Clark v Tieman Industries Pty Ltd
[2011] VSC 500
•4 October 2011
| IN THE SUPREME COURT OF VICTORIA | Not Restricted |
AT MELBOURNE
COMMON LAW DIVISION
PERSONAL INJURIES LIST
S CI 2010 05920
| JOHN CLARK | Plaintiff |
| v | |
| TIEMAN INDUSTRIES PTY LTD | Defendant |
---
JUDGE: | KYROU J | |
WHERE HELD: | Melbourne | |
DATES OF HEARING: | 19-23 September 2011 | |
DATE OF JUDGMENT: | 4 October 2011 | |
CASE MAY BE CITED AS: | Clark v Tieman Industries Pty Ltd | |
MEDIUM NEUTRAL CITATION: | [2011] VSC 500 | |
---
ACCIDENT COMPENSATION – Workplace injuries – Negligence – Breach of statutory duty – Liability admitted – Assessment of damages – Principles for assessing loss of earning capacity – Relationship between pre-existing cirrhosis of the liver and effects of the workplace injuries.
---
| APPEARANCES: | Counsel | Solicitors |
| For the Plaintiff | Mr T J Casey QC with Mr D J Hancock | Arnold Thomas & Becker |
| For the Defendant | Mr J R Moore QC with Ms R L Kaye | Lander & Rogers |
TABLE OF CONTENTS
Introduction and summary....................................................................................................... 1
Evidence and assessment of witnesses.................................................................................. 2
Mr Clark’s personal and work history prior to the accident................................................ 3
Mr Clark’s alcohol consumption prior to the accident......................................................... 4
Mr Clark’s health prior to the accident.................................................................................. 7
Circumstances of the accident................................................................................................. 9
Non-contentious medical evidence......................................................................................... 9
Physical injuries sustained in the accident and hospitalisation until March 2008........... 9
The course of the physical injuries between March 2008 and trial................................. 11
The course of the pre-existing conditions between 15 December 2007 and trial........... 13
Psychological consequences of the accident..................................................................... 15
Mr Clark’s alcohol consumption since 15 December 2007................................................ 15
Mr Clark’s mobility and quality of life since 15 December 2007..................................... 15
Contentious medical evidence.............................................................................................. 17
The cause of Mr Clark’s cirrhosis of the liver................................................................... 17
Effect of the physical injuries on the pre-existing conditions.......................................... 20
Effect of the pre-existing conditions on Mr Clark’s life expectancy................................ 21
Effect of the pre-existing conditions on Mr Clark’s work capacity................................. 22
Assessment of Mr Clark’s damages..................................................................................... 29
Pain and suffering.............................................................................................................. 29
Loss of earning capacity.................................................................................................... 30
General principles for assessing loss of earning capacity........................................... 30
Assessment of past economic loss............................................................................... 33
Assessment of future loss of earning capacity............................................................ 35
Fox v Wood.................................................................................................................. 36
Proposed order........................................................................................................................ 36
HIS HONOUR:
Introduction and summary
The plaintiff, John Clark, claims damages from the defendant, Tieman Industries Pty Ltd (‘Tieman’) for injuries he sustained on Saturday 15 December 2007 as a result of a fall from the back of a truck in the course of his employment with Tieman (‘accident’). Mr Clark relies on two causes of action: negligence, and breach of statutory duty constituted by alleged breaches of regs 3.3.3 and 3.3.4 of the Occupational Health and Safety Regulations 2007.
Mr Clark was assessed as having a ‘serious injury’ for the purposes of s 134AB of the Accident Compensation Act 1985 (‘Act’). He has brought this proceeding in accordance with that section.
The proceeding was originally listed for trial by jury. At the commencement of the trial, I made an order by consent that the trial proceed as a cause. On the second day of the trial, Tieman admitted liability in respect of both causes of action and the hearing proceeded as an assessment.
On the last day of the trial, Tieman conceded that the orthopaedic injuries that Mr Clark suffered at the time of the accident and their effects:
(a) permanently incapacitated Mr Clark from any work; and
(b)permanently aggravated Mr Clark’s pre-existing cirrhosis of the liver (damage to the liver tissue).
At the same time, Tieman abandoned the defence of contributory negligence.
For the reasons that follow, I have assessed Mr Clark’s damages at $532,270, comprising:
(a) General damages: $300,000
(b) Loss of earning capacity – past: $177,700
– future: $ 30,400
(c) Fox v Wood component: $ 24,170
Total: $532,270
Evidence and assessment of witnesses
The only lay witnesses were Mr Clark and his wife, Nancy Clark.
Mr Clark was an honest witness but his evidence was not entirely reliable. Many of his answers were vague and some were contradictory. He could not recall the details of many events and said that he could not remember dates. His memory appeared to be impaired. I formed the clear impression that he understated his levels of alcohol consumption. Where Mr Clark’s evidence about his alcohol consumption was inconsistent with contemporaneous histories that he or Mrs Clark gave to medical practitioners, I prefer the histories.
Mrs Clark was an honest witness. Her memory was better than Mr Clark’s memory, assisted as it was by her diary notes. As Mrs Clark was not cross-examined, I accept her evidence on all issues other than in relation to Mr Clark’s alcohol consumption and medical conditions. Where her evidence about Mr Clark’s alcohol consumption was inconsistent with contemporaneous histories that she or Mr Clark gave to medical practitioners, I prefer the histories. Where her evidence about Mr Clark’s medical conditions and their effects was inconsistent with the medical evidence, I prefer the medical evidence.
Mr Clark called the following medical witnesses:
(a) Dr Michael Huang, Mr Clark’s general practitioner since 2007;
(b)Dr Raouf Bassily, Mr Clark’s treating gastroenterologist from July 1999 until August 2010;
(c)Dr Peter Pritchard, Mr Clark’s treating gastroenterologist and hepatologist from September 2010;
(d)Dr John Colman, a consultant gastroenterologist and hepatologist; and
(e) Mr Stanley Schofield, a consultant orthopaedic surgeon.
Mr Clark tendered medical reports of Dr Huang, Dr Bassily, Dr Pritchard, Dr Colman, Mr Schofield, Dr Michael Epstein, consultant psychiatrist, Dr Ian Jennens, infectious diseases physician, Dr Hary Widjaja, rehabilitation physician, and operation reports from the Epworth Hospital.
Tieman called Dr Paul Gow, a consultant gastroenterologist, hepatologist and endoscopist, who is one of two liver transplant physicians in Victoria. Tieman also tendered medical reports of Dr Bassily, Dr Gow, Mr Owen Deacon, orthopaedic surgeon, Mr Timothy Gale, general and trauma surgeon, Dr Andrew Jakobovits, physician, Dr Stephen Stern, consultant psychiatrist and Mr Michael Shannon, general surgeon.
All the medical experts that were called gave honest and impartial evidence. Each of them was refreshingly frank and helpful. Dr Colman and Dr Gow were particularly impressive.
Mr Clark’s personal and work history prior to the accident
The facts set out at [15] to [21] below are based on the evidence of Mr and Mrs Clark and the histories in the medical reports of Dr Epstein and Dr Stern.
Mr Clark was born in Scotland on 31 August 1949. He left school at 15 years of age and worked in various jobs as a shop assistant and as a labourer in the construction industry. In 1973, he began work as a forklift driver.
In 1969, at the age of 20, Mr Clark began smoking 20 cigarettes daily and drinking four to five standard alcoholic drinks[1] per day including beer and whiskey. He occasionally drank more on the weekends.
[1]According to Dr Huang’s evidence, a standard glass of wine constitutes one standard alcoholic drink and a stubby constitutes 1.5 standard alcoholic drinks.
Mr and Mrs Clark married in 1973. They have two daughters and two granddaughters aged two and four years.
In 1982, Mr and Mrs Clark moved to Australia. From 1982 until 2000, Mr Clark worked in a number of shoe factories and then as a cleaner in the construction industry.
In 1987, Mrs Clark injured her back at work at a shoe factory. Since that time, she has had limited mobility and has been receiving WorkCover payments.
In March 2003, Mr Clark commenced working at Tieman as a cleaner and storeman. Later, he obtained tickets qualifying him to work as a forklift driver, mobile crane operator, rigger and dogman. His regular shifts were from 7.00am until 3.30pm Monday to Friday. However, he regularly worked overtime between 3.30pm and 5.00pm Monday to Friday and either half shifts or full shifts on Saturday. Mr Clark described his work as ‘manual work’ that was sometimes ‘hard’ and ‘heavy’. Mr Clark agreed that, with overtime, the work was ‘quite physical’.
