Wall v Cooper

[2006] WADC 81

JURISDICTION     :   DISTRICT COURT OF WESTERN AUSTRALIA

IN CIVIL

LOCATION:   PERTH

CITATION:   WALL -v- COOPER [2006] WADC 81

CORAM:   YEATS DCJ

HEARD:   13-21 FEBRUARY 2006

DELIVERED          :   31 MAY 2006

FILE NO/S:   CIV 1187 of 2003

BETWEEN:   MELVYN LEE MAXWELL WALL

Plaintiff

AND

TIMOTHY MICHAEL COOPER
Defendant

Catchwords:

Medical negligence - Standard of care - Breach of duty of care - Causation - Dog bite - Pseudomonas infection - Whether broad spectrum antibiotics should have been given - Onset of complex regional pain syndrome.

Legislation:

Nil

Result:

Negligence not established
Provisional findings on causation
Provisional assessment of damages

Representation:

Counsel:

Plaintiff:     Mr M H Zilko SC

Defendant:     Mr J R B Ley

Solicitors:

Plaintiff:     Hoffmans

Defendant:     Clayton Utz

Case(s) referred to in judgment(s):

Bolam v Friern Barnet Hospital Management Committee [1957] 1 WLR 582

Chappel v Hart (1998) 195 CLR 232

Clark v Ryan (1960) 103 CLR 486

Glasgow Corporation v Muir [1943] AC 448

March v E & M H Stramare Pty Ltd (1991) 171 CLR 506

Mount Isa Mines Ltd v Pusey (1970) 125 CLR 383

Naxakis v Western General Hospital (1999) 197 CLR 269

Rogers v Whitaker (1992) 175 CLR 479

Strempel v Wood & Anor [2005] WASCA 163

Wyong Shire Council v Shirt (1980) 146 CLR 40

Case(s) also cited:

Albrighton v Royal Prince Alfred Hospital [1980] 2 NSWLR 542

Bennett v Minister of Community Welfare (1992) 176 CLR 408

Betts v Whittingslowe (1945) 71 CLR 637

Birkholz v R J Gilbertson Pty Ltd (1985) 38 SASR 121

Chamberlain v R (No 2) (1984) 153 CLR 521

Cook v Cook (1986) 162 CLR 376

Dwan v Farquhar [1988] 1 Qd R 234

Footner v Broken Hill Associated Smelters Pty Ltd (1983) 33 SASR 58

Gregg v Scott [2005] 2 AC 176

Hotson v East Berkshire Area Health Authority [1987] 2 All ER 909

McGhee v National Coal Board [1972] 3 All ER 1008

Rufo v Hosking [2004] NSWCA 391

TC by his tutor Sabatino v State of New South Wales [2001] NSWCA 380

1. YEATS DCJ:  The plaintiff's action is for damages for negligence on the part of the defendant plastic surgeon in his treatment of the plaintiff for dog bites inflicted by a pit bull terrier on 21 June 1997.  The parties have agreed quantum except for general damages which I must assess.  Liability is very much in issue.  The defendant admitted he owed the plaintiff a duty of care but denies breaching that duty in his treatment of the plaintiff.  The principal issues are the standard of care, breach of the duty of care and causation.

Factual background

1. The plaintiff is a 61‑year‑old paediatrician.  He graduated from the University of Western Australia in 1972 and did his first year of residency at Sir Charles Gairdner Hospital followed by serving at the Royal Alexandra Hospital for Children in Sydney as a paediatric resident in 1974.  He was a paediatric registrar in New Zealand in 1975 and 1976 and then worked at the Children's Hospital in Dublin until 1977 as a paediatrician registrar.  In 1977 he returned to Australia where he was the registrar at the Prince of Wales Children's Hospital in Sydney and then in 1978 came back to Perth as the senior registrar at Princess Margaret Hospital.  In 1979 he worked at the Child Development Centre in Perth and completed his specialist training as a paediatrician at the end of 1979.  In that year he was admitted as a Fellow of the Royal Australasian College of Physicians in Paediatrics and returned to New Zealand from 1980 to 1987 where he worked as a consultant paediatrician prior to taking up duties as the senior paediatrician and director of child development services for the province of Taranaki.

2. In June of 1997 Dr Wall returned to Western Australia and set up a consulting practice in Kelmscott initially as a general paediatrician but subsequently specialising in neurodevelopment paediatrics.  His speciality is children and adolescents' behavioural, emotional and education problems.  He was a pioneer in the diagnosis and treatment of children affected by ADHD in Western Australia.  Dr Wall continued that work until he ceased working entirely in May 1998 because of complications following surgery for his dog bite.

Dr Wall's injury and treatment

1. Dr Wall was working on 21 June 1997 and was making a home visit.  His patient was a troubled child due to appear in the Children's Court in need of medication as well as counselling concerning the taking of the medication.  He gave evidence he was attacked at about 2 o'clock in the afternoon when he entered a yard where there were three dogs, including a kelpie, a younger dog and a pit bull terrier.  He was first bitten on the left leg by the kelpie; then the pit bull terrier attached itself just below his right knee on the outside of his calf.  Dr Wall was able to shake off the dog and run to the gate but the dog bit him again before he was able finally to get the dog off him and get out of the gate.  In attempting to lock the gate he was bitten again by the dog, with a puncture wound on the middle finger of his right hand.  He was treated with a towel by the owner of the house and an ambulance took him to St John of God Hospital at Murdoch.  Dr Wall was able to see the wound on his leg.  He described it as one large flap that basically ran like a hinge wound parallel with the main bone.  He noticed a loss of tissue because he could see the head of the fibula and also some of the layer of tissue that lines the muscle.  He said the wound was some 10 centimetres long and about 7 centimetres across.

2. There is a dispute as to the time when the dog bite occurred.  Under cross‑examination Dr Wall admitted it may have been a bit later than 2 pm.  Hospital records show (exhibit 3, p 126) that Dr Wall was seen in the emergency department at St John of God Hospital, Murdoch at 4.50 pm.  Dr Wall admitted in cross‑examination that it did not take two or three hours to get to hospital by ambulance.  He said the ambulance arrived quickly in Karawara, and that there were no delays in taking him to hospital.  Dr Cooper gave evidence that he questioned Dr Wall and was told that the dog bite occurred between 2 pm and 4 pm.  As a matter of common sense with no evidence of any delay I am satisfied the dog bite occurred closer to 4 pm than 2 pm that afternoon.

3. At the hospital Dr Wall was examined by the casualty medical officer, a Dr Berkhout.  The defendant was at St John of God Medical Centre that day and was contacted by the emergency physician, Dr Berkhout, who asked if he would mind seeing a colleague who had been bitten by a dog.  Dr Cooper was told by Dr Berkhout that he thought Dr Wall was neurovascularly intact ‑ in other words, there was no major nerve or vessel damage.  Dr Berkhout described the injury as a degloving injury to the anterior lateral aspect of the right leg and a puncture wound to the right hand.  Dr Cooper examined the nursing staff notes which he said described the injury, the nature of the attack, the degree of pain, the patient's appearance, vital signs as well as shorthand notes for examination of the circulation to the leg that was injured.  From what he read in the nursing notes Dr Cooper thought there was no urgency in terms of damage to a major blood vessel and perhaps no neurological damage.

4. Dr Cooper spoke to Dr Wall and examined him but did not take down the dressing on the wound.  He was concerned to avoid unnecessary pain to the patient.  He made his assessment on the basis of the description from the emergency physician, his reading of the nursing notes and his examination of Dr Wall.  That examination he described as a cursory examination of the power of the circulation to his foot and the two pulses, one behind the ankle and one on the dorsal of the ankle.  He also made a cursory examination of the neurological status of the limb.  He did this by brushing his finger against the side of Dr Wall's finger and comparing it with an adjacent digit that was supposedly normal.  He recalled that the sensation in the injured finger was normal.  He then examined the motor and sensory functions of the lower limbs and he said this:

   "I would have tested the anterior tibial muscles to see whether he could dorsiflex the foot; that is, raise the foot.  I would test for sensation in the lower limb.  That would be a fairly crude sensory test, brushing an object such as a pen and saying, 'Do you feel that there is loss of sensation there?' or 'Is that normal?' " (T367).

5. Dr Cooper did this over the top of the foot distal to the injury.  From his test Dr Cooper concluded that the wound was probably consistent with the nature of the injury described.  He recommended Dr Wall have emergency surgery to clean the wound and repair it including any structure damaged within the wound.  According to Dr Cooper, Dr Wall consented to a procedure involving a skin graft for his leg wound and consent papers were signed.  No theatre was available at St John of God Murdoch and Dr Wall was taken by ambulance to the Mount Hospital and operated on at around 7 o'clock.  Hospital records indicate that surgery commenced at 7.15 and finished at 8.15 that evening.

6. In conducting the surgery Dr Cooper was assisted by a general anaesthetist.  He inspected the wound once the plaintiff had been anaesthetised.  That examination was conducted with loupe magnification three times the magnification of his glasses.  At that time he was using optical loupes glued onto the front of his glasses.  He did not need prescription glasses so the loupe glasses that he wore during surgery protected Dr Cooper's eyes and also allowed him to examine the wound more closely.

7. Dr Cooper recalled the wound as "an untidy laceration of the anterolateral aspect of the right lower leg encroaching on the edge of the popliteal fossa and down on the lateral aspect of the calf" (T369).  Dr Cooper said that the popliteal fossa was the back of the knee bounded by the two hamstring muscles and including a number of vital structures.  Dr Cooper said he washed the wound before inspecting it.  So far as the common peroneal nerve was concerned Dr Cooper said: "I would have inspected that because that's in the site of the injury and I deemed that to be macroscopically normal" (T369).  Dr Cooper's recollection was that you could see the common peroneal nerve.  It was magnified three times with loupe magnification and was normal.  Dr Cooper did not perform neurolysis because there was no indication for it.

8. Dr Cooper noted that for his assessment the injury to the right hand was as important as the leg because for a doctor the right hand is a very vital structure.  Dr Cooper said that puncture wounds can be just as dangerous as degloving wounds because a puncture can inoculate some organisms leading to florid infection.  He also noted that it is easy to damage the digital nerve because it is near the skin surface and that could result in a loss of sensation to the finger.  Dr Cooper said that he explored the puncture wound to make sure the nerve was intact and washed out the wound.

9. Dr Cooper gave evidence that he performed lavage and debridement of the leg wound before the skin graft was laid.  He described lavage as a "pulse lavage done with a machine which gave intermittent bursts of saline under pressure".  He found that very effective in removing contamination from the wound.  Dr Cooper also said he "would have" debrided the obvious dead tissue around the leg, but could not recall the amount of dead tissue he removed.  There was an area of skin loss after he had done that, and Dr Cooper elected to lay a skin graft.

10. So far as damage to any sensory fibres was concerned Dr Cooper said that if you tear away a piece of skin as happens in a degloving wound you are going to tear small sensory nerves with it so it is not uncommon to get a patch of numbness just distal to a skin graft site or an area of skin loss.  According to Dr Cooper those small microscopic filaments of nerves are too small to be repaired.

11. Dr Cooper recalled harvesting a split skin graft from the thigh of the injured limb.  He fenestrated the graft, that is made multiple holes in it to allow fluid egress.  Dr Cooper sutured the finger with monofilament non‑absorbable suture and he repaired the right leg wound with absorbable sutures as well as non‑absorbable sutures and the split skin graft.  The skin graft was inset into the skin deficit with staples and then the leg was completely bandaged from ankle to groin.  Dr Wall's right leg was then immobilised by using a plaster of Paris back slab on the posterior of the leg going from the popliteal fossa to the toes.  Primary closure of the wound including the skin graft was completed by 8.15 pm that day.

