Westcott v Minister for Health - [2015] WADC 122

JURISDICTION : DISTRICT COURT OF WESTERN AUSTRALIA
IN CIVIL

LOCATION: PERTH

CITATION: WESTCOTT -v- MINISTER FOR HEALTH [2015] WADC 122

CORAM: MCCANN DCJ

HEARD: 18, 23-27, 30-31 MARCH, 2 APRIL & 22 JUNE 2015

DELIVERED : 23 OCTOBER 2015

FILE NO/S: CIV 1834 of 2012

BETWEEN: DARREN MARK WESTCOTT
Plaintiff
AND
MINISTER FOR HEALTH
Defendant

Catchwords:

Torts - Professional negligence - Medical care in a public hospital - Turns on own facts

Assessment of damages - Turns on own facts

Legislation:

Civil Liability Act 2002 (WA) s 5B, s 5C, s 5P, s 5PBC(1)
Hospital and Health Services Act 1927 s 7

Result:

Judgment for the plaintiff for $933,544.87

Representation:

Counsel:

Plaintiff: Mr G C Droppert & Mr R D McCabe
Defendant: Dr A B Lu OAM

Solicitors:

Plaintiff: Slater & Gordon
Defendant: Jarman McKenna

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

Arthur Robinson (Grafton) Pty Ltd v Carter (1968) 122 CLR 649
Beer v Duracraft Pty Ltd [2004] WASCA 192
Bowen v Tutte (1990) Aust Torts Rep 81‑043
Briginshaw v Briginshaw (1938) 60 CLR 336
CGU Insurance Ltd v Porthouse (2008) 235 CLR 103
Chamberlain v The Queen (No 2) (1984) 153 CLR 521
Chapman v Katheappa [2002] WADC 47
Chapman v Katheappa [2003] WASCA 50
Fox v Percy [2003] HCA 22; (2003) 214 CLR 118
Griffiths v Kerkemeyer (1977) 139 CLR 161
Jones v Dunkel (1959) 101 CLR 298
Le Brun v Joseph & Ors [2006] WADC 200
Makita (Aust) Pty Ltd v Sprowles [2001] NSWCA 305; (2001) 52 NSWLR 705
Medlin v State Government Insurance Commission (1995) 182 CLR 1; 127 ALR 180
Montemaggiori v Wilson [2011] WASCA 177
Pollock v Wellington (1996) 15 WAR 1
Pownall v Conlan Management Pty Ltd (1995) 12 WAR 370
Purkess v Crittenden (1965) 114 CLR 164
Ramsay v Watson (1961) 108 CLR 642
Robinson v Riley [1971] 1 NSWLR 403
Rogers v Whitaker (1992) 175 CLR 479
Sharman v Evans (1977) 138 CLR 563
Strong v Woolworths Ltd (t/as Big W) [2012] HCA 5; (2012) 246 CLR 182
Swick Nominees Pty Ltd t/as Swick Drilling Australia v Norncott Pty Ltd [No 3] [2013] WASC 173
Tabet v Gett (2010) 240 CLR 537
Wade v Allsop (1976) 50 ALJR 643
Watts v Rake (1960) 108 CLR 158
Wilson v McLeay (1961) 106 CLR 523

MCCANN DCJ:

Introduction and background facts

In this matter the plaintiff claims damages for personal injuries for alleged negligence when he was a patient of Fremantle Hospital (the Hospital) between 31 July 2009 and 6 August 2009. Liability and quantum are in issue.
At all material times the defendant had the management and control of the Hospital pursuant to s 7 of the Hospital and Health Services Act 1927. The defendant conducted, managed and maintained the Hospital and employed and/or engaged consultants, specialists, medical practitioners, nurses and other staff for that purpose.
The Hospital conducted a public Emergency Department (ED) at all material times.
The basic facts as found by me are as follows (many were not in contention).
The plaintiff was born on 21 January 1968.
On or about 25 July 2009 he began feeling symptoms of pain and discomfort in his lower abdomen. These did not resolve and he attended his general practitioner (Dr Gary Spurge) on 29 July. He was prescribed oral antibiotics (Cephalexin I, 500 mg, three times per day with meals).
His symptoms worsened to include some vomiting, constipation and diarrhoea.
He was in distress on the morning of 31 July and had difficulty breathing. His wife, Ms Tania Westcott, called an ambulance at 8.31 am.
He was taken to the Hospital by ambulance and arrived at about 9.49 am.
He was triaged by a member of the nursing staff. Later, he was reviewed by ED doctors including an emergency physician, Dr Banham.
Dr Banham took a full history and carried out a physical examination. He decided upon a working diagnosis of acute abdominal sepsis and queried whether a perforated diverticulum was involved. He ordered conservative management including analgesia, hydration and intravenous triple antibiotics (Gentamicin, Amoxicillin and Metronidazole). He also requested chest x‑rays, CT scans of the abdomen and pelvis and a surgical review from Dr Andrew Finlayson.
The plaintiff underwent the CT scan at 2.42 pm. The radiologist, Dr Michael Krieser, diagnosed acute diverticulitis of the sigmoid colon accompanied by a quantity of free fluid in the pelvis, but pointed out that there was a lack of diverticuli outlined on the scan (a contra‑indicator to diverticulitis). His differential diagnosis was sigmoid cancer.
The plaintiff was admitted to the Hospital under the on-call consultant surgeon, Dr Dean Lisewski. Dr Lisewski reviewed him and the CT images at 6.30 pm and formed a clinical impression of an inflamed sigmoid colon with localised pelvic inflammation, likely due to diverticulitis. He pended a decision on exploratory surgery and ordered the continuation of conservative management with close observation and review.
The plaintiff was managed accordingly. Dr Lisewski completed his on‑call session on the morning of 3 August. Consultant surgeon Dr Makin and a senior colorectal registrar, Dr Lau took over responsibility for the plaintiff.
Following a radiological review that morning, the plaintiff's working diagnosis changed from diverticulitis to appendicitis. However, conservative management continued with provision for surgical intervention if his condition deteriorated.
On the evening of 6 August Dr Lau, performed an exploratory laparoscopy. Dr Lau's findings included a thickened and inflamed appendix, the presence of fibrinous exudate, an abscess between the appendix and sigmoid colon, a thickened sigmoid colon and an erythematous terminal ileum attached to the inflammatory mass in the pelvis. In short, there was a large pelvic abscess surrounded by multi‑visceral inflammation. Dr Lau believed that the abscess was secondary to localised perforated appendicitis.
Dr Lau performed a laparotomy, removed the abscess and performed an appendectomy. He also performed a colonoscopy which eliminated any perforation of the sigmoid colon.
The plaintiff suffered acute respiratory complications whilst he was in the operating theatre. He required post‑operative intubation and observation in the intensive care unit (ICU). An ICU bed was not available so he was transferred to Sir Charles Gairdner Hospital (SCGH).
He experienced a complicated recovery and developed pneumonia. He required sedation, and drainage of his right lung and developed pulmonary embolisms. He eventually required a tracheostomy.
He was discharged from SCGH on 2 September but required regular inpatient and outpatient treatment for further complications.
In October 2010 he underwent surgery to repair incisional hernias associated with the laparotomy. In November he developed a serious infection of the surgical wound for which he was hospitalised until 18 January 2011 and again (briefly) in February. He has been left with a number of scars.
He developed psychiatric complications, including depression and post‑traumatic stress disorder (PTSD) arising from when he was conscious in ICU.
He was able to return to work in his information technology business, but he later closed that and took up employment with others. He completely ceased employment and has not worked since January 2014.

An overview of the issues.

It is common ground that the defendant owed the plaintiff a non‑delegable duty to exercise reasonable care and skill in the provision of diagnostic and treatment services at the Hospital. It is also common ground that the defendant was vicariously liable for the negligence of the Hospital staff.
The plaintiff contends that the Hospital staff breached that duty of care by mis‑diagnosing diverticulitis on 31 July and subsequently when, on the clinical and radiological evidence, he should have been diagnosed with appendicitis and treated accordingly, including by early laparoscopic investigation.
The plaintiff contends that the laparoscopy would have identified the appendicitis and the need for an immediate appendectomy, which could have been carried out during the laparoscopy, or via laparotomy if the appendicitis and/or any abscess was found to be advanced. The pelvic fluid collection and any abscess could have been drained at the same time.
The plaintiff contends that the mis‑diagnosis was maintained until at least 3 August and, further and in any event, appropriate treatment was unreasonably delayed at all material times.
He contends that if treatment had not been delayed it is probable that he would have experienced a complete and uneventful recovery within one or two weeks. To be clear about this, he does not advance an argument based on the loss of a chance and relies on Tabet v Gett (2010) 240 CLR 537. He contends that his complicated appendicitis and sequelae were caused by the Hospital's negligence. Those are (not in chronological order):
(i)acute appendicitis;
(ii)respiratory failure;
(iii)deep wound infection;
(iv)pulmonary embolism;
(v)wound breakdown and cellulitis;
(vi)incisional hernia;
(vii)oesophageal reflux;
(viii)scarring;
(ix)hypertension;
(x)psychological trauma.
The plaintiff adduced expert evidence from Professor Kenneth Thomson (a radiologist), Associate Professor John Raftos (a specialist in emergency medicine) and Professor James Toouli (a consultant general surgeon) to the effect that a working diagnosis of appendicitis should have been made in the first instance and urgently assessed by laparoscopy.
The defendant denies that the Hospital and its employees breached their duties of care.
The defendant contends that on admission the clinical situation was one of delayed presentation (ie, a seven day history) of abdominal pain in the region of the sigmoid colon, consistent with diverticulitis. It contends that appendicitis was secondary to the inflammatory process in the sigmoid colon and adjacent structures.
The defendant therefore contends that, having regard to reasonable therapeutic standards, conservative management was correct, even when the working diagnosis changed to appendicitis on 3 August, because the plaintiff's systemic symptoms were improving at that time. The need to proceed to surgery on 6 August only arose because the plaintiff's symptoms deteriorated the previous night.
The defendant adduced expert evidence from Associate Professor John Mackay (a consultant general surgeon) and Associate Professor Andrew Little (a consultant radiologist). Associate Professor Little concurred with Professor Thomson's opinion that the CT scans of 31 July showed evidence of appendiceal inflammation which was consistent with appendicitis, but in his opinion the appearance was secondary to sigmoid colitis.
Therefore, it is common ground that Dr Krieser failed to report evidence of appendicitis, but the defendant contends (in reliance on the evidence of Associate Professor Mackay) that conservative management was appropriate anyway.
To sum up in relation to liability, the issues are, first, whether Dr Krieser's failure to report the evidence of appendicitis was negligent, and secondly whether the overall diagnostic and management plan was negligent.
As to causation, in submissions filed before the trial the defendant sought to advance an argument based on s 5P of the Civil Liability Act 2002 to the effect that the plaintiff's complications were the materialisation of inherent risks of abdominal surgery which could not have been avoided by the exercise of reasonable skill and care by the Hospital. That contention was not pleaded and the need for the defendant to do so arose a number of times before and during the trial. Eventually the defendant elected to abandon the statutory plea whilst maintaining a traverse of the plaintiff's pleadings based on the contention that the complications would, and as a matter of fact did, occur independently of its negligence.
So far as quantum is concerned, the defendant does not dispute that the plaintiff has suffered the physical and psychiatric sequelae referred to above, save for oesophageal reflux which it contends was a pre‑morbid condition. It also contends that he has made a better recovery and has retained more earning capacity than he contends.