Prior to the accident, Mr Clark was happy, friendly and confident. He and Mrs Clark enjoyed going out to dinner and the movies, visiting friends and attending football games and country race meetings. They have a games room with a snooker table at home which Mr Clark used when friends or relatives visited. Due to Mrs Clark’s disability, Mr Clark assisted with domestic duties, such as making the beds, cleaning, vacuuming and gardening.
Mr Clark’s alcohol consumption prior to the accident
Prior to the accident, Mr Clark consumed alcohol at home after work and on the weekends. There were inconsistencies between the evidence given by Mr and Mrs Clark on the amount of alcohol that he consumed and the histories taken by various doctors from Mr and Mrs Clark about his alcohol consumption. There were also inconsistencies in Mr Clark’s evidence about his alcohol consumption. For the reasons set out at [8] and [9] above, the information that Mr and Mrs Clark provided to various medical practitioners prior to the accident regarding Mr Clark’s alcohol consumption is more reliable than the oral evidence of Mr and Mrs Clark.
The parties have agreed on a table setting out the history of alcohol consumption and, to a lesser extent, cigarette smoking, that Mr and Mrs Clark provided to various medical practitioners. Table 1, below, sets out the information as it appears in the parties’ agreed table, but only until the date of the accident. The table contains the following abbreviations: ‘P’ means Mr Clark; ‘GGT’ means Gamma Glutamyl Transferase (an enzyme whose level in the blood is an indicator of liver disease); ‘GP’ means general practitioner; and ‘LFT’ means liver function test.
DATE
EVENT
SOURCE
2000
P drank four to five standard drinks per day in the form of beer and whisky with more at weekends prior to his diagnosis of cirrhosis.
Medical report Dr Colman – 03.02.11
21 April 2001
P smoked 7 -9 cigarettes per day (heavier in the past) and drinks 8-10 drinks per day for some years (beer and sprits).
St Vincent's clinical records (letter from Dr Matthews)
21 April 2001
P was drinking 6-8 drinks per day (beer and spirits)
P smoked 8 -10 cigarettes a day and drank 4-5 beers/a couple of whiskey's a night.
St Vincent's clinical records
St Vincent's clinical records (clinical risk assessment
21 April 2001
P was admitted to ward via accident and emergency with decompensated cirrhosis (likely alcoholic). He normally drinks 3‑4 beers a night and a "couple of whiskey's"
St Vincent's clinical records (progress and special exam sheet)
21 April 2001
P drank 2-3 beers a day and 2-3 spirits.
St Vincent's clinical records (progress and special exam sheet)
24 April 2001 to 10 May 2001
P had remained abstinent from alcohol
St Vincent's clinical records (letter from Dr Watson 10.05.01)
10 May 2001
P advised he needed to remain abstinent from alcohol.
Stopped drinking.
St Vincent's clinical records (out-patient attendance record)
4 September 2003
P was managing to keep his alcohol down to two drinks per week.
Medical report Dr Bassily – 04.09.03
4 March 2004
P's GGT remained elevated which was suggestive that he was still drinking. He was asked to cut down his alcohol to two drinks on Friday and two drinks on Saturday.
Medical report from Dr Bassily to Dr Huang – 04.03.04
5 August 2004
P was still drinking, although much less than before.
Medical report Dr Bassily – 05.08.04
15 February 2005
P's liver function tests had increased which was suggestive he was still drinking alcohol. He had not developed any further ascites or any signs of decompensation but it would not be long before that happened if he continued to drink. He only admitted to drinking eight drinks per week and he was asked to halve the amount of alcohol he drinks and stop, if possible.
Medical report Dr Bassily – 15.02.05
15 April 2005
P was still drinking 7 to 8 cans of beer a day.
Clinical records - GP
2 June 2005
P was drinking 10 cans of beer per week.
Clinical records – GP
19 July 2005
P was drinking 8 to 9 standard drinks per week which was more than he should.
Medical report Dr Bassily – 19.07.05
8 November 2005
GGT remained elevated as he still drank, although his drinking significantly improved. He was quite stable as long as he did not consume too much alcohol.
Medical report Dr Bassily – 08.11.05
2006
P had been advised to cease alcohol however he continued to drink. After seeing Dr Bassily, he reduced his alcohol significantly and only drank beer.
Medical report Dr Colman – 03.02.11
21 June 2006
P's liver function tests gradually worsened with a predominant elevation of the GGT, suggesting he still drank significantly. He was drinking around 10 to 12 standard drinks a week which was more than he should. He was again advised to cut down on alcohol intake as much as possible.
Medical report Dr Bassily – 21.06.06
21 July 2006
P continued to drink 10 to 12 standard drinks a week. His previous LFT's had shown increased GGT.
Clinical records – GP
10 April 2007
P still drank alcohol.
Clinical records – GP
28 May 2007
Noted P still drinking two cans of beer/day. He was encouraged to cut back or quit as it would help problems as well.
Clinical records – GP
19 June 2007
Discussed with P his alcohol intake. He was still drinking around 12 standard drinks per week maybe more. It was explained that he would need to stop completely if he wanted his liver to show any signs of recovery.
Medical report Dr Bassily – 19.06.07
14 August 2007
P had deteriorated due to an increase in his alcohol consumption. He has now started cutting down again on his alcohol which he admits has been creeping up gradually.
Medical report Dr Bassily – 14.08.07
29 November 2007
P was smoking 15-20 cigarettes a day. He was drinking approximately 12 beers per week.
St Vincent's clinical records (admission history)
29 November 2007
P was drinking 12 heavy cans per week.
St Vincent's clinical records
2 December 2007
P was smoking 1 packet of cigarettes a day.
St Vincent's clinical records (short stay patient admission)
4 December 2007
P was drinking approximately 12 cans of heavy beer a week.
St Vincent's clinical records (letter from Dr Nguyen to Dr Bassily)
I should add that Dr Huang, Dr Bassily, Dr Colman and Dr Gow gave evidence that patients with cirrhosis of the liver tend to understate their alcohol consumption. Although the levels of alcohol consumption set out at [23] above may well understate Mr Clark’s alcohol consumption, I will proceed on the basis that those levels are accurate.
Mr Clark’s health prior to the accident
In July 1999, Dr Bassily diagnosed Mr Clark as suffering from iron deficiency anaemia and Hereditary Haemorrhagic Telangiecstasia (‘HHT’). HHT – which is also known as Osler’s disease – is a genetic condition characterised by multiple blood vessel lesions in areas such as the lips, tongue, oesophagus, lungs, liver and gastrointestinal tract. The lesions tend to bleed if they are not treated.
In 2001, a gastroscopy disclosed that Mr Clark was suffering from oesophageal varices and a duodenal ulcer. Oesophageal varices are dilated veins in the wall of the oesophagus which can bleed if not treated. A duodenal ulcer is an ulcer in the small intestine. Dr Bassily diagnosed Mr Clark as suffering from cirrhosis of the liver, ascites (fluid accumulation in the abdominal cavity) and mild encephalopathy (a confusional state). Dr Bassily prescribed diuretics (drugs that restrict fluid accumulation) and advised Mr Clark to reduce his alcohol consumption.
In 2004 and 2005, Dr Bassily treated Mr Clark’s oesophageal varices with banding, a medical procedure involving the placing of rubber bands around the varices (veins) in order to prevent bleeding.
In July 2007, Mr Clark underwent a gastroscopy which revealed portal hypertension (blockage of normal blood flow through the liver) associated with oesophageal varices and portal hypertensive gastritis (inflammation of the stomach lining). A further banding procedure was undertaken in August 2007.
In November 2007, Mr Clark experienced shortness of breath. He underwent another gastroscopy which showed that he continued to suffer from portal hypertension associated with oesophageal varices and portal hypertensive gastritis. He also underwent chest X-rays and a CT scan of the chest and upper abdomen which showed advanced cirrhosis of the liver, a significant right pleural effusion (fluid accumulation in the chest cavity), oesophageal varices and ascites. Mr Clark was also found to be suffering from hypothyroidism (a deficiency of thyroid hormone), malnutrition, hypertension (high blood pressure) and gastro-oesophageal reflux (stomach acid coming up from the stomach into the oesophagus).
In early December 2007, lesions were discovered in Mr Clark’s liver. It was thought that he might have liver cancer. On 14 December 2007, Mr Clark was informed that the lesions were not cancerous. Dr Bassily advised that the lesions were either cirrhotic nodules or arterio-venous malformations related to HHT.
