Tonga and Comcare - [2002] AATA 798

DECISION AND REASONS FOR DECISION [2002] AATA 798

ADMINISTRATIVE APPEALS TRIBUNAL )

) No N2001/0592

GENERAL ADMINISTRATIVE DIVISION          )
           Re      CEDRIC TONGA
  Applicant
           And    COMCARE
  Respondent

DECISION

Tribunal Mr M J Sassella, Senior Member Dr J D Campbell, Member

Date12 September 2002
PlaceSydney

Decision      The tribunal affirms the decision under review. The applicant is not entitled to costs associated with the application.
   [SGD] M J SASSELLA
  Senior Member
CATCHWORDS
WORKERS' COMPENSATION – laceration to shin causing ulceration – whether injury under Safety, Rehabilitation and Compensation Act 1988 – pre-existing deep vein thrombosis and venous stasis – whether employee's disease arose out of or in the course of employment – permanent impairment

Safety, Rehabilitation and Compensation Act 1988 ss 4(1)("ailment", "disease", "injury"), 14, 16, 19, 24, 27

REASONS FOR DECISION

12 September 2002 Mr M J Sassella, Senior Member Dr J D Campbell, Member

THE APPLICATION

This is an application to the Administrative Appeals Tribunal ("the tribunal") by Mr Cedric Tonga ("the applicant"), date of birth 15 June 1943 (T3) for review of a decision by a Comcare ("the respondent") delegate dated 26 April 2001 (T36) affirming:
(a)a primary decision dated 10 November 2000 (T26) refusing a claim for a lump sum payment of compensation in respect of a permanent impairment; and
(b)a primary decision dated 20 December 2000 (T29) to regard the effects of an injury that occurred on 11 March 1993 (T3, T4) as having ceased.

HEARING

The tribunal convened a hearing in this matter in Sydney on 6 February 2001. Mr M Daley of counsel represented Mr Tonga. Ms C E Adamson of counsel represented the respondent. The tribunal heard oral evidence from Mr Tonga and R S A Lord, Professor of Surgery. The tribunal had access to the following documentary evidence:

Exhibit TD1 – Section 37 Statement and associated documents (exhibits T1 – T36) provided by the respondent.
Exhibit A1 – Applicant's statement of facts and contentions, undated.
Exhibit A2 – Report by Dr P Conrad, surgeon, 7 June 2001.
Exhibit A3 – Report by Dr C Selby Brown, orthopaedic surgeon, 24 July 2001.
Exhibit A4 – Report by Dr A R Graham, vascular surgeon, 14 April 1998.
Exhibit A5 – Report by Dr Graham, 9 August 2001.
Exhibit A6 – Dr Graham's clinical notes.
Exhibit R1 – Respondent's statement of facts and contentions, 15 October 2001.
Exhibit R2 – Report by R S A Lord, Professor of Surgery, 10 August 2001.
Exhibit R3 – Report by Professor Lord, 17 August 2001.
Exhibit R4 – Report by Professor Lord, 19 October 2001.
Exhibit R5 – Clinical notes from Prince of Wales Hospital.
Exhibit R6 – Dr Edema's clinical notes.
Exhibit R7 –Dr Graham's clinical notes.
Exhibit R8 – Diagram of venogram, 14 September 1993.
Exhibit R9 – Report of x-ray of applicant's lumbar spine, 16 December 1997.
Exhibit R10 – Report of CT scan of applicant's lumbosacral spine, 22 February 1999.

FINDINGS ON MATERIAL QUESTIONS OF FACT WITH REFERENCE TO THE EVIDENCE AND OTHER MATERIAL IN SUPPORT OF THOSE FINDINGS
the incident

