[2007] NSWCA 335
Paul v Cooke [2013] NSWCA 311
Sydney South West Area Health Service v MD (2009) 260 ALR 702
Source
Original judgment source is linked above.
Catchwords
[2007] NSWCA 335
Paul v Cooke [2013] NSWCA 311
Sydney South West Area Health Service v MD (2009) 260 ALR 702
Judgment (53 paragraphs)
[1]
Judgment
HIS HONOUR: Brendan Hobson was born with Noonan Syndrome, a genetic disorder that prevents normal development in various parts of the body. A person can be affected by Noonan Syndrome in various ways. These include unusual facial characteristics, short stature, heart defects, other physical problems and possible developmental delays. One of the occasional, although not necessarily universal, manifestations of that condition is an unusual or idiosyncratic shape of the chest. Mr Hobson's chest was affected in this way as the result of a severe lordoscoliosis.
Because of Mr Hobson's problems, he gradually developed difficulties in breathing. In short, in lay terms, the limited volume of his chest cavity began progressively to restrict Mr Hobson's ability to fill his lungs with air. By at least November 2009, Mr Hobson's condition had deteriorated to the point where, without surgical intervention, his prognosis was grave. Accordingly, in November 2009, when he was 24 years of age, Mr Hobson was admitted to Royal North Shore Hospital for a brace of operations designed to remedy this defect. The first operation was planned for, and carried out uneventfully on, 13 November 2009. The second operation was originally planned to take place two weeks later. However, in the events that occurred, to which detailed reference appears below, a decision was made to advance that surgery to the evening of 17 November 2009. It was in the course of that second procedure that Mr Hobson sustained a hypotensive insult to his spinal cord that rendered him a paraplegic. That condition is permanent.
Mr Hobson initially maintained that his paraplegia resulted from the negligence of the four separate defendants. The first and third defendants were, however, released by consent from the proceedings on 21 November 2016. The remaining second and fourth defendants are respectively Dr Gray, the orthopaedic surgeon who performed the operation on 17 November 2009, and Dr Sparks, the attending anaesthetist. A decision was made to discontinue the surgery after approximately three hours when it became apparent that Mr Hobson's vital signs had deteriorated alarmingly. He was returned to the intensive care unit. The operation was rescheduled and successfully completed some weeks later.
However, Mr Hobson alleges in general terms that the operation on 17 November 2009 ought to have been aborted earlier when it became apparent that his intraoperative condition was critical and quickly deteriorating. He alleges that he would not have sustained any injury at all if that course had been taken in a timely way. On the contrary, even though the surgery was ultimately cut short, Mr Hobson complains that the remaining defendants negligently persisted with it to the point where the irreparable damage to his spine occurred and significantly well beyond some earlier stage in the operation when it could have been abandoned uneventfully.
These complaints have been the subject of a large series of differently pleaded allegations that culminated in what became the third further amended statement of claim. It is important at an early stage to record the way in which Mr Hobson ultimately particularised his allegations of negligence. As against Dr Gray they are as follows:
1. Failing to ensure the provision of proper and effective spinal cord monitoring at the surgery on 17 November 2009.
2. Failing to delay or postpone (or advise the delay or postponement) of the surgery until the spinal cord monitoring was in place and a baseline reading obtained.
3. Continuing with the surgery when a baseline reading had not been obtained and/or when the readings of the monitoring were abnormal, and/or when the spinal cord monitoring was compromised by the administration of muscle relaxants.
4. Proceeding with such surgery when blind to whether the spinal cord was functioning normally.
5. Failing to halt or advise the halting of the surgery of 17 November 2009 following the earlier episodes of hypoxia and hypotension (occurring at or about 18.50, 19.10, 20.35 and 21.20) and related complications reported in the anaesthetic record between approximately 19.10 and 21.20 that evening.
6. Continuing the operation:
1. when no baseline was established and/or the readings were abnormal; and
2. in the face of the anaesthetic events detailed in (5) above;
3. when the muscle relaxant medication (vecuronium) administered by the anaesthetist has compromised the spinal cord monitoring.
1. Failing to carry out or cause to be carried out spinal cord monitoring effectively or at all.
2. Failing to pause or cease the surgery when either a baseline had not been achieved and/or the results were reported to be abnormal.
3. Failing to have due regard to:
1. Mr Hobson's existing gliosis on his spinal cord at T11/12; and
2. the reduction in the 13 November 2009 surgery of the number of arteries supplying blood to the spinal cord.
1. Failing to delay or postpone (or advise the delay or postponement of) the surgery until such time as Mr Hobson was haemodynamically stable, could be adequately ventilated and spinal cord monitoring was in place.
2. Continuing the surgery with Mr Hobson in the prone position.
3. Commencing the surgery before baseline spinal cord monitoring was established.
The claim against Dr Sparks repeats the first ten particulars of negligence pleaded against the surgeon together with the following five additional particulars:
1. Commencing the surgery before baseline spinal cord monitoring was established, and before Mr Hobson was adequately ventilated.
