Margio v Metropolitan (Perth) Passenger Transport Trust - [2002] WADC 50

JURISDICTION : DISTRICT COURT OF WESTERN AUSTRALIA
IN CIVIL

LOCATION: PERTH

CITATION: MARGIO -v- METROPOLITAN (PERTH) PASSENGER TRANSPORT TRUST [2002] WADC 50

CORAM: WISBEY DCJ

HEARD: 1, 2 FEBRUARY, 4, 5 DECEMBER 2001

DELIVERED : 15 MARCH 2002

FILE NO/S: CIV 4343 of 1996

BETWEEN: JOHN ANTHONY MARGIO
Plaintiff
AND
METROPOLITAN (PERTH) PASSENGER TRANSPORT TRUST
Defendant

Catchwords:

Torts - Negligence - Employer's liability - Trial of preliminary issue as to whether plaintiff suffered carbon monoxide poisoning in course of employment

Legislation:

Nil

Result:

Plaintiff failed to establish that he suffered carbon monoxide poisoning

Representation:

Counsel:

Plaintiff: Mr R I Viner QC with him Mr H.J. Stephens
Defendant: Mr B P King

Solicitors:

Plaintiff: Slater & Gordon
Defendant: Crown Solicitor's Office

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

Ramsay v Watson (1961) 108 CLR 642

Case(s) also cited:

Malec v J C Hutton Pty Ltd (1990) 169 CLR 638
March v E & M H Stramare Pty Ltd (1991) 171 CLR 506

WISBEY DCJ: John Anthony Margio, a bus driver in the employ of the defendant Metropolitan (Perth) Passenger Transport Trust, claims inter alia that on or about 24 February 1995 whilst driving bus registration no UQB 509 he suffered carbon monoxide poisoning. The matter comes before the Court for the determination of the issue whether on 24 February 1995 the plaintiff suffered carbon monoxide poisoning. I have reservations about the appropriateness of the preliminary determination of that issue, but in accordance with the terms of the Order made, and the desire of the parties, have proceeded to do so.

The evidence

The plaintiff

The plaintiff commenced employment with the defendant as a bus driver in September 1989, and was in the course of that employ on 24 February 1995. He previously worked in the visual arts field as a book designer and a sign maker (having had three years training in fine art); had three years training in pottery; and qualified in architectural drafting in 1975. He indicated that good manual dexterity was required in the various areas of training undertaken.
The plaintiff stated that on 24 February 1995 he clocked on at about 3.58 pm, having travelled by car from his home in Leederville to the Causeway Depot. He was assigned a Mercedes rigid body diesel fuel bus No 509 and left the depot at 4.18 pm driving through the City to the intersection of Thomas Street and Kings Park Road. The return journey took him through the City, across the Causeway, and then via Canning Highway, Mill Point Road and Coode Street to the terminus at Edna Street, Como, where he arrived at about 5.13 pm. He left the Como terminus at about 5.28 pm driving to the terminus at Cantonment Street Fremantle. Having arrived at the Cantonment Street terminus at about 6.34 pm he set the electronic ticket machine ready for the next trip and because he felt hot, tried to switch on the air conditioner, but claimed that it was not operational. He left the engine running for a short time so that the air cooler would function, and remained in the bus reading. He restarted the engine about five minutes before the scheduled departure time of 6.55 pm.
Just prior to departure he leaned over to the side to pick up his bag, and as he did so "became very dizzy, my head started spinning, I was nauseous, I had quite a sharp pain in my head". He stated that he was surprised because he had never been sick in his life.
Feeling that he was in no condition to drive, the plaintiff decided to go to another bus to use its radio to summon assistance, but as he stood up to exit his bus he felt that he was losing consciousness and consequently lowered himself to the floor. After partial recovery he exited the bus and moved towards another bus to the rear of it. The driver of that bus, Mr Gary Hewitt, radioed for assistance while the plaintiff sat on the footpath. The plaintiff was evacuated by ambulance to the Fremantle Hospital, and recalled being given oxygen en route.
The plaintiff arrived at Fremantle Hospital at 7.20 pm and was seen by a Dr Banham at 11.00 pm. Dr Banham required him to perform some tests which appear to have been directed to evaluating balance. The plaintiff performed the tests poorly. One test consisting of sketching overlapping polygons appears at p 6, tab 1, Exhibit P1. He also wrote the sentence which appears thereon. He asserted that he performed the test badly. Following assessment he was discharged in the company of a Metro bus officer.
The plaintiff claimed that he slept unusually soundly, not waking until after midday, and when he awoke felt groggy and dizzy when standing, and experienced difficulty walking. He also claimed to be unable to appropriately name common household objects. Because of the symptoms aforesaid the plaintiff took a taxi to Fremantle Hospital where he was seen by a nurse Gannon at about 2.15 pm. He claimed that he told nurse Gannon of the symptoms he had experienced, and in particular that he had a headache and was vague in his thoughts, (ie he claimed that he referred to the refrigerator as a stove, and said his birthday was in July instead of June).
The plaintiff stayed in hospital overnight and was given oxygen. He then consented to and was given hyperbaric treatment in the hyperbaric oxygen chamber. He required sedation whilst in the chamber because he was claustrophobic. Following the first hyperbaric treatment he was asked to again perform the balance tests, and was unsuccessful. He underwent a second hyperbaric procedure on the 27 February, a third on 1 March, and a fourth on 2 March, but without any positive effect. Dr Oxer then referred him to the neurologist, Dr Bajada, who saw him on 9 March 1995.
The plaintiff was adamant that he had never previously experienced such symptoms, and stated that experiencing headaches was a common occurrence in bus driving.
It was pointed out to the plaintiff that the medical records suggest that he told a Dr Wright at Fremantle Hospital that he had a similar episode at home four weeks previously when he felt dizzy, but that it resolved. He was adamant that he had never been sick in his life, and the only explanation he was able to give concerning the notation by Dr Wright was that he might have said he experienced a headache a few weeks earlier, although the only headache he could nominate was "just an ordinary headache". I found his explanation unconvincing and do not accept it. It was also brought to the plaintiff's attention that it was recorded that he had been under stress, and he responded that he had been actively involved in union issues which was fairly demanding on his time, but that it was not stressful.
In cross‑examination the plaintiff's attention was drawn to a letter from Work Cover Western Australia to Dr Oxer dated 25 May 1995 being tab 4, Exhibit P1 where a statement was made that the history given by him to Work Cover concerning the events of the day in question included a statement that whilst driving on that day he had a headache, but that headaches were commonplace when driving. He conceded that he had headaches from time to time, but denied that it was commonplace. He specifically denied suffering frequent headaches, pain behind the eyes, ocular symptoms, or an inability to concentrate. He agreed that he had a work accident in 1994 causing him spinal injuries.
The plaintiff's attention was directed to a recurrence of disability claim form dated 3 April 1992 (Exhibit D1.1) signed by him, in which he recorded "almost constant headaches; aching eyes; neck pain; shoulder pain (sometimes accompanied by pain in arms and fingers); thoracic back pain; bones 'popping' neck, thorax, lower back; lower back pain (sometimes accompanied by sciatic pain and agitated bowels)". When it was put to him that was in conflict with his denial of having suffered constant headaches in the past, he replied that the statement in the document referred to the position in 1992. Alternatively he seemed to claim that he had forgotten about those symptoms.
A further document signed by the plaintiff on 17 November 1992 made reference to frequent headaches, pain behind the eyes, affected vision, and inability to concentrate.
In a recurrence of disability claim form signed by the plaintiff on 2 February 1994 (Exhibit D1.3) he suggests by implication that his symptoms were persisting.
With the overwhelming evidence of persisting headaches, contrary to his earlier denial, the plaintiff resorted to claiming that they were headaches of a different nature.
The plaintiff was unable to recall whether when presenting to nurse Gannon on 25 February 1995 he suggested that he had carbon monoxide poisoning, which is recorded as the presenting complaint on p 17 of tab 1, Exhibit P1. His attention was also drawn to a notation at p 15 of tab 1 that he had stress at work due to union pressure. He was unable to explain that notation which is in conflict with his evidence that he was not suffering from stress prior to 25 February 1995.
Reference was also made to a notation on p 15 of tab 1 which recorded that on admission the plaintiff had a mini mental score 30/30 and was not suffering from diplopia or nystagmus. The plaintiff maintained that he had difficulty balancing, and did experience the other symptoms.
The plaintiff confirmed that whilst driving the bus, the window was open; and that while sitting in it in the depot at Fremantle, both the window and door were open.
When asked to reiterate what happened when he had the spell, he stated that as he was stooping over to the side to retrieve some papers his head started to spin quite violently and he lost track of which way he was facing. He became dizzy and nauseous. He sat up again and felt faint when he went to stand up. He lay on the steps for a moment, and then using the bus for support, proceeded to the bus behind.
The plaintiff was directed to a statement allegedly made by him to the ambulance driver that he had a sudden onset of dizziness and nausea at about 1900 hours, with a loss of balance, but no disorientation loss of consciousness or collapse, and with a slight headache and cool and clammy feeling. He appears to accept that was his account to the ambulance driver.
The plaintiff accepted that when first admitted at Fremantle Hospital he told nurse Esmond that he had become dizzy, lost balance, felt faint and dopey, and become nauseated, and an ambulance had been called. He also agreed that he told her he was under some stress.