Mr Tonga was working for Australian Defence industries on Garden Island in the Royal Australian Navy dockyard as a boiler attendant in 1993 when he had a work accident. He had to climb ladders to open and shut safety valves and test water gauges. The tank was about 20 feet high and Mr Tonga might have to climb the ladder three or four times a day. He was on his feet most of the time. He could sit for up to five minutes at times. He also did general cleaning and painting. His shifts were 12 hours long.
On 11 March 1993 Mr Tonga slipped on a ladder on the way down from the top of the tank. In oral evidence he said that he broke the skin on his left shin. He could see the shin bone. He saw to his own first aid using a first aid box. He worked on while in pain and took Panadol for relief, seeing no doctor. Mr Tonga said that he worked on for four or five weeks during which the leg "wasn't good" but he had bills to pay. In fact, it emerged in cross-examination, Mr Tonga worked on until August 1993 without any sick days. Blisters developed, however, said Mr Tonga, and work proved difficult because of pain. On 22 April 1993 (T9/33) Mr Tonga went to St Vincent's Hospital where the wound was dressed. On 24 June 1993 Mr Tonga saw Dr Edema, his GP, about an infected ulcer on the left lower tibia (T9/28). He did not connect the ulcer to a work incident in dealing with Dr Edema (ex R6). It was only on 27 September 1993 that Mr Tonga told Dr Edema of the work incident (ex R6). In August 1993 Mr Tonga reported to the navy medical centre. The ulcer was no better and had grown larger. He saw Dr Graham, on referral by Dr Edema, for the first time in August 1993 (ex A4) and he gave him painkillers and a letter for his GP. The wound healed after 12 or 13 months.
Mr Tonga said that he used a pad and stocking on the affected leg after the ulcer healed. However, a couple of months later it returned as a boil and opened up. Mr Tonga was made redundant in 1995, at which time the wound was still opened. Tribunal member, Dr Campbell, asked Mr Tonga about the dressings he had applied to the ulcer. Mr Tonga had explained that he used to dress the ulcer four or five times a day. He explained that he had done this without medical advice to do so because the ulcer oozed and smelt. No one had told Mr Tonga that he should dress the ulcer no more than once a day in order to achieve the fastest resolution of the problem.
In cross-examination it emerged that Mr Tonga had lost no days of work after the ulcer re-opened. He then became redundant. He said that he had not worked since the redundancy. The wound closed after he became redundant but pain is still present. The pain was said to be from the knee down in the front of the leg. Sometimes, he said, there was pain at the rear of the left calf muscle. He first felt this pain, which runs to the buttock, in 1994 before the ulcer returned after first healing. Mr Tonga said he has good and bad days, with bad weather and extended carrying and walking making it worse.
Mr Daley in final submissions argued that the effects of Mr Tonga's injury on 11 March 1993 had not ceased. He had an area of scar tissue that was still present and weakened the skin. This had to be guarded. He put that Mr Tonga needed access to compensation under s 16 of the Safety, Rehabilitation and Compensation Act 1988 ("the Act") for reasonable medical expenses associated with the injury. These included creams Mr Tonga bought to apply to the weakened skin area and general medical reviews.
Mr Daley submitted that Mr Tonga attracted incapacity payments under s 19 of the Act because he could not do labouring type jobs or jobs involving walking as a result of his work-related injury.
a pre-existing condition
The respondent opened up an alternative explanation of any ongoing problems with his left leg that Mr Tonga may be experiencing. This was based on evidence that he suffered a deep vein thrombosis in 1986. In summary the evidence on the deep vein thrombosis theory was as follows. On 13 June 1986 Mr Tonga ruptured an Achilles tendon. He spent three days in the Prince of Wales Hospital and was discharged on crutches. He had returned to the hospital in September 1996 complaining of pain from the ankle to the thigh in his left leg. As this material was put to Mr Tonga by Ms Adamson in cross-examination, Mr Tonga said he could recall none of this.
Mr Tonga was admitted to the Prince of Wales on 10 September 1986 with a swollen left foot and leg and stayed in until 23 September 1986. He was diagnosed with deep vein thrombosis. Mr Tonga conceded that he could remember being an inpatient although he later said that he did not remember that. He insisted that he did not recall being diagnosed with deep vein thrombosis. He told the tribunal that he did not know he had deep vein thrombosis when he commenced work at Garden Island and mentioned it to no doctor there. The hospital records showed that he underwent an operation to check on the condition of his veins but Mr Tonga replied that it was only to check on the condition of his Achilles tendon.
Mr Tonga was given the drug Warfarin when he was discharged. He had five outpatient attendances to receive Warfarin on a fortnightly basis. Ms Adamson put to Mr Tonga that Warfarin was prescribed for deep vein thrombosis. Mr Tonga said he thought it was "for his blood" and took it for only a few days.
On 9 March 1987 Mr Tonga had returned to the Prince of Wales because of swelling in his left leg to the ankle and foot, to the front and back of the leg. The left leg was warmer than the right. Foot movements were restricted. Again, Mr Tonga could not remember this. He was in hospital for one night. He had difficulty walking with his left leg, which was painful and swollen. Mr Tonga saw a Professor Huckstepp at the hospital. Mr Tonga was given a heavy duty stocking. Mr Tonga denied this.
Ms Adamson mentioned related matters to Mr Tonga.

