Sant v Tsoutsas [2009] NSWCA 3 (30 January 2009)

Last Updated: 10 February 2009

NEW SOUTH WALES COURT OF APPEAL

CITATION:
Sant v Tsoutsas [2009] NSWCA 3


FILE NUMBER(S):
40473/07

HEARING DATE(S):
31/10/08

JUDGMENT DATE:
30 January 2009

PARTIES:
Steven Sant (Appellant)
Peter Tsoutsas (Respondent)


JUDGMENT OF:
Beazley JA Bell JA

LOWER COURT JURISDICTION:
District Court

LOWER COURT FILE NUMBER(S):
DC 2391 of 2005

LOWER COURT JUDICIAL OFFICER:
Balla DCJ

LOWER COURT DATE OF DECISION:
13/6/07


COUNSEL:
Mr B Toomey QC / Mr SE McCarthy / Mr M Eirth (Appellant)
Mr B J Gross QC / Mr K Kelleher (Respondent)



SOLICITORS:
Albert A Macri Partners (Appellant)
Moray & Agnew (Respondent)

CATCHWORDS:
APPEAL AND NEW TRIAL – duty to give reasons – conflicting expert opinion – experts not called – duty not discharged

LEGISLATION CITED:
Suitors’ Fund Act 1951

CATEGORY:
Principal judgment

CASES CITED:
Ahmedi v Ahmedi (1991) 23 NSWLR 288
Wiki v Atlantis Relocations (NSW) Pty Ltd [2004] NSWCA 174; 60 NSWLR 127

TEXTS CITED:


DECISION:
1. Allow the appeal.
2. Quash the orders made in the District Court and in lieu thereof direct that there be a new trial on the issue of damages.
3. The respondent is to pay the appellant’s costs of the trial and of the appeal. In respect of the costs of the appeal, the respondent is to have a certificate under the Suitors’ Fund Act 1951, if qualified.



JUDGMENT:

THE SUPREME COURT
OF NEW SOUTH WALES
COURT OF APPEAL

CA 40473/07

DC 2391/05

BEAZLEY JA

BELL JA

Friday 30 January 2009

Steven SANT v Peter TSOUTSAS

Judgment

1 BEAZLEY JA: I agree with Bell JA.

2 BELL JA: The appellant was injured in a motor vehicle accident on 27 January 2001. He was aged 21 years. The respondent’s tipper truck which was carrying a load of sandstone collided with the appellant's vehicle, almost completely destroying the rear section of it and propelling it to the incorrect side of the roadway. The appellant suffered injury including to his left ankle as the result of the collision. Liability was admitted and the matter proceeded in the District Court as an assessment of damages.

3 At the time of the accident the appellant was about to complete his apprenticeship as a vehicle body-builder. He was in employment with a firm called Custom Coaches. He participated actively in a number of sporting activities. He was aged 27 years at the date of trial and he had not worked since the accident. He complained of continuing pain in his left foot and he walked with a noticeably distorted, antalgic (pain avoidant), gait.

4 Two doctors gave oral evidence concerning the left ankle injury. Dr Giblin, an orthopaedic surgeon performed a left ankle peroneal tendon stabilising procedure on 19 June 2001. He observed that the appellant had a congenital anomaly in the muscle associated with the tendon, a condition that would become symptomatic from time to time. Dr Giblin considered the instability of the tendon was the result of trauma caused by the accident. Dr Gibbs, a sports physician, commented that the congenital condition typically predisposes a person to recurrent tenosynovitis/tendonitis. Dr Gibbs considered that the appellant had chronic peroneal brevis tendonitis. In his opinion the accident may have caused a flare-up of the condition, which was similar to the flare-ups of the ankle problem that the appellant had experienced from his sporting activities in previous years.

5 Whatever the aetiology of the ankle injury, the procedure conducted by Dr Giblin was successful and it was not in issue that following the appellant’s recovery from it there remained no orthopaedic cause of the continuing left ankle pain or the distorted gait. It was the appellant’s case that both were the result of reflex sympathetic dystrophy (RSD) (in some reports described as complex regional pain syndrome type 1 (CRPS1)). The primary judge did not find that the appellant suffered from RSD.

6 Her Honour found that the appellant had suffered from peroneal tendon problems for a number of years before the accident. (Red 20.W-X) He disclosed that he had sprained his ankle in 1996 in the accident report form. However, in cross-examination a more extensive history of left foot/ankle problems emerged. In the five years before the accident the appellant had attended doctors with left foot/ankle complaints on 12 occasions. Her Honour considered that there was no satisfactory explanation for the appellant’s initial inability to remember this history, and this was a circumstance that had some impact on his credit. (Red 23.M) There were other inconsistencies in the appellant's evidence, which also adversely affected his credit. Her Honour considered that the appellant had exaggerated the level of his incapacity.

7 The respondent conceded that before the accident the appellant’s left ankle congenital abnormality had not significantly interfered with his capacity to work or to play sport. It was not in issue that before the accident the appellant did not limp.

8 Her Honour found that the accident had caused temporary exacerbation of an underlying condition involving the left ankle, which had been extended by psychological/psychiatric factors complicating the appellant’s recovery. She accepted that the appellant had developed low back pain brought about by his altered gait and that this made it difficult for him to stand for long periods.

9 There was no claim for non-economic loss.

10 Her Honour assessed damages in the amount of $483,005.35. She arrived at this sum on the basis of the following assumptions. The appellant would have been earning around $800 net per week had it not been for the accident. He had retained a capacity for work in an occupation such as a product assembler or motor vehicle parts interpreter. The impairment in his earning capacity was assessed at $450 net per week from the date of the accident to the date of judgment. The appellant’s condition was likely to improve markedly with time and psychiatric treatment. An allowance for continued impairment of earning capacity for 10 years from the date of judgment was allowed calculated on the basis of continued net loss of $450 per week, discounted by five percent, with a 15 percent reduction for vicissitudes. Future medical and out of pocket expenses were calculated on the basis of continuing need for 10 years from the date of judgment: four visits per annum to the general practitioner; physiotherapy; and gym membership. The full amount claimed in relation to future psychiatric treatment was allowed.

11 The appellant appeals against the whole of the assessment.

The grounds of challenge

12 The notice of appeal challenges the judgment on 13 grounds. Ground 13 complains that no adequate reasons were given to enable the appellant to understand the matters upon which his case failed.

