveness of treatment and also can cause problems. It works as what we call a Starling resistor. So (indistinct) resistor on your nose, and you’ve got a floppy airway behind it, as you’re trying to draw air through your blocked nose obviously the tube behind it is more collapsible. That’s what is referred to as a Starling resistor type phenomena which might have been happening on him before in early 2010. But look, the surgery was effective for his nose, but unfortunately sleep apnoea, as I’ve said, did get worse. So the nose is important. It can make treatment more difficult. It can make the severity of the sleep apnoea slightly worse than it would have otherwise been if you didn’t have the nose. It also causes you often to mouth breathe, which obviously as you open your mouth, your tongue has a more posterior position, goes back into your throat. Soft palate, there’s no airflow behind your soft palate. You’re not getting any airflow behind your soft palate to keep it out of the way. So then the soft palate gets sucked in behind your tongue, if you like. So we always look at the nose, always want to make sure that it’s sort of as (indistinct) as possible. But look, he actually responded well from the surgery from that point of view, yes. Does that answer your question?
In cross-examination Dr Philpott’s evidence was as follows (Transcript, pp 48-49):
MS OLIVER: Thank you. Doctor, you talked about – that you’ve done two nasal resistance studies, is that right, for Mr Anderson?
DR PHILPOTT: Yes. So we did one in – we did at least two. We probably did three actually but anyway – no, in fact we did another one in January of 2014. So the first one showed a severe impairment. The next two were both normal. So the one in February after his surgery was normal and the one in January 2014 when I did another study on him with the mouth guard in situ was normal.
MS OLIVER: Thank you. That – the results of those nasal resistance studies indicate that the correction of the deviated septum in - - -?
DR PHILPOTT:…Has been effectively treated with the surgery, yes.
MS OLIVER: So because there’s no longer any nasal resistance associated with the deviated septum after that surgery, would it be fair to say then that the deviated septum is not contributing to the sleep apnoea that Mr Anderson is suffering after that surgery?
DR PHILPOTT: Yes.
Dr Sader’s evidence at the hearing was to the effect that he performed septoplasty to repair the Applicant’s deviated septum and the UPPP procedure and turbinate reduction. His evidence was that the UPPP and the turbinate reduction were procedures to modify the natural anatomy of the Applicant (Transcript, p 62). Dr Sader confirmed that after the surgery the Applicant’s nasal airflow was normal. Dr Sader did also make the following comment in examination–in-chief (Transcript, p 63):
MS SORGIOVANNI: … If you’ve got increased nasal resistance, does that increase the likelihood of the tissues in the throat collapsing?
DR SADER: No. No, I don’t think there’s a relationship between nasal resistance and collapsing of the upper airways.
MS SORGIOVANNI: Do the muscles in the throat get weaker over time as you age?
DR SADER: Yes.
Dr Prichard also gave evidence at the hearing. In relation to OSA and its causes, Dr Prichard’s evidence in examination-in-chief was (Transcript, p 87):
MS OLIVER: What is obstructive sleep apnoea?
DR PRICHARD: So the term broken down means that apnoea refers to stopping breathing and sleep intermittently and the obstructive form of apnoea in sleep occurs through intermittent collapse of the upper airway typically starting in the space called the velopharynx between the nose and the back of the mouth behind the soft palate but also behind the tongue and it is usually due to intermittent muscle relaxation and negative pressure collapse of the upper airway.
MS OLIVER: What leads a person to develop obstructive sleep apnoea?
DR PRICHARD: There are generally speaking two broad main causes. There is a demographic cause of putting on weight and so there is a strong relationship between body mass index and particularly weight distributed in around the upper airway as measured by neck circumference, so it is - so weight gain or obesity is one of the causes and secondly, craniofacial structure, so factors like short mandible, high arch palate with an auxiliary constriction, all of those factors contribute to the development of sleep apnoea.
…
MS OLIVER: Does ageing have any part in relation to sleep apnoea?
DR PRICHARD: Yes. So age is very important, so the prevalence of sleep apnoea, that is how common it is in the community and middle age, is roughly five to eight percent depending upon gender and that is of symptomatic sleep apnoea. In the over 65 age group, it increases to as much as 25 percent of the population.
In relation to the link between the Applicant’s broken nose and deviated septum and OSA, Dr Prichard’s evidence was (Transcript, pp 92 – 93):
MS OLIVER: In relation to Mr Anderson, having conducted your assessment of him, did you form a view as to what the likely causation was of sleep apnoea in his case?