12. Dr Cooper prescribed the antibiotic Flucloxacillin.  He did that based on his experience with dog bites and his concern about staphylococcal infection.  He left instructions for intravenous Flucloxacillin to be continued six hourly after surgery while the plaintiff remained in hospital.  Dr Cooper next saw Dr Wall at 9 o'clock the following morning 22 June 1997 and gave orders to remove the drain and for Dr Wall to remain resting in bed continuing intravenous antibiotics and intravenous hydration but to leave the dressings intact.  Dr Cooper said he explained to Dr Wall what was involved in the surgery, what he found exploring the wound, what he had done and his likely convalescence.  Dr Cooper said that he told Dr Wall the dressings should be left intact until Dr Cooper next reviewed him and he would have to keep his leg elevated as much as possible.  Dr Cooper remembered telling Dr Wall that the graft could take a couple of weeks to heal and then there would be a period of rehabilitation.  Dr Cooper said he also explained that Dr Wall would take the intravenous antibiotics but once he went home was likely to convert them to oral antibiotics. 

13. On 23 June Dr Cooper saw Dr Wall again and arranged for his discharge from hospital.  Dr Cooper told Dr Wall that he was going to be away overseas with Interplast Australia doing plastic surgery in Vanuatu and would be back on 6 July.  Dr Cooper said the arrangement he made with the nursing staff on the ward was to see Dr Wall on 7 July in his rooms which was the earliest date that he could see him after returning from overseas.  Dr Cooper said he specifically instructed Dr Wall to try and keep the leg elevated as much as possible, to utilise crutches, to non‑weight bear and to continue the course of antibiotics for five days.  Dr Cooper also said he told Dr Wall that if he were concerned about something going wrong ‑ and that would have been unusual pain, offensive discharge, feeling unwell, those sorts of symptoms ‑ that he should seek attention by contacting Dr Cooper if Dr Cooper was in town and otherwise contacting his deputy.  Dr Cooper's evidence was that he told Dr Wall that during office hours he should contact Dr Cooper's rooms, and that if it was out of hours, the appropriate place to contact would be the nursing station on Jarrah B, the plastic surgical ward at the Mount Hospital.  But under cross‑examination Dr Cooper admitted he could not exactly remember telling Dr Wall that, and that it was "hard to know" (T462).

14. Dr Wall had a different recollection of what Dr Cooper told him before he was discharged from hospital.  According to Dr Wall all Dr Cooper told him was to keep the leg elevated as much as possible but that he could walk with crutches and to finish the course of antibiotics.  Dr Wall agreed the arrangement was that he would see Dr Cooper again in two weeks and the nursing staff made an appointment for him for 7 July.  According to Dr Wall, Dr Cooper mentioned something to the effect that there should not be a problem with infection because he was on antibiotics.  According to Dr Wall he was given no further instructions but was to see Dr Cooper in two weeks.  Dr Wall agreed that Dr Cooper told him he was going overseas.  As events developed Dr Cooper never saw Dr Wall after Dr Wall was discharged from hospital on 23 June 1997.

The development of pain symptoms

1. During the first five or six days following surgery Dr Wall described bearable pain, in keeping with the degree of trauma plus the surgery he had undergone.  But according to Dr Wall on 29 July he started to experience quite a severe aching, a penetrating aching pain, just behind the top of the fibula extending forward a few millimetres.  It was painful enough that he began to feel a bit nauseated.  Dr Wall was somewhat confused about the actual dates and from all the evidence it would appear that the more serious pain began to develop on 30 June.  The following afternoon on 1 July Dr Wall tried to contact Dr Cooper's rooms at 4 o'clock and could not recall whether there was an answering machine but he was unable to speak to anyone.  Dr Wall said he also telephoned the Mount Hospital hoping to learn the name of Dr Cooper's deputy.  At the Mount Hospital he spoke to one of the nursing staff and was told that there was no record of Dr Cooper's deputy.

2. That night the pain became worse and in the early hours of the morning Dr Wall noticed a very unpleasant smell.  When he pulled back the bandage he discovered that the wound was running with green pus.  Dr Wall said he tried again about 8 o'clock that morning, 2 July 1997, to contact Dr Cooper's rooms but was unable to speak to anyone.  He said he could not swear that there was no answering machine but was sure there was not one.  Dr Wall then contacted a general practitioner, Dr Lawrance, and was seen by Dr Lawrance at 9 o'clock that morning.  Dr Lawrance noted that Dr Wall was suffering from secondary wound infection and breakdown after the initial graft and had Dr Wall admitted to Gosnells Private Hospital for bed rest, wound dressing and the administration of a combination of antibiotics, particularly Ciprofloxacin and Clindamycin.

3. Dr Wall remained in the Gosnells Hospital undergoing frequent irrigation with a saline solution using a syringe swirled around the wound to clean up any debris.  There was also debriding and removal of any dead tissue.  Initially the lavage and debriding was done four hourly for two or three days and then continued less often but for the full 10 days that he was in hospital until he saw another plastic surgeon, Dr Allison, on 11 July 1997.  Dr Wall was allowed to return home late on the Saturday but then was readmitted into the hospital the following day under Dr Allison who did further debridement and irrigation of the wound in theatre and then, after two or three days during which there were saline packs in the wound, a second skin graft was laid on 15 July 1997.  Dr Wall remained in hospital several more days and he described the nursing staff rolling and doing various procedures to the skin graft and keeping an eye on it to make sure it did not become infected.

4. Dr Wall gave evidence that after he was discharged from Gosnells Hospital the pain gradually worsened ‑ particularly the aching pain just behind the knee.  He began to develop other pains and unpleasant sensations in his right leg within the week after leaving hospital.  He described them as sharp pains that would occur in unpredictable places particularly down the right side in front of his leg like very severe pin pricks that could then pass downward like an electric shock.  He also experienced unpleasant sensations particularly a burning sensation or coldness in the lower part of his leg plus the aching sensation that persisted in increasingly dense, more severe pins and needles.  He experienced this in his whole right leg and foot.  Dr Wall said that he was unable to obtain any relief and that pain and those sensations have continued even to the present day.

5. Dr Wall said that after the first couple of years he began to experience similar symptoms in his left leg.  The first sign was quite a bit of hair loss on the right side of his right leg and then he noticed that there was hair loss on the left leg like a mirror image.  Dr Wall said that the pain in his left leg comes in massive spasms at night time and can create pain for hours from which he has little relief.

1. So far as work was concerned, despite the pain, Dr Wall went back to work on a part‑time basis after three months.  He worked until the end of May 1998 but the pain was persistent and getting worse and he was unable to cope with the demands of a paediatric practice.  He ceased work entirely in May 1998.

2. Under cross‑examination the plaintiff talked about the severity of his pain.  He agreed that his pain improved over the time he was in Gosnells Hospital and that this was borne out by the fact that he did not always seek analgesia from the nursing staff.  The pain behind his knee was not as bad by the time he was discharged.  He did, however, continue to have the pain and required analgesic relief but not constantly.  Dr Wall said that by the time he consulted Dr Knezevic, a neurologist, in December 1997 his pain had been getting worse for quite a long time.  He admitted however, that up until September when he went back to work the pain had not been terribly bad but it worsened between September and December.  By the time he saw Dr Knezevic in December 1997, Dr Wall was suffering pain behind the right knee as well as stabbing pains in the right leg occurring several times a day as well as the hot and cold burning sensation.

3. Dr Wall gave evidence that his pain symptoms have not diminished in severity between 1997 and the present day but they have changed.  He still suffers from an aching pain in the lateral aspect of his knee every day for a few hours but there is no regular pattern.  It is unpredictable.  He also still suffers a burning sensation in his right leg several times a day that can last from a few seconds to an hour and a half or all day.  He also suffers intermittent sharp pains lasting one second which can occur several times in a row, shooting up and down the leg.  Dr Wall said that his pain was aggravated by activity and emotional changes.  Dr Wall agreed that although the episodes of pain are now less intense he finds their persistence greater.  Over the last five or six years Dr Wall has also begun experiencing pain in his left leg which awakens him at night and can last for two and a half hours and is so intense it can lead to screams of pain as though his bones are being crushed.  That pain is often triggered by the sheets touching his scar.  When the sheets touch any part of his left leg he can suffer this excruciating pain at night time.

Medical evidence

1. A large number of medical practitioners and consultants gave evidence in the course of the trial.  A number of the specialists were treating specialists.  Other doctors and surgeons were called upon to give expert opinions and did not treat or, in some cases, even see the plaintiff.

2. Dr Denis Neil Lawrance is the general practitioner who treated Dr Wall for the infected wound.  He saw Dr Wall on 2 July, immediately put Dr Wall into the Gosnells Hospital and oversaw his treatment on a daily basis by antibiotics, narcotic analgesics to control his pain and both lavage and debridement to clean the wound.  Dr Wall was discharged from the care of Dr Lawrance on 12 July 1997 but the next day returned to hospital under the care of the plastic surgeon, Mr Allison.  Dr Lawrance described the plaintiff as experiencing significant pain when he first presented on 2 July 1997, pain which was unable to be managed without narcotic analgesia.  Oral analgesia was tried but, particularly at night, he required intramuscular analgesia.  Dr Lawrance described the wound as "significantly infected" when he saw it on 2 July.  A swab was taken and it was found to be a pseudomonas infection.  All of the treatment Dr Lawrance supervised while the plaintiff was under his care in Gosnells Hospital was directed at eliminating the infection.  Dr Lawrance said he had hoped to eliminate the infection and release the plaintiff home but because of the significant amount of pain the plaintiff was suffering he contacted Dr Allison.  Dr Lawrance said that he was aware the plaintiff had an appointment to see Dr Cooper on 7 July 1997. Dr Lawrance had a specific recollection of ringing Dr Cooper's rooms about that.  He could not recall if he spoke to Dr Cooper or not.  As a result of the telephone call in discussion with Dr Wall they elected to have a second opinion from Dr Allison.

3. Dr Wally Knezevic, a consultant neurologist, was called to give evidence on behalf of the plaintiff.  Dr Knezevic had treated the plaintiff since first seeing him on 9 December 1997 when he diagnosed persistent pain syndrome which he later described as complex regional pain syndrome.  In a report dated 14 June 2004 (exhibit 3, p 26) Dr Knezevic was asked:

   "What contribution to the development of the persistent pain state is likely to have been made by the setting in of the infection, the wound breakdown and further surgery requiring to be done by Mr Allison?" 

4. Dr Knezevic replied:

   "I think it is very difficult to state what contribution the delay to the treatment of infection would have contributed to the pain syndrome but it is certainly well recorded that persistence of abnormalities, including persistence of pain, predisposes to subsequent development of complex regional pain syndrome and any delay in healing, treatment and rehabilitation is likely to predispose and contribute to subsequent development of a complex regional pain syndrome."

5. Dr Knezevic went on to say that:

   "The best one can say is that it is probably more likely than not, had there not been complications, that the patient would not have developed complex regional pain syndrome" (exhibit 3, p 26).

6. Dr Knezevic was particularly asked about the role infection plays in the development of the pain syndrome and his answer was:

   "Infection, trauma, immobilisation, all of these seem to … be some sort of reinforcing loop and people used to – or some people still consider – that it's the sympathetic nerves that initiate and perpetuate this loop and just simply immobilisation is enough to perpetuate it" (T217).

7. Dr Knezevic gave evidence that the severity of the injury does not necessarily correlate because people with quite trivial injuries can develop regional pain syndrome.  The longer a person has pain and discomfort the more likely it is that the person will develop the syndrome (T217).

8. Dr Knezevic was asked about the likelihood of Dr Wall developing the pain syndrome if there had been no complication but merely the trauma of the dog bite.  His answer was:  "It's possible but relatively uncommon but, you know, I would say less than 5 per cent or something like that."  Under cross‑examination Dr Knezevic conceded that the dog attack may have caused the pain syndrome and in re‑examination was asked how that fit with his original estimate that the chances of it happening from the dog attack alone were 5 per cent.  Dr Knezevic explained that while 5 per cent was sort of a best guess his belief was that:  "with every problem, with more immobilisation, ongoing pain, the longer the duration, the more liable you are to complex regional pain syndrome" (T233).