The hospital records (tab 1, Exhibit P1)

The Emergency Department Nursing Assessment form (p 3) completed by Nurse Esmond noted that the history given by the plaintiff on admission was that he had become nauseous and unwell at work. His presenting complaint was "became dizzy, loss of balance, faint, feels dopey". Her nursing assessment was that he was coherent, pale looking, and complaining of a headache. Breathing was unremarkable, and pulse rate was regular. Nurse Esmond recorded that the plaintiff indicated "he is under some stress at present".
The plaintiff was required to complete a mini mental state examination and returned a perfect score, demonstrating that he did not have cognitive difficulties.
The Department of Emergency Medicine sheet dated 24 February 1995 (p 7) recorded the plaintiff's presenting complaints of nausea, dizziness and "woolly" head; and the emergency physician, Dr Wright, recorded the following history:
"Sitting in bus about to start round when felt dizzy, weak & woolly in head. Lay down on step because felt he might faint. Rang Transperth & said he wouldn't do round, they called ambulance. Developed frontal headache on arrival in ED at 1700, now has settled. Similar episode 4/52 at home – felt dizzy, resolved."
The plaintiff was seen by Dr Banham at 2300 hours when it was recorded that he had a COHb level of 5 per cent. Dr Banham recorded that the plaintiff's onset of symptoms occurred whilst he was sitting in a bus, 20 minutes after the engine had been turned off. It seems from his notes that he considered the possibility of carbon monoxide poisoning, but concluded that carbon monoxide exposure was an unlikely cause of the presenting symptoms. In the result, however, the plaintiff was treated once with normabaric oxygen and four times with hyperbaric oxygen.
It was necessary for the plaintiff to sign a written consent to undergo hyperbaric oxygen therapy, and that document dated 25 February 1995 appears at p 11. His signature does not appear to be different from signatures appearing on Exhibits D1.1, 1.2 and 1.3 which were signed by him on 3 April 1992, 17 November 1992 and 2 February 1994 respectively. The signature appearing on an admission form dated 25 February 1995 (p 13) does appear however to have been made with an unsteady hand.
In Department of Emergency Medicine review notes (p 15) it is recorded that the plaintiff had indicated that he was under stress at work because of union pressure.
In an Emergency Department Nursing Assessment form apparently completed by nurse Gannon at about 14.10 on 25 February 1995 the following notation appears under nursing assessment:
"40yo male bus driver presented to EDFH last pm after feeling dizzy ++ & near collapse whilst in bus @ Cantonment Street Station. Discharged home. Symptoms recurred today – Has some R sided arm weakness c/- headache ++, vague in thoughts & slurred speech (not fully obvious) dizziness & leaning to right side c/- sharp central chest pain overnight, relieved spontaneously. ?Sternum damage from MVA 4 years ago."
Nurse Gannon did not give evidence, and it is not possible to conclude on the basis of the above notation whether or not she clinically detected right‑sided arm weakness or any of the other symptoms of which the plaintiff complained.
In a Hyperbaric Medicine Unit assessment and data form dated 26 February 1995 (p 33) Dr Oxer referred to the plaintiff's complaint of carbon monoxide poisoning and recorded that on examination he was "very anxious, little on examination. Can't exclude CO".

The literature

Hyperbaric Medicine Practice 2^nd ed Kindwall & Wellan

Chapter 20 dealing inter alia with carbon monoxide poisoning contains the following relevant information:
1.In the case of CO poisoning cerebral metabolism is adversely affected by reduction in the oxygen supply to tissue. Numerous mechanisms have been postulated as causing the neurologic tissue damage including arterial hypoxemia, direct cellular toxicity of CO, and reduction of cerebral blood flow. In particular it is suggested that depressed cardiovascular function induced by CO, and a limited cerebral blood flow, may be major factors leading to neurologic cellular damage from CO poisoning.
Hypoxia is the most clearly recognised aspect of CO pathophysiology. Deprivation of O2 to cells occurs in several ways. Arterial blood O2 content is decreased directly due to COHb since CO renders the involved haemoglobin unable to bind O2.
2.(i)Other than a raised COHb level and a history of exposure, there are no truly specific findings from CO poisoning which produces diverse and non‑specific clinical symptoms and signs.
(ii)The COHb level is only an indicator of exposure to CO and does not correlate well with symptoms, or with outcome.
(iii)Physical findings vary greatly in CO poisoned patients. They depend on the time between exposure and presentation at the hospital, as well as the duration of exposure and concentration of CO. The most common physical findings include tachycardia and tachypnoea.
(iv)Many factors impinge on the actual clinical presentation: the concentration of CO to which a patient is exposed; the duration of that exposure; the rate and depth of breathing; the heart rate; and, most importantly, the time between discovery of the patient after the exposure, and arrival at hospital emergency department.
3.CO levels of 1 per cent are normal, due to endogenous production. Levels of more than 5 per cent have been measured in non‑smokers exposed to engine exhaust on freeways. COHb levels above 9 per cent are experienced in heavy cigarette smokers.
4.(i)In connection with the diagnosis of the condition, the general clinical presentation in the early phase is nausea, vomiting, mental confusion, dizziness, and periods of unconsciousness.
(ii)The only specific test for CO poisoning is COHb level but that level is not a true indicator of severity of neurologic or cardiac involvement.
(iii)Neuropsychiatric manifestations of CO poisoning include non‑focal alterations in mental status, seizures, amnesia, apraxia, agnosia, Parkinsonism, cortical blindness, incontinence, and peripheral neuropathy.
5.(i)Generally patients who should be observed in the emergency department or admitted to hospital are those with a COHb level equal or greater than 25 per cent; those with a level greater than 15 per cent where there is a history of ischemic heart disease; pregnant females with a level greater than 10 per cent where the concern is about the affects of CO on the foetus; the presence of metabolic acidosis; abnormal psychometric testing; or history of unconsciousness.
(ii)Early studies have suggested that minimal symptoms were detected at COHb levels of less than 10 per cent. Tightness across the forehead and headache were experienced at levels of between 10 per cent and 20 per cent. Levels of 20 to 30 per cent resulted in a throbbing headache in the temple regions. Levels of 30 to 40 per cent produced severe headache, generalised weakness, visual changes, dizziness, nausea, vomiting, and ultimate collapse. As the levels increased to 40/50 per cent, syncope, tachycardia, and tachypnoea occurred. Levels of over 50 per cent were associated with coma and intermittent convulsions. Above 60 per cent, death occurred due to cardiac depression and respiratory failure.
(iii)It has been documented that COHb levels above 15 per cent increase the risk of myocardial infarction. A 9 per cent COHb level lowers the ventricular fibrillation threshold and also causes intermittent claudication in patients with peripheral vascular disease.
6.(i)Although hyperbaric oxygen therapy for CO poisoning was originally applied only to shorten half life of COHb and provide immediate oxygenation of the tissues, more recent research has revealed that the intra heart and cellular effects are paramount.
(ii)The half life of CO is rapidly reduced by higher oxygen concentrations; in three atmospheres of hyperbaric oxygen, the half life is 23 minutes, versus 320 minutes on air. There appears to be great variations in the half life of CO untreated.
7.Patients may appear to recover from acute CO poisoning, and then develop abnormalities from 1 to 21 days later. Included in the presentation of the delayed syndrome may be aphasia, apraxia, apathy, disorientation, hallucinations, nuchal rigidity, gait disturbances, faecal and urinary incontinence, and bradykinesia. Cognitive and neurologic deficits may also be present.
8.In the hyperbaric oxygen treated group, recurrent symptoms requiring retreatment emerged in a very small percentage, and 92 per cent returned to normal levels.