In his report dated 4 February 2009, Dr Huang stated:
Prior to [the orthopaedic] injuries Mr. Clark has had notable chronic medical conditions including:
1.Chronic alcoholic liver disease leading to cirrhosis of the liver and portal hypertension with associated oesophageal varices,
2.Hereditary haemorrhagic telangiectasia,
3.Vitamin D deficiency,
4.Chronic obstructive airways disease, which I believe is related to his cigarette smoking, (20 cigarettes per day for over 40 years).
5.Hypothyroidism.
…
Leading up to his accident, he was preoccupied by several medical issues. In the 4 months prior to the injury he was requiring banding of oesophageal varices and medical treatment of ascites by his gastroenterologist, Dr Raouf Bassily.
In his report dated 3 August 2011, Dr Gow described Mr Clark’s medical condition as at 14 December 2007 as follows:
As best I can tell from the medical record the patient at this stage had evidence of portal hypertension (varices and hepatic hydrothorax) but well preserved hepatic synthetic function (albumin and bilirubin values were good). Ie: at that stage he had early evidence of hepatic decompensation.
In the same report, Dr Gow stated that, in general, hepatic hydrothorax (ascites tracking up into the right lung) is ‘a manifestation of very advanced, even preterminal liver disease’.
Despite his health problems, Mr Clark regularly worked overtime and had virtually no time off work. As the sole wage earner, he was a motivated and reliable employee.
Circumstances of the accident
As Tieman has admitted liability, I will only briefly summarise the circumstances of the accident.
As stated at [1] above, the accident occurred on Saturday 15 December 2007. On that day, Mr Clark was performing the duties of dogman in connection with the loading of steel ramps known as dock levellers onto a semi-trailer. The loading operation was conducted outdoors in wet conditions. A mobile crane was used to load the levellers onto the back of the semi-trailer by means of hooks at the end of chains that were inserted into eyebolts in each corner of the leveller.
With Mr Clark’s guidance, the mobile crane driver had deposited a dock leveller onto the back of the semi-trailer. It appears that Mr Clark had removed the hooks from three of the eyebolts and was on top of the dock leveller on his way to the fourth eyebolt when he slipped and fell a distance of approximately three metres off the semi-trailer. He landed on his right side on a bare earth surface.
Non-contentious medical evidence
Physical injuries sustained in the accident and hospitalisation until March 2008
Following the accident, Mr Clark was taken by ambulance to the Royal Melbourne Hospital (‘RMH’). He was assessed as suffering from the following injuries:
(a)A comminuted sub-trochanteric fracture of the upper end of the right femur (thigh bone) immediately distal to the hip joint. I will refer to this injury as the hip fracture.
(b)Fractured pelvis involving the right inferior pubic ramus and the right acetabulum.
(c)Burst fracture of the L1 and L2 vertebrae of his lumbar spine. I will refer to this injury as the lumbar spine fracture. Mr Schofield described it as being ‘at the [upper] level of seriousness’.
(d)Fracture of several transverse processes of the spine.
On the day of the accident, Mr Clark underwent surgery for the hip fracture. The treatment comprised the insertion of a rod (described as a ‘gamma nail’) through the shaft of the femur and a single screw device together with cross bolts to hold the femur in its correct vertical position.
On 18 December 2007, Mr Clark underwent surgery for the lumbar spine fracture. He had an anterior spinal fusion with a plate and screws at the lumbar spine L1 and L2 levels and a bone graft. Mr Schofield described the spinal surgery as being ‘at the upper end of … seriousness’.
The fractures to the pelvis and the transverse processes did not require surgery and were treated conservatively.
A number of complications arose during Mr Clark’s initial care at the RMH. The complications associated with the cirrhosis of the liver will be discussed at [56] below. The other complications were as follows:
(a)The prosthetic rod that was used to treat the hip fracture shifted in position necessitating a further operation on the hip on 24 December 2007.
(b)Mr Clark developed an infection at the site of the prosthetic rod, which necessitated surgery under general anaesthetic on 4 January 2008 and again on 12 January 2008 to wash out the wound. Mr Clark was prescribed Bactrim (an antibiotic) to treat the infection.
(c)Mr Clark developed post operative respiratory depression requiring admission to the Intensive Care Unit.
(d)Mr Clark was found to have folate deficiency, hypothyroidism, Vitamin D deficiency and hyperkalaemia.
(e)Mr Clark’s weight decreased from about 80 kilograms to about 55 kilograms.
Mr Clark was bedridden for three weeks. He then used a wheelchair and later a walking frame. He experienced panic attacks and constant pain in his right hip and back. He was prescribed Oxycontin and Endone, which are strong narcotic analgesics, to manage his chronic pain.
On 22 February 2008, Mr Clark was transferred from the RWH to the Rehabilitation Centre at the Epworth Hospital (‘Epworth Rehabilitation’). At the time of the transfer, Mr Clark was ‘50% weight bearing on the right leg’. He underwent physiotherapy, hydrotherapy, occupational therapy and exercise physiology. Initially, he required assistance in the performance of many day-to-day functions.
In-patient rehabilitation treatment at Epworth Rehabilitation assisted Mr Clark to become mobile with the aid of two elbow crutches. He was discharged from Epworth Rehabilitation on 18 March 2008.
The course of the physical injuries between March 2008 and trial
Following his discharge from Epworth Rehabilitation, Mr Clark commenced an out‑patient rehabilitation program at Epworth Rehabilitation. This involved physiotherapy and hydrotherapy three times per week. Gradually, he walked with the assistance of a single elbow crutch.
Mr Clark’s fractures took a long time to heal. The right hip fracture had not fully healed by December 2008. In May 2009, Mr Clark attended the Fracture Clinic at the RMH for X-rays and a CT scan of his right femur, which showed that his hip fracture was still incomplete. A total hip replacement was considered but did not proceed due to the risk of infection.
On 24 July 2009, Mr Clark had surgery at the Epworth Hospital to remove an unstable and un-united segment of the femoral bone and the rod that had been inserted in the femur on 15 December 2007. A steel locking plate and screws were used to secure the damaged bone and healthy bone was grafted to the osseous defect.
In September 2009, Mr Clark developed a serious infection in the right thigh and femur and was re-admitted to the Epworth Hospital. He underwent surgery under general anaesthetic on 15, 18, 24 and 29 September to wash out the wound and cut away dead tissue (debridement). The wound was closed on 29 September 2009.
The infection in the right thigh and femur re-appeared in March 2010. Mr Clark returned to the Epworth Hospital and underwent surgery under general anaesthetic on 12 and 17 March 2010 to wash out the wound. There was a large abscess in the right thigh and approximately 80mls of thick pus was drained and dead skin and tissue was cut away.
By June 2010, the wound had healed satisfactorily and there was no sign of recurrence of infection. However, the metal in Mr Clark’s femur poses an ongoing risk of infection and requires management with permanent antibiotic therapy.
In June 2010, Mr Clark resumed physiotherapy treatment at Epworth Rehabilitation twice a week.
On 30 June 2011, Mr Clark was crossing a main road when he tripped on an uneven surface on the pavement. His physical disabilities from the accident and the position of the crutch prevented him from regaining his balance and he fell heavily on his right side. He was taken by ambulance to the Epworth Hospital. He had soft tissue and muscle damage. He remained in hospital for a week and then spent nine days at Epworth Rehabilitation. After he was discharged, he continued outpatient physiotherapy twice per week until shortly prior to the trial.
In his report dated 1 August 2011, Dr Huang stated that Mr Clark’s daily medications were:
1.Actilax syrup 20 mls twice daily – to overcome medication induced constipation
2.Aldactone and Urex – diuretics to manage fluid retention related to his chronic liver disease
3.Deralin – a medication to help manage his portal hypertension
4.Fucidin, Rifampicin and Bactrim – antibiotic prophylaxis
5.Oxycontin 80 mgm twice daily and Endone 5 mgm up to 5 times daily to manage his chronic pain
6.Oroxine 50 mcg daily – treatment of his hypothyroidism
7.Losec – 20 mgm twice daily – to reduce inflammation and risk of bleeding from his oesophagus.
The Fucidin, Rifampicin and Bactrim prevent a recurrence of the hip infection. Mr Clark is required to take these medications for the rest of his life. He is also required to take the narcotic analgesics (Oxycontin and Endone) for the rest of his life.
