Michael Aaron James (by his next friend Rhonda Dawn James) v Grant - [2009] WADC 201

JURISDICTION : DISTRICT COURT OF WESTERN AUSTRALIA
IN CIVIL

LOCATION: PERTH

CITATION: MICHAEL AARON JAMES (by his next friend RHONDA DAWN JAMES) -v- GRANT [2009] WADC 201

CORAM: MAZZA DCJ

HEARD: 2-5, 8-12, 15 & 17 JUNE 2009

DELIVERED : 22 DECEMBER 2009

FILE NO/S: CIV 56 of 2006

BETWEEN: MICHAEL AARON JAMES (by his next friend RHONDA DAWN JAMES)
Plaintiff
AND
CLAIRE REBECCA GRANT
Defendant

Catchwords:

Damages - Personal injuries - Brain injury - Plaintiff 27 year old man with Down Syndrome - Life expectancy - Future care requirements - Home modification expenses - Future gratuitous services - Equipment and vehicle expenses - Holiday expenses - Future medical expenses - Turns on own facts

Legislation:

Public Trustee Act 1941 s 37, s 38B, s 40
Rules of the Supreme Court 1971 O 70

Result:

Damages awarded to the plaintiff

Representation:

Counsel:

Plaintiff: Mr T Lampropoulos SC & Mr M E Herron
Defendant: Mr D R Clyne

Solicitors:

Plaintiff: Donna Percy & Co
Defendant: K N Allan

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

Malec and JC Hutton Pty Ltd (1990) 169 CLR 638
Morris v Zanki (1997) 18 WAR 260
Pettersen v Bacha (1995) 21 MVR 71
Sharman v Evans [1977] 138 CLR 563
Sosa v Carter [1978] WAR 123
Thurston v Todd [1966] 1 NSWR 321
Todorovic v Waller (1981) 150 CLR 402
Wilson v McLeay (1961) 106 CLR 523

MAZZA DCJ:

Summary

The plaintiff, who has Down Syndrome, was injured on 4 June 1997 when the bicycle he was riding was struck by a vehicle being driven by the defendant. Liability has been admitted. As a result of his injuries, the plaintiff's life expectancy has been shortened and he requires 24 hour care.
My task is to assess damages estimating as best I can a sum which is "most likely to provide fair and reasonable compensation": Todorovic v Waller (1981) 150 CLR 402 per Gibbs CJ and Wilson J at 413. In relation to the cost of accident caused expenses to be incurred in the future, reasonableness must be judged having regard to the benefits which will accrue to the plaintiff: Sharman v Evans [1977] 138 CLR 563 per Gibbs and Stephen JJ at 573.
The parties have agreed many heads of damage. Although there are a number of issues to be decided, the main issues in dispute are the plaintiff's probable life expectancy and whether the plaintiff should receive active, as opposed to passive, care at night.
I have decided that the plaintiff's probable life expectancy is 22 years and that he should have active care at night. I have made other findings concerning aspects of his future care, the provision of future gratuitous services, accommodation, equipment and holidays. I will give the parties the opportunity to consider these reasons and make calculations, where necessary, in accordance with my findings. I propose to make orders on 22 January 2010.

The plaintiff

There is no dispute about the following facts.
The plaintiff was born on 18 January 1982. At the date of the accident, he was 15 years old. He is currently 27.
The plaintiff was born with Down Syndrome. Up to now, he has lived all his life with his parents, Rhonda and Paul James. He has two older sisters, Pauline and Melissa. The plaintiff has always lived in or about the Bunbury/Harvey region. Currently he lives in Eaton, a short distance north of Bunbury. His sisters live independently in Perth.
Down Syndrome is a chromosomal disorder caused by the presence of all or part of an extra 21^st chromosome.
All individuals with Down Syndrome have some degree of intellectual and physical disability. The symptoms of aging occur earlier in people with Down Syndrome. Alzheimer's Disease will eventually affect a person with Down Syndrome and can impact 15 to 20 years before a person in the general population and as early as 40 years of age. However the data as to the precise impact of Alzheimer's Disease is very vague (T304).
The level of intellectual and physical impairment varies substantially between individuals.
The plaintiff's Down Syndrome was, prior to the accident, mild. Physically, the plaintiff was born with a small hole in his heart but this spontaneously healed. Apart from this, he experienced no real health problems. He had no history of epilepsy or respiratory disease.
In terms of his intellectual development, although throughout his school career he spent some of each school day in an education support class, he was also able to participate in some mainstream classes. He learnt to read, write and carry out basic mathematical skills. In her evidence, his mother said that at about the time of his accident, his reading, writing and mathematical abilities were about year 4 level (T157).
The plaintiff, prior to the accident, interacted well with children and was socially active. He played basketball and cricket. At the age of 9 he learnt to ride a two‑wheeler bicycle and motorcycle.
He was able to walk around his neighbourhood on an unsupervised basis and go to the local shop to buy such things as milk and bread. He was assigned and performed household chores. He would catch the school bus. By the time he was 10 or 11 he was a confident swimmer.
Before the accident, the plaintiff was able to wash, dress and toilet himself, cook simple meals and go fishing and camping with his father.
The plaintiff's parents had hoped that after he left school he would be able to enter the wider workforce and obtain employment as a shelf‑stacker, cleaner or as a trade's assistant, albeit that it was recognised that he would require supervision in whatever employment he undertook.
The plaintiff's parents had also hoped that he would leave home in due course and live independently with a friend that he met at school named Casey Sheppard. The hope was that they would share accommodation together.