9. Dr Knezevic has been seeing Dr Wall continually since 1997 and strongly disagrees that he is in any state to return to work.  Dr Knezevic explained that the impairment to Dr Wall's cognitive functioning [due to pain and medications] meant that he would have difficulty concentrating.  In such circumstances a cognitively demanding job like paediatrics would have been impossible for him.

10. Dr Knezevic observed that on most occasions when he saw Dr Wall there had been no improvement and over all the years he has been treating Dr Wall he believes that there was a worsening of pain (T220).  Dr Knezevic entirely rejected the suggestion of Dr Grainger that there was any degree of pain behaviour disorder present.  Dr Knezevic reported on 28 November 2005 (exhibit 3, p 33):

    "I have not seen any features of pain behaviour.  In fact, Dr Wall has been rather stoical and has battled bravely under adverse circumstances despite considerable pain and complete disruption of his previous career and life.  I think he is actually of a rather stoic disposition, quite the opposite of the usual histrionic personality of a patient with abnormal pain behaviour disorder."

11. In his evidence Dr Knezevic said that Dr Wall is a patient who simply endures the pain (T221).

12. Under cross‑examination, Dr Knezevic conceded that he had first seen Dr Wall on 7 April 1997 prior to the dog bite injury in a consultation for pain and numbness in his right foot following a fracture to his right leg in December 1995 some 15 or 16 months earlier.  At that time Dr Knezevic diagnosed a mild digital neuropathy.  However, Dr Knezevic explained that digital neuropathies are quite common, more often related to footwear and that his treatment had consisted of advice on orthotics.  That was the only occasion when Dr Wall consulted him about that previous injury.

13. Dr Knezevic confirmed that he had tested Dr Wall's right leg and foot and that there was no sensory loss to the foot, no loss of motor function and that therefore he was satisfied there had been no damage to the peroneal nerve.  He confirmed that there would have been no advantage in having explored the peroneal nerve during surgery as there was no evidence of any such damage.

14. Under cross‑examination Dr Knezevic agreed that it would be unusual for the persistent pain syndrome to be triggered by infection alone and conceded that he had never encountered infection causing the syndrome.  So far as the trigger for the syndrome Dr Knezevic reaffirmed that the most important trigger was the duration of pain and immobility.  He said that the duration of the immobility related to pain is one of the most important triggers (T231).

15. Dr Knezevic did not disagree with aspects of Dr Crawford's report but he considered Dr Crawford's theory concerning the development of the pain syndrome to be an hypothesis which Dr Knezevic could not say was not true.

16. Finally, so far as foreseeability was concerned, although it was a bit out of his field as a neurologist, Dr Knezevic's opinion was that he was sure that surgeons are well aware that ongoing pain, ongoing immobilisation, ongoing inflammation of the limbs in particular, predisposes people to developing regional pain syndrome and that is why surgeons are well aware of the need to rehabilitate and get patients moving as quickly as possible in all of these situations.

17. Dr Thomas Berrigan, a pain specialist, first saw Dr Wall in July 1998 on referral from Dr Knezevic.  Dr Berrigan diagnosed regional pain syndrome resulting from damage to a branch of the lateral popliteal nerve or a sympathetic dystrophy.  Dr Berrigan confirmed that the lateral popliteal nerve was the same as the common peroneal nerve.  He agreed with Dr Knezevic that Dr Wall had complex regional pain syndrome secondary to the dog bite and subsequent wound infection, treatment and injury to the sensory branches of the peroneal nerve.  Dr Berrigan confirmed that there was no significant injury to the peroneal nerve itself.  That nerve was obviously intact.  If there had been any significant injury to the common peroneal nerve Dr Berrigan expected Dr Wall would have experienced a foot drop.

18. Dr Berrigan treated Dr Wall with a lateral popliteal nerve block followed by right lumbar sympathetic blocks and right chemical lumbar sympathetic blocks.  When those treatments failed to bring long term relief he tried an epidural stimulator.  That brought some relief but, once he implanted the stimulator, and despite repositioning it, it proved to be ineffective.  Dr Berrigan said that this situation happens in about 20 per cent of cases where spinal cord stimulators are inserted; there was good analgesia during the trial process but effective analgesia was not obtained with the permanent procedure.

19. After the failure of all of these treatments and the continuation of Dr Wall's extremely severe pain Dr Berrigan implanted an intrathecal drug pump on 9 November 1999.  The drug pump is implanted under Dr Wall's skin and a catheter goes from the pump subcutaneously around the spine and then into the spine into the cerebral spinal fluid which surrounds the spinal chord.  The pump instils various drugs into the spinal fluid and those are washed down and are absorbed into the spinal chord.  In Dr Wall's case a narcotic analgesic, hydromorphine was used combined with a long‑acting local anaesthetic Bupivacaine.  Dr Berrigan said those are very strong pain drugs.  Since November 1999 Dr Berrigan has reviewed Dr Wall every four weeks to replenish the drug supply in his pump and to check on his pain levels and has found that there has been no improvement.  The strong drugs slightly dull the pain but Dr Wall continues to experience considerable pain despite the drug pump.

20. Dr Berrigan did not agree with Dr Crawford's assessment that there was a connection between the right ankle injury sustained in January 1996 and the development of the regional pain syndrome because in Dr Berrigan's experience regional pain syndrome commences very soon after the incident, almost straight away.  Nor did Dr Berrigan agree with the connection Dr Crawford made between persons suffering ADHD and chronic pain syndromes; he considered such a connection unlikely.  So far as causation was concerned Dr Berrigan said:

    "I found it very difficult to say whether his present condition is due to the initial injury; that is, the dog bite, or the surgical treatment or the infection" (T331).

21. Under cross‑examination Dr Berrigan explained that the most common cause of regional pain syndrome is some damage to the nerve but he conceded that it is possible that something else could have caused it (T337).  Although Dr Berrigan conceded that in his experience regional pain syndrome sometimes can burn out within a few years, he believed it unlikely that that would happen in Dr Wall's case because of the passage of so many years without any improvement in his condition.

22. Ultimately Dr Berrigan's evidence under cross‑examination was that either the dog bite itself or complications which set in afterwards were the cause of the onset of the regional pain syndrome (T341).

23. Dr Peter Conrad is presently an emeritus consulting surgeon at Nepean Hospital, a teaching hospital of Sydney University.  He is very experienced and very highly qualified holding four fellowships including a Fellowship in the Royal Australasian College of Surgeons.  His curriculum vitae shows extensive membership of advisory boards for conferences, both in Australia and overseas, extensive publications and lectures.  He has practised as a surgeon for over 35 years and from 1985 to 1998 was the head of the Department of Surgery at the Nepean Hospital.  He has taught surgical registrars and others in surgical technique and training.  Over the course of his career as a general surgeon he estimated that he had treated upwards of 500 dog wounds.

24. Dr Conrad never examined the plaintiff but he was provided with all the records of treatment, the hospital notes, and the various reports.  Dr Conrad formed the view that the dog bite to Dr Wall's leg undoubtedly damaged the lateral popliteal nerve, mainly the sensory fibres rather than a major injury to the motor fibres of that nerve.  He formed that opinion because of the site of the dog bite overlying the lateral part of the popliteal fossa and the other part of the fibula, an area where the lateral popliteal nerve is particularly vulnerable to injury.

25. In Dr Conrad's opinion no‑one knows whether that damage to the popliteal nerve was repairable or not because based on the surgical notes it was not clear whether Dr Cooper had explored the nerve or not.  Dr Conrad said that if there was a laceration or superficial laceration of the popliteal nerve and it was not repaired then this would have enhanced the possibility of neuroma formation which can lead to the pain syndrome.  Dr Conrad said that most experienced surgeons would definitely have made comprehensive notes about having explored the popliteal nerve and the status of the nerve and such notes were missing from Dr Cooper's surgical notes.

26. After reviewing the whole case Dr Conrad was of the opinion that there were two points of inadequacy in Dr Cooper's treatment of Dr Wall.

    "The first was that in my personal experience and practice and teaching any dog bite or human bite or other animal bite is regarded as heavily infected by bacteria and therefore potentially a wound infection can set in therefore I would never advocate doing a primary skin graft in a bite of that sort.  The second point of criticism that I had was that having done an operation, any operation really, and one that had a potential for going wrong it is absolutely mandatory for any specialist if they then leave their post, so to speak, to provide an adequate deputy to look after potential problems and to adequately advertise the name and contact details of that deputy to anyone that might need that service" (T246‑247).

27. Dr Conrad explained that primary closure means either suturing the skin or skin graft.  In Dr Conrad's opinion primary closure of a wound caused by an animal bite should be delayed except in the case of bites to the face.  In his opinion the wound should be left open and dressed with suitable antiseptics and the patient given broad spectrum antibiotics until the surgeon was satisfied that the wound was clean and could be closed.  In Dr Conrad's experience and practice that would usually take 8 to 10 days.  Dr Conrad conceded that the face has an excellent blood supply and infection can be overcome with antibiotics and for bites to the face a surgeon could get away with primary closure.  But in all other cases good practice would be to delay closure.

28. Dr Conrad explained what he believed should have been done so far as examining the popliteal nerve.  In his opinion Dr Cooper should have performed neurolysis, a procedure where the surgeon gently mobilises the nerve and has a close look at all the surfaces so that if there were any laceration then it could be repaired under microsurgical technique.  Neurolysis, Dr Conrad explained, involves gently cutting the membrane that tethers the nerve, gently mobilising the nerve and looking at it closely under loupe magnification.

29. Dr Conrad strongly disagreed with Dr Baldwin; in Dr Conrad's opinion a primary closure is never an appropriate treatment for a dog bite (except to the face).  In his opinion the majority of the bites will get infected whether the patient is given antibiotics or not.  In his experience the potential for infection when you have primary closure was something known to surgeons.  Dr Conrad said that despite antibiotics ‑ even broad spectrum antibiotics ‑ the majority of dog bites would get infected and reject the skin graft or, if it was sutured, the sutures would simply fall out if primary closure was used.  Dr Conrad was firmly of the view that a broad spectrum antibiotic was the only kind that would be appropriately used for treating dog bite patients and that that was widely known in 1997.

30. So far as Dr Cooper's notes were concerned, Dr Conrad's view was that there should have been a more detailed description of the anatomy and then a sort of ticking off of all the structures that were explored during surgery.  He explained that in any trauma the underlying anatomy – the veins, arteries, nerves, the lateral popliteal fossa should have been examined and mentioned in the notes as inspected.  Dr Conrad criticised Dr Cooper for not mentioning any of these matters in his notes.

31. A major defect in the expert evidence of Dr Conrad was his assertion under cross‑examination that the lateral popliteal nerve is "absolutely not" the same as the common peroneal nerve (T253).  Dr Conrad contended that it was the parent nerve, the lateral popliteal nerve that was likely to have been damaged and he distinguished that from Dr Baldwin's opinion and Dr Knezevic's opinion referring to the lateral peroneal nerve.  Summing up his opinion he said:

    "What I am saying is that … in view of the fact that Dr Wall has had such a major ill effect from a nerve injury on the balance of probabilities that nerve injury was much more likely to have been the parent nerve, the major nerve which is the lateral popliteal nerve rather than a sensory branch.  In my experience if you have a sensory branch avulsion then it is not likely to cause major neuralgia such as Dr Wall has" (T254).