Liability – relevant principles

The plaintiff's claim is based in negligence and is subject to the Civil Liability Act.
Section 5B sets out general principles as follows:
(1)A person is not liable for harm caused by that person's fault in failing to take precautions against a risk of harm unless –
(a)the risk was foreseeable (that is, it is a risk of which the person knew or ought to have known);
(b)the risk was not insignificant; and
(c)in the circumstances, a reasonable person in the person's position would have taken those precautions.
(2)In determining whether a reasonable person would have taken precautions against a risk of harm, the court is to consider the following (amongst other relevant things) –
(a)the probability that the harm would occur if care were not taken;
(b)the likely seriousness of the harm;
(c)the burden of taking precautions to avoid the risk of harm;
(d)the social utility of the activity that creates the risk of harm.
Section 5PB(1) of the Act specifically provides that an act or omission of a health professional is not a negligent act or omission if it is in accordance with a practice that, at the time of the act or omission, is widely accepted by the health professional's peers as competent professional practice. However, whether reasonable care has been exercised is a question for the court. An expert may give evidence of an objective standard that is pertinent to a professional of a relevant kind (CGU Insurance Ltd v Porthouse (2008) 235 CLR 103).
In Rogers v Whitaker (1992) 175 CLR 479, Mason CJ, Brennan, Dawson and McHugh JJ said at (489; emphasis added):
The duty of a medical practitioner to exercise reasonable care and skill in the provision of professional advice and treatment is a single comprehensive duty. However, the factors according to which a court determines whether a medical practitioner is in breach of the requisite standard of care will vary according to whether it is a case involving diagnosis, treatment or the provision of information or advice; the different cases raise varying difficulties which require consideration of different factors. Examination of the nature of a doctor-patient relationship compels this conclusion. There is a fundamental difference between, on the one hand, diagnosis and treatment and, on the other hand, the provision of advice or information to a patient. In diagnosis and treatment, the patient's contribution is limited to the narration of symptoms and relevant history; the medical practitioner provides diagnosis and treatment according to his or her level of skill. …
The notion of 'a single comprehensive duty' extends to the exchange of information within a hospital's health professionals, as the facts and the circumstances require. And the issues must be addressed prospectively rather than with the benefit of hindsight. (But this does not mean that subsequent events cannot be circumstantially relevant).

Evidentiary principles

I am required to make findings on the ultimate issues on the balance of probabilities based on a body of direct and circumstantial evidence.
In a circumstantial case an ultimate fact is taken to be proven if the court is satisfied (ie, can infer) based on the whole of the evidence that it is more probable than not that the fact occurred or exists (Chamberlain v The Queen (No 2) (1984) 153 CLR 521, 536, (Gibbs CJ and Mason J)). By 'more probable is meant no more than that upon a balance of probabilities … an inference might reasonably be considered to have some greater degree of likelihood' than others that are open (Jones v Dunkel (1959) 101 CLR 298, 310 (Menzies J)).
But, being satisfied as to the standard of proof is not an arithmetical exercise. I am required to be actually persuaded as to the probability of a fact being true (Briginshaw v Briginshaw (1938) 60 CLR 336). Nor should I confuse mere conjecture with reasoned conclusion (Jones v Dunkel (305) (Dixon CJ), 309 – 310 (Menzies J)).
Inferences 'from actual facts that are proved are just as much part of the evidence as those facts themselves' (Jones v Dunkel (309) Menzies J)).
I am also mindful that a circumstantial case which is reliant on deduction by a process of elimination is potentially fraught with the fallacy that a hypothesis is correct merely because it is the only one left. Findings must be supported by evidence and an assumption is not evidence (Swick Nominees Pty Ltd t/as Swick Drilling Australia v Norncott Pty Ltd [No 3] [2013] WASC 173).
The assessment of the credibility or reliability of evidence is a multi‑factorial task. The appearance and demeanour of witnesses are relevant factors, but there is a danger in too readily drawing conclusions about truthfulness and reliability solely or mainly from such considerations. Judges are encouraged to 'limit their reliance on the appearance of witnesses and reason to their conclusion, as far as possible, on the basis of contemporary materials, objectively established facts and the apparent logic of events' (Fox v Percy [2003] HCA 22; (2003) 214 CLR 118, [30] ‑ [31] (Gleeson CJ, Gummow, Kirby JJ)).
It is also useful to take into account the cooperativeness and frankness of witnesses and their willingness to make concessions.
An expert is permitted to give evidence of an opinion (which would otherwise be hearsay) with respect to a factual issue which requires expert elucidation if he or she is qualified by training or experience to do so. Opinion evidence is admissible for the purpose of assisting the court to make findings of fact.
Opinion evidence, and findings derived from the same, must be based upon facts or stated assumptions that are proven (or bear sufficient correlation to facts which are proven) and must be explained in such a way that the court can comprehend it and make the necessary findings, or at least understand why it should be adopted or deferred to. (Pownall v Conlan Management Pty Ltd (1995) 12 WAR 370; Pollock v Wellington (1996) 15 WAR 1, 3 (Anderson J); Beer v Duracraft Pty Ltd [2004] WASCA 192 [78] – [80] (McLure J); and Makita (Aust) Pty Ltd v Sprowles [2001] NSWCA 305; (2001) 52 NSWLR 705, [64] (Heydon JA)).
As with lay witnesses, the court is entitled to accept all of a particular expert's evidence, or none of it, or accept some and reject the rest, or simply put it to one side (Ramsay v Watson (1961) 108 CLR 642; 645). In this way findings can be drawn from evidence and opinions of more than one expert, irrespective of who adduced the evidence.
The assistance to be derived from expert evidence, ie, its weight, may also depend to some extent on the degree of specialisation involved in the relevant expert field, because some fields are more esoteric than others.
But, I stress that in very technical or esoteric areas (of which radiology and surgery are examples) the purpose of expert evidence is not to educate the court so that it may then form and rely upon its own view. The court cannot substitute a diagnostic or pathological role for its forensic role.

Meta‑glossary of terms

I have prepared a 'meta-glossary' of terms which is annexure 1 to these reasons and is to be read as part of them. It is based on the evidence as a whole, but mostly that of Professors Toouli, Thomson and Mackay. I have obtained some assistance from Mosby's Dictionary of Medicine Nursing and Health Professions (ANZ ed, 2006 reprint) in relation to non-controversial technical words which were used in the evidence. The prefix 'meta' denotes that the meanings have been adopted by me in accordance with my understanding of the evidence (ie, they are findings). Some terms have also been defined or explained in these reasons.

The organisation of the Hospital

Dr Lisewski explained the Hospital's hierarchy and procedures in 2009.
The Hospital was divided into four units, A, B, C and D. Unit A was the colorectal unit, B was the endocrine and general surgical unit, C was the hepatobiliary unit and D was the emergency unit. As such, when he was on-call emergency patients were admitted under him to the 'Surgical D' unit.
There was no colorectal consultant on call to cover unit A during the weekends. So, as the surgical consultant on call, he was ultimately responsible for all colorectal surgical emergencies as well as general surgical emergencies.
The hierarchy beneath Dr Lisewski comprised senior registrars (ie, trainee consultants such as Dr Lau who was in unit A), registrars and less qualified doctors including residents. As the consultant, Dr Lisewski had the 'final say'.
Moving on to ward procedures, Dr Lisewski explained that a 'handover' meeting occurred every morning at 7.00 am (except on Sundays when it was at 8.00 am), to enable the night staff to hand over to the day staff. All new cases were explained and existing cases were reviewed. The meeting took place in a designated room adjacent to the ED and acute surgical unit. The room was fully equipped with computers and screens.
Ward rounds were then conducted by the senior doctor on duty (assisted by junior staff) in order to see and review each patient. A ward round might be (but was not invariably) described in the notes as a 'consultant's ward round', or a 'registrar's ward round' depending on who was in charge of it. The notes were written up in the integrated progress notes by the most junior doctor present. Dr Lisewski never made any notes on those occasions.
He insisted several times (ts 577, 591 – 592, 610, 611 – 612) that he never missed a ward round in his career as a consultant. He always saw every patient on a ward round every morning, without exception, and he had a statutory and professional duty to do so. ('I would see the sick patients without fail'). I accept that evidence, but it follows from what he said above ([61)] that these visits were not always formal in the sense that sometimes a registrar would be in charge of a true 'ward round'.
Other documentary records included scans, reports, nursing notes, observation charts, test results and the like.
Based on the documentary evidence I have inferred that a specialised ward known as the 'Nurse Specials Unit' (NSU) provided elevated levels of observation and care (see [100] and [157] below) for patients who were very sick but not in need of ICU care.

The anatomy of the intestinal system

The abdominal cavity contains the intestines and other organs such as the bladder, liver, pancreas, gall bladder, spleen, kidneys and glands, as well as fatty tissues. The intestines comprise the large and small intestines (or bowels).
The small intestine lies within the large intestine. It is connected to the stomach via the duodenum and to the large intestine via the ileum and cecum (aka caecum) in the right iliac fossa.
An illustrative diagram of the large intestine (exhibit 30) depicts a loose 3 ½ sided square (the reality is not symmetrical).
Food passes from the stomach into the small intestine, where it is digested. Waste exits and passes through the ileum and into the cecum via the ileocecal valve. It then passes upwards through the right-sided segment of the large intestine (the ascending colon).
The ascending colon flexes at the hepatic flexure and extends horizontally to the left (the transverse colon). The transverse colon flexes at the splenic flexure and descends (the descending colon) to the sigmoid flexure (approximately opposite the cecum).
The sigmoid colon is the fourth (incomplete) side of the 'square' and extends horizontally from the sigmoid flexure to the right to the mid‑line of the abdomen. It then flexes downwards at the rectosigmoid flexure and becomes the rectum.
The ascending and descending colons are fixed to the abdominal wall (the peritoneum) and are therefore relatively static, but the transverse colon is suspended from surrounding mesentery and is more flexible. The sigmoid colon is also a relatively free structure that is attached to mobile mesentery.
The appendix is an out-pouching of the base of the cecum. It is not anchored to any other anatomy and can flex in various directions, including leftwards towards the sigmoid colon or upwards towards the ileum. It is a redundant relic of a bygone stage of human evolution when homo-sapiens enjoyed a vegetable–based diet (as remains the case for some ruminant mammals, such as cattle, which still have a use for it).
The dimensions of a healthy adult appendix are typically 7 – 8 cm in length (Dr Raftos, ts 508) and approximately 6 – 7 mm in internal diameter (Professor Thomson, ts 481; Professor Little, ts 341).
In cross-section (from inside to out) the appendix and sigmoid colon comprise (relevantly) the lumen, mucosal lining, muscularis propria and serosa.
The cecum, appendix and each segment of the large intestine receives a blood supply from arteries which originate from the aorta. Blood is drained and returned to the heart through veins which lie parallel to the arteries.
A third circulatory system known as the lymphatic system lies adjacent to the arterio-venous system and drains fluids that leak from the capillaries of the arterial system into lymph nodes. The lymph nodes produce white blood cells which fight infection. They become particularly active (enlarged) in case of inflammation or infection.