The plaintiff's injuries and their consequences

These facts are not in dispute.
Immediately after the accident, the plaintiff was hospitalised at Bunbury Regional Hospital for three days. There a CT scan taken soon after his admission showed a relatively minor right frontal haematoma to the plaintiff's brain (Dr Peter Walsh 17 July 1999 Exhibit 20 p 169). This type of injury would not normally have produced significant long term problems, but for the plaintiff, it has (Professor Gubbay 2 December 2004 Exhibit 26 p 5). The exact reason or reasons for this are not precisely known. Nevertheless, it is accepted that the plaintiff's brain injury has caused serious and permanent intellectual and physical disabilities.
Shortly after the accident, the plaintiff's parents observed a marked and serious deterioration in his physical and mental health. Most notably, he began suffering from frequent and debilitating seizures, which have been categorised as follows:
1."Blank stares". These are trance like episodes which last for a short period of time but which occur frequently during each day.
2."Drop attacks" or "drop fits". These describe a seizure where the plaintiff suddenly becomes unconscious and falls over.
3."Grand‑mal seizure". This is a major seizure in which the plaintiff, if standing, collapses and where his limbs shake and his body becomes rigid.
In or about December 1997, the plaintiff was diagnosed with epilepsy. It is not disputed that the accident caused the epilepsy.
The plaintiff has suffered, and continues to suffer, epileptic seizures which, notwithstanding various medications and treatments, have proved impossible to control. The plaintiff will continue to suffer on a permanent basis from frequent epileptic seizures. The first two types of seizure can occur on a daily or almost daily basis while grand‑mal seizures occur unpredictably but less frequently, usually at night.
The plaintiff's epilepsy combined with the side effects of his epilepsy medication have resulted in the plaintiff experiencing an increased loss of coordination, reduced intellectual function, slurring of speech, difficulty in swallowing, drowsiness and lethargy, urinary and faecal incontinence and breathing difficulties.
Although the plaintiff returned to school after the accident, he was frequently absent due to his ill health and he ceased all attendance at school in about 2000.
In mid‑2001, probably as a result of aspiration of some of his stomach contents into his lungs, the plaintiff developed severe bilateral pneumonia which led to acute Respiratory Distress Syndrome and acute renal failure. His condition was life threatening and he was on life support for a period of time at Royal Perth Hospital. The plaintiff survived this ordeal and recovered his renal function, however, he did not recover his respiratory function.
After his discharge from hospital and ever since, the plaintiff has required supplementary administration of oxygen on a 24 hour per day basis. Without supplementary oxygen, the plaintiff's oxygen level desaturates quickly to a dangerous level. (Dr de Chaneet, Exhibit 20 p 34) The plaintiff's respiratory dysfunction is not as a result of lung disease, rather he suffers from an accident related condition called alveolar hypoventilation. This is a condition where a person does not breathe in enough because of an abnormality of the ventilatory control of the brain (Dr de Chaneet, Exhibit 20 p 35).
While at Royal Perth Hospital, the plaintiff contracted Methicillin Resistant Staphylococcus Aureus ("MRSA") which is a type of golden staph. The plaintiff's MRSA is chronic and requires frequent antibiotic and topical treatments. The plaintiff is also infectious and those who care for him and come into contact with him, require precautions to ensure that they do not become cross‑infected. The treatment of this condition is complicated because the plaintiff also suffers from chronic and unsightly skin inflammation and sores, particularly, on his back. Because of the risk of cross‑infection, it is necessary to carry out and maintain a rigorous regime of cleaning, washing and showering. This regime includes the plaintiff's body and any surface he comes into contact with.
In 2006, the plaintiff suffered another episode of pneumonia which, although not as serious as the episode in 2001, required him to be hospitalised (Dr de Chaneet, Exhibit 20 p 40).
The plaintiff also suffers from sleep apnoea.
The plaintiff is connected to an oxygen machine known as a concentrator during the day. The oxygen is administered to him by a Hudson mask. When the plaintiff eats or exercises, oxygen is administered by nasal prongs.
In November 2006 the plaintiff was placed on a ventilator at night which is connected to him by a full face mask. This machine was described in the evidence as a BPAP or a VPAP machine. For the sake of consistency I will refer to it as a VPAP machine. This aid has proved most effective in controlling his breathing and oxygen supply whenever he sleeps as well as his sleep apnoea. He will require it for the rest of his life.
The concentrator and VPAP machines are electrically powered. If the electricity supply fails, oxygen is administered to the plaintiff from portable oxygen cylinders. He also uses these cylinders when he leaves the house.
The plaintiff now leads a largely sedentary life and has become obese. He receives regular physiotherapy designed to help his respiratory function and maintain some level of physical fitness. The plaintiff is able to walk short distances and stay upright. I have viewed a DVD lasting approximately 55 minutes entitled "A day in the life of Michael James" which was made earlier this year (Exhibit 2). This DVD shows, amongst other things, the plaintiff performing various exercises including boxing a light‑weight static plastic target, singing and dancing a little. Although not shown on the DVD, he ,from time to time, goes to a pool and swims. As I understand it, this is in the nature of water therapy where he wades or swims with the aid of a foam "noodle" in order to build up his respiratory and muscle function.
Because of the risk of seizure, in coordination and lethargy, the plaintiff uses a wheelchair when he goes out. He has the capacity to self propel the wheelchair for short periods but usually his chair needs to be pushed by someone.
The plaintiff presently has a very basic non‑adjustable fold‑up wheelchair which is placed in a Kia Carnival van which his parents own. He also has a more comfortable, functional and adjustable wheelchair known as a Quickie Iris. This wheelchair does not fit in the Kia van.
The plaintiff is able to do very little for himself. He no longer has the relative independence of function that he had prior to his accident. It is not disputed that he requires constant care 24 hours per day 7 days per week. He must be assisted and supervised in almost every function of his life including dressing, toileting, eating and drinking, recreation and movement.
He is currently under the care of a number of health professionals including his general practitioner, Dr Lee, a neurologist for his epilepsy, Dr Walsh, a urologist for his bladder and continence conditions, Dr Yin, a consultant physician principally to manage his respiratory function, Dr de Chaneet and a specialist in infectious diseases, Dr Golledge.
In addition, the plaintiff receives physiotherapy each week and less frequent assistance from an occupational therapist, a speech pathologist, a dietician, a continence advisor, a podiatrist and another general practitioner who prescribes the plaintiff various vitamins, minerals and probiotics.
The plaintiff will require, for life, access to health professional of the type I have just mentioned and various medications, aids, and equipment to deal with his many health problems and ongoing care.
The effects of the accident have all but destroyed his quality of life. He will never be employed in the paid workforce. His life expectancy, which was reduced because of his Down Syndrome, has been further reduced.
The plaintiff is constantly at risk from the effects of choking and aspiration of his stomach contents into his lungs. This is because the plaintiff has difficulty swallowing his food and drink and also because, during epileptic seizures he loses control of his swallowing mechanism. Aspiration into the lungs can have serious and even fatal consequences because of the risk of infection. In order to alleviate these risks, since about August 2007 the plaintiff has been placed on a regime where his food is cut up into small pieces and lubricated and any fluids he drinks are thickened.
For the past 12 years, the burden of the plaintiff's care has fallen on the very capable shoulders of the plaintiff's mother. She has devoted her life to the plaintiff's welfare and has shown exceptional dedication and competence in looking after him. She has, in this regard, been assisted, when they can, by her husband and her daughters. Without doubt her work has been arduous and stressful.
Presently, the defendant's insurer, the Insurance Commission of Western Australia pays for a carer for the plaintiff for 12 hours per day. At the moment one carer, Carly Brown, cares for the plaintiff for the whole 12 hours 9 days each fortnight. On the other 5 days, two carers share the load with each carer being on duty for 6 hours.
The Disability Services Commission is providing funding for another person to work 22 hours per week. Currently that person does the cleaning and other household chores. This person does not come every day.
The plaintiff's mother provides the care at all other times, including, at night. While she does not stay with him in his room and observe him on a constant one‑on‑one basis, she gets up frequently in the night to check her son and to ensure that his VPAP mask is fitting properly.
Mrs James, at the present time, coordinates the plaintiff's carers and all his medical and other needs. She has a very detailed knowledge of her son's conditions and care requirements. She makes and records medical observations relating to his conditions. These observations are made available to the plaintiff's doctors and other health care providers, and have proved helpful to them.
Mr and Mrs James have recently completed renovations of their house in Eaton which were designed to cater for the special accommodation needs of the plaintiff and his carers. Until these renovations were completed, their house at Pratt Road Eaton was not really adequate for the plaintiff's needs.
At the time that these renovations were planned and undertaken, it was intended that the plaintiff would remain home with his parents. However, those plans have now changed. The plaintiff's mother believes it is now time for her to step back from being her son's carer. The present plan is for a project home to be built for the plaintiff close to where his parents live in Eaton and for that home to be modified for his needs.
With respect to his care, it is proposed that that be taken over by a team of paid carers coordinated by a specialist case manager with the assistance of a registered nurse.