1. Dr Conrad maintained that he was "absolutely" talking about a different nerve from the common peroneal nerve referred to by Dr Scopa, Dr Baldwin and Dr Knezevic.  Dr Conrad went on in great detail to explain (T258):

   "The lateral popliteal nerve is very superficial behind the fibula, that's the thin bone, and is right at the area that the top of the dog bite was at.  The peroneal nerve is further down and is a branch of the lateral popliteal nerve and is purely sensory.  So they have totally different nerves. … What those people that are talking about the sensory fibres of the peroneal nerve, it's much lower down and it's a much more superficial, purely sensory nerve.  They're different nerves really."

2. The defendant opened his case on the basis that the lateral popliteal nerve and the common peroneal nerve were one and the same.  As a result of Dr Conrad's opinion, it was necessary to adjourn the trial in order for cross‑examining counsel to take further instructions. After the adjournment under further cross‑examination Dr Conrad completely resiled from his earlier position.  Dr Conrad agreed that the common peroneal nerve is synonymous with the lateral popliteal nerve, that the lateral popliteal nerve is simply older terminology and that the nerve is now called the common peroneal nerve.  He agreed that the common peroneal nerve divides into two branches, the superficial peroneal nerve sensory and the deep peroneal nerve mixed motor and sensory.  Dr Conrad then re‑stated his position that on the balance of probabilities he considered it more likely because of the amount of neuralgia Dr Wall has had that the original injury was to the main trunk of the common peroneal nerve.  He therefore disagreed with Dr Baldwin and Dr Knezevic.  In Dr Conrad's opinion neuralgia is pain emanating directly from a nerve and if you accept Dr Wall has neuralgic pain then it is not likely to come from damage to just a superficial sensory branch but is more likely to come from damage to a major trunk of the common peroneal nerve.

3. Under cross‑examination, Dr Conrad conceded that he was not a specialist reconstruction surgeon but maintained he had done a large number of skin grafts.  He conceded that his major area of expertise is in the treatment of varicose veins and venal problems but he had other interests particularly after 35 years as a general surgeon and trauma surgeon.  Dr Conrad admitted that he had not treated a dog bite with a skin graft within the last three years but during the last three years he was in practice he would have treated one.  He advocated keeping the wound open (delayed closure) to try and prevent the risk of infection.  He knew of no research in Australia as to the current practice.

4. So far as post‑operative treatment was concerned Dr Conrad had never used primary closure on a dog bite and therefore was unable to give an opinion based on his own experience of whether allowing two weeks before the wound was checked was good practice.  Dr Conrad conceded that the proper practice if a surgeon will be unavailable to his patient would be that he appoint as a deputy another plastic surgeon, give the name of that plastic surgeon to the hospitals where he operates in case his patients ring and leave a message of some sort on the answering machine at his rooms directing patients to that deputy.

5. Under re‑examination Dr Conrad maintained that the majority of surgeons would have the viewpoint of erring on the side of safety and delaying closure and avoiding primary closure in the case of dog bites.  He conceded that it's really only recently that there may have been viewpoints advanced that say that primary closure may be an alternative but, in his opinion, in 1997 secondary closure would have been the majority view.  Dr Conrad was also of the view that by the time there was an offensive discharge it was too late; by that time any skin graft would have disintegrated and it would be highly unlikely that you would be able to save it.

6. Professor William John Spicer is a consultant medical microbiologist and infectious diseases physician at Alfred Hospital in Sydney.  He is also an Associate Professor at Monash University, Honorary Infectious Diseases Physician at Austin Hospital and consultant pathologist at Dorevitch Pathology.  Professor Spicer's curriculum vitae is of considerable length, including 73 journal articles, and 25 books and chapters, the most important of which, is his co‑authorship of "Therapeutic Guidelines: Antibiotic".  The 13^th edition was published in 2005‑2006.  Professor Spicer has co‑authored that book since he and his co‑authors began writing it in 1977‑1978 initially as a little 28 page booklet for use in Victoria but now the largest selling medical textbook in Australia.  Professor Spicer's opinion is that it would be an unusual doctor who did not know of or use the antibiotic guidelines.

7. Professor Spicer's opinion was primarily sought on the issue of the appropriate antibiotic to have been used by Dr Cooper in his treatment of Dr Wall.  Professor Spicer also gave an opinion on the issue of primary closure.  That opinion was objected to as outside Professor Spicer's area of expertise.  In his evidence Professor Spicer explained that from 1966 to 1970 he was the Chief Medical Officer of a hospital in Bangladesh and had a regular surgical list every Wednesday during that period.  He, on numerous occasions, treated dog bites, sometimes the worst kind of bites from dogs infected with rabies.  During his four and a half years in Bangladesh he also did numerous skin grafts because of the number of burn injuries seen in children in that country.  In another book of his Professor Spicer has written on microbiology and infectious disease dealing with major surgical principles.  From the 1960's onward he has been a specialist in wound care and was often consulted by surgeons and others on that issue.  In this case I am satisfied that Professor Spicer is well qualified to provide an opinion in the area of wound care, including the question of primary closure.  It is clear to me that his experience and particularly his advice to surgeons on wound treatment and his writings qualify him as an expert in that field, as well as being an expert on the appropriate antibiotic treatment for dog bites.  (Clark v Ryan (1960) 103 CLR 486).

8. Professor Spicer did concede that it is a question of opinion at times as to whether a surgeon can use primary closure or not on a wound.  If all the omens were favourable and it were a small wound without a puncture that was quickly attended to and there is no deep damage, particularly if it is on a facial area where cosmetic result is important and the right antibiotics were given, then in Professor Spicer's opinion primary closure including a skin graft may be successful.  In this case Professor Spicer considered there were a number of adverse factors including an extensive tearing wound, a delay of five and half to six hours, and possible deep structure involvement.  His opinion was that the prudent course would have been to delay closure and the skin draft.

9. Professor Spicer was eminently qualified to give his opinion on the use of a broad spectrum antibiotic rather than the narrow spectrum antibiotic Flucloxacillin which Dr Cooper used.  In Professor Spicer's opinion, in a medical sense there is almost no argument in this situation.  Professor Spicer referred to the 40 or more organisms found in a dog's mouth and dog saliva, and advised that those organisms fell into three major groups – gram‑positive, gram‑negative and anaerobes.  A narrow spectrum antibiotic such as was used by Dr Cooper is aimed at and effective against gram‑positive organisms but has little activity against gram‑negative and the anaerobes.  Professor Spicer went on to say that broad spectrum antibiotics are just as safe, but are effective against all three major groups.  To Professor Spicer it made no sense at all not to prescribe a broad spectrum antibiotic to Dr Wall.  Professor Spicer tendered an exhibit 3.34.1 which included a table of common bacterial isolates from dog and cat bite wounds, and a table showing the susceptibilities of bacteria frequently isolated from animal bite wounds to particular antibiotics.

10. Professor Spicer was referred to the Cochrane Collaboration (exhibit 9) a report published after he prepared his advice in this matter.  In Professor Spicer's opinion, that report simply does not deal with broad spectrum antibiotics.  What it does support is the fact that narrow spectrum antibiotics do not work with animal bites and that Flucloxacillin normally has not worked in the trials in which it has been used.  According to Professor Spicer the Cochrane Collaboration is silent on the question of broad spectrum antibiotics except for one relatively weak broad spectrum antibiotic, Cotrimoxazole.

11. On the question of primary closure, Professor Spicer referred to a survey of common practice of surgeons in the United Kingdom where the majority of surgeons do not practice primary closure of dog bite wounds except on the face.  In Professor Spicer's opinion the safest thing is unquestionably to leave the wound open because it has been known for a century or more that if you were to close a wound in which there are organisms trapped underneath the closure, whether it is closed by sutures or a graft, the organisms are locked up in the particular area and become inoculated and pus forms.  In these circumstances infection is more likely and more difficult to treat.  Professor Spicer went on to say:

    "Doctors involved in the care of wounds whether general practitioners or specialists would know that there is a greater risk of subsequent infection in closing a wound if there is a possibility of infection in that wound.  If it is a clean wound then it is closed.  If there is a possibility of infection in some circumstances it is closed, in some circumstances it is left open.  The greater the risk of worse infection the more likely it is to be left open" (T291).

12. Professor Spicer went on to say that although the wound would heal after the infection, in general there would be more fibrosis, more scarring, more disfigurement and more involvement of adjacent structures.  He did concede that nerves very seldom get infected, but structures such as bones and joints, and even muscles and arteries or veins can become infected.

13. Under cross‑examination Professor Spicer explained the phenomenal growth of bacteria when infection occurs.  He said that bacteria doubled their numbers every three minutes, so in three and a half hours after an injury, if the bacteria started multiplying straight away they would have increased a thousandfold, and in four and a half hours ten thousandfold, and in five and a half hours one hundred thousandfold.  Therefore if only a thousand organisms were put in the injury by the dog, there would be likely to be more than ten million organisms there within five and a half hours.  In his opinion, the longer the delay between injury and surgery, the more one would tilt towards needing antibiotics.

14. From his book, "Therapeutic Guidelines: Antibiotic" Version 12, (2003), Professor Spicer referred to two pages (exhibit 3.34.2) headed "Bites and Clenched Fist Injuries".  The guidelines stipulate that bites and clenched fist injuries often become infected and the organisms involved in animal bites are named.  The recommended management for animal bites is thorough cleaning, debridement, irrigation, elevation and immobilisation.  The guidelines go on to say that in the case of low risk wounds "antibiotics may not be necessary for mild wounds not involving tendons or joints that can be adequately debrided and irrigated and that are seen within eight hours."  Professor Spicer believed that this was not a mild wound.  He conceded it was not a high risk wound and he agreed that it was treated within eight hours, but it was a very deep wound and he would not put it in the low risk category.  Professor Spicer further pointed out that the surgeon obviously thought that antibiotics were needed and that it was therefore not in the lower category.  The only issue was whether it was better if broad spectrum antibiotics had been given.  Professor Spicer conceded that giving any antibiotic would make it less likely that infection will occur, but noted that broad spectrum antibiotics would have been the appropriate prescription.

15. Professor Spicer was referred to the three Western Diagnostic Pathology reports on swabs taken from Dr Wall's wound (exhibit 3.39, 3.40 and 3.41).  On 2 July 1997 some 11 days after Dr Cooper's closure of the wound, the only infection found was a heavy growth of pseudomonas aeruginosa.  Some 12 days later on 14 July 1997 a swab of the wound found (1) moderate growth of peptococcus species as well as (2) a light growth of mixed coliform bacteria.  However, on 4 August 1997, over a month later, there was again a heavy growth of pseudomonas aeruginosa as well as isolated colonies of staphylococcus aureus.  Professor Spicer conceded that pseudomonas was not an organism that would normally come from a dog's mouth, and that if it did it would be extremely unusual.  In his opinion it is likely that this organism was either put there at operation or as a subsequent contaminant.  He conceded it may not have been present in the wound when it was first seen by Dr Cooper.

16. Professor Spicer admitted that the fact that staphylococcus aureus was not found until August is evidence that it may not have come from the dog.  Professor Spicer conceded that it was more likely than not that that particular organism came into the wound between 2 and 14 July.  Professor Spicer was firm in his view that if broad spectrum antibiotics had been given, they are active against pseudomonas infections and they would have diminished the likelihood of pseudomonas being there.  If the broad spectrum antibiotics recommended had been given at the time of surgery, Professor Spicer's opinion was that would have made it much less likely that pseudomonas would have been present on 2 July because Flucloxacillin is not active against pseudomonas.

17. Professor Spicer was asked about the re‑occurrence of pseudomonas in August after Dr Wall had been treated with broad spectrum antibiotics and he conceded that pseudomonas is one of the most resistant of organisms and many broad spectrum antibiotics do not work against pseudomonas.  Professor Spicer conceded that it is true that even with the administration of broad spectrum antibiotics, the prospect of eradicating pseudomonas is limited.  Nonetheless he believed that it is very important to give the right antibiotics when the smallest number of organisms and the smallest amount of tissue damage has occurred.