DR PRICHARD: So, there were no major cranial facial abnormalities that I can recall and I had first assessed him after he had palatal surgery there was evidence of palatal surgery. I guess the number one issue really was his BMI and neck circumference as risk factors for sleep apnoea. So, he didn’t really have any major nasal issues at that time.
MS OLIVER: You’re aware that Mr Anderson sustained a broken nose in April 1988?
DR PRICHARD: Yes.
MS OLIVER: In your opinion, would that broken nose have contributed to the onset of sleep apnoea that was diagnosed in 2010?
DR PRICHARD: No, for two reasons. One would expect the trauma - the effects of the trauma to have been temporary and, secondly, the bit that’s injured in a fractured nose from trauma of that sort is external to the nasal cavity and most of the literature about the relationship between nasal issues and the development of sleep apnoea, or a contribution to sleep apnoea, relate usually to intranasal issues; that is, that part of the nose that’s within the face.
MS OLIVER: Those intranasal issues that you’re talking about, would they normally occur as a result of trauma or are they naturally occurring?
DR PRICHARD: So, there is naturally occurring septal deviation, for example, that can even result from those defects or, at least, the process of delivery or the cranial facial development. So, for example, if the upper jaw, the maxilla, develops in a way that the hard palate arch is higher then it will tend to cause a bend in the septum. So, there are developmental issues that lead to septum deviation. Secondly, there are other nasal problems that can cause narrowing of the nasal passage and they’re commonly referred to as rhinitis, or nasal inflammation, and they can either be classified as allergic or non-allergic. The non-allergic ones usually result from irritant exposures like smoke or external chemical fume exposures or sometimes they can just be unexplained.
MS OLIVER: Now, in Mr Anderson’s case we know that the surgery corrected his deviated septum, in light of that and that was April 2010, is it fair to say that any contribution that the deviated septum may have had to his sleep apnoea would have been resolved after that surgery?
DR PRICHARD: Yes.
MS OLIVER: Given your assessment of Mr Anderson, even had he not suffered the broken nose, do you think he would likely have developed sleep apnoea?
DR PRICHARD: Probably.
MS OLIVER: And are there particular matters that make you think that he probably would have developed that?
DR PRICHARD: I guess for the reasons I’ve already stated previously about the temporary nature of a nasal fracture and its impact on the nose generally and what part of the nose is involved and, secondly, that there’s no relationship that I could see between him having that trauma and subsequently gaining weight, for example, or having any other factors affecting his upper airway muscle function or size and shape of the upper airway. The nasal trauma is very specific to that part of the nose.
MS OLIVER: So, the other matters affecting the upper airways that lead to sleep apnoea are normally constitutional or part of a natural anatomy; is that right?
DR PRICHARD: Yes, correct.
CONSIDERATION
The Applicant’s closing submissions, correctly in the Tribunal’s view, identified the critical threshold question as follows:
14. It appeared at the hearing that the parties agree that the correct question is if the broken nose and deviated septum contributed to a significant degree to the OSA. The applicant says the broken nose and resultant deviated septum contributed significantly to the OSA based on the Medical evidence which has been summarised above.
Paragraph 15 of the Applicant’s closing submissions refers to the evidence of Dr Philpott as supportive of that contention. Those submissions identify five elements of Dr Philpott’s oral and report evidence. In summary they are:
(a)initial swelling from the broken nose causes swelling that obstructs the nasal passage;
(b)the obstruction on one side causes the turbinates on the other side to enlarge;
(c)the nasal obstruction contributes to air turbulence which contributes to snoring and causes increased nasal pressure which can cause the throat tissue to collapse;
(d)over time snoring injures the throat muscle tissue making it more susceptible to collapse; and
(e)once OSA is established it worsens as aging weakens the muscles and OSA can cause obesity because “sleepy people move less and eat more carbohydrates”.
The Tribunal does not agree. The above was not the thrust of Dr Philpott’s evidence either in his several reports or at the hearing. The Applicant’s submissions conflate the issues of snoring and OSA. While there was evidence that a deviated septum can cause snoring (Dr Sader at the hearing, Transcript, p 63) the evidence established that the surgery conducted by Dr Sader in 2010 completely addressed any issue with restricted airflow caused by the deviated septum. Dr Galton-Fenzi’s evidence as set out in [72]-[75] above was that once the deviated septum was repaired the broken nose and deviated septum could not be considered to be significantly contributing to the Applicant’s OSA. Dr Philpott’s evidence set out in [76]–[77] above was to the same effect, namely, that the surgery addressed the issues caused by the broken nose and deviated septum and that therefore post that surgery in 2010 it could not be said that the broken nose and deviated septum was contributing to the Applicant’s OSA.