Matters which have been agreed

Both parties have provided me with detailed schedules of damages.
All rates and costings have been agreed.
The following heads of damage have been agreed:
•Past and future economic loss including superannuation.
•Past gratuitous services.
•Past travelling expenses.
•Award pursuant to Wilson v McLeay (1961) 106 CLR 523.
•Special damages.
•Increased utility expenses incurred by the plaintiff's parents.
•General damages – agreed at the maximum amount for a most extreme case.
•Trustee expenses including MERs.
I will refer to these matters later in these reasons. Each item is subject to approval under O 70 r 10 of the Rules of the Supreme Court 1971.
It is not disputed that the plaintiff is entitled to damages in some amount in relation to the following items:
•Future medical expenses;
•Future equipment expenses;
•The future cost of thickened drinking fluid;
•The future cost of the plaintiff's bladder and bowel requirements;
•Future attendant care;
•Housing modifications and running costs;
•Holiday expenses;
•Motor vehicle expenses.
As to many of these items, the dispute will be resolved by a determination of the plaintiff's future life expectancy. However, in some of these items the defendant's position is that parts of the plaintiff's claim are not needed or unreasonable or both.

Matters in dispute

1. The plaintiff's life expectancy

The most critical issue for me to resolve is the question of the plaintiff's life expectancy. The amount of damages the plaintiff recovers will depend in large part on how long I think he will live. As most of the items in dispute relate to the cost of his future care, the longer he lives the more his care will cost. This finding will determine the 6 per cent multiplier that must be applied to the calculation of those recurring heads of damage that will be paid for life.
The task which I have to perform is an unenviable one. As will become apparent, although there was agreement as to the factors which potentially reduce the plaintiff's life expectancy and how they might most effectively be alleviated, there were significant differences of opinion between the experts on how long he might live.
All of the experts agreed that the plaintiff's life expectancy, already reduced by Down Syndrome, has been further reduced because of his accident related injuries. A number of experts emphasised how difficult the matter was and how imprecise their estimates were. Dr David Burke, a rehabilitation physician called by the defendant, described such an opinion as an "educated guess" (report 22 May 2009 Exhibit 26 p 3). Dr Eli Gabbay said at T514 that the best he could do was give an "educated estimate". Certainly, no one can say precisely for how long the plaintiff will live.

Some of the difficulties facing a trial judge deciding a person's life expectancy were starkly described by Handley JA in Pettersen v Bacha (1995) 21 MVR 71 at 71‑72:
"The trial judge was exercising an awesome responsibility in determining the plaintiff's probable life expectancy. A significant underestimate could amount to a sentence of death imposed by a civil court. On the other hand, if the judge overestimated the plaintiff's life expectancy, the result would be a windfall for others."
According to the Australian Life Tables 1997 – 1999 the ordinary life expectancy of a male person aged 27 is a further 50.59 years. However, because the plaintiff was born with Down Syndrome, his life expectancy is less then the ordinary male life expectancy.