13 At the hearing Mr BMJ Toomey QC who, with Mr SE McCarthy and Mr MB Eirth appeared for the appellant, distilled the remaining 12 grounds into three propositions:

1. Her Honour, wrongly, treated the question of the mechanism of the ankle injury as determined by her preference for the evidence of Dr Gibbs over that of Dr Giblin.

2. The finding that the appellant had not established that his ongoing disability was a consequence of RSD (Red 34.Q-R) was an inadequate consideration of the evidence concerning RSD, which is a cyclical condition.

3. Her Honour’s finding that it was likely that the appellant's post-traumatic stress disorder (PTSD) and depression would markedly improve over time and with treatment was not supported by the evidence.

In the way Mr Toomey developed the challenge emphasis was on the second and third of these propositions, each of which was illustrative of the general challenge to the adequacy of the reasons.

The challenge to the primary judge’s preference for the evidence of Dr Gibbs

14 The only evidence of the mechanism of the ankle injury came from Dr Giblin and Dr Gibbs. The first ground of challenge was a complaint that her Honour erred in preferring the evidence of Dr Gibbs. It is necessary to refer to the evidence in greater detail before returning to the basis of the challenge.

15 The appellant’s general practitioner, Dr Ramanathan, referred the appellant to Dr Giblin for investigation of his left ankle complaint in April 2001. Dr Giblin obtained a history of the accident. He was not aware of the appellant's history of pre-accident left ankle problems. Dr Giblin observed that the peroneal tendons on the left ankle were clicking and unstable around the posterior of the lateral malleolus. The appellant walked with his ankle held in a rigid fashion, externally rotated. Dr Giblin saw the appellant again on 30 April 2001. The results of a left ankle ultrasound were suggestive of subluxation (partial dislocation) of the peroneal tendons. On 13 June 2001 the appellant was still walking with an unstable pattern, his left leg turned outwards and the peroneal tendons remained unstable.

16 On 19 June 2001 Dr Giblin conducted a left ankle peroneal tendon stabilising procedure. The procedure was successful and the appellant’s progress was satisfactory following it.

17 Dr Giblin reported to Dr Ramanathan, on 29 June 2001, that (Blue 370.K-N):

There was a congenital abnormality with muscle associated with the peroneus brevis, coming down to the posterior aspect of the lateral malloelous. There were adhesions here, probably as a result of the direct trauma. Anyhow this was freed up, and he has a below knee non weight bearing cast on. The tendon sheath was left in tact around the posterior aspect of the lateral malloelous. He is likely to be off work for a further six weeks.

18 On 17 August 2001 Dr Giblin reported that he had re-examined the appellant's foot and ankle and that from an objective orthopaedic standpoint there were no significant signs.

19 In his report to Dr Ramanathan, dated 10 November 2001, Dr Giblin said (Blue 377.K-O):

I have re-examined his foot and his legs and I cannot find any organic pathology. Range of motion is good, tendons are intact and stable and reflexes are fine.

He still walks with a limp.

...

From my perspective, I believe he now should be back at work. I have advised him of this.

20 Dr Giblin described the pre-existing condition as a congenital anomaly; it is not always associated with instability unless something occurs to provoke it. Dr Giblin considered that the accident had provoked it. (Black 227.F-K) He thought that it was unlikely that the appellant had suffered from adhesive tendonitis before the accident because he had been able to play indoor soccer, which involved running, shifting directions and tackling and because of his ability to engage in kick-boxing.

21 Dr Giblin agreed that there had been two surgical options, a tenolysis of the peroneal tendon sheath or a stabilisation procedure. Tenolysis is a tendon release. (Black 247.V-W) It was put to him that he had carried out the tenolysis and not the stabilisation. Dr Giblin said, “it wasn’t a formal stabilisation. It was a de facto stabilisation.” (Black 237L)

22 Dr Gibbs, a sports physician who had been in practice in this field for 22 years, described the appellant's problem as a congenital abnormality of the peroneus brevis muscle and tendon unit. (Blue 758-759) It predisposed the appellant to tendonitis of the peroneal brevis tendon as it runs through its sheath. This condition, if chronic, can lead to adhesions in the sheath. Dr Gibbs considered that the procedure performed by Dr Giblin involved the release of adhesions arising from the chronic tendonitis. In his opinion, the tendon sheath was not unstable and did not need a stabilisation procedure. He explained that usually peroneal tendonitis problems occur because of overuse. The appellant’s history of kick-boxing in the years before the accident could have overloaded the peroneal tendon region. Dr Gibbs did not believe that the accident had caused the appellant's condition, but he said it was quite possible that the accident caused a flare up of the condition, which was similar to the numerous flare ups that the appellant had had from sporting activities in the five years before the accident.

23 The primary judge preferred the evidence of Dr Gibbs to Dr Giblin where the two were in conflict for the following reasons (Red 30.I-31.J):

1. Dr Gibbs is a sports physician. It was clear that he has extensive experience in dealing with athletes with this type of injury.

2. The plaintiff’s general practitioner sent the plaintiff for a second opinion to Dr Harris shortly after Dr Giblin had performed the tenolysis. Dr Harris saw the plaintiff on 27 November 2001 and 8 January 2002. He arranged for the plaintiff to have an MRI scan of his left ankle, which was normal. He concluded that there was no evidence of any significant pathology.

3. Dr Giblin’s opinion in the witness box is not expressed as strongly as in his reports. By 17 August 2001 Dr Giblin was of the view that from an objective orthopaedic stand point there were no significant signs and described the plaintiff’s chief problems as stress and anxiety and a reactive depression.

A bone scan on 7 September 2001 is relied on in these proceedings as evidence of the plaintiff having developed a reflex sympathetic dystrophy accounting for his ongoing condition. However, at that time Dr Giblin, while acknowledging there were some symptoms, considered that the plaintiffs’ RSD was fairly minor with no serious organic problems. He suggested referral to a psychiatrist.

On 10 November 2001 Dr Giblin could not find any organic pathology in the foot or legs, the range of motion was good, the tendons were intact and stable and the reflexes were fine. He then was of the view that the plaintiff’s progress would be quite slow until this case had settled.

4. I formed the view that Dr Giblin saw his role as an advocate for the plaintiff. This was especially apparent in his comments about a research paper relied on by Dr Gibbs. He said he was “interested” to see that it had been published in the British Journal of Sports Medicine and not published locally. He concluded that it may have been rejected by the local publishers.

This comment was unnecessary and illustrated his lack of familiarity with sports injuries. Dr Gibbs said that the journal is one of the three leading international journals.

