CORONERS ACT, 1975 AS AMENDED

SOUTH AUSTRALIA

FINDING OF INQUEST

An Inquest taken on behalf of our Sovereign Lady the Queen at

Adelaide in the State of South Australia, on the 7th and 8th days of July 2003, the 12th day of

August 2003, the 23rd day of September 2003 and the 4th day of December 2003, before

Wayne Cromwell Chivell, a Coroner for the said State, concerning the death of Patricia

Davies.

I, the said Coroner, find that, Patricia Davies aged 34 years, late of

28 Uley Road, Craigmore, South Australia died at The Queen Elizabeth Hospital, Woodville,

South Australia on the 4th day of July 2000 as a result of respiratory failure due to

staphylococcus aureus pneumonia and septicaemia complicated by massive haemorrhage.

1. Introduction

1.1. Patricia Davies was born on 20 June 1966. She was a single mother with two

children. She had a very complex medical history which seems to have centred

around a succession of back injuries described by her father, Mr John Davies, as

follows:

'Some years ago Patricia was involved in a car accident, from which she suffered an injury to her back. She had an operation, which resulted in her having to use crutches. One day she slipped whilst on the crutches, and has had back problems ever since.'

(Exhibit C1a, p2)

1.2. The casenotes from the Queen Elizabeth Hospital (‘QEH’), Exhibit C6a, confirm that

Ms Davies had undergone a lumbar laminectomy in November 1995, as well as a

number of other surgical procedures over the years. The casenotes at that time record

that she was taking a large number of medications, including Zoton, Zoloft,

Sandomigran, Mersyndol Forte, Valium, Temazepam, MS Contin and others.

2

1.3. Ms Davies was also morbidly obese. When she died she weighed 113kgs. She was

only 166cm tall.

1.4. Mr Davies’ statement records that at about 6:30pm on Wednesday, 28 June 2000, he

went to Ms Davies’ house and found her in the bath. He said:

'She told me that she had been there for two days after falling down, and not being able to get up. I took Patricia home to my house to try and get her warm. After about an hour I called the ambulance, and she was admitted to the Lyell McEwin Hospital with a collapsed lung and pneumonia.'

(Exhibit C1a, p1)

1.5. At the Lyell McEwin Hospital, Ms Davies was found to have right lower lobe

pneumonia. She was also diagnosed with rhabdomyolysis (known to the layman as

‘muscle meltdown’) and undetermined abdominal pain.

1.6. It was noted that Ms Davies had burns on both breasts with visible pus on the right

breast. She was prescribed intravenous antibiotics and pain relief.

1.7. Ms Davies was transferred to the Intensive Care Unit, where she was intubated and

ventilated by an anaesthetist. A swab taken of the wound to her right breast later

showed the presence of a staphylococcus aureus infection.

1.8. Ms Davies’ condition began to deteriorate on 29 June 2000. In particular she was

unable to maintain her oxygen saturation at appropriate levels without assistance. It

was decided to transfer her to the QEH Intensive Therapy Unit (‘ITU’).

1.9. Ms Davies arrived at the QEH at about 8:30pm where she was seen by the ITU

Registrar, Dr Peter.

1.10. Dr Sandra Peake is an Intensive Care Consultant at the QEH. Dr Peake described Ms

Davies’ condition on admission to the ITU as follows:

'When she came to Intensive Care, she was critically ill. She had severe respiratory failure, necessitating the need for mechanical ventilation. This respiratory failure was due to pneumonia, which was complicated by the development of what is termed 'ARDS', or acute respiratory distress syndrome, and also complicated by the development of a pleural effusion. In addition, she had, as the cause of her pneumonia, a staphylococcus aureus infection, which had led to her developing septicaemia, and the requirement for drugs to maintain her circulation.' (T225-226)

1.11. Dr Peake told me that Intensive Care Units around the world adopt a standard

classification scale known as the Acute Physiology and Chronic Health Evaluation

3

(‘APACHE II’). She said that the score is an assessment of the severity of illness and

enables the clinician to look at predicted death rates. In Ms Davies’ case her

APACHE II score was 57%, and this did not take into account her obesity, which has

a clear association with increased mortality when compared with non-obese patients,

and her narcotic dependence which also increased the risk of morbidity and mortality

because the use of large doses of narcotics necessary in narcotic-tolerant patients

tends to prolong the duration of ventilation (T227-228). To illustrate, Dr Peake said

that the average length of time spent on a ventilator by patients in her ITU was four

days, whereas Ms Davies was expected to be on the ventilator for ‘some weeks’, and

would probably have required a tracheostomy (T229).

1.12. Dr Andrew Holt is an Intensive Care Consultant at the Flinders Medical Centre

(‘FMC'). At my request he prepared a report assessing the quality of treatment given

to Ms Davies for the purposes of this inquest. Dr Holt gave similar evidence to that of

Dr Peake, saying that morbidly obese patients have an increase in mortality rates of

twofold (Exhibit C8, p1).

1.13. Progress at the QEH

An X-ray of Ms Davies’ chest on 30 June 2000 disclosed the presence of a pleural

effusion on the right side. Dr Troy Browne, an ITU Registrar, inserted an intercostal

drain that afternoon. He described the procedure as ‘uncomplicated’.