Liability: the plaintiff's evidence

The plaintiff testified that initially he had a pain in the right side of his abdomen. He went to see Dr Spurge when it did not subside. The following day he was in too much pain to work and stayed at home. His wife went to see Dr Spurge and obtained some pain medication. That made him feel better for an hour or so, but then he returned to bed.
The following morning (31 July) he could hardly stand or walk and was having trouble breathing. His wife called the ambulance. At that time his pain was predominantly right‑sided, although it travelled all over his abdomen (ts 37).
He testified that he told the ED staff the same thing.
They gave him some morphine on a couple of occasions. He remembers x‑rays and the CT scan being taken and being moved to a ward sometime in the late afternoon. At the time he was still in a lot of pain, had nausea (he thinks he may have vomited), was uncomfortable, hot and struggling to breathe (ts 38).
His memories after that are blurry. The main things that he remembers are being in pain and thirsty and visits from his family. He testified (ts 39) that he was constantly asking for pain medication. He noticed that he felt better for short periods after he took the painkillers, but the pain would return a few hours afterwards (worse on occasions).
His next memory is awaking in ICU at SCGH.

Findings based on the Hospital's records

It is convenient to make some findings based on my construction of the Hospital records before I deal with Dr Lisewski's and the experts' evidence. Except where I have stated otherwise, what follows is based on the ED notes and Integrated Progress Notes. These are contemporaneous records of direct clinical interactions between the plaintiff and members of the Hospital staff. (The emphases, parentheses and intercalations in these reasons are mine unless stated otherwise).
I commence with Friday 31 July.
The plaintiff was triaged by an ED nurse on arrival at the Hospital. He reported a one week history of abdominal pain in the suprapubic region and having attended his general practitioner who prescribed 'Keflex' [sic] for a bowel infection.
A doctor ('John K') took a detailed history at 10.00 am and noted the following:
(i)The plaintiff was a 41‑year‑old male with history of suprapubic pain, vomiting and diarrhoea.
(ii)His presenting symptoms included:
(a)Suprapubic pain of one week's duration, fluctuating in intensity with no radiation of pain.
(b)He had initially experienced constipation, but after four days this switched to diarrhoea.
(c)He started vomiting (non‑bilious) the previous night.
(d)He had experienced fevers, chills and rigors ('++').
(e)He had not passed urine since the previous afternoon.
(iii)He was experiencing abdominal pain (10/10) in the suprapubic and left iliac‑fossa regions, associated with shortness of breath caused by pain.
(iv)He reported a past history of a spinal injury and gastro‑oesophageal reflux disease.
(v)On examination he:
(a)Had a temperature of 38.3, a pulse of approximately 130 and a blood pressure of 155/75.
(b)Weighed 120 kg.
(c)Was in pain, with some respiratory distress.
(d)Was obese in the abdomen.
(e)Was very tender to palpation in the suprapubic and left iliac fossa region. (The pain distribution was illustrated by a diagram).
Bowel sounds were not audible after two minutes. Guarding was noted in the left iliac‑fossa and peri‑umbilical area.
The plaintiff was reviewed by Dr Banham at 10.44 am who noted:
(i)The plaintiff described a history of nine days of abdominal pain which was initially a sharp left‑sided stab which progressively got worse. His pain was now generalised, but worse on the left.
(ii)He reported alternating bowel habits, being constipated at first but then small amounts of loose stool with mucus but no blood.
(iii)On examination the plaintiff was:
(a)Alert with a temperature of 38.3ºC and a pulse of 130.
(b)His abdomen was generally tender with guarding and rebound, maximally in the left iliac fossa. The abdomen was consistent with an elevated Body Mass Index [obesity].
Dr Banham formed a clinical impression of acute abdominal sepsis ('acute abdomen/septic') and queried whether (ie, suspected that) a perforated diverticulum was involved. His plan was for analgesia, triple antibiotics, a surgical opinion and radiological investigation.
At 11.06 am the plaintiff underwent an abdominal x‑ray, the findings of which were:
There is slight distension of the transverse colon with some associated oedema of its wall. The remainder of the abdomen is largely gasless and likely reflecting the presence of fluid within bowel loops. A few fluid levels seen on the erect film are also in keeping with this. This is a non‑specific appearance. The possibility of diverticulitis, as indicated on the request form, could be further evaluated by means of a CT scan if clinically indicated.
At Dr Banham's request the plaintiff was reviewed at 1.00 pm by a surgical registrar, Dr Finlayson. He carried out an examination and noted:
(i)The plaintiff reported a nine day history of lower abdominal pain, initially in the suprapubic region, but he now felt it across the entire lower abdomen.
(ii)He had been vomiting for the last 24 hours.
(iii)He had been constipated for seven days but never had diarrhoea.
(iv)He had had fevers.
(v)He saw his general practitioner 3 days prior, and was commenced on oral antibiotics for a 'bowel infection'.
(vi)The plaintiff reported that he had undergone a colonoscopy 10 years prior for 'polyps', and he had a previous right inguinal hernia repair.
(vii)On examination the plaintiff:
(a)Was dehydrated and sweaty.
(b)His temperature was 38.1, his pulse was 120 and his blood pressure 136/72.
(c)Was obese, tender in the lower abdomen (more so on the right than on the left), with guarding and no rebound. (The pain distribution was illustrated by a diagram).
Dr Finlayson noted that the chest x‑ray showed no free gas and that the abdominal x‑ray showed no obstruction. He noted various test results including a WCC of 15.7.
His clinical impression was possible diverticulitis. The management plan was to refer the plaintiff for a CT scan, admit him to a general surgical ward under Dr Lisewski and continue with conservative management with the addition of prophylactic anti‑coagulant treatment ('Heparin and TEDS').
It is to be noted that by this stage the plaintiff's pain (as reported or observed on examination) fluctuated across his entire lower abdomen.
He underwent the CT scan at 2.42 pm. Dr Krieser was provided with a clinical history of 'left iliac fossa and suprapubic pain for one week ?Diverticulitis'.
Dr Krieser's findings were:
There is an approximately 7 cm segment of thickened distal sigmoid with prominent surrounding inflammatory stranding and a small 2.3 cm pericolic collection of its right margin. There are also 2 tiny locules of free intraperitoneal gas. Several mildly enlarged lymph nodes are seen in the adjacent mesentery and there are multiple enlarged retroperiotoneal nodes. The appearances most likely represent acute diverticulitis complicated by small pericolic abscess and very small perforation. However, no gas filled diverticula have been outlined within the colon. A sigmoid neoplasm remains a differential.
There is a small amount of free ascetic fluid within the pelvis but no large collection is present for drainage.
The small bowel and remaining colon are unremarkable.
The liver, spleen, pancreas, kidneys and adrenal glands are satisfactory in appearance.
Mild/bibasal atelectasis noted.
Dr Krieser's comment was:
Approximately 7 cm segment of thickened distal sigmoid with prominent surrounding inflammatory change, small pericolic abscess and very small performation (2 small free gas locules). Acute diverticulitis is most likely although no diverticula have been outlined on this study. Sigmoid neoplasis [cancer] remains a differential.
At 4.25 pm Dr Banham noted that the CT scan 'shows thickened 7 cm distal sigmoid [and] 2.3 cm paracolic abscess with 2 small locules of free air'. He also noted: 'LNS++'. [The lymph nodes were swollen]. He resolved to inform the surgical registrar (ie, Dr Finlayson) accordingly and I infer that he did so.
The plaintiff was formally admitted to the general surgical unit D under Dr Lisewski.
However, he was not transferred to a general ward. Based on the Hospital records (exhibit 32, pages 96 ‑ 101, 112 – 115, 117, 133, 135, 136, 138, 140, 148, 150 and 152) I find that he was in the NSU until he was transferred to ward B8 South at 6.10 pm on 2 August. It may be inferred that the anaesthetist who assisted at the plaintiff's operation on 6 August had the NSU in mind when the plaintiff began to experience respiratory complications in theatre (see [157]) and that it was an area of relatively high care. This was not emphasised during submissions, but it has important ramifications. It signifies that the plaintiff was not on a general ward on any occasion when Dr Lisewski saw him and that he was under relatively close observation for his first two days and, therefore, his case was regarded as problematic and taken seriously.
The plaintiff was reviewed by Dr Lisewski during a 'ward round' at 6.30 pm. His past medical history was considered and the CT scan reviewed. The following note was made by a junior doctor who must have been in attendance:
Inflamed sigmoid with microperforation.
Not many diverticula seen.
Small 2 cm pericolic collection.
Dr Lisewski's plan was for conservative management overnight and review the following day. He requested that the plaintiff be watched 'closely' and resolved that he would need a 'laparotomy' if he deteriorated. In other words (I infer) the NSU was appropriate and surgery was a possible option.
According to the nursing observations, the plaintiff's temperature between 10.05 am and 9.40 pm was 38.3, 38.1, 35.7, 37.5, 37.6, 38.6 and 38.3. The 38.6 entry was made at 8.30 pm and circled. I note that the temperature fluctuated markedly over the course of the day (ie. -2.6 and +2.9).
The plaintiff also had 'nausea'.
I move now to Saturday, 1 August.
The plaintiff was reviewed at 12.15 am by a nurse who noted:
(i)He had not vomited since being admitted. [Compare his evidence that he thinks he did vomit].
(ii)He was sweating significantly ('sweating +++').
(iii)He was tachycardiac (pulse was110‑120 bpm).
(iv)His blood pressure was 150/77.
He was reviewed by a nurse at 5.00 am who noted that he was 'quite settled and slept well', but remained tachycardiac (100‑110 bpm). It was noted that his temperature had been 38.6ºC at 10.00 pm, but he was 'afebrile' at 4.00 am.
The plaintiff's blood pressure at 6.00 am was 190/87 and the nurse manager was informed. The resident medical officer was busy so the nurse arranged for a medical review in the morning.
At 11.10 am the plaintiff's temperature was noted to be 37.2 ‑ 37.5ºC (37.4 according to the observation chart).
He was reviewed during a ward round at 11.30 am. The notes were written by Dr Anderson but do not specify who took the ward round itself. I find that Dr Lisewski did so (see [348] (vi)).
The plaintiff reported feeling well and his pain and breathing had settled. On examination his blood pressure was 148/66, his pulse was 104 and urine output was noted to be good.
According to the notes, the clinical impression (of Dr Lisewski, I infer) was that the plaintiff was indeed suffering from diverticulitis. A three‑step management plan was ordered, namely to stay on clear fluids, continue antibiotics for seven to eight days and undergo an investigative colonoscopy in eight weeks. Dr Lisewski directed that the plaintiff be moved 'to the ward', that is out of the NSU.
At 7.45 pm the plaintiff was reviewed (probably by a nurse) who noted (amongst many other things) that his temperature was 38.6 (a febrile episode) and now complained of abdominal pain, mostly in the right upper quadrant, although at times it was in the left upper quadrant and suprapubic region. (I pause to note that, according to the plaintiff's chronology, this complaint was made at 12.15 am the next day and the defendant admitted as much in its defence. However, it is an obvious error because the relevant entry in the notes states that the complaint was made at 7.45 pm and Dr Lisewski was cross‑examined on that basis: ts 593. I shall proceed accordingly). It was noted that the plaintiff was to undergo cardiac monitoring and hourly observations (consistent with being in the NSU).
He was seen by a registrar and a nurse at 9.30 pm. His temperature was 37.6 and his heart rate 120. The registrar directed that the plaintiff was to receive 'nil by mouth' with a view to 'possible theatre tomorrow if still unwell'. I infer that the febrile episode earlier in the evening informed the registrar's thinking.
According to the nursing observations, the plaintiff's temperature over the course of the day between 4.00 am and 9.00 pm was 36.9, 36.8, 37.2, 37.4, 38.6 (at 6.00 pm), 37.1, 37.6, 36.8, 36.3, 37 and 37 (exhibit 32, pages 114 and 138).
I move to Sunday, 2 August.
A nurse noted at 5.00 am that the plaintiff 'slept for moderate periods', required OxyNorm twice for pain relief and was afebrile.
He was reviewed during a ward round at 10.35 am. According to the notes, Drs Lau, Owen, Karimpasara and Stewart attended.
Dr Lisewski testified that he also took part because this was his ward round and that Dr Lau joined him at his request to provide a colorectal opinion. I am not satisfied that Dr Lisewski was present (see [348] (viii)).
According to the notes:
(i)The plaintiff's pain was 'still there', but he was now complaining of scapular pain as well.
(ii)'Wabs' [ie, anti‑coagulant medicines] had not been administered for 18 hours. [The emphasis was in the original, so the omission was regarded as significant].
(iii)On examination the plaintiff had some crepitus in the base of the right lung and had shallow breaths. His abdomen was soft with minimal tenderness. His blood pressure was 112/96.
Dr Lau's clinical impression was that the plaintiff was 'improving' and that conservative management should continue, with some mobilisation, physiotherapy and a chest x‑ray.