18. Professor Geoffrey John Riley, Professor of Psychiatry and Head of the School of Psychiatry and Clinical Neurosciences at the University of Western Australia first treated Dr Wall in 1998 on referral from Dr Knezevic.  Professor Riley qualified as a psychiatrist in 1977 in London, but chose to work in general practice in the country until in 1990 he specialised as a consultant psychiatrist.  Professor Riley dealt with Dr Wall for two conditions, his depression and his ADHD.  Professor Riley explained that Dr Wall is undoubtedly genetically predisposed to depressive illness and the recent dog attack has precipitated depression.  It is not only the dog attack but the subsequent severe pain that has been the cause of the depressive illness.  Professor Riley described the current episode of depressive illness as moderately chronic and contiguous.  He expected that if Dr Wall were to suffer no pain, he would expect the depression could be controlled.

19. In a report written on 8 August 2000, Professor Riley made two points.  He was familiar with patients who were malingerers or somatisers whose psychopathology causes them to produce symptoms.  But in the case of Dr Wall, Professor Riley said that there was no neurotic contribution to his symptoms.  There was no abnormal illness behaviour.  Dr Wall was dealing with a severe and distressing symptom with great fortitude.  Professor Riley also referred to Dr Wall as a person of the highest integrity who had spent his entire career working as a specialist in an under‑privileged area dedicated to a most disabled and disenfranchised groups of patients, neither receiving nor seeking any recognition.  He considered Dr Wall to be a highly principled physician.  To that extent he entirely disagreed with Dr Grainger, a neurologist who had reported what he considered abnormal pain behaviour in Dr Wall.

20. Professor Riley also diagnosed ADHD suffered by Dr Wall, and prescribed Dexamphetamine for that condition.  Professor Riley explained that ADHD is co‑morbid with depression.  In his experience they commonly occur together and although it cannot be clearly stated and there have been no clinical trials, there is a fair assumption in the medical profession, that ADHA increases the likelihood of depressive illness.

21. Under cross‑examination Professor Riley was asked to explain how a person suffering with ADHD and depression could have achieved what Dr Wall has achieved, and Professor Riley commented on the high intellect, the ability that Dr Wall had to use cognitive skills, and to overcome his ADHD and qualify as a doctor and a specialist paediatrician as he had done.  He explained however that the onset of the severe pain symptoms meant that Dr Wall needed the Dexamphetamine at this stage in his life because he no longer had the reserves to cope with the ADHD without medication.

22. Dr Michael Baldwin is a plastic and reconstructive surgeon who practices in Sydney.  He is the visiting plastic surgeon at the Prince Henry and Prince of Wales Hospitals and the Sydney Children's Hospital.  He has served on numerous professional committees and has published 10 journal articles and books.  Dr Baldwin did not examine or treat Dr Wall.  He was called by the defendant as a plastic surgeon to provide an opinion on Dr Cooper's treatment of Dr Wall.

23. Dr Baldwin relied on the emergency department nursing assessment of Dr Wall's leg injury (exhibit 3, p 128 plaintiff's book of documents).  According to Dr Baldwin that assessment showed that there was no sensory impairment and there was normal colour, warmth and pulses, meaning no arterial damage to the leg.  The tests for motor power were normal, indicating no damage to either the common peroneal nerve or the superficial peroneal nerve.  The only damage was to the lateral cutaneous nerve of the calf as evidenced in loss of sensation around the wound itself.

24. Given these findings, in Dr Baldwin's opinion, there was no reason to explore the common peroneal nerve.  In particular, he disagreed with Dr Conrad's suggestion that neurolysis should have been carried out.  Dr Baldwin's opinion was that the first rule of medical practice is to do no harm.  There was no reason to explore the common peroneal nerve, and nothing to be gained by doing it.  Added to that Dr Baldwin explained that neurolysis can cause damage, either vascular or neural.

25. It was Dr Baldwin's opinion however that if Dr Cooper did visually examine the common peroneal nerve under loupe magnification as he said in evidence he had done, that a prudent practitioner would have included that in his notes as a negative finding.  But in Dr Baldwin's opinion you could not automatically infer that there was no visual examination of the common peroneal nerve because it was not mentioned in the notes.  Dr Baldwin disagreed with Dr Conrad about that.

26. Dr Baldwin went further in his evidence concerning Dr Conrad's opinion that on the balance of probabilities there was some damage to the trunk of the common peroneal nerve.  Dr Baldwin said that Dr Conrad was wrong about that because there were no distal signs of either motor or sensory impairment other than damage to the lateral cutaneous nerve of the calf.  Dr Baldwin was in complete agreement with Dr Knesevic that Dr Wall had a complex regional pain syndrome secondary to his dog bite, subsequent wound infection, treatment and injury to the sensory branches of the peroneal nerve but no lesion of the trunk of the common peroneal nerve or major peroneal nerve injury.

1. So far as Dr Cooper's surgical notes were concerned, Dr Baldwin disagreed with Dr Conrad that Dr Cooper should have mentioned using loupe magnification.  Dr Baldwin said the use of loupe magnification by surgeons, and especially plastic surgeons, was so common that it was like wearing gloves.  If Dr Cooper had not used loupe magnification that should have been noted.

2. Dr Baldwin relied on the photographs (exhibits 1 and 2) as evidence that there was no scar tissue compressing the nerve in Dr Wall's right leg.  Dr Baldwin conceded that all wounds healed with a scar, that a scar undergoes contracture and eventually relaxes.  He conceded that a contracted scar can cause compression, but if there had been any compression he would expect to see clawing of the toes or some effect on the underlying musculature.  If there were compression of the nerve Dr Baldwin would have expected to see some muscular atrophy so that the leg was less full.  None of that was evident in the photographs.  In Dr Baldwin's opinion there was no evidence of any compression of the nerve from any scar tissue.

3. In Dr Baldwin's opinion, Dr Cooper's treatment of the dog bite was appropriate.  He confirmed:

   "Dr Cooper has treated Dr Wall's dog bite by debridement, lavage and application of a skin graft.  It is my view that this is appropriate surgical treatment.  Debridement by definition is the surgical removal of dead, devitalised and contaminated material back to clean and bleeding tissue.  Dr Cooper has then carried out lavage.  Lavage is the use of copious amounts of saline to wash wounds of their contaminants, both macroscopic and microscopic.  That is common surgical practice for treatment of such wounds.  It is routine in all compound orthopaedic wounds.  It is routine in all major soft tissue wounds.  The application of a skin graft is the use of split thickness skin grafts to cover the resulting defect following the contraction of skin flaps and the deficit left after debridement of the edges to viable tissue.  It is my view that this is appropriate treatment" (exhibit 7.3 at pp 3‑4).

4. Dr Baldwin said that he was in complete agreement with Dr Cooper's use of lavage, debridement and primary closure.  Dr Conrad's opinion that primary closure of animal bites was totally inappropriate was considered by Dr Baldwin to be an extreme view, and not the current practice in institutions in which Dr Baldwin has worked.  His opinion was based on 29 years of practice as a plastic surgeon in Sydney where he has treated some 50 dog bites.  In Dr Baldwin's experience primary closure of bite wounds has been the practice for as long as he has been in practice.  Dr Baldwin conceded that delayed or secondary closure was applicable for agricultural wounds, war wounds including high velocity gun shots and for high speed motor vehicle accidents.  In those cases secondary closure is appropriate to allow a return to the operating room for further debridement and/or cleansing because of the high levels of contamination or major muscle necrosis in such wounds.  But, so far as bites were concerned, Dr Baldwin concurred with Dr Cooper's use of primary closure:

   "It is my view that with bites, whether they be animal or human, provided an adequate debridement to viable tissue has been carried out and provided the wound is cleansed the application of a skin graft, even if it is only a biological dressing, is appropriate.  This is the current practice for treatment of dog bites in institutions in which I work.  Thus, I disagree with Dr Conrad's extreme view" (exhibit 7.3 p 4).

5. Dr Baldwin did not agree that secondary closure reduced the risk of infection as Dr Conrad contended; he has found evidence that delayed closure might increase the incidence of infection.  Dr Baldwin referred to "Surgical Delay in the Management of Dog Bite Injuries in Children; Does it Increase the Risk of Infection? by Akhtar, Smith, McKirdy & Page: 2006: 59 Journal of Plastic, Reconstructive and Aesthetic Surgery, pp 80‑85" (exhibit 8.1).

   "The management of dog bite injuries has evolved over the years.  In the past, accepted surgical practice involved delayed closure or healing by secondary intention.  It was thought that because of the risk of infection, dog bite injury should not be closed primarily.  …  More recently there has been a move to more early and definitive treatment, with authors advocating early washout and debridement of wounds and primary closure.  These changes have arisen from findings that the infection rate increased if treatment was delayed following injury, that debridement reduced the incidence of infection by as much as 30‑fold, and that primary treatment produced the best cosmetic and functional results" (exhibit 8.1 pp 82‑83).

6. Under cross‑examination Dr Baldwin conceded that this research involved 61 children, patients at the Sheffield Children's Hospital, and he conceded that children heal more quickly and have a better blood supply than does an adult lower limb.  He conceded that is a factor to be taken into account on the issue of primary or secondary closure of a bite.  He conceded that lower limbs have a lower blood supply and therefore greater risk of break down of grafts.

7. Dr Baldwin also conceded the gist of the journal article (exhibit 8.1) was to avoid night surgery for children thereby reducing hospital costs.  The article concludes at exhibit 8.1 p 84:

   "Surgeons should feel more comfortable postponing the surgical intervention of dog bites until the following day, knowing that with appropriate pre‑operative treatment of the wounds there is no increase in the rate of infection."

8. Dr Baldwin also referred to the abstract of a journal article "Wound Closure in Animal Bites" downloaded from emj-bmjjournals.com (exhibit 8.2) (Electronic Medical Journal and British Medical Journal).  Dr Baldwin relied on the opinion of the authors that dog bites are most appropriately treated by primary closure after thorough cleansing.  But under cross‑examination Dr Baldwin conceded that of 74 papers looked at by the authors, only one paper had anything to do with primary closure.  In that one study no antibiotics were used and the study excluded puncture wounds, wounds infected at presentation, wounds with other structures involved, and those requiring plastic surgery.  Nonetheless, Dr Baldwin considered the article to be of some assistance in this matter.

9. Dr Baldwin conceded that he knew of no other literature or clinical trials suggesting that delayed closure increased the risk of infection; nor did he know of any literature or clinical trials that primary closure increased the risk of infection and, in his opinion, any such clinical trials would not be allowed for ethical reasons.  He conceded under cross‑examination that there is no literature which supports either primary or secondary closure.  Therefore he conceded that he just does not know if delayed closure might allow time to eradicate infection but, based on his practice and experience in Dr Baldwin's opinion Dr Cooper's primary closure of this dog bite was the appropriate treatment.

10. In Dr Baldwin's opinion, Dr Cooper's arrangements for a deputy in his absence in Vanuatu exceeded usual medical practice because it included giving the names of two plastic surgeons to his secretary and to the Mount Hospital as well as placing a message on his after hours answering machine urging patients in emergencies to consult the plastic surgery registrar at a large teaching hospital.

11. Dr Baldwin said he would have waited two weeks to review Dr Wall's dog bite because he would not want to disturb the dressing or the graft.  After two weeks the wound could have withstood interference, but he accepted there would be no risk in taking off the dressing and examining the wound after one week.  He also conceded under cross‑examination that if the wound had been inspected after one week rather than two weeks, there would be a better chance of picking up the onset of infection.

12. Dr Baldwin agreed that the smell and green pus associated with Dr Wall's wound indicated a significant infection that could lead to the breakdown of the skin graft.