1.14. Dr Holt explained how a pleural effusion, in this case a parapneumonic effusion,

occurs:

'Yes, the pneumonia in the adjacent lung is when tissues are inflamed, the blood vessels particularly the small blood vessels supplying the region become leaky. It allows white blood cells to get into (the) infection and has benefit, but the downside is that a lot of fluid accumulates in infected tissues, and a lot of protein and other inflammatory mediators. That fluid and protein leaks from the circulation of the lung, and then leaks from the lung into the pleural space.' (T186)

1.15. Dr Holt explained the consequences of such an effusion as follows:

'It's a physical volume issue from a respiratory point of view. The more volume it takes up in the hemithorax the less ability for the lung to expand to its appropriate operating or functional volume. So that initial parapneumonic effusion would have been in excess of a litre, and that is a litre of volume that the lung cannot expand and the lung gets compressed or collapsed below its appropriate functional volume.' (T187)

1.16. There is strong disagreement between Dr Peake and Dr Holt as to Ms Davies’

progress from that time forward. I will discuss the disagreement in detail later. It is

4

sufficient at this stage to observe that Ms Davies’ condition remained very serious for

the next three days and she remained paralysed and ventilated throughout that period.

1.17. On 2 July 2000, Ms Davies was seen by ITU Consultant Dr Michael O’Fathartaigh in

company with Registrar Dr Chi-Lam Fung. Dr Fung’s note reveals that although

there had been some improvement in her lung field, particularly on the left side, the

right pleural effusion persisted. Dr O’Fathartaigh’s assessment was that Ms Davies’

respiratory failure was ‘slowly improving’. His plan was to conduct an assessment of

Ms Davies’ respiratory function by ceasing the anaesthetic agent and nitric oxide with

a view to attempting to accelerate her recovery. The note records:

'Re-look at CXR (chest x-ray) tomorrow if persistent (R) pleural effusion US (ultrasound) + drain (underwater seal drain)'

(Exhibit C6a)

1.18. The attempt to wean Ms Davies away from the anaesthetic agent and nitric oxide was

unsuccessful and so these medications were continued.

1.19. On 3 July 2000 Ms Davies was seen by Dr Peake. Although the time at which this

consultation took place is not recorded, it would seem that it occurred between about

10am and 1pm. Dr Peake noted that the underwater seal drain was not

‘swinging/draining’. The reference to ‘swinging’ refers to the oscillating movement

of the water in the drain as a result of changes in pressure within the thorax as the

patient breathes (see the evidence of Dr Holt at T145). There was a disagreement

between Dr Holt and Dr Peake about the significance of this finding. Dr Peake

argued that the failure of the drain to swing indicated that the drain tube was no longer

in the correct position, whereas Dr Holt argued that this finding was entirely to be

expected. I will discuss this issue again later.

1.20. In any event, Dr Peake issued a direction to the Senior Registrar, Dr Peter, to remove

the underwater seal drain and get a chest ultrasound. Dr Peake explained that the

ultrasound was required to assess the need for a further drain (T253).

1.21. An ultrasound of Ms Davies’ right chest at 4:30pm on 3 July 2000 confirmed the

presence of a pleural effusion of an estimated 500mls. On the basis of that, Dr Peake

decided that it was necessary to put in a further underwater seal drain. She said that

she knew that Dr Peter would arrange for Dr Fung to carry out the procedure

sometime during that evening (T255).

5

1.22. Dr Fung inserted the underwater seal drain at around 9:45pm that evening. She made

an extensive note of the procedure and its aftermath in the clinical record as follows

(the words in brackets are my interpretations of the abbreviations):

'ICU Note Retrospective entry Patient seen at 2145

Indication for (R) UWSD (underwater seal drain) – (R) pleural effusion

- for drainage to improve ventilation

Patient paralysed + sedated

Difficult procedure because of adiposity

Unable to locate pleural space with usual 23g (gauge) needle or 19g spinal needle

proceeded to blunt dissection using finger

Aseptic techniques. Patient prepped with Betadine

45 upright (R) arm taped to bed and breast lifted off with Elastoplast

MAL (mid axillary) approximately 5th ICS (intercostal space) small horizontal incision 2cm above old drain site

Blunt dissection with mosquito forceps and finger. Intercostal muscle dissected with finger + upper rib border identified

28F (French) chest tube inserted, trocar used for support only

1st time: No air, No fluid

2nd time: 500mls frank blood + air in UWSD with associated dropping BP (blood pressure) to systolic 58/

Resuscitation button pressed. Dr Peter informed.

Adrenaline minijets administered

Haema cell/NSA 50mls stat

Urgent cross match; check Hb (haemoglobin) 9.2

BP continued to fall despite initial improvement

CPR commenced at approximately 2245 when there was EMD (electro-mechanical dissociation); ongoing adrenalin + noradrenaline boluses + CPR

Bilateral swan sheath via femoral routes inserted by Dr Peter – assisted (?) approximately 1135

Massive transfusion – 20 group specific O-ve blood + then further matched blood 8 units; hand-ventilated at 100% FIO2

Adrenalin + noradrenaline infusion at 100ml/HR each; pupils dilated

BP fluctuated but 60/70 systolic eventually stabilised to 120/60

SB (seen by) Mr Fitridge kindly - for urgent thoracotomy. Left ICU approximately 2255- When leaving ICU: BP 120/60? HR (heart rate):100 per min

Total CPR approximately 15-20 mins. Total resuscitation approximately 60 mins

Operative diagnosis: pulmonary trauma to consolidated (R) lung

6

Despite control of bleeding intraoperatively and stable BP (with total 20+ units ABP) patient was unable to ventilate despite changing to double lumen tube + life declared extinct at 0055.'