24 Mr Toomey submitted that her Honour’s preference for the opinion of Dr Gibbs, a general practitioner specialising in sports medicine, who had not examined the appellant, for that of the orthopaedic surgeon who had examined him and carried out the procedure was perverse. The significance of the difference in the opinion of the two was that Dr Giblin’s opinion was consistent with the appellant having suffered a significant insult to the left ankle in the accident as distinct from a flare-up like those that he had reported in previous years. This underestimation of the extent of the physical injury sustained in the accident, it was submitted, had coloured her Honour’s approach to the assessment of the evidence of RSD.

25 Dr Gibbs described the appellant's pre-existing condition as a congenital abnormality, while Dr Giblin preferred to describe it as a congenital anomaly. Both were describing the same phenomenon. Each agreed that it was a phenomenon that would from time to time become symptomatic. In cross-examination Dr Gibbs deferred to the opinion of Dr Giblin concerning the surgical procedure performed on the appellant. Their opinions differed on whether the congenital anomaly caused the appellant to suffer adhesive tendonitis. Dr Giblin considered that unlikely because of the appellant's ability to play sport before the accident.

26 Whether the impact of the accident introduced instability to the tendon or whether it merely exacerbated a pre-existing condition is not critical. Dr Giblin did not consider that there were any physical sequelae from the injury that he observed following the appellant's recovery from the procedure.

27 The primary judge accepted that the accident was causative of the condition in the left ankle that led to the surgical procedure that was carried out on 19 June 2001. Following that procedure the appellant was immobilised for a time in plaster and on crutches, a circumstance that may have been relevant to the question of whether he developed RSD.

28 The difference between the opinions of Dr Giblin and Dr Gibbs did not bear on the determination of the central question, which was the cause and likely course of the appellant’s deformed gait and persisting left ankle pain. Her Honour’s preference for the evidence of Dr Gibbs was explained. It reflected her acceptance of Dr Gibbs’ lengthy experience in treating athletes with this type of injury. It also reflected her Honour’s assessment that Dr Giblin had in some degree assumed the role of advocate. (Red 30.P-R; 31.E-J) Her Honour’s advantage including in the assessment and evaluation of competing expert opinions is to be given weight: Ahmedi v Ahmedi (1991) 23 NSWLR 288 per Clarke JA (Handley JA agreeing) at 299 –300.

29 I would not uphold the first ground of challenge.

30 Before turning to the second and third grounds, reference should be made to one discrete complaint, which relates to her Honour’s finding that an entry in the general practitioner’s notes of the appellant’s attendance on 24 June 2000 was of treatment of the “left foot”. The entry, a photocopy of handwritten notes, appears to be overwritten. (Blue 406.O-P) There is a capital letter before the word “foot” which is either “L” or “R”. In my opinion it is not possible to conclude that the initial is more probably “L” than “R”. Accepting that it was not open to find that the appellant’s attendance on 24 June 2000 was more probably than not for swelling on the talar aspect of the left foot does not materially bear on her Honour’s determination. There were 11, not 12, occasions over the five years prior to the accident when the appellant was treated for complaints associated with his left foot or ankle.

RSD – the evidence

31 In January 2002 the appellant was complaining of persistent neck pain and pain in the left ankle. He was referred to Dr Sheridan, a neurosurgeon. In a report dated 10 May 2005 Dr Sheridan said that the appellant, “had symptoms consistent with reflex sympathetic dystrophy and skin changes and colour changes in his foot.” (Blue 297.O) Dr Sheridan commented that the appellant had undergone a bone scan which he said, “confirmed a reflect sympathectomy dystrophy in his foot”. (Blue 297.Q-R) Dr Sheridan considered that the appellant's main problem was “persisting problems in his left leg consistent with a reflex sympathetic dystrophy as an after effect of his orthopaedic injury.” It was likely that this would be a permanent injury for which the appellant would need ongoing treatment. (Blue 298.E) He referred the appellant to Dr Salmon, a pain management specialist.

32 In a supplementary report, dated 24 August 2005, (Blue 299) Dr Sheridan adhered to his earlier opinion after reading the report of Dr Ross Mellick.

33 Dr Sheridan reviewed the appellant on 24 October 2005 and, again, on 10 January 2006. In his report dated 2 February 2006, he said that the appellant had persisting symptoms of reflex sympathetic dystrophy and problems with walking due to his left leg pain. He also had persisting neck and lower back pain that was possibly related to his abnormal gait. MRI scans of the spine and ankle did not show any abnormality. Dr Sheridan maintained the diagnosis of a sympathetic dystrophy with the need for ongoing management by a pain management specialist. (Blue 300)

34 Dr Sheridan reviewed the appellant on 15 November 2006. In his report dated 23 November 2006, he said this:

He still has symptoms very typical of a reflex sympathetic dystrophy or complex region pain syndrome. His left foot has atrophic changes with loss of hair, atrophy of his skin and colour changes. He is quite sensitive to temperature changes as well. He has been trying various treatments with the Pain Clinic at Liverpool Hospital, so far they haven’t been helping. He is still quite restricted because of the pain. I discussed with him his options today. He should continue to see the Pain Clinic as they will be his best source of advice. He may well need to consider a spinal chord stimulator down the track if everything else fails. I will leave this however up to Dr Salmon and the Pain Clinic to discuss further. (Emphasis added.)

35 Following this report it would seem that Dr Sheridan was furnished with material which included the appellant’s history of pre-accident left ankle problems. In his final report, dated 28 February 2007, Dr Sheridan stated that he had read material supplied to him, “in particular the history of his injury and his lack of ongoing symptoms”. The material did not alter his previously expressed opinion. In Dr Sheridan’s view, the appellant would have not been able to have participated in activities such as kick-boxing, running, soccer and vigorous dancing if the problem was present prior to January 2001. (Blue 302.O-Q)

36 Dr Salmon, the pain management specialist to whom the appellant was referred, reported to Dr Sheridan on 30 April 2002. He said that the appellant’s most severe pain was in the left ankle, it was constant and varied from a moderate dull ache to a very severe, sharp, burning, stabbing pain, radiating to the calf, but not to the toes. The severe pain was both spontaneous and evoked by prolonged weight bearing and movement. It could last for hours. (Blue 303.U-W) The appellant had given a history that his left foot could swell, feel cold, take on a blue appearance, and was cold sensitive. On examination Dr Salmon reported that the range of movement of the ankle was restricted to 0 – 50 degrees of plantar flexion. The foot was dark, cool, but not moist. There was 2 cm wasting of the left calf. The appellant was left leg dominant. Dr Salmon’s opinion was that (Blue 305.F-I):

Steven has internal derangement of the left ankle and foot as a result of direct trauma, and features of sympathetic dysfunction. He was taking pain medication which he was unable to identify, but it made him drowsy and evoked sweating. I have advised him to take Paracetamol plus Brufen on a regular basis. Arrangements have been made for him to have a left lumbar sympathetic nerve block to assess the sympathetic component of his pain.