The course of the pre-existing conditions between 15 December 2007 and trial
The orthopaedic injuries that Mr Clark sustained on 15 December 2007 and their effects aggravated his chronic liver disease and resulted in the redevelopment of ascites and hepatic hydrothorax (with associated pleural effusion). These conditions required treatment by a pleurodesis (the drainage of fluid by inserting a needle into the pleural cavity) on 23 December 2007, diuretic therapy and fluid restriction. He developed bleeding oesophageal varices which required transfusion and banding on 8 February 2008.
On 27 February 2008, Mr Clark returned to the RMH and had a further four varices banded. He was found to have recurrent anaemia which required a blood transfusion followed by oral iron tablets.
On 1 July 2010, Mr Clark was taken to the RMH and had an umbilical hernia repair. He developed severe ascites.
On 10 August 2010, Dr Bassily performed varices banding surgery at the Northern Hospital.
On 26 August 2010, Mr Clark attended the Emergency Department of the RMH and was found to have ascites, anaemia and renal failure. He came under the care of Dr Pritchard following a referral from Dr Bassily.
On 9 September 2010, Mr Clark had an ascitic tap (the drainage of fluid by inserting a needle into the abdominal cavity) and albumin (protein) infusion. Seven litres of fluid was removed. He had a further ascitic tap on 16 September 2010. He subsequently attended the gastroenterology outpatient clinic at the RMH on a weekly basis to undergo ascitic taps.
In his report dated 9 November 2010, Dr Huang stated:
It is my medical opinion that Mr John Clark’s general physical health is very poor, his prognosis is grave, and life expectancy significantly shortened.
Given his parlous state of health, there is a risk that he could die within a matter of months.
On 11 November 2010, Mr Clark underwent a Transjugular Intrahepatic Portosystemic Shunt (‘TIPS’) surgical procedure to manage the portal hypertension related to his cirrhosis of the liver. Dr Bassily described the nature and purpose of the TIPS as follows:
A TIPS is a shunt. … [T]he main problem is that the increased pressure in the veins in the abdomen, … all the blood coming from the gastrointestinal system has to go through the liver to be filtered. Now, that filter is now scarred so it causes a lot of pressure on these veins which leads to the varices … in the oesophagus bursting and dilating, and the accumulation of fluid in the abdomen. In the old days we used to surgically connect the veins draining the abdomen to the rest of the veins … of the body, to bypass the blockage basically. Now we do this procedure called TIPS where they insert a shunt through the liver to bypass the scarred liver. [The TIPS enables fluid from the liver to be drained] directly into the rest of the circulation.
Initially, the TIPS was not successful and Mr Clark required drainage of a large volume of fluid on a weekly basis.
Dr Pritchard referred Mr Clark to the Austin Hospital for assessment for a liver transplant.
By March 2011, the TIPS had brought about stability in Mr Clark’s liver disease. He has not had any further drainage of fluid since then. Mr Clark was informed that his liver function was too good for him to need a liver transplant. His liver condition continues to be stable. Dr Huang gave evidence that since the TIPS began to operate successfully, Mr Clark’s health had ‘remarkably improved’.
Psychological consequences of the accident
Dr Epstein, who examined Mr Clark at the request of his solicitors, diagnosed Mr Clark as suffering from an accident-related mild chronic Post Traumatic Stress Disorder (‘PTSD’) and a chronic adjustment disorder with depressed mood. Dr Stern, who examined Mr Clark at the request of Tieman’s worker’s compensation insurer, diagnosed Mr Clark as suffering from an accident-related chronic adjustment disorder with depressed mood, but not from PTSD.
As the amended statement of claim, which was filed after the conclusion of the evidence, pleaded that Mr Clark suffered only chronic adjustment disorder with depressed mood, I accept Dr Stern’s diagnosis.
Mr Clark’s alcohol consumption since 15 December 2007
Table 2, below, sets out information that appears in the parties’ agreed table regarding Mr Clark’s alcohol consumption[2] for the period following the accident.
[2]See above [23].
DATE
EVENT
SOURCE
16 June 2009
P was urged to cut down on his alcohol intake.
P's liver function tests had deteriorated and it was suspected it was likely to be due to the fact that he was still drinking quite a bit of alcohol.
Medical report Dr Bassily – 16.06.09
18 September 2009
Note P disappointingly, despite strong advice, again drank alcohol.
Medical report Dr de Crespigny – 18.09.09
June 2010
P completely ceased drinking alcohol.
Medical report Dr Colman – 03.02.11
September 2010
P was not actively drinking.
Medical report Dr Prichard – 14.01.11
Mr Clark’s mobility and quality of life since 15 December 2007
Mr Clark gave evidence that, since the accident and the various operations that he has had for his injuries, his mobility and his capacity to engage in many of his pre‑accident activities have been severely limited. His evidence on these issues was supported by Mrs Clark’s evidence. I accept their evidence, which is summarised below.
Mr Clark now walks with the assistance of a left-handed elbow crutch. He can only walk short distances. He cannot sit for very long because he ‘stiffen[s] up’ and has to stand and move. However, he cannot move much because he ‘gets sore’. As a result of the accident, his right leg is two centimetres shorter than his left leg and he walks with a limp. His ability to bend and stretch is severely restricted, preventing him from performing many household chores. He and his wife receive home help in relation to cleaning and gardening.
Since the accident, Mr Clark’s main leisure activity has been watching television. He no longer plays snooker at home and rarely attends the cinema, country races or the football. He rarely goes out to dinner with his wife. While he still attends family functions, there have been occasions where he has had to leave early by taxi because of the pain.
Mr Clark’s personality has changed. His sense of humour has diminished and he is often irritable. He walks around the house complaining that he is useless and cannot do anything.
Mr Clark is not able to enjoy his granddaughters’ company in the same way that he did prior to the accident. His interaction with them is limited to talking to them, helping them draw and amusing them. He cannot lift them and sometimes becomes impatient and irritable with them.
Mr Clark has constant pain in his back and right leg. He takes strong pain-killers. While he has tried to wean himself off the medication, he has found that the pain is too strong and has thus been forced to resume taking the medication. Dr Huang gave evidence that Mr Clark is addicted to the pain-killers.
Mr Clark does not sleep well. He is restless and wakes up due to pain or to visit the toilet.
While Mr Clark is able to drive, he can only do so for short distances because he does not have full strength in his right leg.
Mr Clark described his life as ‘miserable’.
Dr Huang gave evidence that, since Mr Clark’s liver condition had stabilised in March 2011, ‘his sense of well being’ has improved and he ‘seemed to be … happier, more alert’.
Contentious medical evidence
The cause of Mr Clark’s cirrhosis of the liver
There was conflicting medical evidence about the cause of Mr Clark’s cirrhosis of the liver.
In his report dated 25 February 2011, Dr Gow stated:
In general, in patients with alcoholic liver disease, if they stop drinking and maintain good nutrition, they have an excellent prognosis, surviving potentially for decades. However, patients with symptomatic liver disease secondary to [HHT] relentlessly progress and either need liver transplantation or die from their disease.
…
The clinical course in patients with HHT is highly variable but my feeling would be in a patient who has hepatic hydrothorax (pleural effusion) from portal hypertension from HHT, they would be likely to deteriorate over the next year or two.
…
Ongoing drinking in patients with decompensated liver disease, which Mr Clark had, would be well recognised to clearly be associated with acceleration and deterioration in their liver function.
…
If the liver disease was secondary to alcohol [and Mr Clark had abstained from alcohol consumption and/or reduced his consumption in accordance with the directions from his medical practitioners], I would have expected Mr Clark to be well. If the liver disease was secondary to HHT and he had ongoing moderate alcohol, it is unlikely that that alcohol would have been associated with any significant change in the natural history of the disease.
…
If his liver disease was secondary to alcohol, then chronic sepsis would have likely accelerated the course of his condition. If the liver disease was secondary to HHT, this is already a disease that can progress rapidly. The chronic hip sepsis may have accelerated the natural history by some weeks or months.
In his oral evidence, Dr Bassily agreed with all but the second sentence in the fourth of the above statements. He said that the amount of alcohol required to cause cirrhosis of the liver was much less than the amount required to worsen existing cirrhosis. He added that any amount of alcohol will worsen the cirrhosis. In his report dated 15 March 2011, Dr Bassily stated:
I tend to agree with Dr Paul Gow that [HHT] is probably a contributing factor to the aetiology of [Mr Clark’s] liver disease in addition to alcohol. In [Mr Clark’s] case however, it is difficult to differentiate between the partial contribution of both conditions. He has been diagnosed with decompensated liver disease as early as 2000 and has continued to drink alcohol after that, which would have lead to further deterioration of his liver disease and in addition to that his [HHT] could also lead to progressive liver disease.