A microbiology report (exhibit 32, page 177) became available at 11.02 am which stated that no abnormality had been cultured from blood taken on 31 July and that a further report would be issued if subsequent growth occurred. There was no further report, ie, there was no subsequent growth. This excludes a blood-borne infection on 31 July. Later tests were to the same effect.
The plaintiff was seen by a physiotherapist at noon and by nurses at 12.30 pm, 6.10 pm and 9.10 pm. There were no relevant changes.
According to the nursing observations, the plaintiff's temperature between 4.00 am and 10.00 pm was 36.8, 36.3, 37, 37, 36.5 and 37.2 (exhibit 32 pages 115 and 166). So, he was afebrile all day.
I move to Monday, 3 August.
At 6.00 am the plaintiff told a nurse that the intensity of his pain had not changed since his admission, but it had settled well with OxyNorm and morphine. The nurse noticed that his blood pressure remained elevated and notified the resident medical officer. She noted that the plaintiff remained afebrile and was continuing with intravenous therapy and antibiotics.
Dr Lisewski did not come in for the handover at 7.00 am and it was taken by Dr Finlayson. Soon afterwards the plaintiff's case was discussed at a radiology meeting. Dr Stewart's notes (made at 12.05 pm) read:
Imp:? appendicitis discussed at radiology meeting this am. More likely appendicitis than diverticular disease.
I infer from this that it was decided that appendicitis was a 'more likely' diagnosis than diverticulitis, but the diagnosis was still problematic and the CT scans were not regarded as conclusive.
Dr Stewart reviewed the plaintiff at 12.05 pm. The plaintiff reported 'feeling improved', but was complaining of 'mild discomfort' in the right iliac fossa and was feeling 'lethargic'. He was noted to have been afebrile for the last 24 hours. His blood pressure was 154/96. On examination there was tenderness in the right iliac fossa with no guarding or percussion. (This was diagrammatically illustrated).
The plan was to continue to treat the plaintiff conservatively with intravenous antibiotics and to monitor him for 24 hours, particularly his WCC and temperature. It was noted that if these 'recovered' it was 'likely' that conservative management would continue. A request was made for chest physiotherapy.
A nursing note at 2.50 pm recorded that the plaintiff's observations were stable and he was afebrile.
The plaintiff was reviewed by a registrar (Dr Nazaar, with Drs Anderson and Stewart attending) at 4.30 pm. Under the heading 'Registrar review Surg A' (ie, the colorectal surgery unit) the following was noted:
(i)The plaintiff was 'still drowsy' and complained of mild abdominal pain.
(ii)His WCC was 13 and CRP level 400.
(iii)His observations were stable and afebrile.
(iv)On examination, his abdomen was tender to percussion in the right iliac fossa, with guarding. (This was illustrated by a diagram similar to Dr Stewart's from 4 hours prior).
The clinical impression was 'acute appendicitis' and that the plaintiff needed surgery. A four step plan was put in place including fasting and booking an operating theatre.
Dr Stewart discussed this with Dr Lau at 4.45 pm. Dr Lau ordered continuation of conservative management and for the plaintiff's WCC and temperature to be monitored. Theatre would be 'considered' if the plaintiff became 'unwell'.
According to the nursing observations, the plaintiff's temperature between 4.00 am and 10.00 pm was 36.8, 36.2, 36.3, 37.2 and 37.2.
I move now to Tuesday, 4 August.
The plaintiff was reviewed by Dr Lau during a ward round at 7.45 am. It was noted (under the heading 'W/R Lau Surg A') that he was 'improving', his observations were stable, he was afebrile and he was 'not for theatre'. The plaintiff was to remain in hospital until he was 'better', taking only clear fluids. The longer term plan was a colonoscopy in six weeks [to rule diverticulosis in or out] followed by a review by Dr Makin to consider the results and a possible interval (elective) appendectomy [if diverticulosis was ruled out].
At 11.30 am it was noted that the plaintiff's temperature at 8.40 am was 37.3ºC and that he felt tired. Analgesia had been 'as charted with good effect'.
He had physiotherapy at 2.30 pm.
According to the nursing observations his temperature during the day was 36.7, 37.3, 35.2, 38 at 7.30 pm [a febrile episode] and 37.6 (at 11.00 pm). The swing of -2.1 and +2.8 over three consecutive readings is noteworthy.
I move now to Wednesday, 5 August.
At 7.00 am a nurse noted that the plaintiff's blood pressure remained high overnight and he reported pain in the order of 7/10, for which paracetamol and OxyNorm was given.
He was reviewed by Dr Nazaar during a ward round at 8.00 am and was noted to be 'doing well'.
Later the nursing staff noted that his observations were 'unremarkable'. The plaintiff reported some abdominal pain, for which analgesia was provided.
He was seen by a physiotherapist at 2.30 pm. He reported feeling 'much better than yesterday'. He was able to mobilise to the shower and toilet in the morning.
At 8.20 pm he was seen by a nurse who noted that his observations were stable, with no complaints of pain.
According to the nursing observations his temperature between 3.15 am and 11.30 pm was 37, 36.8, 37 and 38 [a febrile episode].
The plaintiff's inflammatory markers between 31 July and 5 August were as follows (exhibit 33, pages 178 – 181):

31.07.09

Friday

01.08.09

Saturday

02.08.09

Sunday

03.08.09

Monday

04.08.09

Tuesday

05.08.09

Wednesday

White Cells

15.70

14.50

18.20

13.00

14.40

15.60

Neutrophils

13.91

11.79

15.18

9.92

11.52

12.65

C-Reactive Protein

240

380

460

400

260

270

Based on my study of the records, I infer these results for each day were not available until late morning at the earliest.
I move now to Thursday, 6 August.
The plaintiff was seen by a doctor at 12.45 am because his temperature had risen to 38. The doctor wrote that:
(i)The plaintiff was admitted nine [sic: seven] days prior for suprapubic pain which was initially thought to be diverticulitis, but after 'discussion with radiologists' was now thought to be appendicitis. It had been treated conservatively as his symptoms were improving. [This provides reliable secondary evidence of the reasoning of Dr Lau].
(ii)The plaintiff reported experiencing increased suprapubic cramping and diarrhoea 'today' (ie, during the previous 24 hours).
(iii)On examination, the plaintiff's entire lower abdomen was tender on deep palpation, with no guarding or rebound. (Illustrated by a diagram).
(iv)The clinical impression was of 'worsening appendicitis'.
The doctor arranged for blood cultures and urine microbiology and resolved to discuss the plaintiff's case with the surgical registrar (and 'team') in the morning. He envisaged surgery if the plaintiff did not improve.
The doctor discussed the case with the surgical registrar at 5.00 am. They resolved to continue with observation and review the case with the surgical team in the morning.
The plaintiff was reviewed during a ward round at 9.00 am. It was noted that:
(i)He had a febrile episode overnight and was feeling worse.
(ii)On examination he looked 'OK' and was 'sitting out of bed'.
(iii)His heart rate was 115, temperature 37.1 and blood pressure 156/96.
The clinical impression was: '? intra‑abdominal collection/inflammation secondary to appendicitis'.
The plan was to provide the plaintiff with 'nourishing fluid' and discuss his case with Dr Lau, which occurred at 11.00 am. Dr Lau decided that the plaintiff was to undergo a laparoscopy (for investigative purposes, I infer) which might need to be converted to a laparotomy and appendicectomy.
According to the nursing observations and theatre records, the plaintiff's pre-operative temperature during the day was 37.1, 37.3 and 37.6 (pages 144 and 166).
According to the anaesthetic and recovery records, surgery commenced at approximately 8.30 pm. The anaesthetist noted that the plaintiff 'desaturated rapidly while waiting for' the onset of suxamethonium, that is to say, the plaintiff's oxygen levels fell rapidly (meaning respiratory complications developed) whilst the anaesthetic drugs were taking effect and before the surgery itself. At 9.30 pm the anaesthetist noted a conversation with the nurse manager about the plaintiff being admitted to the NSU post-operatively.
Dr Lau performed a laparoscopy which was converted to a mid‑line laparotomy, followed by a colonoscopy and an appendectomy. The entire operation took 4½ hours. Dr Lau's recorded findings were as follows (underlining in the original):
OPERATION DETAILS
Findings fibrinous exudate within pelvis secondary to appendicitis. Thickened inflamed appendix. Local abscess adjacent to appendix/sigmoid colon. Also thickened sigmoid colon and erythematous terminal ileum attached to inflammatory mass in pelvis but likely secondary to localised perforated appendicitis.
Colonoscopy on table prior to dissection of inflammatory mass through to descending colon beyond sigmoid colon thickening.
Mild mucosal oedema within sigmoid colon [ie, there was some internal swelling]. No erythema, no mucosal lesion/CA. [ie, no engorgement with blood and no perforation was seen internally].
After SB [small bowel]/appendix dissected off sigmoid colon, no gas leakage [with] colonoscopic insufflation. Therefore sigmoid colon not resected.
Small bowel examined – no perforation but marked serositis [ie, inflammation of the small intestine].
Procedure laparoscopy → laparotomy (mid-line) → colonoscopy (on table)
Appendicectomy, base transfixed [with] 0 vicryl.
TUBES PACKS DRAINS etc.
19 Fr Blake Drain RIF, Yates drain to S/C closed [with] …. loop PDS/clips.
POST OPERATIVE INSTRUCTIONS:
To ICU, routine obs, NGT – free drainage and hourly UD.
The Hospital discharge letter (signed by Dr Anderson) stated that the colonoscopy 'found simple oedema with no erythema or lesions … thought to be secondary to the local inflammation caused by appendiceal abscess'. There was no reference to gangrene.
As can be seen, two drains were left in the abdomen (including a Blake drain in the right iliac fossa) and instructions were given for the plaintiff to be admitted post‑operatively to ICU for routine observations and drainage. It is common ground that he was admitted to ICU because the anaesthetist decided not to extubate him, that is say, to leave him mechanically ventilated because his respiratory distress had not settled. I infer that no serious concerns were held for the plaintiff's ultimate recovery at this stage.
It is also common ground (and I infer) that the notes signify that an abscess occupied the entire area between the small intestine, terminal ileum, appendix and sigmoid colon and that it was adhering to them.
Further, once the abscess had been removed it was noted that none of the air which had been insufflated into the colon during the colonoscopy leaked from the sigmoid colon. As such, it was decided that the sigmoid colon was not then perforated and did not require resection.
I also find that a large amount of pus was found in the abscess. The evidence for this is contained in the notes of an ICU registrar at SCGH made at 3.10 am on Friday, 7 August:
Intra-op puss+++, perforated appendix, 4.5 hour operation.
Fluid resuscitation with 4 litres.
Surgeons recommend Tazolin ABX.
The emphasised notes do not appear in the Hospital records. I infer that the information was nevertheless communicated to SCGH and is reliable.