37 Dr Salmon wrote a report to Dr Ramanathan, dated 22 January 2004, in which he said (Blue 306.Q-X):

Steven continues to report in left ankle and dorsal foot pain, which is constant and can burn. He experiences swelling with activity, frequent sensation of coldness, and noticeable sweating. He has been unable to afford suitable medication, gym/physiotherapy, or pain counselling. He stated that the rehabilitation provider (work) stopped about July, 2002.

Steven last worked on 27 January 2001, and is a qualified vehicle body builder.

He walks with a left antalgic gait. There is wasting of the left quadriceps and calf, with impaired sensation of the distal left extremity. The foot is cold, pale, moist and of decreased temperature. The range of movement of the left ankle is restricted to 40 degrees of plantar flexion.

Steven continues to have Complex Regional Pain Syndrome Type 1. He has trialled Neurontin, but only 1 per day. He will begin Neurontin after the sympathetic block which is proposed.

38 In his report dated 19 May 2003, Dr Salmon commented on his recent review of the appellant, who continued to have left ankle pain. The appellant had some features of sympathetic dysfunction and was attempting home based exercises. In a report dated 22 September 2003 Dr Salmon advised Dr Ramanathan that he had reviewed the appellant, who continued to have pain in the left lower limb. The appellant was complaining of increasing back and right lower limb pain, which Dr Salmon presumed was the result of the left antalgic gait. The appellant gave a history of sensations of hot and cold in the foot with sweating, colour changes, swelling and tingling and numbness. Dr Salmon observed that (Blue 310.Q-R):

On examination the colours of the feet were equivalent, there was increased circumference at the arch, and decreased circumference at the calf and thigh compared to the right. There was a normal range of flexion, with straight leg raising equivalent. The foot was dry, but cool. There was a non dermatomal impairment of sensation (pin prick).

39 Dr Salmon reported on 3 June 2004 that the appellant was very depressed, and complaining of back and leg pain. At this date he had been reviewed by a psychiatrist because of his depression. The last report in evidence from Dr Salmon is dated 14 October 2004. He had recently reviewed the appellant, who continued to complain of left foot and back pain.

40 The respondent qualified Dr Mellick, consultant neurologist, who examined the appellant on 4 August 2004. There was no indication of any spinal or peripheral nerve abnormality. Dr Mellick was not able to identify any neuromuscular disorder involving the spine or lower limbs. In Dr Mellick’s opinion that there was no evidence of CRPS Type 1 or Type 2. The site of surgical intervention was well healed and there was no localised area of tenderness in the region. He did not consider that the appellant’s symptoms were explicable on the basis of an organic process. In Dr Mellick’s opinion the appellant was not suffering from any abnormality that would prevent him returning to work in an occupation, such as coach building. (Blue 540-544)

41 In a further report, dated 15 October 2004, Dr Mellick commented on his review of the appellant and the reports of Dr Salmon. (Blue 549 – 554) He noted that Dr Salmon had reported wasting of the left quadriceps and left calf in the report of 22 January 2003. In Dr Salmon’s report of 22 September 2003 there was no reference to wasting but to a decrease in the circumference of the calf and thigh on the left side. Dr Mellick found no wasting of the left leg. He assessed the appellant as being right sided dominant and he noted that one would expect some asymmetry of the muscle mass with the muscles on the left being smaller than those on the right. In Dr Mellick’s opinion this degree of asymmetry should not attract comment. Dr Mellick noted Dr Salmon’s examination of the appellant on 22 January 2003 when his left foot was “cold, pale, moist and of decreased temperature” and of 22 September 2003 when the left foot was “dry and cool”. Dr Mellick observed that he had not seen the appellant at this time and was unable to know whether the temperature changes and other features described by Dr Salmon were of sufficient magnitude to justify the diagnosis of CRPS. (Blue 550.T-V) In Dr Mellick’s opinion if the appellant had suffered from CRPS at some time in the past he was not suffering from it when he saw him shortly before writing his report of 15 October 2004. (Blue 551.D-E)

42 The respondent also qualified Professor S Nade, an orthopaedic surgeon, who examined the appellant on 13 March 2007. The appellant walked with a left antalgic gait with some circumduction of his left lower limb. Dr Nade watched him walking in the street after leaving his rooms and he noted that the unusual gait persisted, although the appellant appeared to take full body weight on his left leg while in the abducted and slightly externally rotated position. There was noticeably more wear on the heel of the appellant’s right shoe. (Blue 753.H-I) The appellant had shaved the hair from both of his lower limbs and around his buttocks. He told Dr Nade that he had done this because there was greater hair growth on the right lower limb than on the left. (Blue 753.S-T) Dr Nade examined the left lower limb and observed that it was not discoloured and that there was no swelling about the left ankle and no ligamentous laxity. The temperature on the sole and dorsum on the left foot was slightly lower compared with the right. There was no skin oedema and no alteration in perspiration pattern in his feet. (Blue 754.E-G)

43 Dr Nade concluded that it was most likely that the appellant's abnormal gait was a habit that he had developed. There was no evidence of CRPS. Dr Nade reported (Blue 755.I-L):

A diagnosis of complex regional pain syndrome (CRPS) is based on objective clinical signs, as opposed to symptoms, which are subjective sensations of the individual. In order to state that a person probably has complex regional pain syndrome they should have more than eight of the following signs: skin colour being mottled or cyanotic, skin temperature cool, oedema, skin dry or overly moist, skin texture smooth and non-elastic, soft tissue atrophy, joint stiffness and decreased passive motion, nail changes being blemished curved or talon like, and hair growth changes being falling out, longer or finer, and radiographic signs of trophic bone changes or osteoporosis, and radio-isotope bone scan findings consistent with the CRPS. Mr Sant did not demonstrate eight or more of those signs.