Mr Davies, father, informed

Dr Peake informed

Death reported to Coroner’s

Cause of death

- respiratory failure complicating massive pulmonary bleed

(Exhibit C6a)

1.23. Dr Fung recorded a further note in the clinical record on 4 July 2000 as follows:

'(R) UWSD fell out during CPR. Retrospectively there was little fluid upon chest tube insertions and one wonders whether the US was over-estimating the size of effusion.'

(Exhibit C6a)

1.24. Dr Fung said, when giving oral evidence, that there were two aspects of that note

which were incorrect. Firstly, she said that she used three needles during the

procedure, the 23 gauge, 19 gauge, and a 25 gauge special spinal needle, the last of

which she did not mention in the note (T18). Secondly, she sought to clarify the

reference in her note to ‘45º upright’. She said that it was a reference to the position

of Ms Davies’ arm, and was not intended to suggest that the patient was elevated to

45º, which is an important issue when assessing the size and position of the pleural

effusion (T53).

1.25. Emergency surgery

Mr Robert Fitridge, a Consultant General and Vascular Surgeon and Head of the

Vascular Surgery Unit at the Queen Elizabeth Hospital, was paged just as he was

leaving the hospital and attended at the ITU. He quickly made the assessment that Ms

Davies required an emergency thoracotomy, a surgical procedure whereby the thorax

is entered in order to assess the source of the haemorrhage. The operation

commenced at 11:30pm. Mr Fitridge was assisted by Dr Whalan and the anaesthetist

was Dr Rainbird. He described what he found as follows:

'There was a considerable amount of blood present and ongoing bleeding of the lung itself and this required - the lung itself was oedematous and had micro-abscess in it as you would note from the autopsy report. Then, because the lung wasn't able to be collapsed down because there wasn't a double lumen tube, the lung was still quite distended but I put some stitches of vicral, which is sort of a stitch we use for tying off tissues on a reasonably large needle because the lung is very - it's like a sponge - it's really quite fragile tissue, so it's not like you would say if it was a tendon or muscle

7

where you can actually stitch it. We put stitches in there and tried to control the bleeding basically.' (T71)

1.26. Mr Fitridge described the laceration as follows:

'I think it was less than about 1 cm tear in the lung but there was quite a lot of blood coming out of it. I think one of the questions that was raised was just how deep that was. Basically it's impossible to say because in that situation where you can't collapse a lung and the patient's unstable you just put a stitch in it. We needed to put quite a big stitch in it because the lung was so fragile.' (T89)

He said that the bleeding was controlled after his surgery although Ms Davies was

still hypotensive and it remained ‘a fairly disastrous scenario’ (T71). Following the

surgery:

'the patient became difficult for the anaesthetist to ventilate and they noted some fibrin and blood in the bronchus. The patient became increasingly difficult to ventilate … resuscitation measures were commenced, but really she passed away … at 12:55.'

(Exhibit C7, p4)

2. Cause of death

2.1. A post-mortem examination of the body of the deceased was performed by Dr J D

Gilbert, Forensic Pathologist, on 10 July 2000 at the Forensic Science Centre,

Adelaide.

2.2. In relation to the lungs, Dr Gilbert noted:

'Lungs: A sutured laceration was noted in the lateral interlobar fissure of the right lung between the upper and lower lobes. The cut surfaces of both lungs were congested and markedly oedematous. Foci of pneumonic consolidation with abscess formation were noted in the anterior segments of the right upper lobe and the medical basal segments of the right lower lobe.

Pleural cavities: Pleural drain tubes were inserted via the lateral right 4 th and 5th interspaces. The right pleural cavity contained 200mL of clotted blood. No pleural adhesions were identified. The left pleural cavity was intact and normal.'

(Exhibit C3a, p2)

2.3. Dr Gilbert’s diagnosis of the cause of death was:

'Respiratory failure due to Staphylococcus aureus pneumonia and septicaemia complicated by massive haemorrhage due to lung injury due to chest drain insertion.'

(Exhibit C3a, p1)

8

2.4. Dr Gilbert commented:

'1. Death was due to massive haemorrhage due to laceration of the right lung due to chest drain insertion complicating treatment of Staphylococcus aureus pneumonia and septicaemia.