The Applicant also seeks to argue that, even if the surgery on the Applicant’s nose has resulted in the deviated septum not being a cause of the Applicant’s OSA, the snoring caused, or made more severe, by the deviated septum prior to the surgery caused damage to the Applicant’s throat muscles which still contributes to the Applicant’s OSA. Dr Sader’s evidence was to the effect that prolonged snoring can cause oedema (swelling) in the throat muscles which can “increase snoring and the likelihood of sleep apnoea” (Transcript, p 63) and Dr Philpott’s evidence was that there was some evidence that there was “some kind of wear and tear effect like overuse type injury” to the throat muscles of chronic snorers (Transcript, p 96).
That evidence, however, was more in the realm of the theoretical and there was no evidence that any such damage had been caused to the Applicant’s throat muscles which would now contribute to his OSA. The evidence of Dr Sader, Dr Philpott, Dr Prichard and Dr Galton-Fenzi was that since the corrective surgery on the Applicant’s deviated septum it could no longer be said that the broken nose and deviated septum was contributing to the Applicant’s OSA. Dr Prichard’s evidence (see [80] above) went further and was to the effect that, in his view, the Applicant’s broken nose and deviated septum was not a cause of the Applicant’s development of OSA and that it was “probable” that the Applicant would have developed sleep apnoea in any event.
The Tribunal finds that the medical evidence indicates that, even if the injury suffered by the Applicant in 1988 was at some point the cause of, or contributed, to a significant degree, to the Applicant’s OSA, that is no longer the case. In particular the evidence of Dr Galton-Fenzi at [72] and [74] above, the evidence of Dr Philpott at [60], [76] and [77] above, the evidence of Dr Sader at [78] above and the evidence of Dr Prichard at [79] and [80] above indicate that the operation undertaken by the Applicant in 2010 to, amongst other things, correct the Applicant’s dislocated septum (T8) was successful in addressing the restricted airflow caused by the Applicant’s dislocated septum. The evidence at the hearing of Dr Galton-Fenzi set out in [74] above, of Dr Philpott set out in [77] above and of Dr Prichard set out in [80] above was that since the surgical correction of the deviated septum, the deviated septum the result of the incident in 1988, no longer contributed to the Applicant’s OSA.
As the Applicant correctly identified in paragraph 14 of his closing submissions (see [81] above), the critical issue in this matter is whether the broken nose and deviated septum contributed to a significant degree to the OSA. The Applicant says that the broken nose and resultant deviated septum contributed significantly to the OSA based on the medical evidence. The Tribunal disagrees. The medical evidence was to the contrary. The deviated septum does not, or no longer, contributes to the Applicant’s OSA.
At paragraph 18 of his closing submissions the Applicant makes the following submission:
(a) the duration of the employment;
The evidence established that the deviated septum persisted for almost the whole duration of the Applicant’s employment, namely, between 25 April 1988 and late March or early April 2010 when Dr Chaddy [sic] Sader corrected the deviated septum and performed the UPPP. The factors described at paragraph 15 (a) to (d) herein continued throughout that period of time. The medical practitioners agreed that fixing the deviated septum after the OSA was established does not remedy the condition, presumably because the damage is done and cannot be undone.
(Note: the factors in paragraph 15(a) to (d) referred to by the Applicant are those set out in [82] above)
The Tribunal does not accept that argument. The evidence was that in 1988 the Applicant was hit in the face and most likely suffered a deviated septum. The medical evidence was to the effect that a deviated septum, and the disruption to airflow caused by it, can contribute to snoring which can worsen the OSA. The evidence of Dr Prichard (see [64] above) was that:
Increased nasal resistance contributes to worsening of OSA to some extent, however the relationship between high nasal resistance and OSA is unpredictable.
The evidence of Dr Galton-Fenzi (see [66] above) was:
The evidence suggest that the deviated nasal septum will have had a less than significant effect on the progressively developing condition of “OSA”, which is considered to largely be constitutional - given his excess weight, the natural anatomy of his upper airway, his then smoking habit, and his propensity for sleeping on his back. (A2 at 139-140)
Dr Galton-Fenzi’s evidence at the hearing in relation to the causes of OSA (see [72] above) was:
It's constitutional, so with time everybody develops it, but there are certain contributors to that development which we now know quite well, and generally it's in males; generally it is excess weight; generally it is some other medical conditions, which might be diabetes, but it's largely a progressive onset constitutionally, in our experience.