He had seen Dr Edema on 19 June 1991 about left leg varicose veins (ex R6). Mr Tonga replied that he did not think he had seen anyone about varicose veins.
He saw Dr Edema on 11 February 1992 about left calf and Achilles tendon pain (ex R6).
He saw Dr Edema on 17 August 1992 about varicose veins (ex R6).
He saw Dr Graham for the first time on 14 September 1993 (ex R7). Dr Graham's clinical notes show that deep vein thrombosis was discussed at that session in relation to the history of the ruptured Achilles tendon. On 29 November 1993 Dr Graham noted that Mr Tonga's pain had improved.

Professor R S A Lord, Professor of Surgery, gave oral evidence. He provided the report in ex R2 dated 10 August 2001. He considered that Mr Tonga's pre-existing deep vein thrombosis meant that the work-related ulcer of 1993 took months to heal and proved difficult to heal. The ulcer had fully healed but had left scarring on the anterior ankle. The physical signs on the left leg were consistent with healed venous ulcers and stasis syndrome. There were also varicose veins in the left leg, dating from 1991 or earlier. He said he saw no evidence that Mr Tonga's physical condition with respect to the left lower limb was significantly different from prior to the injury on 11 March 1993. He saw no reason why Mr Tonga could not carry out the same physical occupation as in 1993 before the accident. He said that Mr Tonga was suffering in 2001 from chronic venous stasis syndrome affecting the left lower limb. He said that, in the chronic venous stasis syndrome, recurrent ulceration of the ankle area typically occurs. The ulcer from the work trauma had healed and was no longer relevant. The injury at work had precipitated the ankle ulcer but that had healed. The venous stasis was chronic and would persist indefinitely. The chronic venous stasis syndrome dated from the extensive deep vein thrombosis shown on a venography dated 10 September 1986.
In a second report (ex R3) on 17 August 2001 Professor Lord cast doubt on Mr Tonga's permanent impairment claim. First, Mr Tonga had not, as required in s 24(2)(c) of the Act undertaken all reasonable rehabilitative treatment for the impairment in that he had not taken action to reduce his obesity. Second, Professor Lord saw any permanent impairment as entirely related to the pre-existing venous thrombosis. Third, he did not see the applicant's permanent impairment as attracting a rating exceeding 10% in accordance with table 1.3 of the Guide to the Assessment of the Degree of Permanent Impairment published by Comcare ("the Comcare guide"). This was explained in ex R4 on 19 October 2001 when he wrote that the categories in table 1.3 did not precisely match his condition. The closest was the level with a 10% rating. This read "oedema – persistent and incompletely controlled".
In oral evidence Professor Lord examined the Prince of Wales clinical notes (ex R5) and said that they confirmed that Mr Tonga had had an operation for a ruptured Achilles tendon and this had resulted in an extensive deep vein thrombosis. A venogram showed extensive deep vein thrombosis in the left leg caused by post-operative venous thrombosis. Confinement in a plaster cast can predispose a patient to such an outcome. Complete recovery from a deep vein thrombosis such as Mr Tonga's is rare.
Professor Lord mentioned, in commenting on a venogram (ex R8), that ulceration can follow a trauma or it can occur spontaneously.
Professor Lord referred to Warfarin therapy. He said that Warfarin is usually prescribed after deep vein thrombosis for three months when the likelihood of thrombotic episodes diminishes. However, the deep vein thrombosis leaves the patient's valves in a chronic condition. Professor Lord in cross-examination explained that the Warfarin does not cause the deep vein thrombosis to disappear. It prevents new ones from forming.