44 Dr Nade gave oral evidence at the trial. In cross-examination he agreed that he was aware of Dr Sheridan’s diagnosis of RSD. He said that it is a diagnosis that is not always easy to make, which was why he had listed the accepted criteria. (Black 325.B-D) Dr Nade agreed that if the appellant did suffer from RSD the probable explanation for it was the trauma of the accident because it is not a condition that appears spontaneously. (Black 325.J-M)

45 A bone scan of the appellant's ankle was carried out on 21 August 2001. Dr Patel reported that (Blue 271):

The dynamic study and blood pool study demonstrated mildly reduced vascularity in the left lower leg, ankle and foot.

...

There is reduced vascularity in the left lower leg. There is periarticular increased uptake in the left ankle, subtalar joint and proximal intertarsal joints. These features raise the possibility of reflex sympathetic dystrophy. However, the scan features are not entirely typical of reflex sympathetic dystrophy given the absence of increased uptake in the distal joints of the left foot and in the left knee.

46 Dr Giblin, in his report dated 5 November 2001 which was addressed to the appellant's solicitors, referred to his review of the appellant on 7 September 2001, he went on to comment that, “the bone scan confirmed reflex sympathetic dystrophy”. (Blue 206.H-I) Dr Giblin considered that the appellant's prognosis was guarded and that “stress and depression have occurred and have been attended by reflex sympathetic dystrophy”. (Blue 206.L-M) It is accepted that Dr Giblin was mistaken in understanding that the bone scan performed by Dr Patel confirmed the diagnosis of RSD. Dr Sheridan appears to have made the same mistake. (Blue 297.R)

47 A second bone scan was conducted by Associate Professor Pocock on 25 November 2005. He reported that (Red 32.B-F):

The overall scan appearances do not suggest reflex sympathetic dystrophy. The mild diffuse changes in the right calf and foot most likely effect altered weight bearing.

No other bone or joint abnormality identified to account for the patient’s symptoms.

48 In his report dated 13 October 2005 Dr Giblin recorded the appellant’s history of left leg sweating and of feeling hot and cold. The circumference of each calf was 36 cm on the right and 34 cm on the left. Dr Giblin did not detect any temperature difference between the left and the right lower limbs and the pedal pulses in the lower limbs were preserved, equal and normal. There was no discrepancy in skin colour or hair growth on either leg. The appellant’s history of recurrent symptoms was consistent with RSD. The physical examination showed no evidence of any permanent RSD signs other than muscle wasting. The muscle wasting could be attributed to the soft tissue injuries being allied to a reactive illness behaviour. (Blue 208) It remained Dr Giblin’s opinion that the appellant did have RSD, which he considered to be of an incipient type. It is not recognised by the AMA Guides to Impairment. In the clinical world, incipient or recurrent RSD, is a not infrequent problem, especially in relation to soft tissue injuries. (Blue 209.G) In his clinical experience, RSD in a mild form can be episodic in nature.

49 Dr Davis, an injury management consultant, in his report dated 27 September 2005, noted the appellant's quite marked left-sided antalgic gait. (Blue 330.S) Examination of the appellant's left foot had revealed no significant colour changes, but there was some swelling present. (Blue 331.M) The appellant had developed a documented history of CRPS affecting his left foot, with severe pain, sensory changes, swelling and colour changes. He commented on the obvious wasting in the appellant's left lower limb, which was supportive of the appellant’s functional difficulties relating to that limb. Dr Davis considered that (Blue 333.L-M):

There has obviously been degree of resolution in his CRPS symptoms over time although his prognosis must remain guarded as such pathology follows a variable course and is quite unpredictable.

50 Dr Govind, an occupational physician, examined the appellant on five occasions between November 2005 and February 2006. He reported that the appellant's post-surgical recovery had been complicated with the onset of RSD symptoms. (Blue 345.N) In his report, dated 13 February 2006, Dr Govind recorded that examination of the appellant’s left ankle had not revealed features of allodynia, hyperalgesia or abnormal sweat, all of which are manifestations of CRPS1. (Blue 346.U) At a review on 19 December 2005 an MRI of the left ankle joint revealed no obvious abnormality, however the appellant did present with touch allodynia. This is a phenomenon in which the skin is supersensitive to light touch. The appellant complained of a burning sensation on the plantar aspects (sole) of the left foot. (Blue 347.E-F) Dr Govind noted the MRI excluded obvious bony or joint abnormality of the left ankle, but noted that nerve injuries (CRPS/RSD) cannot be visualised on standard imaging. Dr Govind considered that the appellant would experience pain for the foreseeable future and that he may develop disuse atrophy, contractures or muscle wasting. (Blue 348.G-I)

51 A number of civilian witnesses were called in the appellant’s case. They were unanimous in saying that from the time of the accident the appellant had walked with a noticeably deformed gait. A number described observations of the swelling in the appellant's left foot. David Breakspear, an old school friend, had seen swelling around the top of the foot even up to the lower leg on occasions. (Black 144.N-O) Paul Georgievski said that on two or three occasions he had seen the appellant’s left foot swollen. He said on these occasions the swelling was “huge it wasn’t normal”. (Black 168.P) Noreen Campbell, a trained nurse, had observed that the appellant’s ankle appeared “pretty swollen”. (Black 277.I)

RSD - the judge’s analysis of the evidence

52 The primary judge commenced her analysis of the evidence on RSD by noting the results of the two bone scans, observing that the issue of whether the appellant has RSD had been made more difficult by his failure, and the failure of his legal advisers, to provide the second bone scan to the various doctors who reported on his condition. In particular, Dr Giblin, Dr Sheridan and Dr Govind had not been told of the results of the second bone scan. (Red 32.G-N)

53 Her Honour extracted sections of the report prepared by Dr Giblin, dated 13 October 2005 (Red 32.P-X):

There was no temperature difference that I could detect ... there was no discrepancy in terms of skin colour or hair growth on either leg ... .

On today’s physical examination there is no evidence of any permanent reflex sympathetic dystrophy signs, other than the muscle wasting. The muscle wasting could also be attributed to the soft tissue injuries being allied to a reactive illness behaviour ...

It remains my view that this gentleman did have reflex sympathetic dystrophy as a result of his injury ... .

It has been my clinical experience that RSD in mild form can be episodic in nature. On today’s clinical examination, apart from some muscle wasting, as noted, there was no overt objective evidence of RSD. That is not to say, that it cannot return if the patient was exposed to the appropriate, or inappropriate, treatment program.