13. Dr Baldwin gave evidence that although Flucloxacillin is a good drug belonging to the penicillin family and of particular advantage against streptococcus, it lacks completeness of effectiveness against all the anaerobic organisms and the group of gram‑negative organisms found in a dog's mouth.  For that reason broad spectrum antibiotics would have given greater cover against the multitude of organisms found in a dog bite.  There was no contrary indication in this case not to have prescribed broad spectrum antibiotics.

14. Dr Matthew Crawford is a specialist in pain management, intensive care and anaesthesia, called by the defendant.  Dr Crawford has a private practice at the Prince of Wales Private Hospital in New South Wales, and a public practice at Prince of Wales Public Hospital and Sydney Children's Hospital.  Dr Crawford is highly qualified, widely experienced and has made numerous presentations (52) on pain and pain management between 1983 and 2004.  He is also widely published in 33 books and articles listed in his curriculum vitae.  He holds fellowships in anaesthesia and intensive care, and holds both Australian and foreign qualifications.  Dr Crawford did not examine Dr Wall, but he was provided with all the materials listed in exhibit 6.

15. Dr Crawford explained that the diagnostic criteria for complex regional pain syndrome (CRPS) changed in 1999, and that Dr Wall no longer met those requirements.  His condition would now be diagnosed as a neuropathic pain syndrome, a broader category of which CRPS is a subset.  Dr Wall's symptoms did meet the diagnostic requirement for CRPS in 1997 and Dr Crawford conceded this makes little practical difference and that CRPS remains more commonly used to describe his condition.  It is convenient to use the terminology CRPS rather than neuropathic pain syndrome.

16. In Dr Crawford's opinion some sensory branches of the lateral popliteal nerve would have been injured by the degloving injury, but these were terminal cutaneous branches not a major nerve trunk and could not have been repaired.  He went on to say:

    "It is clear that there was no major injury to the lateral popliteal nerve in that motor, or movement, function was preserved.  As such there was no need to further explore the nerve and to do so may well have caused further injury" (exhibit 6.3, p 3).

17. Dr Crawford explained what is known about the onset of CRPS.  He explained that most patients who develop CRPS have undergone a number of traumatic events, finally leading to the persistence of pain.  Dr Crawford noted Dr Wall's initial injury to his right ankle in December 1995, some 15 to 16 months prior to the dog bite.  That injury was corrected with plaster and resulted in a persistent numbness over the dorsum of his big toe.  Dr Crawford explained that whenever a portion of the body develops numbness or loss of sensation, inhibitory cells which modify the sensory pathways in the spinal cord for that region quickly die or decrease so when he experienced later trauma to that region with the dog bite, his spinal cord would have been primed to transmit pain.  Under cross‑examination Dr Crawford said:

    "His full recovery from all symptoms after the fractured ankle before the trauma of the dog bite made no difference because the partial nerve injury to his ankle caused the death of neurones there to inhibit pain.  The next time there is a painful stimulus, you'll have an increase in the amount of pain transmissions that run through to the spinal cord."

18. Dr Crawford gave his opinion of what caused Dr Wall's CRPS:

    "The condition that he is currently suffering from could easily have been triggered by his initial injuries, even without the infection and the apparent surgical breakdown of his initial wound.  It could also have been triggered off by the breakdown of the wound and subsequent infection and even by the subsequent repair carried out by Dr Mark Allison.  The difficulties that Dr Wall had with his insurance company would also have had a bearing upon his subsequent disability and ongoing pain.  His long standing ADHD may also be a major factor for his subsequent inability to return to work.  The role that Dr Wall's previous ankle injury contributed to his current problems is not and cannot be evaluated, however, it is more than likely that it would have some influence upon his long‑term poor outcome" (exhibit 6.3, p 5).

19. Dr Crawford also explained in his evidence at T438:

    "The way I see things he had a predisposing condition of having had some previous nerve injury to his foot but had globally recovered, as we contest, on sensory function.  I still maintain that from what we know he would have had significant injury to his spinal cord at that stage with the death of inhibitory neurones.  Any further neural insult to that region would very likely set him up for the persistent pain syndrome that he currently has.  He did have a neural insult basically at the time of the dog attack by the removal of the piece of skin.  There are small sensory branches.  From the look of the photograph that I saw, the area of skin loss was about the size of a hand.  The peripheral sensory nerves in that region would have been removed with the skin flap that comes off and that's just the type of sensory insult that predisposed him to the type of condition that he has."

20. Dr Crawford explained the connection he sees between CRPS and Dr Wall's ADHD, anxiety and depression.  He explained that certain chemical transmitters in the central nervous system (serotonin, Noradrenaline and Dopamine) are transmitters concerned in the transmission of pain as well as in anxiety, depression and mood.  There is a reduction in these transmitters in patients with ADHD and in patients who have pain.

21. In Dr Crawford's opinion CRPS would not have been caused solely by the infection.  Trauma is the most common cause and immobilisation is the second most common cause, but infection would have been another nail in the coffin, pushing him further down the road of developing CRPS.  In this case Dr Crawford said the most potent stimulus for the pain syndrome was the injury to minor peripheral branches of the sensory nervous system that occurred at the time of the dog bite.  He disagreed with Dr Knezevic's opinion that the likelihood of him developing CRPS from the dog bite alone without complications would be less than 5 per cent.

22. Under cross‑examination Dr Crawford defended his opinion that emotional factors such as Dr Wall's ADHD, depression, anxiety and the dispute with Lumley Insurance played a role in Dr Wall's CRPS.  He explained that it was well known that patients who had significant emotional issues in their lives have far worse pain problems when injured.  Thus the fact of Dr Wall's suffering from ADHD would make him susceptible to an increase in pain and Dr Crawford expected the ADHD to get significantly worse as it did after the trauma he suffered.  While Dr Crawford found it impossible to tease out the exact trigger in this case, in his opinion ADHD certainly predisposed Dr Wall to developing CRPS.  Such a predisposition is borne out by the increased incidence of things associated with CRPS in patients with ADHD.

23. Under cross-examination Dr Crawford did concede that a patient immobilised in prolonged pain can develop CRPS, but he could not verify pain itself as a factor.  He conceded that in Dr Wall's case the infection, immobilisation and varying pain would all be triggering factors as would the further immobilisation necessitated by the further surgery.

24. Dr Clayton Golledge is a senior consultant in clinical microbiology and infectious diseases at the Queen Elizabeth II Medical Centre, a senior consultant in infectious diseases at Sir Charles Gairdner Hospital, a clinical associate professor at the University of Notre Dame Fremantle and a clinical senior lecturer in the Department of Microbiology at the University of Western Australia.  He is a medical practitioner and a specialist in clinical microbiology and infectious diseases, and is very widely published including 126 journal articles.  Dr Golledge did not examine or treat Dr Wall but was asked to advise on Dr Cooper's treatment of Dr Wall.

25. Dr Golledge explained that the majority of his practice is one of clinical practice in surgical discipline so he sees a lot of skin and soft tissue infections including infected skin grafts.  From the information and reports available to Dr Golledge prior to trial, he formed the opinion that this was not a high risk wound and, based on the therapeutic guidelines, he believed no antibiotics were required.  To Dr Golledge it sounded like a superficial degloving wound and an extensive tearing wound.  He believed it did not fall into the high risk category because it did not involve deep tissue structures.  It appeared to Dr Golledge to have been a superficial wound involving superficial structures.  However, under cross‑examination, Dr Golledge accepted the description of the wound given by Dr Wall himself (at T38) that the wound was 10 centimetres long and 7 centimetres wide, one large flap that was hinged almost parallel with the main bone, from outside to inwards, with a lot of loss of tissue so that the head of the fibula was visible as well as some of the layer of tissue that lines the muscle.  Given that description, Dr Golledge conceded that would not be a superficial degloving wound as he had thought.

26. Dr Golledge said that Flucloxacillin as administered by Dr Cooper does have more than a narrow spectrum of activity and does cover a large number of organisms found in dog bite, particularly the common destructive early organism staphylococcus aureus, staphylococcus intermedius and pyogenic streptococci.  He would describe Flucloxacillin as a moderate spectrum antibiotic.

27. As to Dr Cooper's choice of Flucloxacillin, Dr Golledge said this (T477):

    "I think it's perfectly reasonable.  I think that a number of other practitioners would have done the same thing; in fact there might have been a number of practitioners that would have given no antibiotic at all, so Dr Cooper has clearly taken it a step further than that, perhaps two steps further.  He has not just given nothing.  He has not just given penicillin or Amoxycillin.  He has given a reasonable choice antibiotic, Flucloxacillin, and I would not criticise that."

28. Given Dr Golledge's concession in cross‑examination that this wound was not a low risk superficial degloving injury, this statement of Dr Golledge's opinion has to be approached with caution.

29. Dr Golledge went on to say that the important thing that is overlooked, particularly in Professor Spicer's report, is that debridement and lavage are the cornerstones of the treatment of dog bite.  He went on to say (T477):

    "So removing all the dead and diseased tissue, copiously irrigating the wound to get rid of the bacterial bioburden that would be there as a consequence of these wounds which is not disputed, that is the real crux of what should be done in this case, and antibiotics at best only have an adjunctive role.  They certainly are not crucial to the management of this case."

30. Dr Golledge then considered the question of whether the use of a broad spectrum antibiotic as advocated by Professor Spicer would have prevented the pseudomona aerugnosa infection found in Dr Wall's wound on 2 July (T478):

    "That's a very difficult question.  The way I can best answer this is that we commonly see pseudomonas as a complication of what we call a super‑infection; so the organism infecting the wound later on down the line even in patients given aggressive antipseudomonal antibiotics.  So it's certainly common in a variety of clinical situations including complicated skin and soft tissue infection for a patient to be given an antipseudomonal antibiotic but still develop a pseudomonas infection.  So it is a very common almost every day occurrence, particularly in complicated skin and soft tissue infections, particularly in the situation of burns and particularly in respiratory infection or pseudomonas infections.  It is by no means an absolute preventative; in fact I would say in roughly about half the cases, even despite aggressive antipseudomonal therapy, pseudomonas can still occur.  It's a very opportunistic organism."

1. Dr Cooper is a highly trained and experienced plastic and reconstructive surgeon.  He received his Bachelor of Medicine and Bachelor of Surgery from the University of Tasmania in 1977.  He worked as an intern for a year before becoming a resident medical officer and a locum registrar in anaesthesia in intensive care.  After that he worked for at least three years for the Royal Flying Doctor Service in the north‑west and Kimberley regions before spending 1986 to 1988 as a general surgical registrar at various Perth hospitals, including six months as a plastic surgery service registrar at Royal Perth Hospital in 1987.  In 1988 he served as plastic surgery registrar at Queen Elizabeth Hospital in Adelaide.  Between 1988 and 1991 he was a cardiothoracic registrar and orthopaedic registrar at Royal Perth Hospital and the Mount Hospital.  During 1991 and 1992 he was the plastic surgery registrar and the senior registrar at the University Hospital in Cork, Ireland before becoming a Fellow in reconstructive microsurgery at the Pittsburgh Medical Centre in the United States of America in 1994, and a Fellow in microsurgery at the Buncke Clinic in San Francisco in 1995.

2. He was made a Fellow of the Royal College of Surgeons in 1994 and a Fellow of the Royal Australian College of Surgeon at the end of 1996.  In 1996 he was the senior registrar in plastic surgery at the Sydney Children's Hospital and the Prince of Wales Hospital.

3. Dr Cooper commenced his current practise as a plastic and reconstructive surgeon at the Mount Medical Centre and at Sir Charles Gairdner Hospital in 1997.  For two years he has held an academic appointment at the University of Western Australia where he lectures in surgery and supervises post‑graduate training for plastic surgeons in Western Australia.  For the past five years he has headed the department of plastic surgery at Sir Charles Gairdner Hospital and supervised training.  Dr Cooper admitted that he had commenced his consultancy in plastic and reconstructive surgery in January 1997, just six months prior to his treatment of Dr Wall.