In cross-examination Professor Lord agreed with Mr Daley that any thrombus seen in 2001 was a different thrombosis from in 1986 or 1993. However, he was at pains to point out that there was not only one thrombus in the left leg at any time. He agreed with Mr Daley that there could have been a very small thrombus in 1993, but that resolved quickly. He agreed that a trauma to the leg can produce a further thrombosis and that a trauma to the leg could aggravate an underlying disease process. Professor Lord said that such a trauma associated with severe swelling could affect the "venous returns". Asked about the trauma in March 1993 as described by Mr Tonga, Professor Lord said that Mr Tonga's level of swelling was unlikely to suffice as an indication of a thrombus. Swelling was necessary to compress the veins in the lower leg. There was no evidence in 1993 of any significant thrombus. Mr Tonga took no time off work and did not visit a doctor for six weeks. The ulceration was too superficial.
Professor Lord in turn rejected scenarios proposed by Mr Daley. While it was possible that Mr Tonga had a minor thrombosis in 1993 that dissolved it would not have affected the ulceration or venous hypertension. The trauma was not likely to have aggravated venous hypertension because the wound was superficial. It was not likely that Mr Tonga had a cellulitis that produced an infection, with swelling, above the ankle because Mr Tonga sought no help for six weeks. Cellulitis is a life-threatening condition.
Professor Lord addressed the issue of the thinness of the skin on Mr Tonga's left shin. He said that it was a theoretical possibility that thin skin could expose Mr Tonga to the risk of ulceration from further trauma and that amputation could follow a trauma in one with venous hypertension. Professor Lord deemed this sort of scenario extremely uncommon. Dr C Selby Brown, an orthopaedic surgeon, had said on 22 June 1999 (T20/49, 50) that any further ulceration of any significance may lead to a situation eventually requiring amputation of his left leg at a level to be determined at the time. Professor Lord characterised this assessment as extraordinary. Professor Lord in response to questioning said that there were no creams that Mr Tonga could apply to protect the shin area and that walking would not cause the skin to split.
Mr Daley put to Professor Lord that Mr Tonga had had two ulcers within the general area where ulcers resulting from thrombosis could occur. It seemed that Professor Lord had been unaware of the second ulcer occurring after March 1993. He thought the second ulcer attributable to underlying venous stasis. He did not see it as an incidence of cellulitis.
Professor Lord saw the most likely cause of Mr Tonga's leg pain as degenerative disease of the lumbosacral spine, relying on ex R9 and ex R10.
In summarising the respondent's case Ms Adamson, in addition to the above material suggesting a diagnosis of pre-existing deep vein thrombosis with venous stasis, called the tribunal's attention to the following matters. Mr Tonga had had no ulcer since 1997. He had had little time off work leading up to the redundancy in 1995. After that he saw the Department of Social Security for benefits only after a time. He claimed unemployment payments (rather than a Disability Support Pension) because he was keen to return to work. Later he was paid Disability Pension because of his deep vein thrombosis. Ms Adamson defended the decision that effects had ceased. This had occurred in December 2000, three years after the last incidence of ulcers.
permanent impairment
As regards any compensable permanent impairment affecting Mr Tonga, Mr Daley suggested that Dr Graham's reports on post-1994 treatment showed that the shin area was prone to repeated ulceration. The respondent and Professor Lord were said to be wrong to assume that the ulcers had healed. Mr Daley referred to the report by physician Dr P Stevenson dated 11 July 2000 (T25) where Dr Stevenson diagnosed Mr Tonga as suffering from venous hypertension in the left leg. He saw this as caused by a trauma to the front of the leg in 1993 and post-thrombotic changes to the left leg. He saw the ulcer as healed but the venous hypertension as still present. He noted that the skin on the front of the leg was thinner and more vulnerable than it would have been without the injury, however the venous hypertension was such that, even without the injury at work, Mr Tonga's leg would in no way be normal. Dr Stevenson regarded the trauma-produced ulcer as contributing materially to Mr Tonga's condition in 2000.