In his report dated 3 August 2011, Dr Gow stated:
On the balance of probabilities I feel the cause of Mr Clark’s liver disease is that of [HHT].
…
I feel it is unlikely, even if the patient had abstained from drinking as suggested by St Vincent’s and Dr Bassily, that the patient’s condition would have altered significantly, as I feel on the balance of the medical information I have at hand that the predominant cause of his liver disease is [HHT].
Dr Bassily gave the following further oral evidence. HHT is a rare disease. He currently has one or two patients with the disease and, over the years, he has treated three or four such patients. Those patients experienced significant bleeding which required treatment with cortisone and regular blood transfusions. Mr Clark’s bleeding was from oesophageal varices and relatively mild nosebleeds. Mr Clark’s HHT is mild and, while it was a contributing factor to the onset of Mr Clark’s cirrhosis of the liver, it was not the major factor or a primary factor.
Dr Bassily said that the fact that Mr Clark’s cirrhosis of the liver had fluctuated since it was first diagnosed in 2001 indicated that it may be more related to alcohol consumption than to HHT. This was because HHT-induced cirrhosis of the liver progressively worsens ‘regardless [of] what you do’. While HHT-induced cirrhosis could plateau from time to time, it would not improve. As Mr Clark had experienced periods of improvement, including, in particular, after March 2011, this indicated that alcohol consumption was a significant contributing factor. It also suggested that the contribution of HHT to Mr Clark’s liver condition ‘is not as large as [Dr Gow] suggests’.
Dr Bassily said that, as Mr Clark’s cirrhosis condition was predominantly caused by alcohol consumption, the condition could stabilise with alcohol abstinence.
Dr Gow gave the following evidence. HHT is a rare disease. It is not necessarily related to liver disease. He has treated 10 patients that have had liver-related problems with HHT. The most likely cause of Mr Clark’s cirrhosis of the liver was HHT rather than alcohol consumption. This was because Mr Clark’s alcohol consumption was at the ‘very lower edge for what could go on to cause chronic liver disease’. His diagnosis was supported by the fact that, as at early December 2007, Mr Clark suffered from ascites and pleural effusion. Alcohol consumption could worsen Mr Clark’s cirrhosis condition but would not be a major contributor to the disease.
Dr Gow said that the fact that Mr Clark’s nosebleeds were not serious did not detract from his diagnosis because, in his experience, patients with HHT-induced cirrhosis of the liver did not necessarily have significant bleeding problems that required transfusions. Likewise, the fact that Mr Clark’s condition had exhibited a ‘dramatic improvement’ since March 2011 did not cause him to alter his assessment. The improvement had resulted from the TIPS procedure, expert nutritional advice and the stabilisation of the sepsis of the hip.
Dr Colman gave evidence that it was 95 per cent probable that alcohol consumption was the cause of Mr Clark’s cirrhosis of the liver. However, he also said that, to his knowledge, there was ‘no relevant alternative causative agent for [Mr Clark’s] liver cirrhosis’. He also said that he is not familiar with HHT.
In my opinion, both HHT and alcohol consumption contributed to the onset of Mr Clark’s cirrhosis of the liver and to the progression of the disease. On balance, I accept Dr Bassily’s evidence that the dominant contributing factor was Mr Clark’s alcohol consumption. However, in so far as Dr Bassily’s oral evidence can be interpreted as suggesting that the contribution of HHT was minor, I reject it. While HHT, in comparison to Mr Clark’s alcohol consumption, was a secondary contributing factor to the onset of the cirrhosis of the liver and its progression, it nevertheless was an important contributing factor.
In accepting Dr Bassily’s evidence that alcohol consumption was the dominant contributing factor to the onset of Mr Clark’s cirrhosis of the liver, I have taken into account the fact that Dr Bassily has been treating Mr Clark since 1999 and was more familiar than Dr Gow with Mr Clark’s medical history and treatment. Dr Bassily was aware of Mr Clark’s fluctuating alcohol consumption – as conveyed to him by Mr Clark – and the relationship between that alcohol consumption and the progression of Mr Clark’s cirrhosis of the liver. On the other hand, the written chronology of Mr Clark’s alcohol consumption that was provided to Dr Gow only covered the period from 2000 until September 2010.
Dr Bassily based his assessment that Mr Clark’s HHT did not have as significant an impact on Mr Clark’s cirrhosis of the liver as suggested by Dr Gow on his experience with other patients who suffered from HHT.[3] It was not clear from Dr Bassily’s evidence that the three or four patients that he has treated for HHT also suffered from cirrhosis of the liver. In comparison, the profiles of the 10 patients with HHT that Dr Gow has treated more closely resemble Mr Clark’s profile, in that Mr Clark suffers from both HHT and cirrhosis of the liver. It follows that Dr Gow has broader and more relevant clinical experience than Dr Bassily and is better placed to assess the impact of Mr Clark’s HHT on the cirrhosis of the liver.
[3]See above [84].
Effect of the physical injuries on the pre-existing conditions
As stated at [4] above, Tieman conceded that the orthopaedic injuries resulting from the accident permanently aggravated Mr Clark’s pre-existing cirrhosis of the liver.
In my opinion, this concession was properly made. In the light of the concession and the medical evidence to which I have referred, I find that Mr Clark’s orthopaedic injuries and their effects have significantly contributed to the deterioration in Mr Clark’s cirrhosis and have resulted in some permanent damage to Mr Clark’s liver.
Effect of the pre-existing conditions on Mr Clark’s life expectancy
Dr Bassily gave evidence that Mr Clark’s cirrhosis condition has been rated as ‘Child-Pugh B’, which means that his life expectancy is about five years. He said that as Mr Clark’s current condition had improved, his life expectancy was between five to 10 years, and could possibly be as much as 15 years if he continued to improve. However, Dr Bassily also emphasised that a prognosis about life expectancy was very difficult and depended on a number of factors, including the level of alcohol consumption.
Dr Gow gave the following evidence. As at early December 2007, Mr Clark had manifestations of serious underlying liver disease which was likely to progress and become more significant with time. If the etiology of the disease was HHT, Mr Clark’s life expectancy would be shortened by the disease. He could die or could need a liver transplant within five years of December 2007. However, drawing an exact timeline for the progression of the disease was difficult because HHT is a rare condition and people vary markedly in how their underlying liver disease behaves. If the etiology of the disease was alcohol consumption, then, with abstinence from alcohol consumption, Mr Clark ‘should live to be an old man’. If Mr Clark continued to consume alcohol, then ‘he would get sicker with time’.
At [90] above, I concluded that the dominant cause of Mr Clark’s cirrhosis of the liver was alcohol consumption and that HHT was an important secondary cause. Given this conclusion, and given Mr Clark’s abstinence from alcohol consumption since June 2010, the evidence of Dr Bassily and Dr Gow suggests that if Mr Clark continues to abstain from alcohol, he may live for as much as 15 years from December 2007.
Dr Pritchard gave the following evidence. The TIPS is a bridging procedure. There will be an ongoing, gradual deterioration in Mr Clark’s liver function until a liver transplant takes place. That is why he referred Mr Clark to the Austin Hospital for assessment for a liver transplant. Mr Clark has been assessed as a suitable candidate for a liver transplant. While Mr Clark’s liver is currently too healthy to qualify him to be placed on the active list of transplant recipients, he is on the inactive list of transplant recipients. Should his liver function deteriorate further, he will be eligible for a liver transplant. Without a liver transplant, Mr Clark had a 15 to 20 per cent chance of living for five years.
Dr Colman gave evidence that, with ongoing alcohol consumption, Mr Clark’s life expectancy would be predictably reduced. He said that the greater the amount of alcohol consumed, the worse the outlook would be.
An additional factor that may affect Mr Clark’s life expectancy is that he is a long‑term smoker of cigarettes, with a chronic obstructive airways disease.
In the light of all the above evidence and considerations, I am of the view that it is unlikely that Mr Clark will live beyond December 2020.