Evidence of Dr Mark Neville

Dr Mark Neville has been a consultant pathologist since 1988. He and his staff performed a histopathological examination of the plaintiff's appendix on 7 August 2009. The relevant parts of his report dated 11 August 2009 are as follows:
MACROSCOPIC:
Received in formalin is an appendix which is 88 mm long and 10 mm in maximal diameter. The serosal surface of the specimen appears congested and is a dark mottled purple. There are no mass lesions identified. There are no areas of macroscopic perforation identified. The appendix has a maximal wall thickness of 5 mm. The appendiceal lumen is partially obliterated.
…
MICROSCOPIC:
Sections of appendix show fibrous obliteration of the distal lumen. The patent proximal lumen contains a little mucoid material and the mucosal lining appears intact. A few blood vessels within the lamina propria are showing peripheral margination of polymorphs and isolated interstitial neutrophils are seen. Similar vascular changes are present within the muscularis mucosae and the subserosa. The latter is also showing vascular congestion, poorly developed leukocytoclasis and extravasation of red blood cells. In addition, the serosal surface is partly coated with fibrinopurulent exudate.
CONCLUSION:
Acute appendix, predominantly extrinsic in type, there is no evidence of malignancy.
Dr Neville testified that the macroscopic examination was performed by a trained staff member and involved an examination of the entire appendix with the naked eye. He performed the microscopic examination himself. This involved examining slides of sections of appendix which had been prepared by his assistant.
He explained that the congested, dark and mottled purple appearance of the serosal surface was consistent with the organ having been clamped and thus deoxygenated during the surgery. In other words, the appendix was not gangrenous.
The finding of 'fibrous obliteration of the distal lumen' is a very common incidental finding in adults and was therefore non‑specific. (Associate Professor Mackay concurred: ts 683).
The evidence of 'peripheral margination of polymorphs and isolated interstitial neutrophils' within the lamina propria was evidence of a small amount of low grade, non-specific inflammatory reaction, consistent with an early, evolving, acute inflammation.
His finding that the appendicitis was 'predominantly extrinsic in type' meant that the inflammation of the organ was mainly on the outside which, in his opinion, strongly suggested that the disease was secondary in aetiology.
Dr Neville was not challenged in cross-examination and, overall, conveyed complete confidence and assurance about his findings and opinion. He is very experienced, there was nothing unusual about the case from his point of view and he appears to have encountered no difficulties performing his investigation. His findings that the appendicitis was secondary is consistent with the definition of primary appendicitis (Annexure 2) which predicates an internal obstruction of the lumen of the appendix (for which no radiological or pathological evidence was found) and with Associate Professors Little's and Mackay's interpretation of the CT scans.
In short, there is no reason to doubt or dispute Dr Neville's histopathological findings that the plaintiff's appendicitis was of external (or secondary) aetiology. I find accordingly.

Dr Lisewski's evidence

Dr Lisewski is a Fellow of the Royal College of Surgeons (Ireland) and a Fellow of the Australasian College of Surgeons. He has been a consultant surgeon since 2005.
In 2009 he was employed by the Hospital as a consultant general surgeon on an on‑call basis from 5.00 or 6.00 pm on Fridays until 7.00 am on Mondays.
He testified that he has virtually no independent recollection of the plaintiff or his case (ts 560 – 561). But he has not entirely forgotten about it because he was contemporaneously informed of the plaintiff's complications and complaints and it is the only time in his career that his professionalism has been disputed. He has an actual recollection of being informed by Dr Finlayson of the change to the possible 'cause of the diagnosis' after the radiology review on the morning of 3 August.
For the purpose of giving evidence Dr Lisewski entirely relied on the documentary records and the CT scans. (He was also provided with the expert reports). I make no criticism of him for doing so, but his evidence was essentially a complete reconstruction. As will be seen, it was very unreliable at times.
He initially testified (ts 552 – 553) that he first became involved in the plaintiff's case at a handover meeting at 7.00 am on Saturday, 1 August (ts 552 ‑ 553). He testified (ts 556) that the entry in the notes which recorded that he saw the plaintiff on the ward ('W/R Lisewski') at 6.30 pm on Friday 31 July was actually a record of the Saturday morning ward round and that the recorded time (ie, 6.30 pm) was when the junior doctor made the note itself (ie, on the Saturday evening).
Clearly, Dr Lisewski was completely wrong about this. The notes of the ward round precede entries which were made at 12.15 am and 5.00 am on Saturday, 1 August. The review must have taken place at 6.30 pm on Friday, 31 July, as recorded.
Dr Lisewski accepted his error once it was pointed out to him and endeavoured to explain it (ts 583). He said that the notation 'W/R Lisewski' had initially suggested to him that it was a routine ward round which would have taken place on the Saturday morning after the handover meeting. However, he was occasionally called in to see a sick patient and that is what must have happened at 6.30 on the Friday evening. He said (ts 583):
… It's not in my normal practice to review patients on Friday evening when I take on the on call unless the patient is sick or needs an operation.
With these observations in mind, I return to Dr Lisewski's evidence of seeing the plaintiff, bearing in mind that it is a reconstruction of what occurred.
He testified (ts 553) that he questioned the plaintiff to confirm the history that he had already been given, conducted a physical examination, reviewed the observation chart and discussed the management plan.
He testified (ts 549 – 555) that he regarded the seven-day history of illness as 'really important'. It meant that there was an 'established pelvic sepsis' which was visible on the CT scan. ('Any radiologist will tell you that').
He read Dr Krieser's report (ts 560), reviewed the CT scan and wrote his findings in the notes. His opinion was (ts 572):
… There was a phlegmon [which] … looked to be concentrated on the sigmoid colon. So the sigmoid colon showed signs of severe inflammation. There was an [inflamed] appendix nearby and we entertained the possibility of primary appendicitis but we deferred to think of this as a secondary appendicitis. Because when you've got a focus of infection or inflammation the surrounding organs adhere to that infection to ward off the infection. That's the body's response to internal infection. And so the difficulty I have when we argue about the aetiology is, is it acute colitis or sigmoid diverticulitis or is the problem acute appendicitis. Well, I think if you just look at the CT scan you can't actually tell. I don't believe you can …
… there was a locule of gas which indicates to me a microscopic perforation … There was two of them – adjacent to the sigmoid colon and a common cause of something like that is a micro perforation in a sigmoid diverticulum. And we did see diverticulii and that's where we disagreed with the radiologist.
And that's how we get acute diverticulitis, of course, is that there some micro perforation, otherwise you wouldn't have – you wouldn't get diverticulitis. In this case there was a small abscess. We felt that it was too small for percutaneous drainage …
(Dr Lisewski used the pronoun 'we' in the singular sense, ie he was actually referring to himself, and the above was his assessment.)
Dr Lisewski testified that on clinical examination the plaintiff's 'tenderness was localised, it wasn't generalised' (ts 555) and that the sepsis was too hostile to justify an urgent operation. As such he embarked on conservative management. He said (ts 557):
… The plan was to keep a very close eye on him, that if his objective markers of his unwellness were to deteriorate then we would have to intervene. But my preference was to not operate because of the hostile environment that we were encountering with the delayed presentation to the hospital in the first place.

He testified (ts 571) that he would have done a 'comprehensive' review on the morning of Saturday, 1 August because he always did so on Saturday morning and always saw the sick patients. (I have accepted this evidence: [62], [348] (vi)).
He testified (ts 584) that his findings were the reason he elected 'not to take him to surgery but rather continue along his current management plan'. These included that the plaintiff was afebrile, his abdomen was not as tender as it was on admission and his WCC 'was settling'.
I comment that as at 11.30am on the Saturday Dr Lisewski probably had that day's serology showing that the WCC had fallen from 15.70 to 14.50.
As for Sunday 2 August, he testified that the plaintiff had improved clinically with conservative management. Accordingly (ts 562), his
plan was to continue along this pathway until the patient improved well enough to be discharged from the hospital, and then we could investigate … when the patient had settled down, and if we needed to do an operation, that could be done electively when the patient was well and his healing process would have been … a lot better.
He cited the following evidence to support his assessment that the plaintiff had improved.
First, the test results supported it. After two days of incubation blood taken on 31 July disclosed 'no growth [which] … tells us the patient did not have septicaemia on 31 July' (ts 569). Also, (ts 570), on admission the plaintiff's white cell count was 15.7 which was consistent with a person who was fighting an infection, but it settled over the next three to four days save for a 'slight spike'. The plaintiff's neutrophils showed 'a steady decline' save for 'a bad day on the 2nd, where there was a jump'.
I pause to comment that these serology results would not have been available to Dr Lisewski at 10.35 on the morning of 2 August except for the WCC, neutrophil and CRP for 31 July and 1 August.
Second, save for occasional spikes, the plaintiff was afebrile (ts 577, 579).
Third (ts 579), the plaintiff's subjectively reported pain settled, as did his objective signs of pain (i.e. tenderness to palpation).
Fourth (ts 580), the plaintiff no longer looked as unwell as he did on the Friday. He testified (ts 580):
I see him on Friday - … he's looking unwell. His objective criteria, a fever, rigors, abdominal pains, white cell count are all – look like there's a sick person in front of us. And then literally in 24 hours of … appropriate medical treatment, he's an improved person. Clinically, he's improved, and that reassures me that we're heading in the right direction. There was no point of changing the plan when we're having – when we've got evidence of clinical improvement.
(See also ts 584). He explained the advantages of conservative management followed by investigations and an interval appendectomy.
Dr Lisewski was cross-examined about these reasons.
It was put to him (ts 592 ‑ 593) that the plaintiff's pain pattern changed in that initially it was recorded in the left iliac fossa but there was a report of new pain on the evening of 1 August in the right upper quadrant and (at times) in the left upper quadrant and supra-pubicly. He was dismissive of this evidence.
Firstly, he disputed the underlying premise of the question to the effect that the pain was originally in the left iliac fossa and said that it 'never was'. He said that the plaintiff presented with 'suprapubic pain which radiated across the lower abdomen' which was consistent with the evidence of inflammation which was 'smack bang in the mid-line'. In my opinion the premise of the question was mostly correct, at least in so far as the notes of 31 July are concerned and Dr Lisewski took an unduly self‑serving view of the notes here.
Secondly, Dr Lisewski said that he would attach no weight to a nursing note of a subjective (self‑reported) complaint of pain as opposed to objective evidence gathered by clinical examination (including palpation) by a doctor. Again, I believe that he was self‑serving in this instance. Whilst it makes sense for him to attach more weight to pain elicited on a clinical examination rather than a subjective complaint, it cannot be correct to assert that the latter was not relevant at all.
Dr Lisewski's evidence that the plaintiff was afebrile after 24 hours was challenged (ts 594 – 595) on the basis that his temperature was 38.6 on the evening of Saturday 1 August. He countered this by pointing out that he based his clinical assessment on the temperature chart in which there was no record of the febrile reading. Once again, the documentary evidence does not support him. The observations to which he was directed (exhibit 32, page 138) still showed the 38.6 reading as a dot on a graph and the NSU chart (page 114) recorded the actual figure.
That matter notwithstanding, Dr Lisewski agreed (ts 594) that the fact that the plaintiff's temperature 'spiked' was relevant, but he pointed out that on the Saturday morning it was 37.2 (8.00 am) and 37.4 (11.00 am).
It was put to Dr Lisewski that the objective evidence did not support his view that the plaintiff was getting better on the Saturday and Sunday. It was suggested that the inflammatory markers were at best equivocal and showed that the inflammation and/or infection was not getting better, and that the other evidence which suggested that he was (reduced pain and fever) was consistent with the effect of medications for the same (paracetamol and analgesia respectively).
Dr Lisewski responded:
(i)The diagnostic and management process is multifactorial and involves 'putting together the pieces of the puzzle'. He said (ts 600) that:
We never make a decision based on one variable, these are all variables, they change continuously throughout the patient's admission … We don't respond to an isolated elevation in the white cell count. And he had an infection on board so I'd be surprised if it wasn't'.
(ii)The plaintiff's elevated inflammatory markers were consistent with ongoing sepsis which was not disputed. However, they were only part of the diagnostic puzzle and, as far as he was concerned, the pre‑eminent fact was that the plaintiff's vital signs had improved.
(iii)Paracetamol has 'a very short antipyretic action [and would not] … mask a significant fever' if there was one ((ts 603, see also ts 601). Similarly, a single febrile spike would not 'change my whole course of management' (ts 603).
Dr Lisewski was not cross-examined about his reasons for not proceeding to theatre. To reiterate, these were that the septic conditions were too risky when the plaintiff was first admitted and, as I understand it, the appendicitis was believed to be secondary (in other words, from an aetiological point of view its function was to contain the primary infection and/or inflammation emanating from the sigmoid colon) and as such did not warrant surgical intervention.
Similarly, Dr Lisewski was not asked if he could have, or even did, query the matter with the radiologist (or any radiologist) as happened in the radiological review on Monday morning, 3 August. (It is reasonable to infer that a radiologist was on call over the weekend.)