The expert testimony relevant to life expectancy

Professor Alan Bittles, a human geneticist with a special interest in Down Syndrome, was called by the plaintiff. Since 2000, Professor Bittles has been involved in a number of studies into the life expectancy of persons with Down Syndrome. Professor Bittles said that those studies revealed that there has been "a highly significant increase in the life expectancy of people with Down Syndrome which appears to have commenced during the 1950s, with evidence of an acceleration in the life expectancy from the 1980s onwards." He went on to say that during the period between 1951 and 2000 the life expectancy of a person with Down Syndrome increased by an average of 0.94 life years per calendar year. He said that this rapid rate of increase has "probably slackened" and is no longer at this level (T300). He said that the difference in life expectancy between people with Down Syndrome and the general Australian population has narrowed to approximately 20 years.
Professor Bittles was provided with information about the plaintiff's schooling and general health prior to his accident. In his opinion the plaintiff "was very probably in the upper range of achievement for persons with Down Syndrome with mild intellectual disability (IQ range 55 to 69)". Professor Bittles also noted that the plaintiff had "relatively minor physical problems" associated with his Down Syndrome before the accident. He concluded that prior to the accident, the plaintiff would have had "a mean life expectancy of approximately 65 years". At T303, he characterised this estimate as "realistic".
Although other experts, notably Dr Buckley and Professor Gubbay, referred to shorter pre-accident life expectancies, each acknowledged that their information was out of date and deferred to Professor Bittles' expertise. Based on Professor Bittles' opinion, I estimate the plaintiff's pre‑accident life expectancy as 65 years. In other words, prior to the accident, he could have reasonably expected to live another 38 years having already attained the age of 27.
The plaintiff's case is, having regard to all of the circumstances and all of the expert opinion, that a reasonable estimate of the plaintiff's remaining life is 29 years.
The defendant's case is that the plaintiff is likely to survive another 15 to 18 years. Mr Clyne, submitted that, 18 years was a just estimate. Mr Clyne submitted that if I decided 18 years was too short, I should discount any higher figure for adverse contingencies.
I will examine, in greater detail, the expert evidence on the subject of the plaintiff's life expectancy. However, all of the expert opinion recognised that the main risks to the plaintiff's life expectancy are alveolar hypoventilation and epilepsy. In addition, other risk factors were acknowledged. The most significant of these were:
(i)respiratory tract infections generally including those caused by the spread from the plaintiff's skin infections;
(ii)the plaintiff's difficulty swallowing; and
(iii)the plaintiff's sleep apnoea.
The plaintiff's medical problems are various and complex. While each risk factor can be identified separately, I recognise that they are, to some extent at least, inter‑related. For example, during an epileptic fit, a loss of muscle control may result in the plaintiff swallowing mechanism being further compromised with an increased risk of aspiration. Another example is that the plaintiff's anti-epilepsy medication depresses his respiratory drive and so contributes to his alveolar hypoventilation.
The plaintiff has alveolar hypoventilation. It is not disputed that because of this condition, the plaintiff is at risk of developing pulmonary hypertension and consequent right heart failure.
Dr Eli Gabbay, a respiratory physician with a special interest in pulmonary hypertension was originally retained by the plaintiff to provide expert evidence in this case. In the end, he was called by the defendant. Dr Gabbay saw the plaintiff on two occasions, on 15 July 2005 and 14 May 2009.
Dr Gabbay explained that low oxygen levels caused by alveolar hypoventilation can constrict the pulmonary blood vessels from the right side of the heart to the lungs. As a result, the walls of these vessels thicken and pressure within them rises. This puts additional pressure on the right side of the heart. The right side of the heart, unlike the left side, is not used to higher pressure levels and minor elevations in pressure can cause the right ventricle to dilate. This can cause the right ventricle to fail leading to cardiac death.
Dr Gabbay said that the best way to diagnose pulmonary hypertension is by echocardiogram although, he said, by the time the condition is diagnosed it is usually quite advanced. In 2006 the plaintiff had an echocardiogram which did not reveal the existence of pulmonary hypertension.
Dr Gabbay said the best measure to lower the risk of pulmonary hypertension and consequent right heart failure was effective oxygen therapy and in particular the nightly use of the VPAP machine. While there are drug therapies, there is as yet, he said, no good data as to their effectiveness in treating the type of pulmonary hypertension the plaintiff is at risk of developing.
Dr Gabbay's opinion in 2005, before the plaintiff commenced VPAP therapy, was that there was a 60 per cent risk over 10 years that the plaintiff would develop these conditions (report 10 March 2006, Exhibit 20 p 64).
However, in light of the successful introduction and use of the VPAP machine every night Dr Gabbay's view was that the plaintiff's long term prognosis had significantly improved. Under cross-examination from Mr Lampropoulos, he said that the plaintiff's risk of developing pulmonary hypertension in the next 10 years was in the order of 30 per cent (T529). When asked about the reference period of 10 years, he said that he used that period when dealing with his patients who had undergone lung transplants and that it was easier to say what was likely to happen in 10 years compared to what was likely to happen in a year (T525). He said that once severe pulmonary hypertension is diagnosed, death from heart failure would likely occur within 5 years or so (T531). He was not asked about the risk of pulmonary hypertension developing over a period longer than 10 years.
In Dr Gabbay's report dated 12 May 2009 (Exhibit 24 - the date of this report is incorrect, the report refers to Dr Gabbay's review of the plaintiff on 14 May 2009 and so must have been written after that date) he said that the plaintiff had made good progress since he had last seen him in 2005. Dr Gabbay acknowledged that the plaintiff was receiving appropriate therapy on VPAP with supplemental oxygen. He remarked that Dr de Chaneet was in a better position than he to comment on the adequacy of the current therapy being used to control the plaintiff's alveolar hypoventilation. He made the point in this report that there was no evidence of any pulmonary hypertension or right ventricular dysfunction.
In Dr Gabbay's report dated 3 June 2009 (Exhibit 23) he said:
"The primary long term risk is the development of progressive respiratory failure and subsequent cor pulmonale with pulmonary hypertension and right ventricular dysfunction and subsequent death from progressive right ventricular dysfunction or sudden cardiac arrhythmia."
At T514 when asked to explain this, he said:
"…. – what is likely to happen with Mr James over time is that even with the best therapy, the VPAP, it's not the same as not having alveolar … hypoventilation. So he will … always, even with good therapy, not be normal. And over time, this will result in this vascular change that I was talking about earlier in the lungs' circulation. That actually is what cor pulmonale means. It means the development of pulmonary hypertension secondary to lung disease. And so, … there will be changes in Mr James' pulmonary vasculature … and progressive remodelling and constriction and progressive elevation in pressures and subsequently problems with the right side of the heart."
Dr de Chaneet, the plaintiff's treating respiratory physician, in his report dated 21 May 2009 (Exhibit 20, p 46) acknowledged that there was a risk that the plaintiff would develop pulmonary hypertension, but did not assess the chance of the condition developing. He was not asked in evidence to assess the chance in his evidence, and he did not specifically comment on Dr Gabbay's estimate as to the plaintiff's life expectancy.
With respect to the plaintiff's epilepsy, there is no question that it is severe. Despite the best efforts over a long period of time by his neurologist, Dr Peter Walsh, it has proved impossible to control and there is nothing to indicate that it will be controlled in the future.
The plaintiff's epilepsy poses several threats to his wellbeing. The first is that he may suddenly collapse and injure himself. In late 2007 the plaintiff had a seizure whilst standing beside a therapy pool and as a consequence he fell into the pool landing on his head and the back of his neck. He suffered a fracture to his neck at the T1 level which has subsequently healed. This episode is a sobering reminder of the risk of serious injury caused by the plaintiff's epilepsy. The second risk posed by epilepsy is the risk of aspiration. The plaintiff's frequent fitting could result in what Dr Gabbay described as "chronic aspiration", that is, aspiration of small amounts of stomach matter which over time damages the lung. Although the plaintiff has suffered two serious episodes of acute pneumonia, the first of which was thought to be as a result of aspiration, there is no evidence of lung damage relating to chronic aspiration. The third risk posed by the plaintiff's epilepsy, according to Professor Sasson Gubbay, the specialist neurologist called by the defendant, is an increased chance of a condition known as Sudden Unexpected Death in Epilepsy. At T567, referring to this phenomenon, he said:
"Nobody knows quite the mechanism of that. It's probably a cardiac type of death, and it occurs relatively frequently in patients with severe epilepsy who have also got other problems, such as in this case."
I now turn to the other risk factors.
Because the plaintiff's respiratory system is compromised he is generally more susceptible to common respiratory infections. The effect of those infections can be serious for the plaintiff. Dr Gabbay assessed the possible effects of respiratory infections as varying from mild to potentially life threatening. Further, the undisputed evidence of Dr Clayton Golledge, who has been treating the plaintiff on a regular basis since 2004, is that the plaintiff has, what he described as "established, very abnormal skin" (T406) and that he has chronic MRSA. Dr Golledge was of the view that the plaintiff will not be cured of his skin conditions and he will require antibiotic and topical treatment for life. Although relatively rare, MRSA can get into the lungs and cause pneumonia (T413). Further, regular antibiotic treatment can, Dr Golledge said, deplete the gut flora and render the plaintiff susceptible to super infection by drug resistant organisms (T406). Dr Gabbay said that there was a risk that sepsis from his skin lesions may spread to the lungs and cause respiratory infections (report 12 May 2009, Exhibit 24 at p 2). I accept these opinions.
With respect to the plaintiff's ability to swallow, this was assessed by Adele Beadman (now Adele Jane), speech pathologist, in July 2007. His ability to swallow was poor and he was assessed at being of high risk of aspiration and choking (report July 2007 Exhibit 18 p 16). There is no evidence and I find that the plaintiff's ability to swallow will improve. However, he has, as I have already observed, been placed on a special diet to alleviate these risks.
There is no dispute that the plaintiff suffers from mild obstructive sleep apnoea (report of Dr Carol Huang 7 November 2006 Exhibit 20 p 140). The stark risk posed by sleep apnoea is that the plaintiff will stop breathing during his sleep. Dr de Chaneet in his report dated 4 April 2006 (Exhibit 20 p 35) referred to a report given to him by the plaintiff's mother that the plaintiff had, in the past, stopped breathing at night. I find this condition is being effectively controlled by the use of the VPAP machine.
The plaintiff has received excellent medical care not just from his mother and the various medical practitioners he has consulted but from other health care professionals such as speech pathologists, physiotherapists, nurses, carers, and occupational therapists.
The various risk factors facing the plaintiff have been treated as follows.
Of all the risk factors, the one which has proved most difficult to effectively treat is, as I have already mentioned, epilepsy. Initially, the plaintiff's epilepsy was treated by his paediatrician, Dr Lawrence Hu, with the anti-epilepsy drug, Epilim. In time, the Epilim dose was increased by Dr Hu. In 1999, Dr Hu referred the plaintiff to Dr Walsh who has continued to treat the plaintiff. It is clear from Dr Walsh's reports and from his evidence that the plaintiff has been treated with various anti‑epileptic medications in changing dosages. Despite these efforts, control of the plaintiff's epilepsy remains as elusive as ever and he will remain on a regime of anti-epilepsy treatments for the rest of his life.
In relation to the plaintiff's alveolar hypoventilation, as I have already mentioned, in 2001 oxygen therapy was commenced and in late 2006, the plaintiff began using the VPAP machine. Fortunately, the plaintiff has taken well to VPAP therapy. The VPAP machine provides the plaintiff with both ventilation and oxygen. It monitors his rate of breathing and the amount of oxygen being delivered to him. Should either of these things drop below optimum level, say if there is a mask leak, the machine emits an alarm. The mask is intrusive but the plaintiff has got used to it and sleeps comfortably with it. In order for the machine to be effective, the mask must fit properly. There is a danger that the mask can be inadvertently moved during sleep through tossing and turning and its performance compromised. While the alarm will sound in the event that the machine's performance is compromised, Mrs James' evidence was that the sound of the alarm was "very light" (T111) and that sometimes the machine takes a while to sense a leak big enough to affect him (T111).
Dr de Chaneet described the plaintiff's respiratory health since he began VPAP treatment as "very stable" (report 21 May 2009 Exhibit 20 p 46). Dr Gabbay, the defendant's respiratory physician, having initially expressed doubts about the plaintiff's ability to tolerate the VPAP therapy, frankly admitted in his evidence that he had been wrong about this and agreed that VPAP therapy has resulted in "good control of his alveolar hypoventilation" (report 12 May 2009 Exhibit 24).
While it is true that the plaintiff's current treatment regime is keeping his respiratory function stable, I find he nevertheless remains at risk of developing pulmonary hypertension and right heart failure as a result of his alveolar hypoventilation. Dr de Cheneet in his report dated 21 May 2009 expressly recognised the risk. Dr Gabbay said in his report dated 12 May 2009 that even with control of the plaintiff's alveolar hypoventilation with VPAP therapy, he remains at risk of the development of pulmonary hypertension and right sided heart failure. Professor Gubbay said under cross‑examination that while the plaintiff's respiratory condition was stable, it is nevertheless, as he put it, "fairly severe" (T578).
In relation to the plaintiff's risk of contracting respiratory tract infections, he will always be at risk of contracting such infections. Dr Gabbay's evidence was that as the plaintiff's respiratory disease progresses he will become susceptible to infections which may not currently affect him (T517). What effect any individual infection will have on the plaintiff is difficult to predict. A factor which is likely to impact on this is his level of care and the effectiveness of any antibiotic therapy prescribed to him. Plainly, proper care and effective drug treatment will reduce the risk posed by respiratory tract infections but the risk can never be eliminated.
With respect to the risk of respiratory tract infection caused by a spread from the plaintiff's skin infections, I am satisfied that the plaintiff is being well cared for in this regard as a result of the meticulous cleaning regime of the plaintiff's body and his home. In addition, the plaintiff is receiving and will continue to receive appropriate topical treatments and regular antibiotic treatment. These will alleviate, but not completely eliminate, the risk to the plaintiff's respiratory health posed by the spread of his skin infection to his lungs.
In relation to the plaintiff's difficulty swallowing, the aspiration controls which I have already mentioned along with measures to ensure that the plaintiff regularly coughs and keeps his airways and lungs clear will, in my opinion, reduce the risk posed by aspiration. Nevertheless, the risk cannot be eliminated. The danger posed to the plaintiff's health as a result of aspiration cannot be underestimated. Aspiration can, as I have already mentioned, result in choking or can trigger an episode of pneumonia. This risk has been further reduced by the plaintiff being watched whenever he eats and drinks. However, aspiration may occur during an epileptic seizure at a time when the plaintiff is not being watched or asleep. As Dr Gabbay put it in his report dated 14 April 2008 (Exhibit 20 p 67):
"there is the risk of a significant respiratory infection with aspiration of gastric or other content during an uncontrolled epileptic seizure. Such an infection could prove fatal but the risk that this will develop is not predictable."
In relation to the plaintiff's sleep apnoea, this condition seems well controlled by the VPAP machine. While the plaintiff's sleep apnoea remains a risk to the plaintiff, I do not think it poses a great risk to his life expectancy.
I will now outline the expert evidence estimating the plaintiff's life expectancy.
Dr Stephen Buckley, a rehabilitation specialist called by the plaintiff, estimated that the plaintiff could expect to live another 32.64 years. He said that he thought the plaintiff's expected pre-accident life expectancy was 64 years of age. He noted that the plaintiff was presently 27. Accordingly, he said, the plaintiff could have expected to live another 37 years pre-accident. He said that he would deduct from that 37 years, 2 per cent to take into account the plaintiff's epilepsy which amounts to a deduction of 0.74 years. After making that deduction, the plaintiff, he said, could expect to live for another 36.26 years. From this, Dr Buckley would deduct a further 10 per cent to take into account the plaintiff's respiratory problems. This amounts to another 3.62 years. This leaves, on Dr Buckley's estimate, the plaintiff with an expectation that he will live another 32.64 years.