Effect of the pre-existing conditions on Mr Clark’s work capacity
Dr Colman gave the following evidence. The fact that, prior to the accident, Mr Clark was suffering from oesophageal varices that required banding and hepatic hydrothorax (with associated pleural effusion) indicated that he had an advanced liver disease which was potentially pre-terminal, particularly with continuing alcohol consumption. It was ‘remarkable’ that, with these conditions, Mr Clark was able to work in December 2007. It was more than likely that, with continuing consumption of alcohol, Mr Clark’s condition would progressively deteriorate leading to death. On the other hand, abstaining from alcohol consumption can lead to a patient becoming stable and being able to live a normal life.
Dr Colman agreed that, in the light of Mr Clark’s medical conditions prior to the accident, his capacity to perform the type of work that he did at Tieman would become ‘more and more limited’. The following exchange then took place between Mr Jeffrey Moore QC, who appeared with Ms Roslyn Kaye for Tieman, and Dr Colman during cross-examination:
[Mr Moore:][O]n balance … are we talking about a year or perhaps a couple of years you might reasonably anticipate not being able to press on?
[Dr Colman:] With work or with life?
[Mr Moore:]Yes, with work?
[Dr Colman:] Yes, a short time I would have thought.
[Mr Moore:]Is your concept of a short time maybe a year or two?
[Dr Colman:] Yes, but it’s difficult to be certain about that, and balance of probabilities aside it’s still very difficult to speculate on a timeframe.
In his report dated 25 February 2011, Dr Gow stated:
As stated previously, in cirrhosis secondary to alcohol where people stop drinking, generally they remain very stable … and people can continue working. People with HHT deteriorate potentially over months to years which would result in significant functional decline such that a person in Mr Clark’s occupation would find it very hard to perform physical duties. This would be expected to occur any time I feel in the year or two following the development [of] the pleural effusion from his liver disease.
In oral evidence, Dr Gow said that most people who are suffering from the conditions that Mr Clark suffered in early December 2007, irrespective of their cause, would be incapable of performing the work that he then performed. In relation to the impact of Mr Clark’s conditions as at early December 2007 on his ability to continue working, Dr Gow gave the following evidence-in-chief:
[Mr Moore:][A]re you able to, again doing the best you can, identify first of all the apparent state of health on the presentation as at early December 2007, and what it probably would mean to a man who was working as a physical worker … being a dogman, forklift driver, labourer, sweeper, what would you foresee for him in terms of his capacity to keep up that sort of work?
[Dr Gow:]I think there's a big spread of what can happen. It's conceivable with very good medical care that two or three years down the track he could have been still very well. The TIPS procedure he had inserted at the Royal Melbourne Hospital may if done earlier have resolved a lot of his complications earlier on, but it's also conceivable that he could have had a relentless progression and been extremely unwell a year or two after that presentation.
…
[Mr Moore:]So absent the fall, absent the injuries, but if he continued consuming intoxicating liquor in the pattern that you had identified in the information given to you, would that, in your opinion, have any likely contributing factor or impact on his capacity to work?
[Dr Gow:]Yes.
[Mr Moore:]How does that fit in with your prognosis of - look, a couple of years maximum?
[Dr Gow:]I feel the primary cause of his symptoms and of his liver disease was the genetic condition. … I feel alcohol has made perhaps a small component to the presentation and therefore would make a small component to the potential progression if he was to keep drink[ing] six or eight units a day.[4]
[Mr Moore:]… So would it interfere one way or the other with your prognosis of doing the best you can, two years work into the future was probably going to be the case?
[Dr Gow:]To a minor degree, yes.
…
[Mr Moore:]If this condition … was found or concluded to be at the end of the day in fact alcohol induced, and given the presentation as at December 2007, and HHT was a factor but not the causative factor just an additional complication, would you still see him being able to manage labouring work for several years or some years or roughly how long, if he kept drinking?
[Dr Gow:]And had the accident you mean?
[Mr Moore:]Without the accident?
[Dr Gow:]Without the accident, if it's liver abuse from alcohol, and he kept drinking I would doubt he could work, you know, more than a year or two perhaps after 2007.
[4]Dr Gow explained that one can of heavy or full-strength beer contains about 1.8 units of alcohol.
Dr Gow was not cross-examined on the above evidence-in-chief.
In evidence-in-chief, Dr Bassily said that, due to Mr Clark’s pre-existing condition, in early December 2007, he ‘wouldn’t have been able to do the same … heavy duty work’. In cross-examination, Dr Bassily agreed that, just before the accident, Mr Clark ‘would be having difficulty’ carrying out the type of work that he was performing at Tieman.
In evidence-in-chief, Dr Bassily was not prepared to estimate how long Mr Clark could have continued to perform his duties at Tieman after December 2007 if he abstained from alcohol consumption. He said that he was not qualified to give that evidence. In cross-examination, Dr Bassily agreed that, with continued alcohol consumption, Mr Clark’s liver condition, in the absence of the accident, would probably involve ‘ongoing progressive decline in liver function’ and ‘ongoing progressive decline in…will power [and] physical capacity to do things and manage things generally’.
Dr Pritchard did not give evidence on this issue.
Mr Terence Casey QC, who appeared with Mr David Hancock for Mr Clark, submitted that I should not accept the evidence of Dr Colman and Dr Gow that the state of Mr Clark’s cirrhosis of the liver just prior to the accident was such that, in the absence of the accident, he would only have been able to continue working in his then current role for one to two years. In the case of Dr Gow, this was said to be because his diagnosis of the etiology of Mr Clark’s cirrhosis of the liver was incorrect. In the case of Dr Colman, this was said to be because his evidence was based on the inaccurate premise that, as at early December 2007 and independently of the accident:
(a) Mr Clark suffered from oesophageal varices which required treatment by way of banding; and
(b) Mr Clark suffered from pleural effusion which required treatment by way of drainage of the fluid.
In relation to the oesophageal varices, Dr Gow gave evidence that, but for the accident, Mr Clark would have required further banding. Dr Bassily gave evidence that he was not sure whether the varices had been banded prior to the accident. On the basis of this evidence, I am not satisfied that the banding took place prior to the accident.
In relation to the pleural effusion, Mr Clark gave evidence that the fluid had been drained prior to the accident. Dr Bassily referred to medical records from St Vincent’s Hospital dated 29 November 2007 which indicated that Mr Clark suffered from pleural effusion and that this was treated on that day by draining the fluid from his chest. On the basis of this evidence, I am satisfied that, prior to the accident, the fluid in Mr Clark’s chest was drained.
Mr Casey also submitted that Mr Clark’s prognosis was more positive than Dr Colman and Dr Gow suggested because of Dr Bassily’s evidence that the damage to the membrane that separates the abdominal cavity from the pleural cavity had apparently healed after the fluid in Mr Clark’s chest was drained. Dr Bassily gave evidence that where the membrane is damaged, fluid in the abdomen (ascites) can track up into the pleura (hepatic hydrothorax) and cause pleural effusion. He said that where the membrane repairs itself and is sealed, it stops ascites going back into the pleural cavity. Mr Casey contended that, as the membrane had healed itself, this had an important bearing on Mr Clark’s capacity to work.
Mr Casey also contended that the evidence of Dr Colman and Dr Gow was based on the assumption that Mr Clark would have continued consuming alcohol even if this began to interfere with his ability to work. He said that, given Mr Clark’s work ethic and need to provide financially for his family, Mr Clark would have stopped consuming alcohol if it affected his work.
In my opinion, the matters set out at [110] above do not detract from the evidence of Dr Colman and Dr Gow about the effect of Mr Clark’s pre-existing liver condition upon his ability to continue to perform his pre-accident duties in the absence of the accident. Both doctors described Mr Clark’s pre-accident liver condition as very serious and both were surprised that he was able to perform his duties at Tieman while suffering from that condition. Dr Bassily’s evidence was broadly consistent.
I am satisfied that Dr Colman and Dr Gow’s evidence would have been the same if they had been informed that the fluid from Mr Clark’s chest had been drained on 29 November 2007.
I am also satisfied that Dr Bassily’s evidence about the repair to the membrane separating the abdominal cavity from the pleural cavity would not have affected the prognoses of Dr Colman and Dr Gow. Dr Bassily’s evidence was not put to Dr Colman because he gave evidence before Dr Bassily. Dr Bassily’s evidence was, however, put to Dr Gow. Dr Gow acknowledged that it was unusual for hepatic hydrothorax to occur only once, but this did not cause him to alter the substance of his evidence about the causes and effects of Mr Clark’s pre-existing cirrhosis of the liver.