The Tribunal also notes the following evidence of Dr Galton-Fenzi quoted at [74] above:
MS OLIVER: Your conclusion here, if I understand correctly, is that in Mr Anderson's case, because of his other constitutional factors, the broken nose or deviated septum, would have had less than significant effect on him developing sleep apnoea, is that correct?
DR GALTON-FENZI: I'd have to say that.
MS OLIVER: So in all likelihood, even if he hadn't broken his nose, he would have developed sleep apnoea, do you believe?
DR GALTON-FENZI: Yes…
Contrary to the Applicant’s submission, what the evidence established was that OSA is multi-factorial, primarily related to weight, fat deposits and laxity of muscle associated with aging. The proposition that because the deviated septum was corrected and the Applicant still suffers from OSA, now 30 years after his nose was broken, is evidence that the “damage is done and cannot be undone” is non-sequitur. The fact that the correction of his deviated septum did not cure the Applicant’s OSA is, in the Tribunal’s view, more indicative of the fact that the deviated septum was not, by 2010, the cause or even a significant contributor, to the Applicant’s OSA. What is clear on the medical evidence is that since the deviated septum was corrected, it and the incident on April 1988 are not contributing to any, or any significant degree to the Applicant’s OSA.
The Applicant also sought to argue that the UPPP “is known to cause scarring” (paragraph 9 of the Applicant’s closing submissions). How this is linked to the Applicant’s deviated septum is not clear given that UPPP is a procedure to remove tissue from the area around the patient’s soft palate, however, the whole purpose of the UPPP is to increase the airflow to lessen the pressure and decrease the likelihood of muscle collapse around the soft palate. The evidence does not support the Applicant’s assertion that the operation, and the scarring caused, “adds to the problem as it narrows the airway instead of increasing it” (paragraph 9 of the Applicant’s closing submissions). That was not the evidence and the only direct evidence in relation to the scarring was the evidence of Dr Sader. His evidence was that the scarring was “quite limited” (Transcript, p 66) and that when he examined the Applicant two weeks after surgery there was nothing about the scarring that would be cause for concern. His evidence was also that the UPPP dealing with the soft palate tissue is an operation addressing the patient’s natural anatomy and that it was “not something that has been affected by the broken nose” (Transcript, p 66).
In answer then to “the correct question”, as the Applicant puts it in paragraph 14 of his closing submissions, is that the broken nose and deviated septum do not contribute significantly (or at all) to the Applicant’s OSA. Put another way, in the context of the issues as the Applicant has identified them (see [29] above), there is no existing nexus between the Applicant’s OSA and his employment by the Commonwealth.
Given that finding the other issues identified by the parties as set out in [28] and [29] above largely become irrelevant. The gateway for any liability on the part of the Respondent under ss 24 or 27 of the DRC Act is that the injury for which compensation is sought relates to the Applicant’s employment by the Commonwealth. It is therefore unnecessary for the Tribunal to consider the legal arguments raised by the parties as to whether any impairment is to be assessed on a treated or untreated basis, or as to whether Part 1 of the approved guide can be used to assess the level of impairment suffered by the Applicant.
The Applicant argues that the OSA is a disease, as that term is defined in s 5B of the DRC Act, that was contributed to, to a significant degree, by the Applicant’s employment by the Commonwealth (paragraph 13 of the Applicant’s closing submissions). While it may have been the case that up to the time of the correction of the Applicant’s deviated septum in 2010, the deviated septum contributed to the Applicant’s OSA, the medical evidence, in the Tribunal’s view, establishes that that is not the case now, nor was it at the time that the reviewable decision was made.
CONCLUSION
For the reasons set out above, the Tribunal finds that the Applicant’s OSA is not contributed to, to a significant degree, by the Applicant’s employment by the Commonwealth and that therefore no compensation is payable under s 24 or s 27 of the DRC Act. The Tribunal therefore affirms the reviewable decision.
I certify that the preceding 98 (ninety-eight) paragraphs are a true copy of the reasons for the decision herein of Deputy President Boyle
......[sgd]..................................................................
Associate
Dated: 8 November 2018
Date(s) of hearing: 14 and 15 August 2018 Counsel for the Applicant: Ms Sorgiovanni Solicitors for the Applicant: Soul Legal Counsel for the Respondent: Ms Oliver Solicitors for the Respondent: Sparke Helmore Lawyers
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