While I acknowledge Dr Buckley's expertise in the area of rehabilitation medicine, he is not an expert with respect to either epilepsy or respiratory medicine. I do not accept his estimate of life expectancy. I think he has underestimated the effects of epilepsy and the plaintiff's respiratory problems.
Dr Walsh's evidence about life expectancy was, quite properly having regard to his specialty, restricted to the adverse effects of epilepsy. He deferred to the opinion of Dr Gabbay as to the influence the plaintiff's respiratory problems had on his life expectancy. Dr Walsh noted an article in the respected journal "Brain" published in 2004 which, based on a UK study, suggested that a person who develops epilepsy as a result of trauma at about the age of 15 years and who is still alive 12 years later could expect a reduction of normal lifespan of approximately 6 years. Dr Walsh, noted that the plaintiff's pre-accident lifespan was limited by his Down Syndrome to between 60 and 65 years. He thought it was reasonable to think that the plaintiff's epilepsy might shorten his life expectancy to approximately 55 to 60 years of age (report 22 May 2009 Exhibit 20 pp 186‑187, T349‑351).
Dr de Cheneet did not offer a precise opinion as to the plaintiff's life expectancy. In his report dated 14 November 2006 (Exhibit 20 p 39):
"With luck and good management, Michael's life expectancy may be many years however, unfortunately, it would only take one episode of intractable seizures with respiratory complications to end his life."
Dr David Burke, a rehabilitation physician called by the defendant, said in his initial report dated 22 April 2008 (Exhibit 26) that on the basis that the plaintiff's pre-accident life expectancy was approximately 50 years, this had been substantially reduced because of his accident related epilepsy and respiratory dysfunction. In his later report dated 25 May 2009, he said:
"The reduction in life expectation of patients due to severe epilepsy and pulmonary disease is outside my area of expertise."
He went on to say that, in his view, the opinions of specialist neurologists and respiratory physicians should carry the most weight because they are the areas which have the most impact in the assessment of the plaintiff's life expectancy. I accept this opinion.
Dr Gabbay has consistently expressed difficulty in estimating the reduction in the plaintiff's life expectancy due to all the plaintiff's respiratory problems including alveolar hypoventilation.
In his report dated 12 May 2009, at p 2, he identified the risks of respiratory tract infections, alveolar hypoventilation and sepsis from his skin infections spreading to the plaintiff's lungs as the most significant respiratory problems which potentially threaten his life. He concluded at p 3:
"As frequently stated, I am not in a position to comment on Mr James' life expectancy from his brain injury, epilepsy or Down Syndrome.
The risk from a respiratory cause of death is significant, but his life expectancy is difficult to estimate. I believe that taking into account the potential respiratory problems, a reasonable estimate of Mr James' median life expectancy would be in the order of a further 18-23 years of life."
In other words there is a 50 per cent chance the plaintiff will live shorter than this period and a 50 per cent chance he will live longer (T535).
Dr Gabbay provided a further report to the defendant's solicitors dated 3 June 2009 in which he was somewhat less optimistic of the plaintiff's life expectancy expressing the median life expectancy of the plaintiff to be an additional 15 to 20 years. The change in his opinion was caused by Dr Walsh's opinion in his report dated 22 May 2009 which confirmed that the plaintiff's epilepsy was unlikely to ever be controlled and his perusal of the Sir Charles Gardiner Hospital file relating to the plaintiff's admission in 2006. In that file Dr Gabbay noted a significantly elevated CO² level in a test done on the plaintiff on or about 31 October 2006 which lead him to believe that the plaintiff's respiratory function was worse at that time than he had first thought. However, in cross-examination when referred to other CO² readings he accepted that the elevated reading could have been a mistake and he returned to the estimate of median life expectancy, having regard to his respiratory function, as being 18 and 23 years (T545). He said that in medical terms the difference between 15‑20 years and 18‑23 years was "a pretty minor change" (T540).
Dr Gabbay agreed with the proposition put to him in cross‑examination the longer that a person survives after a condition has developed the greater is the chance that he will live beyond the median expectation (T546).
Dr Michael McComish, consultant physician, did not give evidence at trial but his report dated 17 March 2009 (Exhibit 20 p 155) was by consent tendered in evidence pursuant to s 79C of the Evidence Act. With respect to the plaintiff's life expectancy, in his opinion, the plaintiff's pre‑accident life expectancy was 64 years. He identified the main risk factors which will threaten his life expectancy as alveolar hypoventilation, epilepsy and "his overall neurological impairment". In his report, he said that a 10 per cent reduction to something like 58 years for his respiratory condition would be a reasonable estimate. He said that he agreed with an earlier opinion of Dr Walsh that only a small reduction in his life expectancy should be made for epilepsy. He said that the plaintiff's neurological impairments reduce further "but slightly" his life expectancy. Dr McComish said that "to ensure the best outcome [with respect to life expectancy] Michael James will require permanent care of the sort that he has obtained from his parents and others since the accident." He went on to say "there is a clear correlation between the level of care and life expectancy … but I doubt there would be any gain from increasing the level of care from that which he is receiving at present…".
Dr Ong, who was the plaintiff's general practitioner and who treated him for almost 10 years said in his report dated 13 November 2006 Exhibit 20 p 168 that the plaintiff's life expectancy has been considerably shortened, but he was unable to give a figure as to the plaintiff's post‑accident life expectancy.
Professor Gubbay, a neurologist, was called by the defendant. Professor Gubbay has provided five reports dated 22 August 2000, 16 August 2002, 2 December 2004, 7 April 2009 and 12 May 2009. These reports are all contained in Exhibit 26. Professor Gubbay saw the plaintiff on 22 August 2000 and on 2 December 2004. Professor Gubbay has not seen the plaintiff since then and is not his treating neurologist.
In his report dated 2 December 2004, he estimated that the plaintiff's epilepsy and respiratory failure "might mean that his life expectancy might be as short as a further 5 to 15 years. This figure could well be modifiable by a respiratory physician who would have some estimate of prognosis". This estimate was given on the erroneous assumption that the plaintiff's pre-accident life expectancy was 50 years.
In his report dated 7 April 2009 Professor Gubbay said:
"Unlike Dr Buckley I believe that his severe seizures for which he had been taking multiple anticonvulsant drugs are likely to cause a much more significant reduction of life expectancy then 2 years. Evenmoreso (sic), I believe that his respiratory insufficiency is likely to be the most important of all his life limiting factors. It is not really pertinent to subtract the reduced life expectancy from epilepsy together with the reduced life expectancy from respiratory insufficiency from his already reduced life expectancy from Down Syndrome. Rather it is that we should consider his life expectancy as of now to be reduced by a combination of his epilepsy and his non-accident related respiratory insufficiency. This then needs to be compared with a background life expectancy which Professor Bittles believes is possibly as long as 65 years.
Like Dr Buckley I seek clarification in regard to the reduced life expectancy resulting from respiratory failure.
Michael James is now aged 26 years. When taking all these matters into consideration I think it is likely that there will be a reduction of his life expectancy by 15 to 20 years ie that there would be a 50 per cent chance of his survival to the age of 45 or 50 years.
It is hardly scientific to quote accurate figures of life expectancies for the two factors which are operative in this regard namely severe epilepsy and respiratory insufficiency then subtract the sum from the life expectancy that might have been applicable before the motor accident. One can only provide a general estimate according to one's experience in his or her own area of expertise.
Overall my opinion in this matter has only been modified by the rather higher then expected life expectancy of uncomplicated Down Syndrome as expanded by Professor Bittles. However life expectancy is likely to be much shorter as described above when taking into consideration his severe epilepsy and respiratory insufficiency."
The effect of Professor Gubbay's opinion on life expectancy was that, he like Dr Gabbay, thought his median life expectancy was between 18 and 23 years. Although Dr Gabbay's estimate was with regard to the plaintiff's respiratory problems only.
In evidence-in-chief, Professor Gubbay explained the first paragraph of this extract. He said that risk factors have a negative effect on each other so that their combined effect is greater than a simple accumulation of their negative effect. He described this effect as geometric rather than arithmetic (T573-4). Professor Gubbay's expertise is the field of epilepsy. He has, and claimed, no expertise in respiratory medicine. It was evident in cross-examination that Professor Gubbay, while having some appreciation of the plaintiff's respiratory condition, did not have the detailed knowledge either Dr Gabbay or Dr de Chaneet. Further although he assumed that the plaintiff was receiving a modified diet, exercise and physiotherapy he had not been made aware of these developments. Nor was he aware that the plaintiff had been successfully using the VPAP machine. Finally he had not seen the plaintiff since late 2004.