54 Her Honour noted that Dr Giblin had been sent the bone scan and that in his later report, dated 24 January 2007, he had not commented on whether the appellant had RSD. (Red 33.E)

55 Her Honour went on to refer to the reports of Dr Sheridan (Red 33.G-34.F):

The reflex sympathetic dystrophy was diagnosed by Dr Mark Sheridan, neurosurgeon. The plaintiff relies on the opinion of this doctor in asserting that some or all of the disability in his left foot is caused by RSD.

In a report dated 23 November 2006 Dr Sheridan referred to having reviewed the plaintiff on 15 November 2006. He then mentioned a number of symptoms. I decline to find that Dr Sheridan is recounting his findings on examination as submitted by counsel for the plaintiff.

Dr Sheridan described the plaintiff as having symptoms typical of a reflex sympathetic dystrophy. These were loss of hair, atrophy of his skin, colour changes and sensitivity to temperature change. I do not understand the plaintiff to assert that he has any loss of hair. He has shaved the hair on his legs. He said he did this because the hair on his right leg was longer than on his left leg. The plaintiff did say that his foot and ankle would change colour and become clammy and sweaty. The plaintiff called three friends to give evidence. They described the swelling but did not mention any change in colour. The plaintiff’s father said that he had seen the ankle area a bluish colour a few times. His brother has never even seen the ankle swollen. In view of my findings as to the plaintiff's credit I am not persuaded that there is any significant ongoing issue with the ankle or foot changing colour.

Dr Sheridan was sent some documents in January and March 2007 and asked to comment. In neither supplementary report does he expressly mention the second scan. In the first report he comments on whether the plaintiff’s earlier symptoms are of any relevance. In the second report he simply said that Dr Gibbs report did not cause him to change his opinion. Accordingly I have not been assisted with his opinion in relation to the second bone scan.

Dr Sheridan referred the plaintiff to Dr Salmon for pain management. He diagnosed a complex regional pain syndrome type 1 which is RSD. That doctor also relied on the history given to him by the plaintiff in relation to his symptoms. His reports refer to examinations of the plaintiff which do not refer to any change in colour. The doctor’s last report was prepared before the plaintiff underwent the second bone scan. (Emphasis added.)

56 Her Honour went onto note that the appellant had seen Dr Govind, who had proceeded on the basis that he was suffering from RSD. Her Honour noted that Dr Govind relied on the history given to him by the appellant and that he had not commented on the second bone scan. (Red 34.G-I) She noted that Dr Mellick had not found any symptoms of RSD at the time of his examination and that Associate Professor Jones considered the appellant had sustained a relatively minor injury and that he displayed a bizarre walking pattern. She observed of Associate Professor Jones that, “[h]e considered that the appearances did not confirm the diagnosis of RSD although there were symptoms that might indicate that such a diagnosis would be made.” (Red 34.L-P)

57 Her Honour concluded that the appellant had not discharged the onus of showing that his ongoing disability was a consequence of RSD. (Red 34.Q-R)

58 The grounds of appeal contained a challenge that the primary judge erred in concluding that the appellant did not suffer from RSD and that in so concluding she had ignored evidence of the existence of the condition, including its episodic nature and that she had made incorrect findings on the unchallenged evidence of Dr Sheridan. The contention that it was an error not to find that the appellant suffered from RSD was not pressed at the hearing. The challenge was to the sufficiency of the analysis of the conflicting expert evidence and to the failure to address the evidence that RSD can be intermittent. Specific complaint was made of her Honour’s refusal to accept that Dr Sheridan was describing his findings on examination in his report of 23 November 2006 (the highlighted passage at [34] above). It was noted that Dr Sheridan had not been required for cross-examination and in these circumstances it was submitted that it was not open to have found this issue against the appellant. It was also submitted that her Honour wrongly approached Dr Salmon’s reports on the basis that he had been reliant on the history and not on clinical observations.

59 It is true that Dr Sheridan’s evidence was unchallenged in that he was not required for cross-examination. Neither was Dr Mellick required for cross-examination and Dr Mellick’s opinion did not support a finding of RSD. The case proceeded, as is common in motor accident claims in the District Court, with the tender of conflicting medical reports without the doctors giving oral evidence. The only doctors who gave oral evidence were Dr Giblin, Dr Gibbs and Dr Nade. Both Dr Giblin and Dr Gibbs provided some support for a diagnosis of RSD but this was not the focus of their evidence. Her Honour was confronted with the common difficulty facing judges in the District Court of coming to a reasoned conclusion based on the conflicting opinions of expert witnesses who were not tested in cross examination. The complaint that she rejected the unchallenged opinion of Dr Sheridan does not address the way in which the trial was conducted.

60 Her Honour had reservations about the appellant’s credibility and considered that he had exaggerated his complaints. Significant to her rejection of the diagnosis of RSD was her view that those who favoured the diagnosis were dependent on the history obtained from the appellant. In this respect there is substance to two of the criticisms that Mr Toomey made. Dr Sheridan recorded in his report of 23 November 2006 that the appellant's left foot had atrophic changes with loss of hair, atrophy of his skin and colour changes and that he was quite sensitive to temperature change as well. (Blue 301.M-N) It was open to her Honour to place no significance on the hair loss since there was evidence that the appellant shaved the hair on his lower limbs. Nonetheless, the basis for rejecting Dr Sheridan’s report of skin and colour changes and sensitivity to temperature is unexplained. The report was of the results of Dr Sheridan’s review of the appellant, which was conducted on 15 November 2006.

61 In the highlighted concluding passage at [55] above, her Honour says that Dr Salmon relied on the history given by the appellant and that his reports did not refer to colour changes. In two respects this passage appears to be incorrect. Dr Salmon was not dependent on the appellant’s history alone and he did refer to a change in colour in the left foot. He recorded the results of his examination of the appellant in his report to Dr Sheridan of 30 April 2002, which included that the left foot was “dark, cool, but not moist”. He also noted impaired sensation in a non-dermatomal distribution of the distal limb and 2 cm wasting of the left calf. (Blue 304.J-K) In his report of 22 January 2003 Dr Salmon comments on the results of a recent review of the appellant in which he described wasting of the left quadriceps and calf with impaired sensation of the distal left extremity. The left foot was cold, pale, moist and of decreased temperature. (Blue 306.U-V) In his report dated 22 September 2003 Dr Salmon described the left foot as having been “dry, but cool”. (Blue 310.R) He again recorded the decreased circumference of the left calf and thigh compared to the right. The colours of the feet on the occasion of this visit were equivalent.