Occupational Medicine – Clinical Smoke Inhalation - Shusterman

1.Carbon monoxide produces tissue hypoxia by interacting with biological molecules and interfering with normal O2 transport or utilisation. CO exerts its toxic action by its competitive and allosteric effect on oxygen, binding with haemoglobin. Haemoglobin binds CO with over 200 times the avidity than with O2.
The decreased O2 carrying capacity of haemoglobin is probably the dominant mechanism of CO toxicity under normal circumstances.

2.The clinical manifestations of CO intoxication are many and include such non‑specific symptoms as headache, nausea, and light-headedness. The major targets of CO intoxication are the central nervous system, the cardio vascular system, and the heart. Most often the earlier symptoms of CO intoxication are referable to the central nervous system and include headache, fatigue, and light-headedness. At higher COHb levels, vasodilation – a compensory response to decreased O2 carrying capacity, produces flushing, tachycardia and lowered systemic blood pressure. With progressive increasing COHb levels, headache, light-headedness, and decreased vigilance are followed by nausea, vomiting, decreased coordination, syncope, coma, convulsion, and finally death.
3.In table 2 "Acute Health Effects of CO Exposure" it is indicated that at COHb levels below 10 per cent there are no symptoms; between 10 and 20 per cent slight headache, fatigue, and light‑headedness; between 20 and 30 per cent, moderate headache, nausea, impaired fine manual dexterity, abnormal visual evoked response, flushing and tachycardia; between 30 and 40 per cent, severe headache, nausea and vomiting, hypertension, ataxia; between 40 and 50 per cent, syncope; between 50 to 65 per cent coma and convulsions; and over 65 per cent lethal if not treated.
4.The range of neurological and neuropsychiatric findings after significant CO intoxication include not only personality and memory disturbances but also a Parkinsonian like syndrome including tremor, rigidity, and abnormal postural reflexes.
5.Persons requiring hyperbaric treatment generally include those with altered consciousness and/or documented COHb levels in excess of 25 to 40 per cent.

Occupational Medicine: Carl Zenz – Carbon Monoxide - Eric P Kindwall

1.Carbon monoxide has an affinity for the haemoglobin moiety of the blood approximately 200-300 times that of oxygen; but most importantly, it enters the tissues and attacks the cytochrome system causing clinical morbidity and eventual mortality.
Carbon monoxide produces tissue hypoxia, and along with it the expected changes in function and, if prolonged and severe, histopathologic changes that are associated with hypoxia.
2.COHb levels frequently do not correlate well with the patient's clinical appearance. A person engaged in vigorous activity will note the onset of symptoms and signs more quickly than a sedentary person. The symptoms and signs do not correlate well with the absolute level in the blood.
3.When the tissues of the body become hypoxic, the heart must supply more blood by increasing both its rate and its output. Consequently the heart should be considered the first target organ in carbon monoxide poisoning because of the necessity for increased cardiac output.
4.On the basis of present data it is impossible to state what level of carbon monoxide in the blood will produce permanent pathological changes in human beings, but:
5.Blood COHb levels below 15 per cent due to acute exposures rarely produce any symptoms; beyond 15 per cent, the patient may complain of headache and nausea; at levels above 25 per cent there may be electrocardiographic changes; and at levels of 40 per cent a person generally has a history of having been unconscious.
6.A basic rule of thumb is that persons having a COHb level of or in excess of 25 per cent require treatment in a hyperbaric chamber.

Relevant to the issue required to be determined by me, the literature establishes the following propositions of fact:
(a)hypoxia, resulting from the deprivation of 02 in the blood, thus preventing its distribution to body cells generally, is the primary consequence of CO poisoning.
(b)CO poisoning is ubiquitous and produces diverse and non‑specific clinical symptoms and signs.
(c)COHb levels up to 10 per cent are experienced quite commonly in some members of the community without the production of deleterious consequences.
(d)it is unusual to experience incapacitating symptoms when the COHb level is less than 25 per cent.
(e)residual symptoms following hyperbaric treatment are unusual, save in the case of acute poisoning.
(f)although the COHb level is not a true indicator of pathological consequences, it is indicative of expected symptoms.