Plaintiff's submissions on life expectancy

Mr Lampropoulos submitted that epilepsy and alveolar hypoventilation, if it develops into pulmonary hypertension, are the main threats to the plaintiff's life expectancy.
As to the appropriate method of assessing the plaintiff's life expectancy, Mr Lampropoulos submitted that I should not look at each risk factor in isolation, assess its reduction in life expectancy and then add those reductions. Mr Lampropoulos submitted that to do so would be, as he put it, to double or triple discount the same risk factor because the risk factors overlap.
However, Mr Lampropoulos submitted that I should not, as Professor Gubbay suggested, multiply the effects of the risk factors. On this point, he submitted that a possible geometric effect was not put to other medical witnesses and Professor Gubbay was mostly in the dark about the precise nature of the plaintiff's respiratory condition and had not seen the plaintiff for a long time.
Mr Lampropoulos submitted that I should take what he described as "an holistic approach" rather than focus on statistical and medical judgments alone.
With respect to alveolar hypoventilation, Mr Lampropoulos pointed to the unchallenged evidence that the plaintiff had not yet developed pulmonary hypertension and there was no evidence of heart problems. Mr Lampropoulos submitted that there were positive developments in respect of this condition in recent years. In 2001 oxygen therapy was commenced. In 2006, VPAP therapy commenced which the plaintiff tolerates well. In addition to these measures, Mr Lampropoulos pointed to the exercise and physiotherapy regimes and aspiration controls which have been put in place for the plaintiff's benefit, and Dr de Chaneet's opinion that the plaintiff's respiratory health had been very stable since the introduction of VPAP.
Mr Lampropoulos drew my attention to Dr Gabbay's evidence that the risk of the plaintiff developing pulmonary hypertension was in the order of 30 per cent in the next 10 years. He submitted that, in effect, this meant that it was not probable that the plaintiff would develop pulmonary hypertension in that time.
With respect to epilepsy, Mr Lampropoulos submitted that there should only be a modest reduction in relation to its possible effects upon the plaintiff. Mr Lampropoulos submitted that the greatest risk with respect to epilepsy was aspiration as a result of an epileptic fit. Mr Lampropoulos submitted that quality care for the plaintiff would minimise the risk that aspiration poses to the plaintiff.
Mr Lampropoulos referred me to the evidence of Drs Walsh, Buckley and McCommish whom, he submitted, suggested that epilepsy has only a small negative effect on the plaintiff's life expectancy.
Mr Lampropoulos recognised that Professor Gubbay thought that the effect that epilepsy had a greater effect reducing the plaintiff's life expectancy however, he submitted that I should not accept Professor Gubbay's opinion because he had not seen the plaintiff for five years and did not have sufficient knowledge of the plaintiff's overall health.
Mr Lampropoulos submitted that although Dr Gabbay believed that the plaintiff's median further life expectancy was between 18 and 23 years, it was more likely that the plaintiff would have a better life expectancy than this median range, having regard to the plaintiff's stable respiratory health and the high level of care he could expect in the future. Mr Lampropoulos submitted that the plaintiff had survived 12 years since the accident, so he had a greater chance of living beyond the median expectancy. Mr Lampropoulos noted the opinions of Dr Buckley and McCommish as to the plaintiff's life expectancy were more optimistic then Dr Gabbay.
Having regard to all of these things, Mr Lampropoulos submitted that I should assess damages on the basis of a further life expectancy of 29 years.

The defendant's submissions on life expectancy

Mr Clyne submitted that I should accept Dr Gabbay's evidence which he said was to the effect that leaving aside epilepsy, the plaintiff's life expectancy having regard to alveolar hypoventilation and its consequences alone was between 18 and 23 years.
Mr Clyne submitted that there was no evidence to the contrary. Mr Clyne referred to Dr de Chaneet's evidence in particular and noted that he did not provide a contrary opinion.
Mr Clyne placed particular emphasis upon Dr Gabbay's report dated 14 May 2009 where he identified the significant respiratory risks faced by the plaintiff.
Mr Clyne submitted that the starting point in terms of life expectancy is 18 to 23 years as proffered by Dr Gabbay having regard to his alveolar hypoventilation only. Mr Clyne submitted that other risks, most notably epilepsy, but also sleep apnoea, recurrent respiratory infections and MRSA further reduce the plaintiff's life expectancy.
Mr Clyne submitted that the plaintiff's epilepsy was serious and referred me to the evidence of Dr Peter Walsh and in particular his report dated 22 May 2009 and to the evidence of Professor Gubbay.
Mr Clyne submitted that having regard to the starting point set by Dr Gabbay based only on the plaintiff's alveolar hypoventilation and taking into account all the other risk factors, the plaintiff's likely life expectancy was a further 15 to 18 years. Mr Clyne said that the defendant's position was, erring on the side of conservatism, that the plaintiff was likely to live another 18 years. Mr Clyne submitted that I should assess the plaintiff's life expectancy on the basis of Professor Gubbay's evidence that the various risk factors have a geometric effect.
Mr Clyne submitted that all calculations of future loss should be subject to a reduction of 10 per cent to allow for negative contingencies. Mr Clyne submitted that this was required to recognise the risk that each and everyone of the conditions which threaten the plaintiff's life could cause his demise at any time and that from the age of 40, by virtue of his Down Syndrome, he will develop Alzheimer's Disease. Mr Clyne submitted that if I come to the view that the plaintiff has a longer life expectancy than 18 years, a higher figure for negative contingencies should apply.