62 Her Honour said that she took into account Dr Giblin’s report which I have extracted at [53] above. However, she did not explain how she took it into account. The only discussion of Dr Giblin’s diagnosis of RSD was the observation that he had not commented on whether the appellant suffered from RSD in his report dated 24 January 2007, which was prepared after he had been sent a copy of the results of the bone scan. It is to be observed that in the January 2007 report Dr Giblin said that he had no reason to change the general thrust of the comments and opinions expressed in his earlier reports. (Blue 213.H) In his oral evidence Dr Giblin appears to have adhered to his diagnosis of RSD. (Black 233.D-H) There is no explanation for the rejection of Dr Giblin’s opinion that the appellant suffered from RSD, which was of an incipient or recurrent type. (Blue 209.F)

63 Mr BJ Gross QC, who with Mr KJ Kelleher appeared for the respondent, drew attention to Dr Nade’s report, which is extracted at [43] above. His point was that none of the doctors on whom the appellant relied identified eight of the diagnostic signs of RSD which Dr Nade set out as requisite to the diagnosis. The difficulty with this submission is that the transcript of Dr Nade’s evidence, to which reference is made at [43] above, does not convey that Dr Nade went so far as to say that Dr Sheridan was wrong to make the diagnosis in the absence of identification of eight or more of the signs. Dr Nade’s comment on Dr Sheridan’s diagnosis was to say that RSD is a difficult diagnosis to make. Dr Nade was aware of the bone scan performed by Professor Pocock. He did not say that the negative result of the scan excluded the diagnosis. Her Honour’s analysis of the conflicting evidence concerning RSD makes no reference to the report or oral evidence of Dr Nade. Her rejection of the diagnosis made by the treating doctors, that the appellant was suffering from RSD, was substantially based on the absence of objective signs consistent with the condition given that she did not accept the appellant's report of symptoms as reliable. In these circumstances the unexplained rejection of Dr Sheridan’s report of the appellant's presentation at his 23 November 2006 review and the error in assessing Dr Salmon’s diagnosis as being wholly dependent on the history, undermines the conclusion.

The psychiatric evidence

64 Her Honour found that the appellant had loved his work and had felt significant grief at losing his employment. She rejected the respondent’s primary case, which was that the appellant's symptoms were fabricated.

65 The appellant was seen by Dr Canaris, a consultant psychiatrist, at the request of his solicitors. Dr Canaris described the appellant as having been through a life-threatening event of the highest order of magnitude. The appellant showed evidence of PTSD, which was not surprising given the magnitude of the trauma. His presentation had been complicated by the emergence of moderate to severe depression, which is a frequent accompaniment of PTSD. Dr Canaris concluded his report saying (Blue 323.V-X):

I cannot envisage this man making a rapid recovery. Indeed he may not recover at all given the lengthy period that has elapsed between the accident and the present assessment. Psychiatric treatment may palliate but probably not 'cure'.

66 Dr Sydney Smith, a consultant psychiatrist, assessed the appellant for the respondent. Dr Smith obtained a history of intrusive thoughts, flashbacks and nightmares from the date of the accident. The appellant reported having become phobic about being in a car, that he avoided reminders of the accident, that he suffered panic attacks and had become hyper-vigilant. If the history was accepted, Dr Smith considered the appellant had PTSD. Dr Smith noted that the appellant had been counselled by Ms Deane in 2002 on pain management strategies. (Blue 683.N-Q) Her Honour appears to have accepted that Dr Smith’s diagnosis was supportive of PTSD when viewed against a background of the observations made by Ms Deane in the period following the accident.

67 Dr Smith concluded his report as follows (Blue 683.T-684.D):

If it is true that from the time of the accident he has suffered PTSD symptoms complicated by depression and substance abuse then he is in need of psychiatric care. He should be tried on antidepressant medication in combination with counselling, behavioural therapy approaches to overcome his phobias, and treatment of his substance abuse.

This may best be done on an inpatient basis for a period of three or four weeks followed by outpatient treatment. He would then require regular supervision by both a psychiatrist[] and a Drug & Alcohol counsellor, with regular urine testing to ensure that he is not continuing to abuse drugs. Such an intensive program could involve the 40 – 50 sessions of care suggested by Dr. Canaris, however, this number should be shared between the psychiatrist and Drug and Alcohol counsellor.

68 Ms Deane, clinical psychologist, reported to the rehabilitation adviser at AAMI CTP, on 14 January 2002 that the appellant was suffering a significant degree of depression, feeling generally low and lacking motivation. He complained of problems sleeping, irritability, weight gain, decreased appetite and lethargy. At times he described feeling hopeless, helpless and worthless. (Blue 527.M-O) He appeared to excessively avoid many activities because he was fearful of experiencing more damage. (Blue 527.U-V)

69 Dr Moore, a consultant psychiatrist, assessed the appellant for the Motor Accident Authority on 18 October 2004. She diagnosed chronic PTSD. (Blue 839.L-M) She noted that the appellant had not had any definitive treatment for the condition and given the time that had elapsed since the accident it was not likely that treatment would be of much benefit to him. Dr Moore considered the appellant required treatment for his depressive condition and unless and until he was adequately treated for this condition he was unlikely to be able to move on with his life and that his prognosis would be poor. The appellant’s intolerance for antidepressant medication and ongoing moderate to heavy alcohol use created considerable doubt about his future recovery. (Blue 839.G-K) In Dr Moore’s opinion the appellant suffered from a major depressive disorder of moderate severity which was secondary to his chronic PTSD. (Blue 839.L-M)

70 Dr Akkerman, a psychiatrist, assessed the appellant for the Motor Accidents Authority on 16 December 2005. Dr Akkerman noted the appellant's current symptoms included getting upset when thinking about the accident; avoidance; flashbacks; startles easily; hyper vigilant particular when in a car; feels different from others and has a restricted affect. He did not have a sense of shortened future and he exhibited no psychogenic amnesia. (Blue 730.M-S) In Dr Akkerman’s opinion the appellant embellished his symptoms. (Blue 731.J) Dr Akkerman diagnosed the appellant as suffering an adjustment disorder with depressed and anxious mood. This condition was unlikely to change substantially and by more than three per cent with or without medical treatment. Dr Akkerman estimated the appellant's whole person impairment for the purpose of the Motor Accidents Authority at five per cent. Dr Akkerman considered that with appropriate treatment the appellant's condition will improve markedly. (Blue 733.J-M)

The primary judge’s analysis of the psychiatric evidence

71 Her Honour’s analysis of the psychiatric evidence is set out below (Red 35.L-36.H):

He has also reacted to the pain from the injury at the time of the accident. He also experienced a potentially life threatening event.