Andrew Craig Harper

Dr Andrew Craig Harper practises as an occupational physician, and stated that his general work related to examining persons to assess work related problems. Dr Harper is trained as an epidemiologist in public health, and has taught and done research in that area, including assessing people suffering from chemical exposure. He stated that as an epidemiologist he had experience in looking at medical research data and clinical evidence to make an assessment of the probability of a person having a disease relating to a specific cause – what he described as evidence based medicine.
Dr Harper stated that when inhaled, carbon monoxide binds with haemoglobin reducing the capacity of the blood to transport oxygen in the body and liberate it through tissues. In addition carbon monoxide has a direct toxic effect on body cells, and can disturb the cardiovascular system affecting the effectiveness of cardiac output. He concluded that it was probable that the plaintiff had carbon monoxide toxicity as a result of exposure on 24 February 1995. That toxicity manifested itself in terms of symptoms and signs which the plaintiff experienced at the bus depot, and over the following days, some of which were residual. He described the plaintiff's symptoms as dizziness, disturbance of vision, unsteadiness, nausea, cognitive problems, difficulty with gait, upper limb disturbance, and tremulous when performing a mini mental state evaluation. He stated that the disturbed gait, tremor, and weakness of the left hand, were signs.
Dr Harper stated that the literature identified symptoms such as visual disturbance, altered manual dexterity, and headaches, as being associated with carbon monoxide poisoning, and referred to the article by Shusterman tab 9, p 477, table 2 Exhibit P1. He correctly identified that the table suggests that some of the symptoms of which the plaintiff complained were only expected to be experienced by a person with a carboxyhaemoglobin (COHb) of 20 to 30 per cent. He commented that the symptoms experienced by the plaintiff were consistent with the clinical research cited in the literature relating to carbon monoxide poisoning, but having regard to the plaintiff's level of COHb that does not seem to be correct. He acknowledged that symptoms were non‑specific and had to be looked at in their clinical context – that is by taking a global view of a patient's condition and his circumstances. He stated the most common premonitory signs of carbon monoxide poisoning were headaches, nausea and occasional breathlessness; with the subsequent development in a person remaining in a carbon monoxide atmosphere, of muscle weakness, dizziness and confusion, leading to unconsciousness.
When addressing the fact that the plaintiff's COHb level was 5 per cent, Dr Harper noted that it was indicative of the fact that the plaintiff had been exposed to carbon monoxide, and that the level would have been higher at the time of exposure. The level of COHb did not closely correlate with the clinical severity, and there were examples in the literature of markedly varying clinical states in patients exposed to carbon monoxide with high and low COHb levels. He suggested that the conclusion to be reached from the literature was that the severity of the toxicity could not be diagnosed on the basis of the COHb level. That view does not seem to accord strictly with the literature put into evidence.
The reason Dr Harper had concluded that the plaintiff suffered from carbon monoxide poisoning was:
"The development of these symptoms was in association with a source of carbon monoxide poisoning, coupled with a reading in his blood that, yes, he was exposed. He did have clinical signs of neurological toxicity, some of which have persisted, and in this man the medical practitioners caring for him have not identified any alternative diagnosis which can explain the development of these symptoms as they occurred and the persistence of them."
Dr Harper discounted a vasovagal episode, or anxiety, as providing a satisfactory basis for the plaintiff's condition, since neither would explain the subsequent development of neurological symptoms and signs.
Dr Harper examined the plaintiff on three occasions in 1995 and twice in 1996.
He disagreed with views expressed in a report by Dr Wong that there were no clinical signs of carbon monoxide poisoning stating:
"This man has had a problem which developed on the specified date and his condition was acknowledged by the treating doctors and he was treated accordingly."
Dr Harper did not consider the history of symptoms provided by the plaintiff in the workers' compensation forms to be of diagnostic consequence.
In his report dated 20 July 2000 (tab 8 Exhibit P1,) Dr Harper expressed the view that the plaintiff had carbon monoxide induced Parkinson's disease.
Dr Harper stated that at his first consultation the plaintiff referred to the fact that he was experiencing the usual type headaches in 1994, and that he commonly had headaches when driving a bus. Dr Harper stated that the plaintiff did not refer to having experienced a similar incident four weeks prior to 24 February 1995, but that he had indicated that some eight weeks earlier he had developed a headache at the end of the day's work. He agreed that the fact that the plaintiff returned a perfect score on the mini mental test demonstrated that he was alert and fully orientated, and that the 60/60 sharpened Romberg result demonstrated normal proprioception. He agreed these were objective clinical signs.
Dr Harper confirmed that hypoxia was a term applied to the condition that resulted when the binding of carbon monoxide on the haemoglobin inhibited its capacity to absorb oxygen and deliver it to body tissue; and agreed that hypoxia was a prerequisite to tissue damage. He acknowledged that the primary organs susceptible to hypoxia were the heart and brain. He accepted that he was not an authority on vascular responses to hypoxia, and did not have experience in hyperbaric and/or acute medicine. He agreed with counsel that a person suffering from hypoxia experienced an increase in pulse rate as the body attempted to adjust to the reduction in oxygen supply (tachycardia), and/or some increase in breathing rate (tachypnoea). His view was that those symptoms did not necessarily accompany carbon monoxide poisoning if the hypoxia was not of sufficient order to compromise the cardiovascular system.
Dr Harper agreed that his diagnostic approach to the issue had been to carry out some research on the question of carbon monoxide poisoning, examine reports and hospital notes, and then arrive at a conclusion regarding the probable cause of the plaintiff's symptoms. He accepted that cigarette smokers have baseline COHb levels ranging from 2 to 8 per cent. He stated that he was not aware of any literature or other information suggesting that Parkinsonism could result from cigarette smoking. He accepted that headache was one of the early non‑specific manifestations of exposure to carbon monoxide.
When it was suggested to Dr Harper that one would not expect a person with a COHb level of less than 10 per cent to experience symptoms, he seemed unwilling to respond directly, because I suspect he regarded the answer as not supporting the opinion he had advanced. He resorted to the proposition that current environmental health experience suggested that people suffered adverse physical consequences from lower exposure levels of toxins than previously thought due to the intracellular toxic effect of chemicals.
He agreed that he was not aware of any medical recording of a person with lower than 10 per cent COHb presenting with neurological sequelae, and accepted the categorisation in the literature that below 20 per cent COHb was mild, 20 to 40 per cent was moderate, 40 to 60 per cent was severe, and above 60 per cent extremely severe.
Dr Harper summarised his reasoning at T 256 as follows:
"The clinical notes have been one of a bus driver who gets the non‑specific symptoms of headache and dizziness, a bit confused, feels a bit faint, goes to the hospital and there is some degree of weakness identified on the left side. He writes his name in a very squiggly manner. He is asked at one point in the early presentation to do the mini mental assessment and he draws two polygons which were a bit out of shape and would have been the sort of ones that you would expect of, say, a 12 year old kid. Mr Margio is an artist and we see that there are signs then of some degree of loss of dexterity therefore clinically – and then we have got a COHb level of 5 per cent taken some time after he came to hospital, presumably being in clean air and having some oxygen. We therefore have a situation which is suspicious of carbon monoxide poisoning. So we begin with the symptoms, we end up with a COHb of 5 per cent and in an exploration of his clinical circumstances there wasn't an alternative diagnosis sufficiently strong to deter the clinicians in charge of his case to ultimately treat him with hyperbaric oxygen. That's the reasoning that one would go through. It's the reasoning that I have in fact gone through."
He agreed that he would have expected the symptoms to have come on at the time of maximum exposure, but was not troubled by a delay of 20 minutes between when the plaintiff stopped the bus engine and experienced symptoms. He was prepared to accept Dr Joyce's conclusion that the COHb level would have been about 7 per cent at the time of exposure. He would not accept that hypoxia was a necessary by‑product of the toxic effect of carbon monoxide, stating that it was possible to have a toxic effect at a cellular level. He considered that acidosis was more related to hypoxia than to a cellular insult.