Expert evidence and further factual findings in relation to liability

Radiological issues

The fundamental questions in relation to the radiological issues are: what did the CT scans disclose and did Dr Krieser accurately report them?
All of the medical witnesses were qualified to address these issues to varying degrees, and I have not ignored any such evidence when it was relevant. However, it is appropriate to primarily consider the evidence of the two experts, namely Professor Thomson and Associate Professor Little.
Each was asked to replicate the process as it applied to Dr Krieser. However, their reports (especially that of Associate Professor Little) were more lengthy and condescended to details to an extent which, I infer, would be regarded as atypical for a routine radiology report.
Professor Thomson is Director of Radiology at the Alfred Hospital in Melbourne. He has been a radiologist since 1974. His report dated 6 July 2012, a three page email exchange between he and Associate Professor Little in February 2015 and a further report dated 10 March 2015 were received in evidence (exhibits 19B, 19D and 19E).
He reported as follows on his examination of the CT scans (exhibit 19B).
CT Scan abdomen and pelvis dated 31 July 2009.
Contrast enhanced axial scans were performed in a portal venous phase from the lower portion of the thoracic cavity to the pelvis. Coronal reconstructions of the abdomen and pelvis were performed from the axial data.
There is evidence of minor dependent atelectasis in the basal portion of both lungs. The liver, gallbladder and pancreas and spleen have a normal appearance.
There is no evidence of diverticula disease or diverticulitis. [ie. he examined the sigmoid colon and, a fortiori, there was nothing relevant to report].
There is an extensive inflammatory mass in the region of the caecum, appendix and terminal ileum with very extensive fat stranding. There is marked mucosal thickening in the cecum and appendix and the terminal ileum is collapsed. The tip of the appendix extends almost to the mid-line of the left edge of the mass. Near the tip of the appendix there are two small bubbles of gas consistent with a contained perforation presumably of the appendix. The inflammatory mass extends to the margin of the sigmoid colon and there is a little free fluid in the right paracolic gutter and pelvis with inflammatory stranding of the mesentery of the sigmoid and a small amount of free fluid in the left paracolic gutter.
The cecum is mildly dilated measuring 5.7cm in diameter but the remainder of the colon and the small bowel are not dilated.
The kidneys are normal in appearance but there are numerous para-aortic lymph nodes, some on which are in the 1 – 1.5cm range consistent with an inflammatory response.
In my opinion the most likely diagnosis is appendicitis with rupture and abdominal surgery would be indicated. The reasons for this opinion are the free bubbles of gas, evidence of mucosal oedema in the ileocaecal area identification of the appendix within the region of inflammation, free fluid, the significant degree of fat stranding and the presence of large numbers of lymph nodes.
The differential diagnosis would include Crohn's ileitis but this would be expected to have much more inflammatory wall thickening in an acute stage and perforation would be less likely. Ileocaecal inflammation from bacterial infections such as Yersinia.Enterocolitica may give a similar appearance in terms of the ileum and cecum but the degree of the fat stranding would be less prominent and usually it is associated with watery diarrhoea. Caecal diverticulitis may mimic appendicitis but there is usually a diverticulum visible. The features do not suggest lymphoma as the wall thickening whilst significant is not excessive and para-aortic lymph nodes are not markedly enlarged.
Further clinical history would also be helpful. Lifestyle factors may indicate the likely immune state or HIV, a history of prior abdominal pain, recognition of fever and or leucocytosis would also be helpful. In my opinion the presence of free gas would however result in a laparotomy.
Associate Professor Little is radiology consultant at St Vincent's Hospital in Melbourne. He qualified as a specialist in 1992. He has made a sub‑speciality of abdominal imagining and intervention (which enhances his qualifications as an expert in my assessment).
His report of 5 October 2014 was received in evidence as exhibit 23. In par 10 he said that the 'key factual findings of the CT examination' as he would have reported them are as follows. (I have corrected some mis‑numbering):
(i)There is a postero-basal inflammatory change in both lung bases with associated atelectasis.
(ii)There is a moderate amount of peri-hepatic free fluid.
(iii)The liver is of uniform continuation without evidence of portal vein thrombosis or hepatic abscess formation.
(iv)There are an increased number of lymph nodes in the porta-hepatis space with the largest measuring 22 mm. The additional nodes measure between 7 and 15 mm in their short axes. There is also prominent lymphadenopathy in the porto-caval space.
(v)There is a small amount of perisplenic free fluid.
(vi)There is short segment proximal sigmoid colon transmural thickening with florid oedemateous infiltration of the sigmoid mesenteric fat. These features are consistent with focal colitis. The proximal sigmoid colon enhances with intravenous contrast and the lumen is eccentrically narrow.
(vii)There are a number of small extra luminal gas locules within the mesenteric fat. There is no evidence of any large volume intraperitoneal free gas.
(viii)There are an increased number of lymph nodes in the para-aortic retro- peritoneum adjacent to the inferior-mesenteric artery origin and also in the mesenteric fat in the right iliac fossa within the ilio‑colic chain. All these nodes measure < 10 mm in size.
(ix)The proximal small bowel loops are mildly dilated.
(x)The distal small bowel loops are decompressed.
(xi)The colon is decompressed.
(xii)The appendix is well visualised and is on the periphery of the inflammatory process which has as its epicentre, the sigmoid mesentery and the proximal sigmoid colon. The appendix is mildly dilated measuring approximately 8 -9 mm (normal size: 6 mm).
(xiii)There are one or two sigmoid diverticula, but the degree of diverticula disease is not extensive.
(xiv)In addition to adenopathy described above, there is prominent adenopathy within other various anatomic space:
(a)Cardiophrenic
(b)Gastro-hepatic omentum (see pelvic wall D inguinal)
(xv)There is a small volume of pelvic free fluid.
(xvi)There is a small focus of fluid adjacent to the right lateral aspect of the mid sigmoid colon, measuring approximately 2.5 cm by 3.3 cm. The margins of this fluid are ill-defined and not enhancing suggesting it has yet to evolve into a focal constrained fluid collection.
(xvii)There are a number of important negative findings
(a)There is no evidence of ascending peri-venous inflammatory change surrounding either the superior or inferior mesenteric vein.
(b)There is no evidence of extra hepatic or intra hepatic portal pyaemia.
(c)There is no evidence of a loculated pelvic fluid collection at this stage.
(d)There is no evidence of an evolving or established hepatic abscess.
(e)There is no evidence of a foreign body perforation within the sigmoid colon (eg fish bone or tooth pick). However, with this degree of inflammation, a foreign body perforation may be obscured.
(f) There is no evidence of extensive diverticular disease, with only one or two obvious sigmoid diverticula.
(g)There is no evidence of appendicolith within the appendix.
Associate Professor Little continued to give his opinion:
(i)Mr Westcott presents with an inflammatory focus within the pelvis. The differentiation is between whether the primary inflammatory event involves the sigmoid colon and secondly involves the appendix and its surrounding soft tissues or is primarily appendicitis with secondary sigmoid colitis.
(ii)I strongly favour sigmoid colitis over appendicitis on the imaging findings, but would seek further clinical context for the patient's presentation and whether there was any relevant past history. For example I would enquire whether the patient presented with a classic clinical features of appendicitis, namely initial peri‑umbical pain, which moved to McBurney's point.
(iii)The specific features favouring sigmoid colitis are:
(a)There is circumferential thickening of the sigmoid colon with associated eccentric luminal narrowing.
(b)The inflammatory change is focused more within the sigmoid mesentery with the sigmoid colon at its epicentre.
(c)While it's clear the appendix is inflamed, the degree of inflammation with the sigmoid mesenteric fat and surrounding the sigmoid colon is out of proportion to the mild increase in the trans-serosal diameter of the appendix, which measures approximately 8 – 9 mm which is only just above the normal trans-serosal diameter of 6 mm.
(d)The appendix is well seen precisely because the retroperitoneal fat surrounding it is not profusely inflamed, which would be unusual if the appendix was the cause of this degree of pelvic inflammation.
(e)Focal fluid, which is yet to organise into a formal collection is within the sigmoid mesentery as adjacent to the inflamed sigmoid colon, rather than immediately surrounding the appendix.
Associate Professor Little continued to point out that the plaintiff's relatively young age and the lack of overt, extensive and pre-existing diverticula disease was unusual and he would not invoke it as the 'definite aetiology [of the colitis] without consideration of other causes' and, as such, 'it would be prudent to reimage or endoscope Mr Westcott when his acute symptoms resolved to rule out an underlying colonic malignancy or lymphoma which has become inflamed and subsequently perforated'.
To summarise the issue between the experts, Professor Thomson said that the primary pathology was centred in the region of the cecum, appendix and terminal ileum and made a diagnosis of appendicitis with no significant involvement of the sigmoid colon at all. He favoured an immediate laparotomy. On the other hand, in Associate Professor Little's opinion the pathology was focused on the sigmoid colon with a diagnosis of sigmoid colitis and secondary appendicitis. He favoured conservative management and an elective colonoscopy later.
The experts conferred with each other and the outcome was as follows (exhibit 19D).
There is a contained perforation of a viscus in the pelvis with fluid and several lymph nodes consistent with inflammatory change. A/Prof Little's opinion is that this is sigmoid colitis and [in Professor Thomson's] opinion … it is appendicitis.
Our opinions differ only in the organ, not the site and nature of the problem.
In the absence of the clinical examination findings, and based on the limited information on the request of the CT, A/Prof Little has recommended observation, more imaging and endoscopy. [Professor Thomson's] opinion was that a laparotomy was indicated.
We are moving outside our joint area of expertise suggesting appropriate treatment based only on a single examination, but both of us consider that the plaintiff needs something more than this CT scan.
Thus, both experts agreed that the plaintiff's CT scan demonstrated appendicitis, but they differed as to whether sigmoid colitis was involved in the primary aetiology. Both would not rule out some form of operative investigation or intervention, but Associate Professor Little was more conservative as to the timing (as were Drs Lisewski and Lau and Associate Professor Mackay). Both would defer to the surgeons as to the ultimate management.
I turn now to their oral evidence.
For logistical reasons Professor Little testified before Professor Thomson and, at my request, it fell to him to explain much of the anatomical terminology. It is therefore convenient to set out his evidence first, and at some length.
Both witnesses systematically analysed the CT scans on screen in court and noted relevant findings as they would in their own practice (with additional explanation for the court) by moving through the images from the superior (upper) to inferior (lower) abdomen.
Associate Professor Little testified in the present tense as follows.
There is evidence of basal changes in both lungs with a small amount of pleural fluid (atelectasis) which signifies that some ill-defined inflammatory or infective process has occurred.