The plaintiff was assessed by Dr Canaris, psychiatrist, in 2004. At that time he diagnosed a post-traumatic stress disorder complicated by the emergence of moderate to severe depression. He concluded that the plaintiff's physical and psychological problems were mutually aggravating one another.

Dr Sydney Smith reviewed the plaintiff at the request of the defendant in October 2004. Based on the history given to him by the plaintiff he also diagnosed a post-traumatic stress disorder complicated by depression and substance abuse.

The plaintiff was also assessed by two psychiatrists at the Motor Accidents Service. In 2004 Dr Moore diagnosed a post-traumatic stress disorder and depression. Dr Akkerman saw the plaintiff on 16 December 2005. He diagnosed an adjustment disorder with anxious and depressed mood caused by the accident. He did not consider that the symptoms were all that severe and believed that with appropriate treatment the plaintiff’s condition would improve markedly.

I accordingly am of the view that the plaintiff's symptoms since the date of the accident were precipitated by physical injury which has been complicated by a post traumatic stress disorder and depression. The overall impression I gained from the witnesses, in particular Mr Karpik and Ms Campbell, is that there has been an improvement over time. He is taking medication.

I consider that it is likely that his post traumatic stress disorder and depression will markedly improve over time and with treatment. Accordingly it is also likely that there will be a corresponding improvement in his gait and overall disability.

72 Her Honour took into account the evidence of Mr Karpik and Ms Campbell in concluding that there had been an improvement over time. Edward Karpik’s son and the appellant had been friends since the appellant was aged around 18 years. The appellant visited the Karpik family home regularly and watched television or played games on a Playstation. Mr Karpik agreed that on these occasions the appellant seemed to be in a pretty good mood. (Black 269.U-V) Ms Campbell had known the appellant for nine or 10 years, he was friendly with her stepson. She considered that the appellant's depression at the date of trial was not as bad as it had been a couple of years earlier but that he was still withdrawn compared to the way that he had been before the accident. (Black 277.T-U)

73 Her Honour accepted the diagnosis of PTSD and depression and assessed damages on the assumption that both conditions would markedly improve over time and with treatment with a corresponding improvement in the appellant’s deformed gait. The complaint is that the finding of marked improvement appears to be based on the report of Dr Akkerman, who rejected the diagnosis of PTSD.

74 Mr Gross acknowledged that her Honour had not spelled out the basis for her partial acceptance of the appellant’s case. He submitted that the appellant's credibility had been a central issue at the trial and that her Honour had made adverse findings in this respect. In light of these findings it was open to her to deal with the psychiatric evidence more briefly than might otherwise have been the case. He put it this way (T'cpt 49.32-39):

It’s really a question of whether her Honour’s gone far enough to spell out how her Honour got to those end points and our submission is that such brevity was allowed in looking at duration [ongoing impairment of capacity for 10 years] because in a situation where a plaintiff bears an onus yet the credibility has been impaired so one doesn’t have the capacity to make those clear mathematical projections based upon known facts, it does become difficult for a trial judge to define an in-between position in a way that is detailed and going beyond merely summarising the various positions.

75 The reservations which the primary judge expressed concerning the appellant’s credit do not explain the basis of the conclusion with respect to the psychiatric evidence. It is true that the assessment for the future could not be carried out with mathematical precision. However, it is necessary for the parties and this Court to understand the basis upon which the assessment, that there would be continued impairment of capacity for 10 years fully resolved by the end of the closed period, was reached. Her Honour accepted that the appellant had a significant level of impairment, which on her findings was the product of his psychiatric condition. None of the doctors who diagnosed PTSD were of the opinion that this condition was likely to markedly improve with time and treatment. Dr Canaris and Dr Moore considered that given the interval of time since the accident and the lack of timely treatment of the condition it was unlikely that the appellant would overcome his PTSD.

76 The diagnosis of PTSD was complicated by the diagnosis of depression and substance abuse. Dr Moore’s report is consistent with a view that with psychiatric treatment for the depression the appellant would be able to “move on”. Her Honour did not refer to Dr Moore’s report in this respect. The finding, that it was likely that there would be marked improvement, in the relatively brief analysis of the psychiatric evidence appears to be an acceptance of Dr Akkerman’s opinion. It is difficult to reconcile acceptance of his prognosis with her Honour’s acceptance at the same time of the diagnosis which he rejected.

77 It is not necessary to re-state the principles governing the obligation to give reasons with respect to conflicting expert evidence. They are collected in the judgment of Ipp JA (Bryson JA and Stein AJA agreeing) in Wiki v Atlantis Relocations (NSW) Pty Ltd [2004] NSWCA 174; (2004) 60 NSWLR 127 at 135-138 [56]- [68]. It is sufficient to note the obligation to engage with the evidence and to explain why the evidence of one expert is preferred over that of another.

78 In the result, the analysis of the evidence of RSD including the diagnosis of incipient or recurrent RSD was inadequate. The evidence of the three treating doctors was rejected for reasons which were not explained beyond the conclusion, in the case of Dr Sheridan and Dr Salmon that they were entirely dependent upon the history obtained, and in the case of Dr Giblin that he had not maintained the diagnosis after receiving the results of the bone scan. These conclusions are flawed for the reasons earlier given. It does not follow that the diagnosis of RSD is one that was established on the balance of probabilities. Important to the way the challenge was put on appeal, was the evidence of Dr Giblin concerning the recurrent nature of RSD. The primary judge was in some respects critical of Dr Giblin whom she assessed as partisan. Her Honour was also critical of aspects of the evidence of the appellant and the evaluation of his evidence is plainly critical to the assessment as a whole. I am persuaded that the challenge to the judgment has been made good however it is not appropriate that this Court itself assess the appellant’s damages. It is regrettable but in the circumstances there is no alternative but to direct that there be a new trial on the issue of damages.

1. Allow the appeal.

2. Quash the orders made in the District Court and in lieu thereof direct that there be a new trial on the issue of damages.

3. The respondent is to pay the appellant’s costs of the trial and of the appeal. In respect of the costs of the appeal, the respondent is to have a certificate under the Suitors’ Fund Act 1951, if qualified.

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LAST UPDATED:
30 January 2009