David Anthony Joyce

Dr Joyce is the head of the department of clinical pharmacology and toxicology at the Sir Charles Gairdner Hospital; the clinical director of the drug assay and toxicology laboratory at the West Australian Pathology Centre; and Associate Professor of pharmacology at the University of Western Australia. His report of 16 August 1995 is tab 17, Exhibit P1. The report indicates that the plaintiff was seen by Dr Joyce on 26 July 1995. It appears that the plaintiff told Dr Joyce that on the day of the incident it was hot and humid, and that he began to feel off colour towards the end of the drive to Fremantle.
Dr Joyce recorded the plaintiff's history of symptoms, at the time of his examination the only abnormality detected being "a relatively coarse action tremor of the upper limbs which was absent at rest and was more prominent on the left, at least while it was being demonstrated". Dr Joyce considered that the initial symptoms described by the plaintiff were consistent with mild to moderate intoxication with carbon monoxide, although they were non‑specific, and viral illnesses, vasovagal episodes, heat exhaustion and other disorders could present an indistinguishable picture.
Dr Joyce considered that the plaintiff's COHb level at the time of exposure was probably of the order of 7 per cent, and stated that a level of 5 per cent was equivalent to that which might be achieved by the regular smoking of one packet of cigarettes per day. He said that on the balance of the evidence a blood concentration of 5 per cent of COHb suggested that an event of exposure had occurred, but that it was either at a relatively low level, or in the relatively distant past, and could reflect normal occupational exposure. It was his view that the likelihood of acute irreversible neurological damage was low in a patient who had not been poisoned severely enough to cause an alteration in conscious or intellectual state, or a disturbance in acid base balance. He agreed that carbon monoxide poisoning was recognised as producing delayed neuropsychiatric effects. He noted that the plaintiff did develop an illness for which carbon monoxide could not be excluded as causative, and which was otherwise unexplained, and therefore on balance concluded that the plaintiff had suffered carbon monoxide poisoning. On the basis that the plaintiff's neurological disorder was the result of carbon monoxide exposure, Dr Joyce expected a near complete recovery.
In evidence Dr Joyce confirmed the views expressed in his report, and I formed the view that his conclusions were to an extent a result of an acceptance of the conclusions of Drs Oxer and Bajada. He stated that having had the advantage of Dr Wong's reports, and giving the matter further consideration, he had come to the conclusion that "the evidence here is pretty knife edged".

Serge Bajada

Dr Bajada is a specialist neurologist who saw the plaintiff on referral from Dr Oxer on 9 March 1995. In his report of that date (tab 14, Exhibit P1,) Dr Bajada appears to have accepted Dr Oxer's diagnosis of carbon monoxide poisoning. Dr Bajada noted that the plaintiff claimed never to have previously suffered migraine, seizures, or giddy spells, although he had experienced a headache in the previous few months, which he attributed to injuries that he had received in an accident in 1990.
Dr Bajada noted that at the time of his examination the plaintiff was very much improved, and the only remnant symptom appeared to be an intention component tremor in the left upper limb. Dr Bajada was happy to accept that the findings were attributable to carbon monoxide poisoning, and stated that there were some features of extrapyramidal disease down the left side, and to a certain extent a cerebellar component. He arranged a CT scan, and an EEG, the results of both being unremarkable, and reported on 23 March 1995 that the plaintiff was ready to go back to work.
In evidence‑in‑chief Dr Bajada pointed out that the extrapyramidal system was that governing the fine controlling of motor function, and was the system that was affected in conditions such as Parkinson's disease. He noted that the cerebellum is the organ in the brain that controls the balancing mechanism in the body.
In cross‑examination Dr Bajada confirmed that his speciality did not involve him in the diagnosis of carbon monoxide poisoning, and as a consequence he relied upon Dr Oxer's diagnosis. He stated:
"The striking thing about this gentleman is that the signs were quite florid and the symptoms to my mind were, from a diagnostic point of view, not the important things. This man had what we call extrapyramidal disease or, in another terminology, a form of Parkinsonism."
Later in the cross‑examination Dr Bajada said:
"Here is a man who presents to me with very florid signs of extrapyramidal disease and this is manifested by the rigidity of his limbs and the tremor in his limbs and the way that he walks, all very abnormal neurologically. I then have to make a diagnostic assessment as to which category he fits into and my thinking at the time was very clearly this man does not have a straightforward Parkinson's disease. He did not fit the typical presentation of that condition."
He went on to say that finding no other cause for the extrapyramidal disease drew him to the conclusion that the symptoms resulted from carbon monoxide poisoning. When his attention was addressed to the fact that the plaintiff had a similar episode some four weeks prior to the incident he stated that he had no record of it, but that the plaintiff was an individual who would be prone to those sort of symptoms, being basically of an anxious personality type.

When pressed in cross‑examination Dr Bajada stated that the plaintiff had very clear signs observable by the examining practitioner, and that he was not basing his diagnosis on the plaintiff's complaints, but on what he found on examination. He stated that he had not been influenced by Dr Oxer's views, the position simply being that Dr Oxer sent him a person who was complaining of neurological problems, and he examined him and made the diagnosis of carbon monoxide affecting his extrapyramidal and cerebellum function.
He confirmed that he had not seen anything in the literature identifying cases where there had been the onset of neurological symptoms in a person with a COHb level of less than 10 per cent, although he pointed out that the response of individuals to toxins was individualistic, stating "we know that 60 per cent COBh for 30 minutes will kill you, but what we don't know is what happens at the bottom end".
Dr Bajada was of the view that the plaintiff had neurological signs in his limbs that were impossible to feign or to have an hysterical or functional basis. He felt that the plaintiff's features did not fit a typical young person with Parkinson's disease, leaving him with a diagnosis that fitted quite well with recorded cases of Parkinsonism following carbon monoxide exposure.

Barry David Gunn

Dr Gunn, a medical practitioner, had experience in emergency and hyperbaric medicine and had clinical experience dealing with carbon monoxide poisoning. He was asked by the Crown Solicitor's Office for an opinion as to whether the plaintiff had suffered carbon monoxide poisoning. His assessment was based upon his expertise and the medical documentation. In a report to the Crown Solicitor's Office dated 14 December 2000 (tab 24, Exhibit P1) he set out the history and expressed the opinion that the plaintiff did not have carbon monoxide poisoning because there was no loss of consciousness; neurological and psychometric examination and testing was normal; there was no metabolic acidosis; the COHb level was less than 25 per cent; and there were no changes evident on ECG. He was also influenced by the fact that the plaintiff had experienced similar symptoms four weeks earlier, had been under a lot of stress, and the symptoms of which he complained commenced 20 minutes after the bus engine was stopped. He considered that a vasovagal attack was a more likely cause for the plaintiff's symptoms.
In evidence he stated that stress could explain the plaintiff's symptoms. He stated that a carbon monoxide poisoned person would demonstrate altered neurological symptoms and signs including, if hypoxic, an increase in both heart and respiratory rate. Dr Gunn said that he would have expected symptoms to have manifested themselves at the time of poisoning. He indicated that his researches had not shown any case of someone with mild carbon monoxide exposure going on to develop Parkinsonian type symptoms.
It was put to Dr Gunn in cross‑examination that he did not possess the requisite qualifications to make a diagnosis and he disagreed pointing out that his work as an emergency medical specialist brought him into contact with people suffering from carbon monoxide poisoning. In particular he had worked with a senior registrar in a hyperbaric unit for a period of two years. He agreed that the literature identified Parkinsonism including tremor as possible neurological sequelae of carbon monoxide poisoning. He confirmed that prior to writing his report he had discussions with Dr Wong who was then director of the hyperbaric unit.
It was put to Dr Gunn that the plaintiff's presenting complaints of nausea, dizziness, loss of balance and "woolly" headiness were premonitory symptoms of carbon monoxide poisoning, to which he responded that they could be but were more likely to be symptomatic of other conditions such as a vasovagal incident. He was not prepared to accept that the plaintiff's COHb level would have been significantly higher than 5 per cent, because carbon monoxide had a long half life. He agreed that he paid no regard to the Fremantle Hospital notes subsequent to the second day of the emergency admission (that is subsequent to 25 February 1995). He agreed that a person suffering carbon monoxide poisoning need not present with all the signs of loss of consciousness, abnormal neurological signs, abnormal psychometric testing and metabolic acidosis, but stated that whilst each of them need not be present, if the position was that none of them were present there was no indication of carbon monoxide poisoning. He was prepared to accept that the unsteady drawing of two polygons might be a sign of neurological abnormality.
Dr Gunn seemed to accept that he might have interpreted the notes of the treating doctors in a manner favourable to his opinion. He also agreed that he had not seen reports from Dr Oxer stating:
"The decision of whether or not he was or was not poisoned is made by his emergency department presentation; predominantly the presentation on 24 February, his initial presentation. As an emergency physician that's when I would make my diagnosis."