2. The deceased had a past medical history of morbid obesity, chronic pain, narcotic dependence and depression. She was admitted to the Queen Elizabeth Hospital on 29 June 2000 with acute respiratory failure due to right lower lobe pneumonia and Staph aureus septicaemia after being found in a bathtub at home unable to move for two days. She was admitted to Intensive Care where she was noted to be difficult to ventilate, required inotropes and was commenced on antibiotics. A right-sided underwater seal drain tube was inserted on 30/6/2000 to drain a pleural effusion. She required continuing ventilatory support from 1/7/2000 to 3/7/2000. The chest drain was removed on 3/7/2000 but an ultrasound examination later that day indicated the presence of approximately 500 mL of residual fluid and a further right-sided chest drain was inserted late that evening. The procedure was technically difficult because of the deceased’s obesity. The insertion was immediately complicated by frank haemorrhage from the tube (500 mL) and a drop in blood pressure. Resuscitation was commenced immediately and an urgent thoracotomy was organised. Cardiopulmonary resuscitation followed by massive transfusion was required to stabilise her pre-operatively. The thoracotomy commenced at about midnight 3/7/2000. A perforation of consolidated right lung attributable to the chest drain insertion was noted and oversewn. The haemorrhage appeared at that point to have been controlled. As the chest wound was being closed, however, haemorrhage into the airways was noted. A double lumen endotracheal tube was eventually passed after 2 unsuccessful attempts but the deceased by this stage could not be ventilated adequately and she went into cardiac arrest and died at 0055 hours 4/7/2000.

3. Insertion of chest tubes may be complicated by lung laceration or perforation particularly if the lung is consolidated or bound to the chest wall by pleural adhesions and can be technically difficult to perform in a markedly obese patient.'

(Exhibit C3a, p4-5)

3.1. Mr Fitridge told me that, on the appearance of the laceration, he thought it would have

been caused by the thoracostomy tube rather than any of the seeker needles used by

Dr Fung. He said:

'I think it would have been by the chest tube rather than the needle itself. I think a needle … you just see a little micro-puncture hole, I suppose. It’s unlikely that would cause the sort of bleeding that this sort of generated … I think if the lung's very fragile and the lung itself is adherent then it really doesn't take - it's very fragile. So the chest tube itself, although it's plastic it's actually reasonably firm so it could certainly tear the (lung), especially if you were giving it a gentle push.' (T90)

3.2. Mr Fitridge’s opinion is consistent with the evidence of Dr Fung, who told me that

when she inserted the tube she had withdrawn the sharp-ended trocar (a penetrating

9

instrument which can be inserted through the tube and used for penetrating tissue

without the need for prior dissection). She said:

'The procedure itself is a simultaneous advancing and withdrawing (the trocar) one because you don't want to leave the trocar in even the subcutaneous tissue unless you absolutely have to. So what would have happened is that I would have advanced the tube quite rapidly and withdrawn the trocar at the same time. So from my recollection I did not have the tip protruded and I certainly made note of the fact that the trocar was away from the plastic end of the tube itself when I inserted it.' (T98)

3.3. Dr Holt accepted that the laceration to the right lung was unlikely to have been caused

by a seeker needle, and acknowledged that Mr Fitridge was in a better position than

others to form that judgment (T138). Dr Holt added that it is likely that the injury

occurred at the time of the second insertion of the tube by Dr Fung (T140). Dr Peake

agreed (T307).

3.4. Dr Holt told me that the research articles he produced established that it was quite

uncommon to pierce the lung with a catheter tube alone, even in a patient with

diseased lungs, but he acknowledged that it is possible and he is unable to say that it

could not have occurred in this case (T182). He said that, particularly if the lung had

been adherent to the chest wall (and there is no way to tell that this is the case until

the procedure is undertaken) the risk of injury is increased, and injury can happen

with the best technique and the most experienced operator (T220).

3.5. In light of those opinions, I accept that the laceration to Ms Davies’ right lung which

was the acute event in the course of Ms Davies’ already critically ill state, and which

culminated in her death, was caused by the insertion of the thoracostomy tube by Dr

Fung when she inserted it for the second time on 3 July 2000.

4. Issues arising at inquest

4.1. First thoracostomy - 30 June 2000

Dr Holt said that it was quite appropriate to perform a thoracostomy into Ms Davies’

right pleural space on 30 June 2000 having regard to the volume of the pleural

effusion as a result of her pneumonia and evolving adult respiratory distress syndrome

(ARDS) (T186-188).

10

4.2. Dr Holt said that, having been inserted, the first thoracostomy tube ‘did its job’ by

draining a large parapneumonic effusion. However, he argued that the fact that it had

stopped swinging and draining was not a reason to insert a second one. He said:

'The fact that it had stopped draining intermittently and then continuously stopped swinging was totally expected. A drain will only swing when it’s entering a space (where) the changes in pressure in the thorax are transmitted to it. If the lung becomes completely re-expanded up against the chest wall and up against the chest drain, it will stop swinging because it will be blocked by the expanding lung. It can also be blocked by fibrin or protein in the parapneumonic effusion. So that I don’t see the fact that the first tube stopped working was at all relevant to the decision to put the second drain in … the drain in that position would still be acting as a safety valve if the lung ruptured and air escaped which is a particular risk staphylococcus pneumonia and if I had been placed in that position with that chest drain in that position not swinging and not moving I would still have left it there because she was still requiring relatively high ventilator pressures and the risk of a rupture of the lung and air escaping was there. But at some point that chest drain would have reached the point where … the likelihood of it being a potential source of infection was outweighing the benefit. I wouldn’t have classified that point in time with that chest drain at three days.' (T145-7)

4.3. Dr Peake rejected this view. She argued that the cessation of swinging or draining

could have been due to the fact that the tube had moved, so that it was no longer

within the pleural cavity. Otherwise, the tube could have become blocked or kinked

thereby rendering it ineffective (T241). She said:

'Any invasive device in a patient is a potential source of infection, so if the tube wasn't serving any purpose, then it would be removed and that would be standard for all invasive devices that we use; that when they are no longer serving their purpose they would be removed, to prevent infection developing.' (T241)

4.4. Dr Peake accepted that it was useful to leave the drain in to prevent a pneumothorax,

as Dr Holt suggested, but she argued that the first drain had already fulfilled that

purpose and that:

'Normally if a drain stops working you may leave it in for one day or two days but after that it would definitely be taken out.' (T242)

4.5. Dr Peake pointed out that Dr O’Fathartaigh had examined Ms Davies on 2 July 2000

and directed that if a chest X-ray revealed the presence of a persistent effusion in the

right lung, then an ultrasound should be performed to verify its presence and then a

further underwater seal drain inserted. She explained:

'The reason the plan was determined was because Ms Davies was really not improving and, as I said previously, the longer you're on a ventilator the more at risk you are of

11

other complications going wrong. We, in intensive care, have a belief: that if you're not getting better, you're actually getting worse, and that being said, because she wasn't getting better, that plan was to do the various things that were needed to improve her recovery.' (T245)

4.6. Use of fibrinolytics

Dr Holt said that instead of inserting a second thoracostomy tube, the clinicians at

QEH, if they were concerned about the size of the persistent effusion (which he would

not have been), could have resorted to the use of fibrinolytic drugs as an alternative

approach. He said:

'I raised the issue of thrombolytics in my report because there were alternatives to re-inserting a second thoracostomy tube. If you've read the accompanying readings you will be aware that the opinion as to the utility of fibrinolytic varies and that in fact the benefit of it is highly likely to be related to how early you use it, because the benefit is that a parapneumonic effusion contains a number of inflammatory substances that cause the pleural space to become loculated or walled off in certain ways so that even though you have a drain in part of the effusion there is fibrin and other material blocking the connection between two parts of the effusion. This process occurs fairly rapidly and you will see from the readings that some experts advocate using the thrombolytics on a high risk parapneumonic effusion from the moment that a thoracostomy tube is inserted. Notwithstanding that on 3 July if there was a sense that there was an effusion there that was no longer in connection with this chest drain that was considered necessary to drain it would have been certainly a safer and likely effective manoeuvre to have tried first of all.' (T147-148)

4.7. As to the use of fibrinolytic medication, it would seem that, if it is to be used at all, it

should be used as soon as the thoracostomy tube is inserted, because Dr Holt

acknowledged that once the damage is done by the fibrin and other material, this

damage cannot be reversed, but further damage can be prevented (T198).

4.8. Dr Peake disagreed strongly with Dr Holt’s opinion in this regard. She pointed out

that there was no evidence that Ms Davies’ effusion had become loculated, or

infected, and in those circumstances, the use of fibrinolytics was not called for. She

said:

'There are no studies in the literature that have looked at the use of intrafibrinolytics for simple non-loculated, non-infected effusions. The only studies which are available in the literature relate to an infected and complicated infusions and in actual fact when I say the only studies there are only two randomised controlled trials in the literature. Looking at the question of intrapleural fibrinolytics versus a standard chest drain. Both those studies are very small, with 24 and 31 patients. Small studies are statistically inherently biased and more likely to show a positive result. They are single centre studies and were not

12

undertaken in critically ill patients on ventilators in Intensive Care. Moreover, the Cochran Review, which is a systematic review of intrapleural fibrinolytics looked at those two studies and their conclusions were there's insufficient evidence to support the use of intrapleural fibrinolytics in loculated or infected effusions. As I said, we weren't even dealing with infected or loculated effusions. This is a simple non-complicated effusion. So the whole question of intrapleural fibrinolytics is to my mind irrelevant because that wasn't the sort of effusion we were treating.' (T258)

4.9. Dr Peake said that she had undertaken extensive inquiries with colleagues both in this

State and interstate:

'Since reading Dr Holt's report I have spoken with professors of Intensive Care in the Royal North Shore, Prince of Wales Hospital, Royal Melbourne Hospital, Prince Alfred Hospital, St Vincent's Hospital, Royal Perth Hospital and Charles Gardener Hospital and have been told by all of them they would not use an intrapleural fibrinolytic for a simple non-loculated non-infected effusion.' (T258-259)

4.10. It can be seen that I have the opinions of two highly qualified and experienced

consultants in intensive care expressing conflicting points of view. On the basis of Dr

Peake’s evidence, her view is in accordance with mainstream medical opinion on the

topic and for that reason alone, even if Dr Holt’s suggestions do have scientific merit

which is as yet not proven in the scientific literature, there is no reason for me to

criticise the clinicians at the QEH for failure to use fibrinolytics in this situation.