In addressing impairment issues, Dr Stevenson spoke only of Mr Tonga as having suffered a contribution to the impairment of his lower limb as a result of the injury even though he would have had an impairment without the injury. He did not explain the impairment. Referring to table 1.3 in the Comcare guide he found the impairment to be less than 10%. He would have liked to boost that rating to account for Mr Tonga's reclusive lifestyle. He seemed unaware of the structure of ss 24 and 27 of the Act. Section 27 will take account of such matters in the assessment of non-economic loss, however, as a first step the employee must be rated on a largely functional effects basis in accordance with, in this case, table 1.3. Section 24(7) of the Act provides for no compensation for permanent impairment if an employee's rating under the Comcare guide is under 10%.
Mr Daley relied greatly on the views of Dr Graham, Mr Tonga's treating vascular surgeon. On 14 December 1997 (ex A6/20) and 9 August 2001 (ex A5) Dr Graham considered that Mr Tonga's left leg pain might have come from a change in posture while walking, caused in turn by his chronic, painful ulceration. The ulceration was, however, well healed. He saw it as unlikely that Mr Tonga could return to his former labouring work because of risk of further injury to the leg.
Mr Daley referred also to Dr P Conrad, a surgeon, who reported on 1 June 1999 (T28/80) and 23 June 1999 (T28/82). Dr Conrad attributed 80% of Mr Tonga's loss of efficient use of the left leg below the left knee to the fall in March 1993. Addressing table 9.5 of the Comcare guide, he found a 20% whole person impairment "due to the ulceration on his left leg" because Mr Tonga could rise to a standing position and walk but had difficulty with grades, steps and distances. On 7 June 2001 (ex A2) Dr Conrad confirmed his assessment as 80% of 20% in accordance with table 9.5 of the Comcare guide. He dismissed the notion that this table was inappropriate and the appropriate table was table 1.3.
Dr C Selby Brown, an orthopaedic surgeon, rated Mr Tonga as having a 20% whole person impairment in accordance with table 9.5 (ex A3). Oddly, however, in his examination of Mr Tonga Dr Selby Brown found no significant restriction to the full ranges of motion in Mr Tonga's left knee, left ankle or left hind foot. He had full ranges of movement in all joints and digits of the left foot and marked venous varicosities in his left leg. The doctor saw Mr Tonga again on 17 July 2001 (ex A3) and made similar findings. He again defended using table 9.5 in assessing whole person impairment and confirmed the earlier assessment. In addition, he addressed table 1.3 and assessed 15% or 20% on the basis that Mr Tonga probably should be regarded as having recurrent superficial phlebitis (venous inflammation) as he stated that he noticed a pink colour around the previously noted area of venous eczema. He "certainly" had a persistent and incompletely controlled oedema (accumulation of fluid). Although there was no present evidence of superficial transient ulceration he considered Mr Tonga to have a very marked potential for such to occur if it were not for Mr Tonga's management of this area. The healed ulcerated area was covered with very thin and very fragile skin and, in Dr Selby Brown's opinion, any amount of ambulatory activity or any direct trauma at all to the area would cause break down of this very thin and fragile skin. "He would therefore appear to have 15% whole person impairment and possibly even 20% … under Table 1.3." This situation had been in existence only since the injury in March 1993 when previously he had been able to work and engage in mini marathon, bikeathon, jogging and weight lifting activities despite his deep vein thrombosis.