Harry Frank Oxer

Dr Oxer is a specialist anaesthetist and in hyperbaric medicine. He was for a period of time the director of the Hyperbaric Medicine Unit at Fremantle Hospital, and whilst there appears to have been involved directly or peripherally in the treatment of 276 cases of carbon monoxide poisoning. With specific reference to the plaintiff, he stated that from a diagnostic point of view it was necessary to take into account the history prior to his emergency presentation, and the subsequent treatment and medical assessments. He said the literature demonstrated clearly that a person with carbon monoxide poisoning might experience secondary neurological difficulties for anything up to 30 days afterwards. He qualified this by saying that the literature showed that some people started developing signs and symptoms from one to 10 days or more after exposure to carbon monoxide.
Dr Oxer stated that his first involvement with the plaintiff was on 26 February 1995 when the plaintiff was given hyperbaric treatment. He stated that it was difficult to conclude the plaintiff's symptoms were of vasovagal origin because he still had symptoms three days after the incident. He stated that the plaintiff's presenting symptoms were consistent with carbon monoxide poisoning, and the fact that symptoms appeared to develop was not inconsistent, as the literature referred to many cases where there was delayed development of neurological symptoms following carbon monoxide exposure.
Dr Oxer referred to the mini mental test as a fairly crude assessment of cognitive function, and expressed the view that had he known of the plaintiff's fine art background he might have attached more significance to the drawing of the overlapping polygons as he would have expected the plaintiff to have performed better. That was based on an acceptance of the fact that the plaintiff was normally capable of very precise work. He also considered that the sentence written by the plaintiff "the quick brown fox jumps over the boring test" was not written with precision, although it is difficult to see why he would so conclude.
Dr Oxer expressed the view that a person could be significantly poisoned although having a quite a low level of COHb.
The hospital records, and Dr Oxer's evidence, indicate that the plaintiff did not attend the hospital on 28 February 1995 as arranged, but reattended on 1 March 1995. It appears that he telephoned the hospital on 28 February indicating that he was not experiencing balancing problems or dizziness. When seen by Dr Oxer on 2 March 1995 the plaintiff was complaining of headaches, difficulty concentrating, and floppy feet when walking, the latter symptom being observable. At that stage Dr Oxer was perplexed by the plaintiff's fluctuating condition because most people treated for carbon monoxide poisoning recovered. Dr Oxer stated that if they did not get better they either had some residual damage caused by the carbon monoxide, or there was some other reason. It was because of that view that he referred him to Dr Bajada.
I got the impression from Dr Oxer that he was having some difficulty explaining the situation on the basis of carbon monoxide poisoning, although he stated that the literature made it clear that carbon monoxide poisoned persons could develop neurological problems 1 to 10 days after exposure.
Dr Oxer exposed his reasoning by saying:
"If you have got somebody who presents, who hasn't had anything like this before, with a sudden onset of problems which include neurological problems, be they symptoms or signs, and has also been exposed to a raised level of carbon monoxide and there is no obvious other possible explanation, then the likely deduction is that the carbon monoxide has in fact caused the symptoms."
When addressing the significance of the supposed similar episode approximately a month earlier, Dr Oxer said it did not alter his opinion. That appeared to be because he was anxious to downplay the significance of what had allegedly taken place – in fact proceeded on the basis that nothing had occurred. His readiness to dismiss that event leaves me with some disquiet as to his evidence generally.
Dr Oxer's reports dated 13 April 1995 and 30 May 1995 appear as tabs 3 and 4, Exhibit P1.
In the report of 13 April 1995 he recorded that apart from a COHb level of 5 per cent on presentation, there was little else to find, save that the plaintiff was an anxious man, who came with his even more anxious mother. The report goes on to refer to the fact that the plaintiff was complaining that his feet flopped when he walked, but does not suggest that was objectively established.
In the report of 30 May 1995 Dr Oxer suggested that carbon monoxide poisoning could come on at any time following inhalation, and that he would have expected a more complete remission from symptoms after treatment with hyperbaric oxygen.
In cross‑examination Dr Oxer agreed that the literature, when referring to cases of delayed neurotoxic sequelae, were dealing with persons surviving acute carbon monoxide poisoning, but asserted that acute meant no more than "just happening and not severe". If acute is given that meaning it would seem to be inconsistent with the concept of delayed neurotoxic onset. He agreed that in the publication "Hyperbaric Medicine Practice" (2ed by Kindwall & Another) the authors asserted that "survivors of serious CO poisoning may develop neurological and psychiatric sequelae such as dementia, Parkinsonism, amnesia and depression". Dr Oxer suggested that that did not exclude such symptoms being experienced by persons with low level exposure, although clearly his experience did not seem to support the assertion. He also indicated that he tended to see people some time after admission and that by then they were not suffering tachycardia or tachypnoea.
It was put to Dr Oxer that at a party at the Parmelia Hotel on 5 September 2000 he expressed a view to Dr Wong that the plaintiff had not suffered carbon monoxide poisoning. His recollection was that he had said something to the effect that there was no way they would ever know whether he had been poisoned, although he said that his subsequent researches suggested his initial diagnosis had been correct. It was put to Dr Oxer that he had a telephone conversation with Dr Wong on 13 September 2000 when he expressed the view that Mr Margio's Parkinsonism was not due to carbon monoxide exposure. He agreed that there had been a telephone discussion, but stated that he probably expressed the view that there was no evidence demonstrating what its cause was.
Dr Oxer agreed that a smoker usually had between 3 and 10 per cent COHb following a period of smoking, but pointed out that there were documented cases where persons with levels lower than those of a smoker had undoubtedly suffered poisoning. The current approach was that the level of COHb did not necessarily correlate with the level of poisoning. He claimed to have seen patients with levels of less than 10 per cent COHb who had treatment for symptoms of dizziness, lack of balance, and lack of concentration, although it was less common.
Dr Oxer agreed that Mr Margio's complaint of flopping feet, which was probably made between the third and fourth treatments, was unusual, and that his symptom development was not what he expected to see following hyperbaric treatment.
Dr Oxer was referred to the article by Dr Kindwall at p 505 where the author stated that blood COHb levels below 15 per cent rarely produced any symptoms. He pointed out that the article was written pre‑1994 and stated that the present view seemed to be that the level of COHB was not a good indicator of the level of poisoning.
Although he agreed that the primary purpose of administering oxygen was to remove the carbon monoxide from the blood, Dr Oxer stated that it was also administered to persons who virtually had 0 levels of COHb but still had signs and symptoms, which appeared to respond to treatment. It appears that the administration of normabaric oxygen was to remove carbon monoxide from blood and hyperbaric oxygen to remove carbon monoxide from blood and tissue.
In re‑examination Dr Oxer said:
"If you have got a person who has suddenly developed symptoms and later developed signs and you have a raised carbon monoxide level and you have no other explanation of this, and carbon monoxide is known to cause neurological signs and symptoms when inhaled, I think you have to put the two together and say there is a high probability that carbon monoxide was the cause of the signs and symptoms."