4.11. Was the patient’s condition improving ?

Dr Holt argued that, in his opinion, an apparent improvement in Ms Davies’ condition

mitigated against the need to undertake a second thoracostomy. He pointed to the

following factors:

Her lung function was improving which was related to the increased ventilator

pressures, the administration of diuretic medication to dehydrate the lung and to

the administration of nitric oxide which has an instant effect of improving lung

function. He said:

'… I still feel that there had been significant improvement in her respiratory function, from a point where when she arrived at the Queen Elizabeth hospital she was in danger of dying from respiratory failure, to the point where even following the cessation of nitric oxide, she had lung disease that was compatible with her survival, with time and continued resolution of the pneumonia.' (T144-145)

Of course, the successful draining of the large pleural effusion by the first

thoracostomy was also a factor in the improved lung function (T145);

13

The signs were that Ms Davies’ infection was resolving. In his report Dr Holt

said:

'The patient’s temperature had improved to a point that she was running a low grade fever only. Her temperature was in the range of 37.3º to 37.9ºC. In addition the patient’s white cell count, which is an index of control of infection, was showing a progressive fall from a peak 15 x 109/L on the 30.06.2000 to 9.3 x 109/L on the 03.07.2000 (normal range 4.0 – 11.0 x 109/L).'

(Exhibit C8)

4.12. Once again, Dr Peake joined issue with Dr Holt in relation to these assertions.

Although she conceded that Ms Davies’ white cell count had come down over the first

24 to 36 hours, Dr Peake pointed out that her ‘PF ratio’, which is a ratio of the oxygen

in the patient’s blood to the inspired oxygen concentration, had remained extremely

low, in the order of 85. She explained:

'Patients who have a PF ratio less than 200 have a much more severe lung injury, and that is then termed “ARDS”.' (adult respiratory distress syndrome) (T230)

4.13. Dr Peake also pointed out that after the initial drop in the white cell count as a result

of the prescription of antibiotics, the count then doubled over the next several days as

Ms Davies developed a secondary infection which Dr Peake described as ventilator-

associated pneumonia. She explained that ventilation decreases a patient’s immune

competency so that they are at risk of developing pneumonia, and the longer the

patient is on a ventilator, the greater the risk of developing ventilator-associated

pneumonia (T232).

4.14. She explained that this process is independent of whether the patient had pneumonia

to start with. If the patient did have pneumonia initially, however, the damage to the

lungs puts him or her at greater risk of suffering secondary pneumonia (T232).

4.15. As to the white cell count, it would appear that Dr Holt has based his opinion that Ms

Davies’ infection was resolving upon a misinterpretation of the laboratory results.

When he stated that Ms Davies’ white cell count on 3 July 2000 was 9.3, he was

actually reading the results of an analysis of a sample taken on 1 July 2000, the results

of which were printed on 3 July 2000.

4.16. In fact, the white cell count on 1 July was 9.3, on 2 July it was 11 and on 3 July in the

morning it was 17.7. Noting the increase, Dr Peake ordered a further white cell count,

14

and a sample taken at 4pm on 3 July showed a continuing rise to 20.1. The normal

range is 4.0 to 11.0 (see T234-236 and T284 and Exhibit C9a).

4.17. Without going into further details, Dr Peake said that several other indicators of

improvement/deterioration were also negative. For example, Ms Davies’ lung

compliance, her need for muscle relaxants and the persistence of a fever all suggested

that Ms Davies’ condition was deteriorating rather than improving (T247-251).

4.18. Dr Peake said that on the basis of the above considerations, Ms Davies was facing a

prolonged course of artificial ventilation and this called for measures to be taken to

improve her ventilatory status in order to give her the best chance to improve (T320).

4.19. On the basis of the above evidence, I conclude that Ms Davies’ condition was not

improving, and in fact was deteriorating substantially as the secondary

ventilatory-associated pneumonia developed. Consequently, it was appropriate to

take whatever measures were available to improve her ventilatory status to give her

the best chance to survive a prolonged course of ventilator-assistance.

4.20. Coagulation studies

Dr Holt said that it would have been prudent to have carried out coagulation studies

before a ‘predictably difficult procedure’ in the form of a thoracostomy was

performed on Ms Davies (T164).

4.21. Dr Peake said that Ms Davies’ platelets had been measured only a few hours earlier,

and these were normal. She said that there was no clinical evidence of coagulopathy

and so further coagulation studies were unnecessary (T275).

4.22. The only time that coagulopathy became an issue was during the latter stages of Mr

Fitridge’s operation, and he said that was likely to have been the result of the bleeding

and consequent loss of clotting agents following the laceration of the lung (T72). On

the basis of that, I conclude that a coagulopathy study before the thoracostomy was

performed by Dr Fung was unlikely to have produced an abnormal result.

15

4.23. Dr Fung’s experience

Dr Holt said that there were a number of reasons why Dr Fung should not have

proceeded apart from the issue of whether the procedure was medically necessary,

during the evening of 3 July 2000:

This was a difficult procedure because the patient was morbidly obese, and it was

likely that the lung was up to and opposed to the chest wall making it harder to

find the pleural space (T166);

The procedure was being performed late at night;

Dr Fung was unsupervised;

Dr Fung was insufficiently experienced.

4.24. Mr Fitridge also said that technically, it would have been a very difficult exercise

having regard to Ms Davies’ size, and the fact that her condition was so unstable

(T91).