Further, I am not persuaded that, prior to June 2010, Mr Clark would have had sufficient self-control to cease consuming alcohol if it started to affect his capacity to work. Tables 1 and 2 indicate that, prior to June 2010, the only period in which Mr Clark abstained from alcohol consumption was when he was hospitalised or under close medical supervision in the months following the accident.[5]
[5]See above [23] and [69].
Although Dr Colman and Dr Gow did not agree about the cause of Mr Clark’s cirrhosis of the liver, they both agreed that, if the cause was alcohol consumption and Mr Clark continued to consume alcohol after December 2007, then in the absence of the accident, Mr Clark would have been able to continue to perform his pre-accident duties at Tieman for one to two years. Dr Gow was of the opinion that, as HHT was the cause of Mr Clark’s cirrhosis of the liver, his estimate of Mr Clark’s work capacity would be affected only to a minor degree by whether or not Mr Clark continued to consume alcohol.
The estimates provided by Dr Colman and Dr Gow were based on their expectation of what a typical labourer with Mr Clark’s pre-existing conditions would be expected to do. I accept their evidence about the position of a typical labourer. However, neither Dr Colman nor Dr Gow treated Mr Clark. Each of them only saw him on one occasion which, in my opinion, was insufficient to enable them to form an accurate assessment of whether Mr Clark was a typical labourer. In the light of Mr Clark’s strong work ethic and general resilience in the face of his conditions, he was far from a typical labourer. Mrs Clark described him as a ‘workaholic’. Accordingly, Dr Colman’s and Dr Gow’s prognoses have only partial application to Mr Clark.
On the other hand, irrespective of the cause of the cirrhosis, as at early December 2007, Mr Clark had a seriously damaged liver. In addition, notwithstanding his awareness that continued alcohol consumption could severely affect his health to the extent of ending his life, he continued to consume significant amounts of alcohol during 2009 and in the first half of 2010.[6] This alcohol consumption further weakened his liver and diminished his work capacity. Importantly, so did the progressive effects of his HHT.
[6]See above [69].
In all the circumstances, it is likely that, in the absence of the accident, Mr Clark would have continued performing the same duties (including overtime) at Tieman until December 2009 and that he would have performed the same duties without overtime until December 2010. After that time, it is likely that Mr Clark would have been able to continue working for another year if Tieman halved his pre-injury hours (inclusive of overtime) and assigned him lighter duties. He could well have continued until December 2012 on reduced hours and lighter duties. I do not believe that there was any prospect of Mr Clark being able to work in any capacity beyond December 2012.
Assessment of Mr Clark’s damages
Pain and suffering
Mr Clark is entitled to damages for pain and suffering, loss of amenities of life and loss of enjoyment of life as a result of the orthopaedic injuries that he suffered on 15 December 2007 and their effects, including the aggravation of the pre-existing cirrhosis of the liver.
I have already summarised the lay and medical evidence in relation to the nature of the physical injuries and their effects. The back and hip conditions will limit Mr Clark’s daily activities for the rest of his life with no prospects of improvement. He will continue to suffer severe pain and will be permanently dependent on narcotic analgesics. His infection-prone hip will also require permanent management with antibiotics. The restrictions on his domestic and social activities will persist for the rest of his life. So will the psychological consequences of the injuries to which reference was made at [68] above.
Mr Casey submitted that, in view of the seriousness of Mr Clark’s injuries and the significant diminution in his quality of life, the Court should award general damages of $300,000.
Mr Moore submitted that the Court should award general damages of $250,000. This was inclusive of an allowance of $75,000 for exacerbation of the pre-existing liver condition, reduced by one-third because of Mr Clark’s alcohol consumption since the accident.
In my opinion, the matters to which I have referred at [38] to [55], [68], [70] to [79], [94] and [124] above necessitate a substantial award of general damages. In arriving at an appropriate figure, it is necessary to take into account that there has been aggravation of the cirrhosis of the liver due to Mr Clark’s consumption of alcohol after the accident – despite Mr Clark knowing that this could kill him – and the ongoing effects of the HHT. Also relevant is the evidence regarding the effects of the cirrhosis of the liver on Mr Clark’s life expectancy.[7]
[7]See above at [95] to [101].
In all the circumstances, the appropriate amount for general damages is $300,000.
Loss of earning capacity
Mr Clark is entitled to be compensated for loss of earning capacity caused by Tieman’s negligence and breach of statutory duty.
Mr Clark gave evidence that he enjoyed his work at Tieman and planned to work there until at least 65 years of age and to undertake overtime if it was available. I accept that, if Mr Clark’s health had permitted him to do so, he would have worked until 65 years of age and would have worked overtime when it was offered.
Mr Clark has not worked since the accident. As stated at [4](a) above, Tieman has conceded that the orthopaedic injuries that Mr Clark suffered at the time of the accident and the effects of those injuries have permanently incapacitated him from performing any work.
In assessing Mr Clark’s past economic loss and future loss of earning capacity caused by Tieman’s negligence and breach of statutory duty, the Court is required to take into account other events and conditions unrelated to the orthopaedic injuries which may have, regardless of those injuries, adversely affected Mr Clark’s capacity to earn income.[8] In making this assessment, I will apply the principles set out at [133] to [140] below. Although I have expressed those principles by reference to negligence, they apply with equal force to breach of statutory duty.
[8]Acir v Frosster Pty Ltd [2009] VSC 454 (7 October 2009) [262] (‘Acir’).
General principles for assessing loss of earning capacity
The defendant must take the plaintiff as found, in his or her physical, mental, social and economic circumstances (‘eggshell-skull principle’).[9] This principle exists independently of the remoteness principle and the rule that the defendant does not need to foresee the extent of the type of injury to the plaintiff which is otherwise foreseeable.[10]
[9] Smith v Leech Brain & Co Ltd [1961] 2 QB 405, 414-5.
[10] Nader v Urban Transit Authority (NSW) (1985) 2 NSWLR 501, 536-8.
Where physical injuries caused by the defendant’s negligence are sustained by a plaintiff with a pre-existing condition, those physical injuries may aggravate or accelerate the plaintiff’s pre-existing condition. For example, the injuries may hasten the progression of the condition or shorten the plaintiff’s life expectancy. The defendant is only liable for the degree of aggravation or acceleration of the plaintiff’s pre-existing condition.[11]
[11]Nominal Defendant v Gardikiotis (1996) 186 CLR 49, 54; Purkess v Crittenden (1965) 114 CLR 164, 168 (‘Purkess’).
The plaintiff at all times bears the legal onus of proving the nature, extent and duration of the injuries sustained due to the defendant’s negligence.[12]
[12]Purkess (1965) 114 CLR 164, 167-8; Pastras v Commonwealth [1967] VR 161, 164.
Where the defendant’s case is that the Court should reduce the damages to be awarded to the plaintiff for his or her incapacity on the ground that the incapacity would, in any event, have resulted, in whole or in part, from some pre-existing condition, the position with regard to onus of proof is as follows:[13]
(a)Once the plaintiff has established a prima facie case that his or her incapacity has resulted from the defendant’s negligence, an evidential onus of proof shifts to the defendant to introduce evidence – as part of its substantive case or by way of cross-examination in the plaintiff’s case – that the plaintiff’s incapacity is wholly or partly the result of the pre-existing condition or that incapacity, either total or partial, would, in any event, have resulted from the pre-existing condition.
(b)In the absence of such evidence by the defendant, if the plaintiff’s evidence is accepted, the plaintiff will be entitled to an award of damages and no issue will arise as to the existence of any pre-existing condition or its prospective results or as to its relationship with the plaintiff’s incapacity.
(c)In order to discharge the evidential onus, it is not enough for the defendant merely to suggest the existence of a progressive pre-existing condition or a relationship between any such condition and the plaintiff’s incapacity. The defendant must introduce evidence of both the pre-existing condition and its future probable effects or its actual relationship to the plaintiff’s incapacity which, if accepted, would establish with some reasonable measure of precision what the pre-existing condition was and what its future effects, both as to their nature and their future development and progress, were likely to be.
(d)If the defendant discharges the evidential onus of proof, it is for the plaintiff, upon the whole of the evidence, to satisfy the Court of the extent of the injuries caused by the defendant’s negligence.
[13]See, Purkess (1965) 114 CLR 164, 167-8; Seltsam Pty Ltd v Ghaleb [2005] NSWCA 208 (1 September 2005) [93]-[112] (‘Seltsam’).