4. Dr Cooper has treated dog bites in the metropolitan area, in Australasia, and in the United States of America where most significant dog bites or animal bites are managed by plastic and reconstructive surgeons.  He estimated that he has been doing 700 to 1,500 hundred operations per year since 1988, and that quite a few involve skin grafts.

5. Dr Cooper placed Dr Wall on Flucloxacillin because based on his experience, he was concerned about staphylococcal infection.  Dr Cooper described Flucloxacillin as a low cost drug.  He has found it unusual if a patient is sensitive to it.  And it covers many of the organisms Dr Cooper was concerned about in the dog bite, particularly staphylococcus aureus in the post‑operative period.  It was Dr Cooper's belief in 1997, and it continues to be his belief, that the efficacy of giving broad spectrum antibiotics in dog bite cases is still not proven.  He considered lavage and debridement the prime action to prevent infection in a dog bite case.  From his experience and teaching, Dr Cooper believed that the sooner you lavage and debride, the less likely it will be that you will get a post‑operative infection.  Dr Cooper does not prescribe antibiotics in all dog bite cases; he said with a small puncture wound to the face he might just wash the wound and suture it.  But in this case he concurred with Dr Conrad that because this more extensive wound was to the leg, he believed antibiotics were required.  Furthermore, Dr Cooper did not believe any antibiotic used would have prevented the appearance of pseudomonas.

6. Dr Cooper said he was always concerned about pseudomonas infection because it is probably the second commonest reason for losing a skin graft.  It would be a possible contaminant but not from the dog's mouth.  Dr Cooper admitted in his evidence that he recognised the possibility of infection.  He said in surgery there is always a risk of infection.  He denied that Flucloxacillin was a narrow spectrum antibiotic.  He classified it as a limited spectrum antibiotic.  Dr Cooper denied that it would have been safer to use a broad spectrum antibiotic for three reasons (T425):  (1) They are more expensive; (2) They are more prone to cause cross sensitivity; and (3) They are more prone to breed resistant bacteria.

7. Dr Cooper believed that the broad spectrum antibiotic Ticarcillin recommended by Dr Golledge could not be prescribed without permission from PBS in Canberra.  He understood PBS would have required a positive wound swab.  Dr Cooper understood that the reason for this was to prevent the community becoming awash with resistant organisms that PBS deliberately focuses on targeting antibiotic therapy to specific drugs.  Dr Cooper was firmly of the view that you do not give antibiotics to prevent pseudomonas when there was no infection of any kind at the time of surgery.  He said the suggestion a doctor should do that was heresy.  Dr Cooper stated that broad spectrum antibiotics are, by their nature, expensive.  Generally it was necessary to ring PBS in Canberra for permission to use them, and necessary to prove there is a pseudomonas infection before approval is given.

8. Dr Golledge confirmed that Ciprofloxacin as administered to Dr Wall in Gosnells Hospital under the care of Dr Lawrance was not freely available in 1997.  It could only have been prescribed with approval from Canberra when the presence of pseudomonas or another multi-resistant organism was proved.  Dr Cooper could not have prescribed it at the time of his surgery as there was no pseudomonas infection at that time.

9. On the other hand, the broad spectrum antibiotic Ticarcillin preferred by Dr Golledge for treating this dog bite was freely available in 1997 as a general benefit, and was not a terribly expensive antibiotic on the PBS scheme.  Dr Cooper could have prescribed it.  Dr Golledge concurred with Dr Cooper's evidence that Flucloxacillin is not a narrow spectrum antibiotic but, rather what he referred to as a "moderate" spectrum antibiotic effective against a large number of organisms found in a dog bite, particularly the common destructive early staphylococcus organisms.  In Dr Golledge's opinion, Dr Cooper gave a "reasonable choice antibiotic Flucloxacillin and I would not criticise it" (T477).

10. Professor Spicer's evidence on this point was that although Flucloxacillin was effective against the gram‑positive organisms found in a dog's mouth, it was not effective against the gram‑negative organisms and the anaerobes found in a dog's mouth.  I accept that evidence and exhibit 3.34.1, the table showing the susceptibility of dog bite bacteria to particular antibiotics.  Professor Spicer conceded that pseudomonas was not an organism that would normally come from a dog's mouth, and if it did it would be very unusual.  But, broad spectrum antibiotics are active against pseudomonas, and in Professor Spicer's opinion, if a broad spectrum antibiotic had been given at the time of surgery, it would have made it much less likely that pseudomonas would have been present on 2 July.  Dr Golledge said that the use of a broad spectrum antibiotic would have made it "less likely" that the pseudomonas would have been present on 2 July – not "much less likely" as Professor Spicer contended.  In Dr Golledge's opinion while "less likely" the use of a broad spectrum antibiotic probably would not have made a great deal of difference.

11. According to Professor Spicer Flucloxacillin is not active against pseudomonas.  Dr Golledge on the other hand gave evidence that Flucloxacillin was effective against pseudomonas – at least in laboratory conditions.  He was asked in examination‑in‑chief what antipseudomonal antibiotics the plaintiff had been given prior to 4 August 1997 when a second heavy growth of pseudomonas was detected, and Dr Golledge replied at T480:

    "The plaintiff had had at least a course of Flucloxacillin which had been tested by the Western Diagnostic Pathology and found to be susceptible in a laboratory at an appropriate dose so that is … (Dr Golledge was interrupted by a question to explain what 'susceptible in an appropriate dose' meant).  What it means is that this antibiotic was tested in a laboratory against the organism on agar plate on petri dish to see whether there was a zone of inhibition around an antibiotic disc to show that in theory, at least in the laboratory conditions, that the organism is being inhibited and killed by the antibiotic.  Now, that of course doesn't always match the clinical situation but that gives the clinician the best guess guide as to what's likely to be susceptible and resistant."

12. In Professor Spicer's opinion, even with the administration of broad spectrum antibiotics, the prospect of eradicating pseudomonas is limited.  Dr Golledge said it is common for a patient to be given an antipseudomonal antibiotic and still develop a pseudomonas infection.  That occurred in this case; Dr Wall developed another pseudomonas infection on 4 August 1997 when a heavy growth of pseudomonas aeruginosa was detected, despite his earlier treatment with antipseudomonal antibiotics.

13. The plaintiff has failed to establish particular 6 in its strict terms.  While I accept Professor Spicer's, Dr Golledge's and Dr Baldwin's opinions that a broad spectrum antibiotic was not administered, that is not what the plaintiff has pleaded.  The plaintiff has pleaded that Dr Cooper arranged for narrow spectrum antibiotics only to be administered.  I accept the evidence of Dr Golledge and Dr Cooper that Flucloxacillin is not a narrow spectrum antibiotic.  While it is not a broad spectrum antibiotic, it is properly a limited spectrum or a moderate spectrum antibiotic.  But I do not believe I should hold the plaintiff strictly to his pleading on this point.  The real issue joined at trial was whether Dr Cooper breached his duty of care to Dr Wall by prescribing Flucloxacillin rather than a broad spectrum antibiotic, and that is the issue that I must address.

14. The plaintiff's pleading alleges this breach occurred "pre‑operatively, operatively and post‑operatively".  On the facts in this case there was little time prior to Dr Wall's surgery for Dr Cooper to have administered any antibiotics pre‑operatively.  There was no evidence led or relied upon by the plaintiff in his submissions suggesting the need for antibiotics prior to surgery.  I have found the surgery commenced at 7.15 pm, less than four hours after the dog bites.  The Flucloxacillin appears to have been started intravenously during surgery because Dr Cooper said he "continued" it six hourly after surgery.  There seems nothing in the evidence to support the plaintiff's pleading of any failure "pre‑operatively".

15. There are a number of contra indicators for the use of broad spectrum antibiotics. These were explained by Dr Golledge at [120] above and Dr Cooper mentioned them in his evidence at [173] above. In exhibit 12 Dr Golledge's written opinion, he had said:

    "While it is true that all bite wounds, especially those of human origin, have the potential to become quickly infected.  It is by no means mandatory that all these bite wounds are treated with broad spectrum antibiotics … ." 

16. I am satisfied that Dr Cooper did administer a moderate spectrum antibiotic rather than a broad spectrum antibiotic.  In this case that took place as part of Dr Cooper's overall treatment of Dr Wall.  Dr Cooper appropriately and adequately lavaged and debrided the wound before he laid the skin graft.  That treatment was done very promptly within four hours of the dog bites.  Professor Spicer's "Therapeutic Guidelines: Antibiotic" suggest that antibiotics may not be necessary for low risk wounds – mild wounds not involving tendons and joints that can be adequately debrided and irrigated, and that are seen within eight hours.  Dr Cooper's treatment fit within those Guidelines; the wound was adequately debrided and irrigated, and seen well within the eight hours.  Dr Cooper recognised however, that it was not a "mild wound".  The degloving injury was too deep.  But it was not in the category of a high risk wound within the Guidelines either.  That was Dr Cooper's opinion supported by the evidence of Professor Spicer and Dr Golledge.  This dog bite fell somewhere between a low risk dog bite where no antibiotic may be necessary and a high risk wound where antibiotics are needed.  Dr Cooper chose to administer antibiotics and his decision to do that is supported by other practitioners who gave evidence.  The only issue is whether he breached his duty of care by not administering a broad spectrum antibiotic.

17. There is no question that infection was a foreseeable risk of surgery.  Dr Cooper admitted that there is a risk of infection with all surgery, and he admitted there was the risk of contracting a pseudomonas infection in all surgery, quite apart from the special risks associated with the 40 organisms found in a dog's mouth when treating dog bite.  The issue is whether Dr Cooper's choice of Flucloxacillin in these particular circumstances breached the standard of reasonable care and skill in Dr Cooper's provision of professional treatment for Dr Wall's dog bites.  While under Dr Cooper's care, Dr Wall did not develop any infection from any organism in the dog's mouth.  That in itself would tend to indicate there was no breach of Dr Cooper's duty of care.  But Dr Wall developed a heavy pseudomonas infection while under Dr Cooper's care.  Was it a breach of Dr Cooper's duty of care to have prescribed Flucloxacillin in these circumstances?  I do not accept that it was unreasonable for Dr Cooper to prescribe Flucloxacillin.  While there is always a risk of pseudomonas infection, I do not accept that a surgeon's duty of care requires the giving of broad spectrum antibiotics to every patient undergoing surgery.  It seems to me that could be the effect of an adverse finding about Dr Cooper's treatment on this issue.  And that would be wrong.  I accept that broad spectrum antibiotics are contra indicated for a number of reasons stated by both Dr Cooper and Dr Golledge.  I accept Dr Cooper's evidence that among other factors, broad spectrum antibiotics are more prone to breed resistant bacteria.  That in itself provides a compelling reason not to over prescribe broad spectrum antibiotics, and certainly not in every case involving surgery.  Keeping Dr Wall immobilized in hospital longer for intravenous administration of a broad spectrum antibiotic with all the associated risks of side effects as Dr Golledge advised would be another important factor supporting the reasonableness of Dr Cooper's decision to prescribe Flucloxacillin.

18. Dr Baldwin's evidence as a practitioner, a Fellow plastic surgeon, was of considerable significance when he described Flucloxacillin as a "good drug" particularly effective against streptococcus but lacking completeness in its effectiveness against all the organisms found in a dog's mouth.  His evidence that he would have prescribed a broad spectrum antibiotic, and that there were low cost broad spectrum antibiotics freely available in 1997 was particularly persuasive.  I accept that Dr Cooper was wrong in his understanding about that, and I accept that his evidence about that has the appearance of recent invention in an effort to justify his use of Flucloxacillin for dog bite.