4.25. Dr Holt said that he would have been ‘very loath’ to have left a senior critical care

trainee at FMC with this type of procedure unsupervised ‘to the point that I would

want to be readily available to be consulted’ (T169). He added:

'I'm imagining a patient of that weight, body mass, that would have alerted to me to difficulty and I would not have been wanting a registrar, senior or otherwise to be doing it at that time of night without the ability to stop and seek advice in presence … Personally I would want to be in a position where I could intervene or be asked for direct supervision if not being present throughout the entire procedure myself. ' (T170)

4.26. Dr Peake, on the other hand, disagreed with Dr Holt’s analysis. She pointed out that

Dr Fung was already a qualified physician and cardiologist, and was six months short

of qualifying as a specialist intensivist as well. She had declined the position of

Senior Registrar for rostering reasons only, and was regarded by the consultants at

QEH as technically competent (T262-263).

4.27. Dr Peake said that it is not unusual for the clinicians at QEH to be dealing with

morbidly obese patients. She said that studies had shown that more than 30% of their

patients weighed more than 100 kilograms (T266). She said it was not the practice of

the Unit to directly supervise Registrars if the Registrar is considered competent and

experienced in the procedure (T266).

16

4.28. Dr Peake disagreed strongly with Dr Holt’s criticism of the hour at which this

procedure was conducted. She pointed out that the ITU at QEH did not work 9am to

5pm, that if it was considered that a procedure was necessary it was done at the

earliest available time, that she was always available to consult with Dr Fung by

telephone if necessary, and there is always a surgeon in the hospital should an

emergency have arisen. She said:

'No, I disagree. There are two types of procedures in Intensive Care, ones which are immediately life threatening and yes, this was not immediately life threatening, and then there is the rest of the procedures and the rest of the procedures are done at the time that they are indicated and at the first available opportunity. They are not left to wait until daylight hours, because that's not how you treat Intensive Care patients. The whole point about treating our patients is that we are continually paying attention to detail; we are continually optimising their management. We are continually reviewing their management. That's why we review the patients three times a day, more if needed. We are continually going around, assessing, changing our treatment plan, and a treatment plan that you made it for entirely appropriate at 9 in the morning may be completely inappropriate three hours later because of the nature of the patients. You do things when they are needed.' (T267)

Dr Peake also pointed out that the incidence of complications with this procedure is

only around 3%, and that includes simple complications such as the misplacement of

the catheter. She described major complications such as the one suffered by Ms

Davies as ‘extremely rare’. She said that she had never seen such a complication in

her clinical experience (T268).

4.29. As to Dr Holt’s practices in relation to trainees, Dr Peake said that FMC has a

‘different, and more restrictive’ approach to training from almost every other

Intensive Care Unit in Australia (T332).

4.30. Once again, I am faced with a clear dichotomy of views between two highly qualified

and experienced clinicians. Dr Holt is a Senior Consultant in critical care medicine at

FMC, and he is a member of several committees charged with monitoring standards in

clinical care. Dr Peake is a Senior Consultant in Intensive Care at the Queen

Elizabeth Hospital, and she also holds a number of important positions in education

and training for intensive care medicine.

4.31. It seems to me, that in every teaching hospital it is necessary for consultants to form a

judgment about whether it is appropriate to entrust a trainee, whether junior or senior,

with performing a procedure unsupervised. I think that there will always be

17

differences of approach to such highly specialised training. It is likely that eminent

specialists will disagree from time to time, as has happened here. In the particular

circumstances of this case, and particularly having regard to the fact that Dr Fung was

unusually highly qualified for a person in her position, I see no grounds for criticism

of Dr Peake on the basis that she allowed Dr Fung to perform this procedure on Ms

Davies without direct supervision.

4.32. Seeker needles

Dr Holt said that, in general, seeker needles are used to identify the presence of a

pleural effusion to confirm that it is appropriate to place the thoracostomy tube in a

particular position (T149). This is consistent with Dr Fung’s entry in the clinical

record:

'Unable to locate pleural space with usual 23g needle or 19g spinal needle therefore proceeded to blunt dissection using finger.'

(Exhibit C6a)

It will be recalled that Dr Fung explained that she, in fact, used three needles,

including a 25 gauge special spinal needle as well as the other two.

4.33. When she gave evidence, Dr Fung said that she did not use the needles to identify the

presence or absence of a pleural effusion, but rather:

'The needles were used to identify the ribs which were the basic landmarks for intercostal space I needed to get to.' (T100)

4.34. Dr Holt said that he was unable to see any benefit in using a seeking needle to locate a

rib as described by Dr Fung - he said that it would have been more appropriate to

simply proceed with dissection, and the rib should have been located as part of that

process (T150). This is in fact what occurred after Dr Fung abandoned the use of the

needles.

4.35. Dr Holt agreed that the issue concerning the seeker needles, which occupied a

considerable amount of time during the inquiry, is something of a red herring in terms

of the causation of the injury to Ms Davies’ lung. However, he suggested that:

'I guess it goes some way to my feeling that given the difficulty of the insertion there may not have been necessarily the appropriate experience at that point in time to proceed with it under ideal circumstances.' (T155)

18

4.36. Dr Peake said that it was open to Dr Fung to use seeker needles if she considered that

appropriate, and pointed out that Dr Fung accessed the pleural space without

complication during the first insertion of the thoracostomy tube. She argued that the

use of the seeker needles was not an indication of Dr Fung’s inexperience (T270).