Legal principles relating to life expectancy

It is impossible to predict with mathematical or scientific precision the plaintiff's life expectancy. I must approach the task of predicting the plaintiff's life expectancy having regard to the principles laid down by the High Court of Australia in Malec and JC Hutton Pty Ltd (1990) 169 CLR 638. In that case, Deane, Gaudron and McHugh JJ said at 642‑3:
"A common law court determines on the balance of probabilities whether an event has occurred. If the probability of the event having occurred is greater then it not having occurred, the occurrence of the event is treated as certain: if the probability of it having occurred is less then it not having occurred is less than it not having occurred, it is treated as not having occurred. Hence, in respect of events which have or have not occurred, damages are assessed on an all or nothing approach. But in the case of an event which it is alleged would or would not have occurred, or might or might not yet occur, the approach of the court is different. The future may be predicted and the hypothetical may be conjectured. But questions as to the future or hypothetical effect of physical injury or degeneration are not commonly susceptible of scientific demonstration or proof. If the law is to take account of future or hypothetical events in assessing damages, it can only do so in terms of the degree of probability of those events occurring. The probability may be very high – 99.9% - or very low – 0.1 %. But unless the chance is so low as to be regarded as speculative – say less then 1% - or so high as to be practically certain – say over 99% - the court will take that chance into account in assessing the damages. Where proof is necessarily unobtainable it would be unfair to treat as certain the prediction which has a 51% probability of occurring, but to ignore altogether a prediction which has a 49% probability of occurring. Thus, the court assesses the degree of probability that an event would have occurred, or might occur, and adjust its award of damages to reflect the degree of probability. The adjustment may increase or decrease the amount of damages otherwise to be awarded."
Brennan and Dawson JJ agreed with the judgment of Deane, Gaudron and McHugh JJ and added at 640:
"…we think it undesirable for damages to be assessed on the footing of an evaluation expressed as a percentage. Damages need not be assessed by first determining an award on the footing that the hypothetical situation would have occurred and then discounting the award by a selected percentage. Damages founded on hypothetical evaluations defy precise calculation."
My task is to estimate the plaintiff's life expectancy, already reduced by Down Syndrome, having regard to the various accident caused risk factors which confront the plaintiff along with the measures which have been taken and which will be taken, as far as I can predict, to deal with these factors and his overall care into the future. I must, approach this task paying careful attention to the expert evidence. However, I am not bound to accept one or other opinion of life expectancy. In Thurston v Todd [1966] 1 NSWR 321 each of the presiding appeal judges, Wallis P, Jacobs and Holmes JJA, made the point that the learned trial judge, in that case, was not bound to select one of a number of conflicting opinions as to the plaintiff's life expectancy. It was said that having regard to the imprecise and somewhat speculative nature of predicting life expectancy, it was open to the trial judge to make his own judgment on the matter, having regard to all of the circumstances including the expert medical evidence.

Fund managers charge a fee for this expertise. This fee is levied against the entire fund under management and is deducted from the fund before any benefit is paid to an investor. This fee is called an MER, which is an acronym for Management Expense Ratio. An MER is the percentage of funds under management levied as fees by a fund manager. It is not a fee levied by or against the Public Trustee. The return to the Public Trustee is net of the MER.
There is controversy about whether MERs should be paid by the defendant or should be an expense shouldered by the plaintiff. There are arguments both ways and no binding decision has been delivered.
The defendant has offered $350,000 by way of Public Trustee's fees but makes no offer with respect to MERs. If MERs were awarded the total amount of the Public Trustee's fees and MERs would be substantially more than $350,000. The defendant's position is if the plaintiff does not accept the $350,000 which has been offered it will seek to further litigate the entire issue of fees on the basis that the plaintiff's need for fund management and investment advice was caused not by the accident but rather by his pre‑existing Down Syndrome.
The parties' position is, rather than litigate the issue, they wish me to approve the sum of $350,000 as a sum which represents an amount for all fees whether levied by the Public Trustee or MERs.
In my view this is appropriate. This litigation should be finalised not prolonged. The parties have fully considered their positions. It is to the plaintiff's benefit for the matter to be resolved without litigation and the sum of $350,000 is not, in all of the circumstances, unreasonable.

Summary of findings

1.Damages should be assessed on the basis that the plaintiff will live to the age of 50 years, that is, another 22 years calculated from his next birthday [172].
2.As the plaintiff's case:
(a)A case manager will be required to work 8 hours per month for the first three months and 4 hours per month thereafter [178].
(b)A registered nurse will be required to work 10 hours per week [186].
(c)A multi‑skilled carer will be required to work 4 hours per day 7 days per week [189].
(d)The plaintiff will require 24 hour care from a carer on an active basis [209].
(e)Multi‑skilled carers and the plaintiff's personal carers require 6 hours of education per year based on a roster of nine staff [215].

3.As to home modification expenses:
(a)The total sum I allow for the provision of extra internal and external space and the carer's room and bathroom is $158,800 [226], [232] and [233].
(b)The total sum I allow for other housing modifications is $44,900 [249] and [250].
(c)I allow $30,555 for professional fees with respect to the building modifications in (a) and (b) above [251].
(d)I disallow the claim for the swimming pool and spa [264].

4.As to future gratuitous services to be provided by Mrs James I allow 2 hours per week [273].
5.As to holiday expenses I allow $60,000 [285].
6.As to equipment and motor vehicle expenses:
(a)The plaintiff requires two wheelchairs, the Quickie Iris and the Glide Series 6 electric wheelchair. The Quickie Iris will need to be replaced every 5 years and the Glide Series 6 every 7 years [300‑301] and [310].
(b)The plaintiff requires a VW Crew Van modified for his needs to be replaced every 5 years [307‑9].

7.As to future medical expenses:
(a)GPs consultations to be costed at $99 per visit [313].
(b)Dr Walsh's consultations to be costed at $93 per visit [314].
(c)I disallow the claim for visits to a respiratory physician in addition to Dr de Chaneet [315].
(d)Dr Golledge's consultations to be costed at $110 per visit [316].
(e)The claim for the vitamins, minerals and probiotics prescribed by Dr Bullen is allowed [320].

8.As to the items agreed at the outset of the trial I approve them pursuant to O 70 r 10 of the Rules of the Supreme Court 1971. Specifically I approve the amount for trustee's fees including MERs at $350,000.

I will hear the parties with a view to the filing, prior to 22 January 2010, of a schedule of damages in accordance with my finding. I will also hear the parties with respect to costs.