Having considered the evidence and also examined evidence of the open market, Mr Thompson concluded that in general terms the plaintiff's earning capacity produced a greater rate of return for labour when he was salaried compared to when he owned and operated Tandaz.
Based on Mr Thompson's undisputed findings the parties submit that past economic loss should be assessed as follows:

Period Type of loss Plaintiff's submission Defendant's submission

Up to 30 June 2010 Increased external labour to the business $37,085 $37,085

1 July 2010 – 30 June 2012 Gratuitous services in the business provided by Ms Westcott
$37,440

(Based on Mr Thompson's calculations, page 27 and using the pre‑tax figure rather than the after-tax figures)
Nil

1 July 2012 – 22 June 2015 Lost earnings (after deduction of actual earnings) $106,192.40 $75,916.64

As to the period 1 July 2010 – 30 June 2012, the only issue is the plaintiff's claim for gratuitous services in the business ($37,440) because Ms Westcott increased her IT contribution to the business. This coincided with the cessation of external labour and the closure of the retail premises for which she was previously responsible. This claim is additional to the claim for gratuitous services referred to in exhibit 3 which covers the period 2 September 2009 to 31 July 2012. Mr Thompson assumed 10 hours per week for the period covered in his report whereas the amount referred to in exhibit 3 was six hours per week.
Ms Westcott testified as to the nature and need of her additional input into the business when the plaintiff was incapacitated. Her time was effectively an input to the business or, alternatively, evidenced the imposition which the plaintiff's injuries had on his earning capacity. In my opinion it is compensable and the only issue is quantum.
I favour a global amount to reflect the wide number of variables, not the least of which is the issue of the amount of additional time put into the business by Ms Westcott. In my opinion a sum of $30,000 is justified.
The defendant accepts $106,192.40 as a starting point in respect of the period 1 July 2012 to 22 June 2015, but contends that there should be a deduction of 50% because of 'the plaintiff's failure to mitigate his losses'. The defendant submits that the plaintiff acted unreasonably in failing to seek psychological counselling through Medicare on a GP Mental Health Treatment Plan (of which he would have been aware from the expert reports). This argument is not supported by the evidence. The plaintiff testified, and I accept, that he ceased employment in January 2014 because of his inability to cope with his work. (He ceased work for six months in 2012 for the same reason). The exact circumstances of his departure from Absolute IT Solutions are not entirely clear, but I am satisfied that he was not coping with his work and was emotionally very volatile. When seen by Dr Edwards‑Smith on 23 May 2014 and again by Dr De Felice on 19 January 2015 he was deemed to be unfit for work. I accept their findings.
There is no evidence to suggest that the plaintiff's employment prospects have improved since he saw Dr De Felice and, as will be seen, I am not satisfied that he will be fit for any kind of employment for some time.
I note that the plaintiff did not allow a reduction for the period when he and his wife travelled overseas. This is problematic because it was a voluntary decision and involved a long overdue holiday from work. However, as Medlin illustrates, a reasonable, subjective decision to opt out of employment for injury‑related reasons can be compensable. I am satisfied that this is such a case.
I am therefore satisfied that the amount claimed by the plaintiff for loss of earning capacity between 1 July 2012 and 22 June 2015 should be allowed, namely $106,192.40.
Based on the methodology used by the parties, this award should include an allowance for lost superannuation, but not interest.
The award in respect of economic loss up to 22 June 2015 is $173,277.40.
I turn now to future economic loss.
Based on Mr Thompson's projections (assessed as at 28 February 2015 and inclusive of superannuation) assuming total incapacity at a weekly rate of $1,224.20 net per week a retirement age of 67, the plaintiff's original earning capacity was $752,395.
Mr Droppert accepted that the plaintiff had some retained earning capacity in that it is probable that he will regain some capacity for work if he responds well to treatment for his PTSD and depression and/or regains better physical functioning from his targeted exercise programme.
In the result, he submitted that the loss of earning capacity should be assessed at 50%, hence the claim for $376,192.50.
The defendant submitted that from a physical point of view the plaintiff is capable of returning to full time work in the IT industry and that his PTSD and depression are treatable. As such, it submitted that a period of one year's loss of future earning capacity would be sufficient.
In my opinion the following facts and findings are particularly relevant:
(i)It is most unlikely that the plaintiff will be able to return to employment in the near future. I have found that he has been wholly unfit for work since early 2014 and he has significant physical and psychological treatment and retraining needs.
(ii)It is likely that he will return to the IT workforce in about 2 years in some capacity.
(iii)At that time the plaintiff will need to 'ease' back into employment and will need to be selective and work within some physical and psychological restrictions. For instance, from a physical point of view he may need to commence by working from home. Therefore whilst on the evidence employment opportunities in IT are readily available (see report of Professor Mulvey, exhibit 11), there is a real and not speculative possibility that he will be less competitive than other people (see Wade v Allsop (1976) 50 ALJR 643, 647 (Stephen J)).
(iv)He will always be susceptible to a psychiatric relapse which, combined with his permanent pain, could always affect his productivity and longevity in the workfoce.
Mr Droppert's submission is consistent with the approach mandated in Bowen v Tutte (1990) Aust Torts Rep 81‑043. It is attractive in that it predicates flexibility as to future developments. But it is difficult to judicially fix upon an appropriate discount for retained earning capacity. Mr Droppert contends for 50%, but on what basis? Has the plaintiff lost half of his earning capacity? That would certainly be justified if he does not benefit from rehabilitation, re‑training and an assisted return to work and is limited to part‑time employment 'at a lower degree of complexity'.
Mr Thompson determined that the plaintiff's future loss of earning capacity would be $291,799 if he was wholly incapacitated for employment up to 30 June 2017 (2 years 4 months) and was thereafter able to earn the average that he earned when he was working with Perfect Computer Solutions and Absolute IT. On the assumption that the period of total incapacity continued to 30 June 2019 the loss would be $453,682. The amount contended for by Mr Droppert falls within that range.
In my opinion Mr Thompson's calculation of the loss for two years and four months ($291,799 or 38% of the total loss) is an appropriate starting point because it provides for a lengthy period for the plaintiff to re‑train and recover job ready fitness. But, it is on the low side because the plaintiff will always be susceptible to relapse and some loss of competiveness in the market‑place. I assess the lost earning capacity at 45%.
Accordingly, future economic loss (including superannuation) is assessed in the sum of $338,577.75.

Non‑pecuniary loss

The plaintiff's quality of life has been severely affected by pain, reduced mobility, psychiatric distress and the loss of many occupational, intimate and recreational pleasures that he previously enjoyed. His scarring is markedly worse than it would have been if he had been treated in a timely way in the Hospital.
In my assessment a significant award is warranted for the physical injuries viewed by themselves when one has regards to his lengthy and at times confronting recuperation and his ongoing pain.
His psychiatric injuries have also had a significant effect upon him. His close relationship with his spouse has been affected and virtually effaced in terms of its intimate aspects. He has nightmares, flashbacks, is emotionally unstable and labile. The enjoyable aspects of his life are now a shadow of what they were.
Having said that, my findings predicate that in the longer term the plaintiff will recover in some domains. So, for instance, he will be employed in his chosen career, albeit without the same sense of achievement and independence which he formerly enjoyed.
Mr Droppert submitted that an award of not less than $150,000 was appropriate.
Dr Lu submitted that an award of $75,000 was appropriate. In my opinion such a sum would be within the range for the plaintiff's physical injuries alone.
It follows that it is necessary for the award to be substantially higher, whilst avoiding over compensation because of the co‑morbidity of his injuries.
Bearing in mind that in the longer term some resolution of the symptoms of depression and PTSD can be expected, I am not satisfied that this case warrants an award in the order of magnitude of $150,000.
The award is $125,000.

Summary of assessment of damages

In summary, damages are assessed as follows:
(i)Special damages to date   $ 18,000.00
(ii)Wilson v McLeay allowance   $   7,425.12
(iii)Gratuitous services to date  $ 60,000.00
(iv)Future gratuitous services and allied needs      $ 92,500.00
(v)Home modifications  $ 37,500.00
(vi)Equipment   $   6,000.00
(vii)Future treatment   $ 29,907.01
(viii)Past and future travel  $   5,000.00
(ix)Past loss of earning capacity  $173,277.40
(x)Future loss of earning capacity  $338,577.75
(xi)Non-pecuniary loss  $125,000.00
Total $893,187.28

Interest on past losses

I assess interest on (i), (ii), (iii) and (ix) from 11 August 2009 to judgment as follows:
$258,702.05 x 3% x 5.2 years = $40,357.59.

Conclusion

The plaintiff is entitled to judgment against the defendant for damages and interest in the sum of $933,544.87.