4.37. Mr Fitridge told me that even if Dr Fung had hit a major blood vessel using one of the

needles she had utilised, it was unlikely to have caused a massive haemorrhage having

regard to the fine bore of the needles (T96).

4.38. In all those circumstances, I am not prepared to conclude, from the facts that Dr Fung

used three different seeker needles during the thoracostomy procedure, and that she

abandoned their use and reverted to a normal dissection technique, were indications

that Dr Fung lacked experience or expertise in carrying out -the procedure.

4.39. Suitability of forceps

Dr Holt also mentioned that the forceps used by Dr Fung were not ideal to puncture

the intercostal membrane during the course of the thoracostomy procedure because

the end of the instrument was, in his opinion, ‘too sharp’ (T219).

4.40. However, Dr Fung told me that she used her finger to separate the membrane, and this

would have prevented any injury to the lung (see Dr Holt’s supplementary report,

Exhibit C8a, p4).

4.41. Dr Gilbert, the Forensic Pathologist also noted that:

'The lateral aspect of the right 5th rib had been neatly divided apparently as part of the thoracotomy procedure.'

(Exhibit C3a, p3)

4.42. On the basis of that evidence, I find that there is no ground for criticism in relation to

the forceps used by Dr Fung in the course of the thoracostomy procedure.

4.43. First thoracostomy attempt unsuccessful – 3 July 2000

Dr Holt said that when the first thoracostomy tube did not swing or drain, it would

have been more appropriate to have waited rather than repeating the procedure. He

said:

'… given the fluid was posteriorly or back behind the lung, given that the fluid was likely to be posterior and behind the lung, that there may have been no fluid evident out of the tube straight away. It may not be apparent that you're necessarily anything would happen for some time until you were hooked up to the underwater seal bottle you might then

19

begin to see the level swing as evidence that you're in the chest after a period of time. So I don't know whether she - it was not apparent to me from the interview whether she did hook it up to the underwater seal bottle to determine whether there was any swinging and for how long she did this. But in my experience it's not uncommon to put a chest tube in the right spot and therefore there to be nothing apparent coming out of the tube for some time.' (T159-160)

4.44. Dr Holt said that if Dr Fung thought that she was not in the right place, it would have

been prudent to have stopped and obtained a chest X-ray, which may have told her

with more certainty whether she had the tube in the pleural space or not (T160).

4.45. Dr Holt said that the difficulty with knowing the position of the tube in such a patient

was compounded by the fact that Dr Fung was inserting the thoracostomy tube only

one to two centimetres away from the first thoracostomy performed on 30 June 2000,

and that having regard to the amount of adipose tissue in the area, she may have been

encroaching on the previous pathway (T159).

4.46. Dr Fung explained that she removed the first tube because:

'My recollection was that I interpreted the tube either being blocked at the end by lung tissue or I had not positioned it correctly where the fluid is.' (T61)

4.47. Dr Peake said that in her opinion, Dr Fung’s actions were entirely appropriate. She

said that if Dr Fung thought that the tube was extra-pleural, then it was entirely

appropriate to try again with another tube (T272). In particular, she did not agree

with Dr Holt that Dr Fung needed to obtain a chest X-ray before proceeding, she said

that it was necessary for Dr Fung to place the second tube in without delay to guard

against tension pneumothorax (T273). In any event, Dr Peake said that it was

unlikely that a chest X-ray would have been useful in these circumstances (T316).

4.48. In the event, both Dr Fung and Mr Fitridge raised the possibility that, in retrospect,

the ultrasound was misleading and that the fluid in Ms Davies’ chest was actually

within the lung, rather than in the pleural cavity (see Dr Fung’s note on 4 July 2000 in

Exhibit C6a, and Mr Fitridge’s evidence at T75). Of course, Dr Fung had no way of

knowing this at the time.

20

5. Conclusions

5.1. This has been a very difficult and troubling inquest. Clearly Ms Davies’ death was

brought about by a combination of an acute event, namely the laceration of her right

lung during the thoracostomy procedure, superimposed upon the fact that she was

already gravely ill. It is clear that the acute event precipitated, or at least hastened her

death.

5.2. In that context, I have before me the opinions of two highly respected and

experienced specialists in intensive care which are opposed to each other on complex

areas of intensive care medicine.

5.3. On the evidence before me, I have rejected the criticisms of Dr Fung in all aspects of

her performance of the thoracostomy procedure. It would seem that the injury

occurred as a result of the thoracostomy tube impacting on the lung surface, thereby

causing a laceration of tissue, which had already been severely compromised by an

infection and was much more susceptible to injury. The fact that the tissue may also

have been adherent to the wall of the pleural cavity would also have increased its

susceptibility to injury.

5.4. In those circumstances, I have no criticism of Dr Fung, nor do I criticise the

consultants at the QEH, and Dr Peake in particular. On the evidence before me, Dr

Fung was an appropriately qualified and experienced clinician to carry out the

procedure in question, the procedure was performed with due competence, and the

tragic outcome was the result of a combination of factors which could not have been

avoided in the circumstances of the time.

Key Words: Hospital Treatment; Thoracostomy

In witness whereof the said Coroner has hereunto set and subscribed his hand and

Seal the 4th day of December, 2003.

Coroner

Inquest Number 14/2003 (1638/2000)