The Court distinguishes between proof of historical facts (that is, what has happened in the past) and proof of future possibilities and past hypothetical situations (that is, what would or might have happened). The civil standard of proof applies to the former but not to the latter.[14]
[14]Malec v JC Hutton Pty Ltd (1990) 169 CLR 638, 642-3 (‘Malec’); Sellars v Adelaide Petroleum NL (1994) 179 CLR 332, 349-50, 353, 355, cited in Acir [2009] VSC 454 (7 October 2009) [263]-[264].
In the case of historical facts, the Court determines on the balance of probabilities whether an event has or has not occurred, and makes an assessment of damages on an ‘all or nothing’ approach in relation to that event.[15]
[15]Malec (1990) 169 CLR 638, 642-3.
However, in the case of future or hypothetical events, which are generally not amenable to proof, the court takes a different approach. The Court takes these events into account in the assessment of damages in terms of the degree of probability of their occurrence. That is, except in the extreme cases of mere speculation or practical certainty, the Court makes an estimate of the likelihood that an event would have occurred in the past or might occur in the future and adjusts its award of damages accordingly to reflect the degree of probability.[16] This approach is based on the principles set out in Malec v JC Hutton Pty Ltd[17] (‘Malec principles’).
[16]Malec (1990) 169 CLR 638, 642-3; Seltsam [2005] NSWCA 208 (1 September 2005) [103], cited in Acir [2009] VSC 454 (7 October 2009) [263], [265].
[17](1990) 169 CLR 638, 642-3.
The principles discussed at [136] above about the evidential onus of proof are qualified by the Malec principles.[18] In Seltsam Pty Ltd v Ghaleb,[19] Ipp JA, with whom Mason P agreed, explained the interrelationship between the evidential onus principles and the Malec principles as follows:
Where a defendant alleges that the plaintiff suffered from a pre-existing condition, the evidential onus as explained in Watts v Rake and Purkess v Crittenden remains on the defendant and must be discharged by it. Nevertheless, to the extent that the issues involve hypothetical situations of the past, future effects of physical injury or degeneration, and the chance of future or hypothetical events occurring, the exercise of ‘disentanglement’ discussed in those cases is more easily achieved. That is because the court is required to evaluate possibilities in these situations – not proof on a balance of probabilities.
Without intending to give an exhaustive list of possibilities, it may be that, had the defendant’s negligent act not occurred, a pre-existing condition might have given rise to the possibility that the plaintiff’s enjoyment of life and ability to work would have been reduced and to a susceptibility to further injury; in addition, other causes entirely unrelated to the defendant’s negligent act might have contributed to the plaintiff’s ultimate condition.
Appropriate allowances must be made for these contingencies. A proper assessment of damages requires the making of a judgment as to the economic and other consequences which might have been caused by a worsening of a pre-existing condition, had the plaintiff not been injured by the defendant’s negligence. A pre-existing condition proved to have possible ongoing harmful consequences (capable of reasonable definition) to the plaintiff, even without any negligent conduct on the part of the defendant, cannot be disregarded in arriving at proper compensation.[20]
[18]Seltsam [2005] NSWCA 208 (1 September 2005) [104].
[19][2005] NSWCA 208 (1 September 2005).
[20]Seltsam [2005] NSWCA 208 (1 September 2005) [105]-[107] (emphasis in original).
Assessment of past economic loss
The parties have agreed that Mr Clark’s earnings at the time of the accident were $842 gross plus $388 gross in overtime plus $76 gross in superannuation.
Table 3, below, sets out the parties’ agreed calculations of loss of past earnings.
PERIOD
LOSS OF EARNINGS
AMOUNT
15/12/07 – 30/6/08
30 weeks @ $1,022
$30,660.00
1/7/08 – 30/6/09
52 weeks (with 4% increase applied)
$876 + $403 =$1,279 less $288 tax = $991 + $78 = $1,069 x 52$55,588.00
1/7/09 – 30/6/10
52 weeks (with 3% increase applied)
$902 + $415 = $1,317 less $297 tax = $1,020 + $81 = $1,101 x 52$57,252.00
1/7/10 – 30/6/11
52 weeks (with 3% increase applied)
$929 + $427 = $1,356 less $304 tax = $1052 + $84 = $1,136 x 52$59,072.00
1/7/11 – 23/9/11
12 weeks (with 4% increase applied)
$966 + $444 = $1,410 less $323 tax = $1,087 + $87 = $1,174 x12$14,088.00
$216,660.00
Mr Casey submitted that, but for the accident, Mr Clark would have been able to continue his work at Tieman, with overtime, until 65 years of age.
Mr Moore submitted that, in the light of the evidence of Dr Colman and Dr Gow, Mr Clark’s loss of past earnings should be assessed on the basis that he would have continued to work and earn income at the rates set out in Table 3 until December 2009.
At [122] above, I concluded that, notwithstanding Mr Clark’s pre-existing conditions, but for the accident, he:
(a)would have been able to continue performing the same duties with overtime until December 2009;
(b)would have been able to continue performing the same duties without overtime until December 2010;
(c)would have been able to continue working until December 2011 if Tieman halved his pre-injury hours (inclusive of overtime) and assigned him lighter duties;
(d)could well have continued working until December 2012 on reduced hours and lighter duties; and
(e)would not have worked in any capacity beyond December 2012.
In arriving at these conclusions, I was mindful of the onus of proof principles set out at [135] to [140] above. I was satisfied that Tieman had discharged the evidential onus of establishing with some measure of precision what Mr Clark’s pre-existing condition was and what its future effects, both as to their nature and their future development and progress, were likely to be. Tieman did so principally through the evidence of its sole witness, Dr Gow, and the cross-examination of Dr Colman and Dr Bassily. Once I was satisfied that Tieman had discharged the evidential onus, I looked at the evidence as a whole in reaching the conclusions set out at [122] and [145] above.
Given Mr Clark’s resilience in working extensive overtime while suffering from a serious liver condition, there was no real prospect that health issues other than his pre-existing conditions would have intervened to cut short his ability to work full‑time at Tieman prior to December 2009 or on reduced hours prior to trial.
The Malec principles must be applied in resolving the hypothetical question of what income Mr Clark would have earned until 23 September 2011 if the accident had not occurred. Having regard to the conclusions set out at [145] and [147] above, it is appropriate to provide for a discount of 18 per cent to the calculations set out at [142] above.
It follows that, with some rounding off, I assess Mr Clark’s loss of past earnings at $177,700.
Assessment of future loss of earning capacity
The parties have calculated Mr Clark’s future loss of earning capacity until 65 years of age in the capital sum of $168,586.
Mr Casey submitted that, in the light of the matters set out at [110] to [114] above, I should accept that, but for the accident, Mr Clark would have worked until 65 years of age and that the discount to be applied to the capital sum set out at [150] above – to deal with normal vicissitudes and the possible effects of Mr Clark’s pre-existing liver condition – should not exceed 20 per cent.
Mr Moore submitted that, having regard to the evidence of Dr Colman and Dr Gow, no allowance should be made for future loss of earning capacity.
In the light of the conclusions set out at [122] and [145] above, the Malec principles warrant a discount to the calculation of future loss of earning capacity in the order of 77 per cent. Judging by the regular overtime that Tieman offered to Mr Clark, it appears that he was well regarded and that his job was secure. Given that Mr Clark was highly motivated and was the sole wage earner in the family, there was no prospect that he would voluntarily cease work prior to normal retirement. Accordingly, it is not necessary to provide any additional discount for the vicissitudes of retrenchment or early retirement. However, it is appropriate to add a discount of five per cent to take into account vicissitudes such as the non‑availability of light duties at reduced hours (whether at Tieman or elsewhere) and the absence from work due to accidents unrelated to employment or illnesses unrelated to the effects of the cirrhosis of the liver (such as diseases related to cigarette smoking).
Applying a total discount of 82 per cent to the capital amount of $168,586, with some rounding off, produces a capital sum of $30,400 to compensate Mr Clark for future loss of earning capacity resulting from the accident-related injuries and their effects.
Fox v Wood
Tieman has calculated the total amount of taxation that Mr Clark has paid on worker’s compensation payments at $24,170. Accordingly, the Fox v Wood[21] component of the pecuniary loss damages is $24,170.
[21](1981) 148 CLR 438.
Proposed order
I propose to give judgment in favour of Mr Clark in the amount of $532,270, comprising $300,000 for pain and suffering damages and $232,270 for pecuniary loss damages. I will hear from counsel on the precise form of the judgment and in relation to interest and costs.
---
4
9
0