Ms Adamson argued that Mr Tonga was not eligible for a permanent impairment payment because any impairment was not attributable to his employment. It was instead the result of the underlying deep vein thrombosis. This was effectively Professor Lord's assessment in admitting that Mr Tonga may merit a 10% rating under table 1.3. Ms Adamson argued that table 9.5 did not apply in this case because it can be used only for musculo-skeletal conditions. However, she argued, even if it did, Mr Tonga attracted a rating of only 10%.
Ms Adamson commented on Dr Graham's theory that Mr Tonga's left leg pain was an orthopaedic condition brought on by Mr Tonga's posture as adopted to protect his shin. She argued that Dr Graham presented this as only a possibility and did so without having seen exhibits R9 and R10. Exhibits R9 and R10 were the results of investigations of Mr Tonga's lumbar and lombosacral spine in 1997 and 1999. In summary, in 1999 following ultrasound, it was found that Mr Tonga had marked gaseous degeneration at L4/5 and L5/S1. No disc bulges or herniations were evident at any of the levels examined. There was a spondylolisthesis of L5 on S1 with bilateral pars interarticularis defects and there were facet joint degenerative changes of a mild degree at L4/5 and L5/S1.
Ms Adamson submitted that the medical evidence throughout depended on the extent of an accurate medical history each doctor had available. She noted that Professor Lord had the most comprehensive information in that he had access to the Prince of Wales clinical notes (ex R5). His evidence, it was suggested, was to be preferred.
Ms Adamson made general submissions as to Mr Tonga's credibility. She referred to various indications. When he saw Dr Stevenson in 2000 he denied any previous significant injury to his leg (T25/68). He admitted to the ruptured Achilles tendon when playing squash but said that when operated on it had healed up completely. He told Dr Stevenson he had returned to a full level of activity after that and until 1993. This was most unlikely because Mr Tonga's weight was very high in 1993. He denied any blood clot in his leg after the Achilles tendon repair. In oral evidence he had said that he took Warfarin for only four days. He had said that he had no problems after the 1986 tendon repair operation. He had said that everything changed in 1993. Ms Adamson suggested that the true picture was that everything actually went bad in 1986. There were a number of instances in his oral evidence (noted above in paragraphs 9-13) where he either dissembled or gave unreliable responses. Ms Adamson submitted that the absence of documented symptoms between 1986 and 1990 could not be presumed in his favour to indicate that Mr Tonga had no symptoms, given the unreliability of his evidence.
tribunal's formal findings
There is no argument against the proposition that on 11 March 1993 Mr Tonga suffered an injury in accordance with s 4(1) of the Act. When he fell on the ladder and cut open his shin he sustained an injury (other than a disease), being a physical or mental injury arising out of, or in the course of, his employment. Comcare recognised this on 18 October 1993 when it accepted Mr Tonga's compensation claim (T10). The primary issue for the tribunal is whether the effects of that injury had ceased on 12 December 2000 when Comcare decided that the effects had ceased.
In essence the argument that the effects had ceased consisted of the proposition that Mr Tonga's ulcers had been healed with no recurrence since 1997 (ex A6/20). Any continuing vulnerability on Mr Tonga's part was attributable to his deep vein thrombosis, a disease he had contracted before 1993 and not a disease that arose out of or in the course of his employment.
An alternative theory was that Mr Tonga has an ailment (as defined in s 4(1) of the Act) in the form of thin skin on his lower foreleg that was brought about as an after-effect of the ulceration caused by the fall at work. An ailment is broadly defined in the Act as any physical or mental ailment, disorder, defect or morbid condition (whether of sudden onset or gradual development). An ailment can be a "disease" in accordance with s 4(1) of the Act if it is an ailment or an aggravation that was contributed to in a material degree by the employee's employment by the Commonwealth or a licensed corporation.
Professor Lord was of the view that Mr Tonga's physical condition with respect to the left lower limb was not significantly different from prior to the injury on 11 March 1993. He saw Mr Tonga as fit for his pre-injury duties. Professor Lord told Mr Daley that it was extremely uncommon for thin skin to expose a person such as Mr Tonga to risk of ulceration from further trauma. The tribunal is aware that several other doctors adopted a rather different view, accepting that the thinness of the skin could expose Mr Tonga to the risk of further ulceration from trauma to his shin. However, the tribunal noted that it had been five years since Mr Tonga had last had such a problem and it seemed unlikely that he had not at some time during that period knocked the shin against some or other object. The tribunal noted also that Professor Lord is a professor of surgery with a specialty in vascular surgery. In that regard his assessment of the likelihood of various scenarios coming about was firmly based. In addition, as Ms Adamson pointed out, Professor Lord had, to judge from what was before the tribunal, the benefit of the most detailed history of Mr Tonga's pre-existing condition.