ANNEXURE 1
Meta-Glossary of Terms
Abscess - A contained (focal) collection of inflammatory fluid (exudate) or pus which develops its own covering or wall of fibrinous tissue.
Antibiotics - Drugs which treat and kill bacterial infections. There are many hundreds of antibiotics and their use can overlap (ie. treat different bacteria). 'Triple antibiotics' refers to a combination of three which cover most bacteria which exist in the bowel (as given to the plaintiff).
Appendicitis – Inflammation of the appendix: see Annexure 2
Bacteria – Organisms which occur naturally in tissues and spaces throughout the body. Migration of bacteria can cause and/or spread infection.
Colitis – Inflammation of the colon
Colonoscopy – An internal examination of the rectum, sigmoid colon and other colons carried out by passing a guided scoping device (an endoscope) along and through the lumen. The device is inserted into the bowel per rectum after the bowel has been inflated (insufflated) with air.
CT scan – Computer tomography which provides a series of monochromatic images of internal tissues in axial (cross-sectional) and coronal (horizontal) slices. In the plaintiff's case oral and intravenous contrast was administered to outline areas of the bowel and blood vessels.
Distal – A point furthest from the head, so the distal end of the appendix is that which is furthest from the cecum.
Diverticulitis (see Annexure 2) – Inflammation of one or more diverticula. It can affect a segment of bowel or a single diverticulum. It is not of itself an infection, that is to say, it is not of itself bacterial in aetiology. It is usually treated conservatively (by bowel rest) and settles within four or five days. Antibiotics also have a therapeutic role, although the reason for their efficacy is not understood.
Diverticulosis - The condition of having one or more diverticula. It is most common in late – middle age and is usually benign and asymptomatic (95% of cases). Typically a person has a number of diverticula rather than just one.
Diverticulum (pl. diverticuli or diverticula) - An abnormal, out-pouching of the colon which creates a communication between the lumen and the serosa. It occurs where there is weakness of the muscle wall and is caused by pressure generated during peristalsis.
Diverticulitis and diverticulosis can be identified by colonoscopy (when the outpouchings are visualised in the mucosa of the lumen), by laparoscopy/laparotomy (when the outpouchings are visualised in the serosa) or by CT scans (when the outpouchings are visible as a pale grey‑white blobs or spots).
Erythema (adj. erythematous) – an area of redness caused by engorged blood.
Fascial planes – Connective tissues of the peritoneal cavity.
Fat-stranding – Water-logged (ie oedematous) fat. It is evidence of inflammation.
Febrile – Fevered, ie a body temperature in excess of 37.5 C. Normal temperature range is 36.5 – 37.5 C. Professor Toouli testified (ts 401) that a normal temperature was 36 – 36.5, but others (including those who treated the plaintiff if the clinical notes are any guide) allowed of the higher limit, which I accept.
Fibrin – A reactive substance produced by the body to control (ie contain) an area of inflammation.
Fibrinous exudate – Inflammatory exudate which contains fibrin.
Focal - Constrained or adopting to an anatomic region (ie. walled in by surrounding structures or tissues).
Free gas – Gas bubbles or locules (usually digested air) which have escaped from a hollow viscus (such as the intestines).
Gangrene (adj. gangrenous) – Dead tissue.
Guarding - An anticipatory or pre-emptive tensing (consciously or unconsciously) of the muscles; eg to avoid pain associated with palpation.
Hernia – A defect in the musculature of the abdominal wall which permits the internal contents to push through creating a bulge under the skin.
Iliac fossa(s) – An anatomical term describing the area in the lower sides of the abdominal cavity (left and right).
Inflammatory exudate – Free fluid emanating from inflamed tissue. Inflammation attracts blood to the relevant area and as part of that pathological response immature, leaky vessels produce an inflammatory exudate containing various organisms including granular tranularcytes and white blood cells.
Inflammatory markers – Organisms or chemicals measured from blood serology which are associated with inflammation and infection. They include white blood cell count (WCC), neutrophils (which fight bacterial infection) and C‑reactive protein (CRP). Elevated levels provide evidence of inflammation or infection.
Incisional hernia – A hernia in the area of a surgical scar.
Laparoscopy - A surgical procedure in which an endoscope is inserted through a small (approximately 1 cm) incision in the skin (usually at the umbilicus) to facilitate internal visualisation. Additional incisions of (approximately 0.5 cm) are also made for the insertion of instruments to enable the surgeon to manipulate the endoscope or carry out procedures.
Laparotomy - A surgical procedure involving the making of an incision in the abdomen through which the surgeon can use instruments and carry out open surgery.
Lumen – The void or tunnel of a hollow viscus.
McBurney's point * – a site situated in the normal area of the appendix in the right lower quadrant of the abdomen.
Mesentery – Curtain-like linings in the abdomen. The mesentery of the appendix contains that organ's sole artery.
Meso-colon – Fatty tissue in the mesentery surrounding the colon, principally containing the blood and lymphatic systems.
Mucosa – (and sub-mucosa) - The inner lining of the wall of an organ.
Muscularis propria – The muscle layer or coating of an organ.
Neuropathy * - inflammation or degeneration of peripheral nerves.
Oedema (adj. oedematous) – An abnormal collection of fluid.
Omentum – A fatty apron which extends over the colon and into the pelvis.
Para or peri – a prefix meaning 'around' or 'adjacent to'
Para-colic gutters - Spaces adjacent to the ascending and descending colons.
Peristalsis – The motor function of the bowel which causes the propagation of fluid and digestive material through the bowel.
Peritonitis – An inflammation and/or a bacterial infection of the peritoneal cavity or the peritoneum resulting from the uncontrolled spread of inflammatory exudate (eg, a ruptured abscess). Peritonitis can be local (confined to an area of the peritoneal cavity) or general (throughout the peritoneal cavity).
Phlegmon – An inflammatory mass preliminary to the formation of an abscess.
Proximal – A point nearest to the head. So the proximal appendix is that part which is closest to the cecum.
Pus – A liquid which is created from white blood cells that have invaded a collection of inflammatory fluid.
Rigors - Shivering caused by the body preserving heat during a fever; hence the patient feels cold whilst febrile.
Secondary (as in secondary condition) – A condition (sequela) which results from some other condition. So, secondary inflammation is the sequela of a primary inflammation elsewhere.
Sepsis - An inflammation involving bacterial infection. Symptoms of sepsis include fever, tachycardia, rigors, hypertension. Symptoms of gross sepsis include a 'high fever … (40, 41), gross tachycardia … pulse 120 plus, 150, 160, a swinging fever, high then low, rigors' (Associate Professor Mackay, ts 656).
Septicaemia occurs when septic bacterial organisms migrate to the blood stream and multiply. They generate and secrete toxins which produce secondary effects. Untreated these can include acute cardiac failure, renal failure, respiratory failure and death.
Seroma * - A lump or swelling.
Serosa – The outer lining of an organ, eg the outer lining of the appendix.
Supra-pubic – Describing the area of the lower abdomen immediately above the pubic bone in the pelvic girdle.
Swelling - An inflammation of connective tissue.
Tachycardia – An elevated heart rate. A normal range is 70 – 80 beats per minute, depending on the fitness of the patient.
The peritoneal cavity - The cavity of the abdomen. The peritoneum is the cavity lining.
Ventral * - pertaining to a position towards the anterior surface of the body; frontwards (cp 'dorsal').
Viscus – An organ; thus, a hollow viscus is a hollow organ such as the colon or appendix.
* Definition taken from Mosby's Dictionary of Medicine, Nursing and Health Professionals.

ANNEXURE 2

Diagnostic criteria for appendicitis and diverticulitis

Appendicitis

Appendicitis occurs when the lumen of the appendix becomes obstructed. The most common causes of obstruction are faecaliths (small 'stones' formed when calcium salts and faecal debris become layered over time around a nidus of faecal material within the lumen of the appendix) and enlargement of lymphoid tissue within the wall of the appendix (in conditions such as Crohn's disease, gastroenteritis, amoebiasis, viral infections, measles, etc). Less common causes of obstruction include foreign bodies and tumours. Obstruction of the lumen of the appendix leads to distension of the appendix with accumulated intraluminal fluid. The distension causes ineffective lymphatic and venous drainage which allows bacterial invasion of the appendiceal wall and, as the appendicitis progresses, peritonitis develops because of the bacterial infection. Eventually the gangrenous appendix will perforate and spill pus and faecal material into the peritoneal cavity, causing a more generalised peritonitis and abscess formation.
The typical history of appendicitis is of a gradual onset of abdominal pain, loss of appetite, nausea, and one or two vomits over 12 to 24 hours. Diarrhoea may be present. The pain is initially central in the abdomen and then moves to the right lower abdomen. Physical examination reveals right sided abdominal tenderness and a low grade fever. The white cell and neutrophil counts usually show a mild elevation and the ESR and CRP are elevated above normal. The standard imaging investigations for adults with a suspicion of appendicitis are pelvic ultrasound, whose sensitivity varies from 80% to 95% depending on the patient and the operator, and abdominal CT scan which is about 95% sensitive for appendicitis.

The most common complication of appendicitis is rupture of the inflamed appendix. The appendicitis attracts the omentum to the inflamed appendix so that when the appendix ruptures, the leak of bowel contents is contained by the omentum and does not initially extend into the general peritoneal cavity. The contained bowel contents become infected by bacteria from the bowel within 12 to 24 hours and an abscess develops. The symptoms of appendicitis often settle to an extent after perforation occurs but the contained abscess will eventually leak or rupture into the general peritoneal cavity, usually after several days, and the patient will become critically ill with peritonitis.
The clinical features of a contained perforation of the appendix include:
•abdominal pain, usually on the right,
•nausea, vomiting,
•constipation or diarrhoea,
•abdominal distension,
•tachycardia,
•low grade fever,
•right sided abdominal tenderness, guarding, and rebound tenderness,
•elevation of the white cell and neutrophil counts and the CRP.

From a radiological prospective the diagnostic criteria are as follows (see Professor Thomson's report, exhibit 19C):
Acute appendicitis manifests as enlargement of the appendix to a diameter greater than 6 mm; thickened wall with enhancement; periappendiceal fat stranding; and, sometimes, focal thickening of the terminal ileum or cecum. Conversely, patients with mild isolated appendiceal dilation (˂ 9 mm) are unlikely to have appendicitis. In addition, fewer than one‑third of patients with an identifiable normal appendix surrounded by inflammatory stranding or fluid will have appendicitis. A focal defect in the wall of the inflamed appendix, an appendicolith outside the appendix, a periappendiceal fluid collection, or extraluminal air near the appendix indicates perforation of the appendix. In such cases, the appendix may be difficult to see.

Diverticulitis

Diverticulosis is the outpouching of the mucosa of the large bowel. It is most common in individuals eating a low-fibre western diet, in which case it is thought to be caused by increased pressure within the bowel to move hard stool. The incidence of diverticulosis in western advanced societies is about 60% by age 85 years. The presence of colonic diverticula is usually asymptomatic until complications occur. The most common complication is diverticulitis, in which the neck of a diverticulum becomes blocked, causing pressure to increase within the diverticulum. This increasing pressure causes inflammation and ischaemia of the wall of the diverticulum which eventually perforates. The inflammation that precedes perforation attracts the omentum to the diverticulum. The omentum envelopes the diverticulum so that when the diverticulum perforates, the perforation is contained by the omentum and does not initially extend into the general peritoneal cavity. The contained bowel contents become infected by bacteria from the bowel within 12 to 24 hours and an abscess develops.
The clinical features of a contained perforation of the colon include:
•abdominal pain, usually on the left,
•nausea, vomiting,
•constipation or diarrhoea,
•abdominal distension,
•tachycardia,
•low grade fever,
•left sided abdominal tenderness, guarding, and rebound tenderness,
•elevation of the white cell and neutrophil counts and the CRP.

The diagnosis of diverticulosis is made by visualising diverticula either on abdominal CT scan or at colonoscopy. The diagnosis of diverticulitis is made by visualising diverticula with associated abdominal stranding with or with a collection of pus or free gas on abdominal CT scan. It is neither safe nor reasonable to diagnose diverticulitis in the absence of diverticula on abdominal CT scan.
From a radiological perspective, the diagnostic criteria are as follows (Professor Thomson, exhibit 19C):
Multi-detector row CT findings usually consist of asymmetric or circumferential thickening of the cecal wall, focal pericolic inflammation, and demonstration of diverticula. Inflamed diverticula are usually located at the level of maximum pericolic inflammation over appendicitis. Pericecal lymph nodes adjacent to the focal area of cecal thickening are more commonly seen in patients with cancer than in those with diverticulitis.

31.07.09 Friday	01.08.09 Saturday	02.08.09 Sunday	03.08.09 Monday	04.08.09 Tuesday	05.08.09 Wednesday
White Cells	15.70	14.50	18.20	13.00	14.40	15.60
Neutrophils	13.91	11.79	15.18	9.92	11.52	12.65
C-Reactive Protein	240	380	460	400	260	270

Period	Type of loss	Plaintiff's submission	Defendant's submission
Up to 30 June 2010	Increased external labour to the business	$37,085	$37,085
1 July 2010 – 30 June 2012	Gratuitous services in the business provided by Ms Westcott	$37,440 (Based on Mr Thompson's calculations, page 27 and using the pre‑tax figure rather than the after-tax figures)	Nil
1 July 2012 – 22 June 2015	Lost earnings (after deduction of actual earnings)	$106,192.40	$75,916.64