Brian Robert Dare

Dr Dare is a specialist in occupational medicine and Head of the Department of Risk Management at Royal Perth Hospital. He was asked by the defendant to express an opinion as to whether the plaintiff suffered carbon monoxide poisoning, and his opinion is contained in his reports of 4 January 2001 and 12 January 2001 (tabs 26 & 27, Exhibit P1), being based on perusal of reports and medical documentation identified in his first report.
Dr Dare considered that there was no clinical evidence of carbon monoxide poisoning, stating that on admission to the Emergency Department the plaintiff was complaining of non‑specific symptoms which could relate to a myriad of medical and psychological conditions. He noted that on physical examination, and particularly neurological examination, the plaintiff was completely normal, inconsistent with a person suffering from carbon monoxide poisoning whose expected presentation would have been of altered state of consciousness, abnormal neurological examination, abnormal psychometric testing, raised heart rate, abnormalities on ECG, and a metabolic acidosis.
Dr Dare considered that too much emphasis had been placed on the plaintiff's COHb level, which he did not consider unusual for a person who had been exposed to traffic fumes in his everyday work. He reported:
"A diagnosis of carbon monoxide poisoning is based on a history of significant carbon monoxide exposure, and associated symptoms and signs such as altered consciousness, abnormal neurological and psychometric examination, metabolic acidosis, associated respiratory, blood pressure and ECG abnormalities and COHb levels greater than 25%. Mr Margio had none of the criteria to establish carbon monoxide poisoning."
In his second report he dealt with the consequences of carbon monoxide poisoning stating:
"Carbon monoxide exerts an effect on the body by binding with haemoglobin and forming COHb, and therefore decreases the amount of oxygen delivered to the tissue. However, carbon monoxide also has a direct toxic affect on cells, and it is this effect, as well as the effect of reducing oxygen delivered to the cells, whereby carbon monoxide causes its damage to tissue. There is no doubt that someone who suffered carbon monoxide poisoning could suffer transient or irreversible damage, but in the case of Mr Margio I consider there was no evidence that he had carbon monoxide poisoning, and therefore no mechanism to result in any irreversible damage."
In evidence‑in‑chief Dr Dare pointed out that research in which he had been involved demonstrated that carpark attendants working all day in a traffic environment often had levels of 10 per cent COHb, and levels of that order were not uncommon.
In cross‑examination Dr Dare stated that he had worked for the Adelaide transport authority for a couple of years and had never encountered a bus driver with carbon monoxide poisoning, pointing out that the buses were rear engined and he would not accept that a driver would get sufficient exposure to be poisoned. He agreed that although the plaintiff's symptoms were non‑specific, they were consistent with carbon monoxide poisoning. He estimated that the plaintiff's COHb level at the time of exposure could have been of the order of 7 per cent. Nevertheless he did not consider that very high for someone in an urban environment with a transport job. He pointed out that the literature suggested that one would not expect symptoms until the COHb level was of the order of approximately 15 per cent, and until that level was reached the exposure could not be described as causing poisoning, which necessarily signified toxicity.
Dr Dare said that in his view, based on the medical records, the most likely scenario was that due to stress and anxiety or a similar cause, the plaintiff felt faint and lay down at work, and that his ongoing symptoms were more likely related to ongoing stress and anxiety. He referred to the similar episode recorded as occurring about a month earlier in support of his view.

Robert Manching Wong

Dr Wong is the present Director of the Fremantle Hospital Hyperbaric Unit and has considerable experience in hyperbaric medicine and associated disciplines. He was asked by the defendant to express an opinion as to whether the plaintiff suffered carbon monoxide poisoning, and as a consequence reviewed the plaintiff's hospital file and issued reports dated 7 April 2000 and 4 September 2000 (tabs 21 & 22, Exhibit P1).
In his report of 7 April 2000 Dr Wong set out the medical history, noting the plaintiff's presenting complaints, and commenting that it was of interest that he complained of a similar episode at his home four weeks previously. Dr Wong referred to the fact that the literature indicated that COHb levels of more than 5 per cent had been measured in non‑smokers exposed to engine exhaust on freeways, and he did not consider that a COHb level of 5 per cent would in itself indicate carbon monoxide poisoning. His view was that for a diagnosis of carbon monoxide poisoning to be made, it was necessary for there to be clinical symptoms and signs of poisoning, the most common being tachycardia (fast heart rate) and tachypnoea (fast breathing rate). He stated that if the plaintiff had suffered carbon monoxide poisoning he would not have expected him to be alert and to perform the mini‑mental test and the sharpened Romberg test perfectly. He considered that delayed onset of symptoms arising from carbon monoxide poisoning was abnormal.
Dr Wong favoured a diagnosis of vasovagal attack, and thought there was a very slim chance that the plaintiff had carbon monoxide poisoning. He stated that the plaintiff's bicarbonate level did not indicate acidosis, which commonly accompanied carbon monoxide poisoning. His view was that carbon monoxide poison patients who required hyperbaric treatment usually had a COHb level well in excess of 25 per cent, and presented with an altered conscious state, positive focal neurological signs, abnormal ECG results, and an indication of metabolic acidosis, and were unable to successfully perform a mini‑mental test. Dr Wong regarded the plaintiff's presentation and regression whilst subject to treatment, inconsistent with his experience of persons suffering carbon monoxide poisoning. His view was that on the history given it was not possible to conclude that the plaintiff was suffering from carbon monoxide poisoning when he presented at Fremantle Hospital. The plaintiff's symptoms were consistent with an anxiety disorder, tension headaches and/or hyperventilation. Dr Wong reported that it was only survivors of serious carbon monoxide poisoning who developed neurological sequelae such as dementure, amnesia, depression, and Parkinsonism. He had not experienced anyone with a 5 per cent COHb level and no abnormal physical findings on presentation to hospital, who having been given hyperbaric treatment, subsequently developed neurological symptoms. Also that most patients who presented with carbon monoxide poisoning responded to treatment and recovered fully, save for those who had severe symptoms on presentation, and who had a long delay between exposure and treatment.