Mr Daley had relied on Dr Stevenson's views in T25. However, the tribunal found Dr Stevenson's report somewhat confusing. First he thought that the skin on the front of the leg was thinner and more vulnerable than it would have been without the injury. He did not explain how he came to that conclusion, how he assessed the relative thickness of the skin. He then said that the venous hypertension, a condition unrelated to Mr Tonga's employment, was such that, even without the work injury the leg would in no way be normal. His assessment appears to the tribunal not very different from Professor Lord's.
Dr Graham in his reports endorsed the view that Mr Tonga's shin was vulnerable to fresh ulceration but he did not in his reports refer to the skin in that area being thinner than elsewhere or thinner than previously. Indeed, in a number of the reports in earlier years he saw Mr Tonga as fit to return to work or as becoming fit to return.
Dr Selby Brown adhered to the view that Mr Tonga's skin was thin (ex A3) and did explain how he formed that view. However, his findings are adversely affected by his ready acceptance that there was a wholesale change in Mr Tonga's life in March 1993. He had a less than ideal history of Mr Tonga's condition before 1993 and he accepted Mr Tonga's assertion that engaged in marathons and bikeathons up to March 1993 despite his being described as obese.
This is a matter that must be resolved by the tribunal preferring one medical view over another. The tribunal considers that Professor Lord was in the best position to provide the most reliable assessment.
The conclusion from this finding is that Mr Tonga probably has no ailment as such, in that his leg is the same now as if he had not had the injury in 1993.
This effectively disposes of the permanent impairment claim. If Mr Tonga's leg is the same now as if the employment-related trauma never occurred, any impairment he has is not related to an injury under the Act, as required by s 24(1) of the Act. Another way of stating this is to indicate that the decision that Comcare has, since 12 December 2000, been no longer liable to pay compensation to Mr Tonga in accordance with s 14(1) of the Act deprives Mr Tonga of success in claiming in respect of a permanent impairment. However, the tribunal should say something of the arguments made on permanent impairment.
First, the tribunal finds that the only table in the Comcare guide relevant to Mr Tonga's condition is table 1.3 on "varicose veins, deep vein thrombosis, oedema, ulceration". This is in the part of the Comcare guide headed "cardio-vascular system". The tribunal finds that table 9.5 is not applicable in the absence of an injury involving the "musculo-skeletal system". That is the section of the guide in which table 9.5 is located. In support the tribunal refers to the "Introduction" to the musculo-skeletal tables at page 9 of the Comcare guide. The introduction states that tables 9.1 to 9.6 "are intended to be used to assess impairment arising from specific joint lesions or amputations". Mr Tonga's problems with his lower left limb were caused by the alleged thinness of the skin on his left shin. That is in no way a joint lesion or amputation.
Dr Graham and Ms Adamson both suggested that Mr Tonga's left leg pain was possibly orthopaedically caused. However, Dr Graham thought it stemmed from Mr Tonga's posture when walking. The respondent produced the reports in ex R9 and ex R10, seen by Professor Lord, that indicated degenerative changes in Mr Tonga's spine unrelated to his employment. The tribunal finds that the evidence presented by Professor Lord is to be preferred to the theory, unsupported by any objective evidence, presented by Dr Graham. Were Mr Tonga's lumbosacral problems employment-related, it would have been appropriate to apply table 9.5.
So far as table 1.3 is concerned, Professor Lord was prepared to allow an assessment of 10% because of oedema incompletely controlled. However, as found earlier, there is no compensable injury any longer to support this being an employment-related condition. The same applies to the other assessments under table 1.3 such as Dr Selby Brown's apparently generous assessment in ex A3.
CONCLUSION
The tribunal has found that the effects of the compensable injury suffered by Mr Tonga on 11 March 1993 had ceased by 12 December 2000, the date on which Comcare decided that they had ceased. Mr Tonga is not, therefore, eligible for incapacity payments, compensation for medical expenses associated with his left leg or for compensation for any alleged permanent impairment of his left leg.
DECISION
The tribunal affirms the decision under review. The applicant is not entitled to costs associated with the application.
I certify that the 48 preceding paragraphs are a true copy of the reasons for the decision herein of Mr M J Sassella, Senior Member and Dr J D Campbell, Member
Signed:         .....................................................................................
  Associate
Date of Hearing  6 February 2002
Date of Decision  12 September 2002
Counsel for the Applicant        Mr M Daley
Solicitor for the Applicant         Brydens Solicitors
Counsel for the Respondent    Ms C E Adamson
Solicitor for the Respondent    Australian Government Solicitor