19. This issue is narrowly balanced.  In his closing submission Senior Counsel for the plaintiff referred to the evidence of all the medical practitioners called to give evidence, that each would have given a broad spectrum antibiotic.  That included not only Dr Conrad and Professor Spicer who were called by the plaintiff, but also Dr Baldwin and Dr Golledge who were called by the defendant.  But the test for medical negligence is not what other doctors say they would have done in the same or similar circumstances (Strempel v Wood).  From what was said in Strempel v Wood if I were to treat this evidence as decisive, I would be in error because such an approach adopts a variant of the Bolam principle (Strempel v Wood [28] ). Instead I must judge the matter myself applying the standard of an ordinary skilled person exercising and professing to have the special skill of a plastic surgeon, and I must determine as a matter of fact whether the duty of care has been breached.

20. In this matter I am particularly persuaded by Dr Golledge's opinion that Flucloxacillin was a reasonable choice antibiotic that he would not criticise.  Although the issue is narrowly balanced, accepting as I do the contra indicators for the giving of broad spectrum antibiotics and Dr Cooper's reasons for giving Flucloxacillin, and applying common sense, I am not persuaded that the standard of reasonable care in the treatment of Dr Wall for this dog bite required the prescription of a broad spectrum antibiotic.  Therefore the plaintiff has failed to establish particular 6 of the particulars of negligence.

Provisional findings on causation

1. In March v E & M H Stramare Pty Ltd (1991) 171 CLR 506 the "but for" test for causation was rejected by the High Court and the majority held that the question of whether conduct is a cause of an injury is to be determined as a question of fact by reference to common sense and experience. Considerations of policy and value judgments necessarily enter. The decision in March v Stramare was unanimously endorsed by the High Court in Chappel v Hart (1998) 195 CLR 232. Before the defendant can be found responsible for the plaintiff's injury, the plaintiff must prove that the defendant's conduct or omission caused or materially contributed to his injury. In Western Australia, although the burden of proof remains on the plaintiff to prove causation, there is a shifting of the onus of proof in some circumstances. In Strempel v Wood [2005] WASCA 163 McClure J said at [49]:

   "If an injury occurs within an area of foreseeable risk, then, in the absence of evidence that the breach had no effect, or that the injury would have occurred even if the duty had been performed, it would be taken that the breach of the common law duty caused or materially contributed to the injury".

2. As McHugh J said in Chappel v Hart at [27]:

   "Before the defendant will be held responsible for the plaintiff's injury, the plaintiff must prove that the defendant's conduct materially contributed to the plaintiff suffering that injury.  In the absence of a statute or undertaking to the contrary, therefore, it would seem logical to hold a person causally liable for a wrongful act or omission only when it increases the risk of injury to another person.  If a wrongful act or omission results in an increased risk of injury to the plaintiff and that risk eventuates, the defendant's conduct has materially contributed to the injury that the plaintiff suffers whether or not other factors also contributed to that injury occurring".

3. In this case the defendant's approach to the issue of causation was different from that of the plaintiff.  The defendant submitted that any breaches of Dr Cooper's duty of care could go no further than causing or materially contributing to the onset of Dr Wall's infection and therefore the plaintiff's case must fail because it cannot be established on the balance of probabilities that the infection caused the plaintiff's pain syndrome.  On the other hand the plaintiff submitted that the Court must approach the question differently, and suggested that any failure on Dr Cooper's part to exercise reasonable care as alleged in the particulars of negligence was likely to have caused or materially contributed to the onset of Dr Wall's pain syndrome because the infection caused the breakdown of the skin graft and led to Dr Wall's immobilisation in Gosnells' Hospital from 2 July to 24 July.  There is evidence from a number of the experts that immobilisation is causative of the pain syndrome.

4. I accept the plaintiff's analysis of this issue.  This is a chain of causation case.  It is not the pseudomonas infection, but the inevitable results of that infection, leading to prolonged immobilisation that it is suggested caused or contributed to the onset of the pain syndrome.  I agree with the defendant that there is no evidence that could satisfy me that the infection standing alone caused or contributed to the pain syndrome.  But that is no answer.  I accept the plaintiff's submission that the onset of the infection was the first link in a chain of events inevitably leading to the prolonged immobilisation of the plaintiff and the onset of the pain syndrome.

1. On the issue of causation Dr Cooper's alleged negligence need not be the sole cause of the pain syndrome so long as the plaintiff proves that the negligence materially contributed to the onset of the pain syndrome, or increased the risk of the plaintiff contracting the pain syndrome.

2. It is readily apparent in this case that the dog bite itself cannot be removed as a cause of the onset of the pain syndrome.  The dog bite clearly started the chain of causation.  Dr Berrigan's evidence was that either the dog bite or its complications were the cause of the onset of the regional pain syndrome, while Dr Grainger's opinion was that the dog bite alone may have caused the onset of the pain syndrome.  In Dr Knezevic's opinion there was less than a 5 per cent chance that that was the case, but Dr Crawford disagreed with Dr Knezevic about that.

3. I was particularly assisted by Dr Knezevic's opinion that any delay in healing, treatment and rehabilitation is likely to predispose and contribute to subsequent development of a complex regional pain syndrome, and that surgeons are well aware that ongoing pain, immobilisation and ongoing inflammation of the limbs in particular, predisposes people to developing regional pain syndrome.

4. Dr Crawford's opinion was also of considerable assistance.  He discussed three possible "triggers" for Dr Wall's regional pain syndrome:

   (1)The initial dog bites even without infection, or

   (2)The breakdown of the skin graft with the infection, or

   (3)The subsequent repair carried out by Dr Allison.

5. Dr Crawford also referred to a number of "predisposing" conditions particular to Dr Wall including his previous nerve injury to his right foot and his ADHD.  Factors such as this do not assist me however.  They are more akin to the issues in the "egg shell skull" cases.  At law a defendant takes the plaintiff as he finds him so that while Dr Wall may have been more susceptible to developing the pain syndrome because of his earlier foot injury, and while the ADHD may have had an adverse effect on Dr Wall's experience of pain and may go someway to explaining why he still experiences excruciating pain despite heavy ongoing medication, nonetheless, Dr Wall only developed the pain syndrome after the dog bite, and it is the triggers for the onset of the pain syndrome that must be considered.

6. Dr Crawford also gave evidence that emotional factors such as depression, anxiety and Dr Wall's dispute with Lumley Insurance played a role in the onset of his pain syndrome, but I found his evidence about these emotional factors, including ADHD provided an explanation for Dr Wall's heightened pain experience but did not support the proposition that any of these emotional factors alone or together caused or materially contributed to the onset of the pain syndrome.

7. Dr Crawford agreed the pain syndrome would not have been caused solely by the infection.  I accept Dr Crawford's evidence that trauma is the most common cause and immobilisation is the second most common cause for the onset of regional pain syndrome.  Under cross‑examination, Dr Grainger agreed that immobilisation can cause regional pain syndrome.  That opinion is consistent with the opinions of Dr Crawford and Dr Knezevic.

8. Taking account of all the expert evidence I am satisfied that prolonged pain and immobilisation can cause or contribute to the onset of the pain syndrome.  I am satisfied that the dog bit alone did not cause the onset of the syndrome.  Other factors were involved.  I am satisfied that the pseudomonas infection led to the breakdown of the skin graft, and that in turn led to the prolonged immobilisation of Dr Wall's leg while he was hospitalised during July.  If I had been satisfied that Dr Cooper breached his duty of care by laying the skin graft before he had ensured that all infection was eradicated or by failing to arrange a review for two weeks, or by failing to arrange for a deputy or by failing to give the plaintiff any advice or instructions prior to discharge, I would have found that all or each of these wrongful acts materially contributed to the onset of the regional pain syndrome by causing or materially contributing to the onset of the infection and the breakdown of the skin graft which resulted in prolonged pain and immobilisation.

9. The position is somewhat different with the alleged wrongful act of failing to prescribe a broad spectrum antibiotic.  Professor Spicer's opinion was that if broad spectrum antibiotics had been given, that would have made it "much less likely that pseudomonas would have been present on 2 July".  Dr Golledge said it would have been less likely but it probably would have made no difference.  I accept and rely on Dr Golledge's expert evidence about the nature of pseudomonas, what he called a "super–infection" infecting the wound later down the line even in patients' given aggressive antipseudomonal antibiotics.  I accept his opinion that "in roughly half the cases even despite aggressive pseudomonal therapy, pseudomonas can still occur" (T478).  And I note this happened in this case when Dr Wall experienced another heavy growth of pseudomonas infection in August, despite aggressive antipseudomonal treatment during July.  I also accept Dr Golledge's evidence that a pseudomonas infection is not a rare event.  It happens "almost on a daily basis" (T487) at a big teaching hospital like Sir Charles Gairdner where patients develop pseudomonas infections despite what would be deemed "appropriate antibiotic cover" (T487).

10. Another factor is Dr Golledge's evidence that at least in laboratory conditions pseudomonas is susceptible to Flucloxacillin (T480).  Professor Spicer held a different opinion.  This aspect of Dr Golledge's evidence was never put to Professor Spicer during his cross‑examination.  This failure weakens Dr Golledge's evidence about this and I do not rely on that part of Dr Golledge's evidence.

11. Taking account of the nature of the pseudomonas super‑bug and relying on Dr Golledge's opinions, I am satisfied on the balance of probabilities that Dr Cooper's failure to give a broad spectrum antibiotic increased his risk of the onset of a pseudomonas infection but I am satisfied that the risk remained irrespective of the giving of a broad spectrum antibiotic, and that Dr Wall was just as likely to develop a pseudomonas infection whatever antibiotic was given.  In this case there is evidence the injury would have occurred even if the duty had been performed and therefore the evidential onus did not shift (Strempel v Wood [49] ).

12. For these reasons I provisionally find that failure to prescribe a broad spectrum antibiotic did not cause or materially contribute to the onset of the pain syndrome.

Provisional assessment of damages

1. The parties have agreed damages in the amount of $1,300,503 not including general damages for pain, suffering and loss of amenity which I must assess.

2. Dr Wall has experienced severe pain from the pain syndrome since 1997 with similar symptoms developing in his left leg – excruciating pain that he experiences during the night – since about 1999.  No‑one suggests the pain syndrome will run its course or abate.  Dr Wall can look forward to living with this for the rest of his life.  The severity of his pain is such that he has considered amputation of his leg, but realises that would not necessarily alleviate the pain.

3. I accept that Dr Wall may be experiencing a heightened level of pain because of factors personal to himself such as ADHD, but that does not lessen the need to compensate him as much as monetary compensation is able to do for the extreme and prolonged pain he has suffered and will continue to suffer.

4. The pain syndrome has had a devastating effect on his personal life and on his career.  He was a leading specialist paediatrician looking after youngsters with ADHD.  Not only that work but his research and his participation in national and international forums have been ended by the pain syndrome.  He was writing papers and a book, but the onset of the pain syndrome meant he could not sit and type and he could not concentrate sufficiently to complete his book or research.  He has had to forego overseas travel because of the pain he experiences in flight.  He had to stop work completely in 1998 because of his inability to concentrate due to the pain and drugs that he was experiencing.

5. He is left with a very limited existence and is dependant on heavy doses of morphine based pain killers with little time or energy to enjoy any of the normal day to day pleasures of life.  I was glad to hear that he is still able to undertake some wood‑work in his workshop but it is very reduced from what he was able to achieve before he was injured when he built wooden toys, fine furniture and complete kitchens in his workshop.  Now he is only able to spend two to two and a half hours a day in his workshop without having to rest because of the pain.  He enjoyed walking before he was injured but now is unable to engage in that exercise.

6. Taking account of the severity and duration of his pain, the loss of his career and the loss of the amenities in his life, I provisionally award the amount of $450,000 for general damages.  Therefore I award total provisional damages of $1,750,503.