In his report of 4 September 2000 Dr Wong responded to Dr Harper's report, rejecting the proposition that the plaintiff suffered Parkinsonism as a neurological sequelae to carbon monoxide poisoning, and stating that the Parkinsonism was a coincidental finding. He reported:
"I do not dispute that the symptoms could also be attributed to CO exposure. However, in my experience in the management of CO poisoned patients, I've not come across anyone who has no clinical signs whatsoever, (unless one infers that all examining doctors who examined Mr Margio were incompetent and missed out on clinical signs which were easily detectable) … Mr Margio was alert and fully orientated in time and space. Mini‑mental test was 30/30, sharpened Romberg test was 60/60. All observations, BP, pulse rate etc. were normal. Clinical examination was normal. There was no loss of consciousness, no memory loss, no neurological signs. Although arterial blood gases were not done, bicarbonate level was normal, thus there was no acidosis. EGC was normal, in sinus rhythm at a rate of 68/min. … If Mr Margio was not a bus driver, I doubt if anyone would have even suggested CO poisoning as a diagnosis. … Perhaps Dr Harper could also explain the reasons why Mr Margio experienced a similar episode at home four weeks prior to his presentation at the hospital."
In evidence‑in‑chief Dr Wong confirmed that his diagnosis was based on the plaintiff's hospital file, including a report by Dr Oxer and reports from Dr Bajada. Dr Wong stated that he considered that there had been carbon monoxide poisoning when a person was exposed to it to a level such that it caused disturbance in normal physiological function. He referred to three conditions being hypoxia, cellular toxicity, and oxidation, as mechanisms in poisoning.
Dr Wong said that hypoxia was due to carbon monoxide combining with haemoglobin and not allowing oxygen to be delivered to the body. He described four types of hypoxia, stating that the one relevant to this case was anaemic hypoxia the result of a high level of COHb limiting the capacity of haemoglobin to carry oxygen. He stated that the plaintiff was not hypoxic because if he was he would have experienced tachycardia together with other signs; and if he was sufficiently hypoxic he would have metabolic acidosis (the latter being excluded by the ascertained bicarbonate level). He also pointed out that a pulse rate of 68 was totally inconsistent with hypoxia.
Dr Wong expressed the view that a person suffering carbon monoxide poisoning would experience symptoms simultaneous with the maximum exposure.
He referred to the earlier incident about which the plaintiff had allegedly complained, and speculated that it might have been indicative of idiopathic Parkinson's disease which was a progressive disorder. He pointed out that carbon monoxide induced Parkinsonism was very rare, this being confirmed by a number of research studies to which he made reference. He confirmed the view expressed in his reports that the diagnostic procedures carried out upon admission to hospital were indicative of a person unaffected by any disease or physiological or psychological disturbance, stating that the plaintiff returned a perfect score on the mini‑mental test, was alert and orientated in time and space, had a normal ECG with no tachycardia, a bicarbonate level of 25 indicating a normal acid based balance, and 5 per cent COHb. He expressed the view that if the plaintiff had carbon monoxide poisoning he should have presented with abnormal clinical signs, being slightly dizzy, return an abnormal mini‑mental test, have focal neurological findings, tachycardia, be disorientated and be unable to do the sharpened Romberg test.
Dr Wong referred to his discussions with Dr Oxer in the latter part of the year 2000 and claimed that Dr Oxer then expressed the view that the plaintiff had not been poisoned.
Dr Wong did not attach diagnostic significance to the plaintiff's polygon drawings and/or his handwriting. He was emphatic that if a person had hypoxia there would be an increased pulse rate; and probably an increased respiratory rate, stating that if the ingestion of carbon monoxide was not sufficient to compromise the cardiovascular system so as to cause an increased pulse rate, there was no potential for neurological damage.
When asked to address the presenting history of headaches, Dr Wong stated that in his experience in the management of carbon monoxide poisoning in the hyperbaric chamber, most patients presenting with headaches improved, and the headaches did not return. In the plaintiff's case he felt that the returning headache indicated that it was the result of anxiety, or another condition. Dr Wong disputed the view expressed by Dr Oxer that cardiac abnormalities were not common, pointing out that he had done a clinical audit of 78 cases and that 47 per cent of the patients had a tachycardia pulse rate over 100. He was also firm in his view that neurological signs consistent with carbon monoxide poisoning were experienced only in those who had suffered significant poisoning; and further that delayed neurological sequelae was not common and appeared to be restricted to persons who were significantly incapacitated.
In cross‑examination Dr Wong agreed that a person who suffered carbon monoxide poisoning would not necessarily have metabolic acidosis, and that persons could suffer carbon monoxide poisoning and exhibit a COHb level of less than 25 per cent. He stated that it was very unusual for a person who had suffered carbon monoxide poisoning not to have tachycardia, because the mechanism of poisoning was hypoxia, which caused tachycardia. In his experience he had not seen anyone who had CO poisoning who had not had tachycardia, although he conceded that depending upon the time that elapsed between the exposure and hospital assessment, the tachycardia may have subsided. He would not agree with the proposition that a person who suffered carbon monoxide poisoning from exposure might not necessarily get symptoms immediately, although he seemed prepared to accept that there might be some delayed neurological sequelae. He agreed that the plaintiff's presenting complaints of dizziness, loss of balance, feeling faint, dopey and nauseated, described symptoms which could be the result of exposure to carbon monoxide. He agreed that headache was also a symptom that could be related to carbon monoxide poisoning although it was also consistent with anxiety. When his attention was directed to the medical history that the plaintiff had a good night's sleep following normabaric treatment Dr Wong pointed out that it was inconsistent with poisoning, as the literature demonstrated that carbon monoxide poisoning severely disturbed sleep.

Findings

The plaintiff carries the burden of establishing on the balance of probabilities that he suffered carbon monoxide poisoning in the course of his employment on or about 24 February 1995. That involves a consideration of the expert evidence, and more particularly a weighing of the probabilities. As the Court put it in Ramsay v Watson (1961) 108 CLR 642 at 645:
"That some medical witness should go into the box and say only that in his opinion something is more probable than not does not conclude the case. A qualified medical practitioner may, as an expert, express his opinion as to nature and cause, or probable cause, of an ailment. But it is for the jury to weigh and determine the probabilities. In doing so they may be assisted by the medical evidence. But they are not simply to transfer their task to the witnesses. They must ask themselves 'are we on the whole of the evidence satisfied on a balance of probabilities of the fact'?"
That very clearly identifies my task.
I found Dr Wong's evidence and reasoning compelling and consistent with the literature. He gave his evidence clearly and carefully. It was obvious that he is a person of considerable intellect who has a broad and exact appreciation and understanding of his medical discipline, augmented by careful and thorough research of the matters about which he spoke. Further his evidence and conclusions accord with logic and commonsense.
As I have already indicated the literature, based as it is on extensive research, is eloquent of the fact that it would be very unusual for a person whose exposure to CO had been such that his COHb level was less than 10 per cent, to suffer pathological consequences. Further it demonstrates that the expectation based on medical experience is that the development of neurological and cognitive disadvantage consequent upon carbon monoxide poisoning is expected only in cases of acute poisoning where the COHb level is in excess of 25 per cent. In general it is only persons with such levels who are considered for and require hyperbaric treatment.
The cognitive assessment of the plaintiff upon presentation to the emergency department, together with the absence of tachycardia or tachypnoea, was inconsistent with acute CO poisoning; as indeed was the fact that such symptoms as he allegedly experienced were not manifest for some time after the point of a maximum exposure.
There appears to be little doubt that the plaintiff has a condition described as Parkinsonism, the cause of which is presently unidentified. The literature, together with the research experience of practitioners such as Dr Gunn and Dr Wong, did not reveal examples of persons developing Parkinsonian type symptoms consequent upon mild carbon monoxide exposure.
I have no hesitation in concluding that the plaintiff suffered a similar episode to that which caused him to present to the emergency department on 24 February 1995, approximately one month earlier. That would have been of diagnostic importance to Dr Wright and it is unlikely that his notes made on 24 February 1995 would be inaccurate. Those notes were tendered by consent, and in those circumstances I am entitled to rely on them. I reject the plaintiff's evidence that he did not mention such an episode to Dr Wright. It is probable that his denial is indicative of an appreciation by him of the fact that the previous episode raises doubt as to the validity of his contention that the incident on 24 February 1995 was connected with carbon monoxide exposure. The fact that Doctors Harper, Bajada and Oxer reached their conclusions without an appreciation and proper consideration of the diagnostic consequences of the earlier incident necessarily affects the validity of their conclusions.
There can be no doubt that the plaintiff had an exposure to carbon monoxide on 24 February 1995 but I am not satisfied on the balance of probabilities that it resulted in poisoning – that is that it had pathological consequences and was responsible for the symptoms alleged which caused him to present to the emergency department, and/or the symptoms which developed thereafter.
The preliminary question is answered in the negative.