2. Failing to ensure complete and effective spinal cord monitoring in the 17 November 2009 operation.
3. Continuing with the operation in the face of the abnormalities shown on the anaesthetic record referred to above.
4. Failing to inform the treating surgeon that a probable cause of the failure of the spinal cord monitoring was the use of the chosen anaesthetics and muscle relaxants and that an alternative which did not affect the monitoring should be used.
5. Failing to inform the surgeon that the likely cause of Mr Hobson's ventilation problems was him being in a prone position and this could not be solved by any approach other than turning him supine.
It can be seen that most of these allegations are common to the case against both Dr Gray and Dr Sparks. By reason of their separate roles, however, they necessarily raise slightly different considerations. This is discussed more fully later in these reasons. It will be obvious that spinal cord monitoring is alleged to be a significant element in Mr Hobson's case against both of these defendants. This procedure therefore requires at least a rudimentary explanation.
[2]
Spinal cord monitoring
Based upon the articles and associated literature to which my attention has been drawn, I take at least the following general matters concerning spinal cord monitoring, in its application to the facts of the present case, to be uncontroversial.
Spinal cord monitoring, as the name suggests, is a procedure or technique designed to monitor the intraoperative integrity of a patient's spinal cord during surgery. This is done by the stimulation and measurement of motor evoked responses via electrodes connected to the patient's extremities. These signals are generated at various appropriate and convenient stages of the operation so as to provide information to the surgeon about whether the spinal cord has or may have been surgically damaged. Single or repetitive pulse stimulation of the brain in this way causes the spinal cord and peripheral muscles to produce neuroelectrical signals known as motor evoked potentials. This technique obviates the need to arouse the patient from an anaesthetised state in order to check whether the patient's spinal cord may have been damaged in any way.
The role of intraoperative monitoring in spinal surgery is to evaluate the integrity of the nervous system continuously while patients undergo procedures that have the potential to cause injury to the nervous system, particularly the spinal cord and spinal nerves. Since patients are under general anaesthetic, techniques for examining the nervous system are limited to those that can be applied to an unconscious subject. The task of monitoring personnel is to identify neural irritation or injury at a time when the surgeon can take steps to reduce or reverse it and to define the nature of the injury in a way that will allow the surgeon to complete the procedure without risking further injury. Ideally, this is done in an efficient manner without interfering with the flow of the operation or producing unnecessary interruptions.
The risk of neural injury has long been recognized, and several other manoeuvers have been devised to try to detect and correct problems before they become irreversible. Electrophysiological intraoperative monitoring techniques have evolved, and now offer timely evaluation and feedback to the surgeon at a point where interventions can be taken to prevent irreversible neural damage. The aetiology of neural injury is varied, and mechanisms can range from structural compromise related to abnormal spinal anatomy to instrumentation-related injury and vascular insufficiency. The structures at risk include peripheral nerves, spinal roots, and spinal cord.
The decision to perform intraoperative monitoring involves many factors, and the approach to monitoring is a team effort that includes the surgeon, monitoring personnel, and the anaesthetist. These factors presumably include an assessment of the risk of injury from a given operative procedure. That risk can vary from highly likely to none at all, and the decision to monitor in any given case will generally be that of the surgeon and the monitoring team. Since there are a variety of monitoring techniques and strategies, the surgeon and the monitoring team must also determine which neural structures are at risk so the appropriate monitoring protocol can be used.
It will be apparent that spinal cord monitoring is far more complicated than this brief description is able to communicate. I have included the description in order to aid in the understanding of what follows. No part of the foregoing description concerning spinal cord monitoring in general, or references to its use in this case in particular, is intended in any way standing alone to inform or determine the remaining liability issues in Mr Hobson's cases against either Dr Gray or Dr Sparks.
[3]
Background
In 2008 or 2009, Mr Hobson was told that he should have an operation to straighten his thoracic spine. He had by that time developed some difficulty breathing and had also developed an intermittent problem with wheezing. He was told that the operation might assist with this breathing problem and also straighten his back. He was referred to Dr Gray at Royal North Shore Hospital. They met several times.
Dr Gray told Mr Hobson that the operation would be carried out in two stages. One or more rods would be inserted to straighten his spine, held in place by screws. He was also told that spinal cord monitoring could be performed if Mr Hobson was a private patient. Mr Hobson recalls being told by Dr Gray, "The spinal cord monitoring will monitor the function of your spinal cord during the operation and tell us if the signal is too low or too high".
Mr Hobson was placed under general anaesthetic on 17 November 2009 but has no other relevant recollection of events until sometime in mid-December when he "realised something wasn't right". Somewhat extraordinarily, he was not told formally what had happened to him until early in January the following year.
[4]
Dr Gray's evidence
Dr Gray first saw Mr Hobson on 21 August 2009 at the Spine Clinic at RNSH. He noted that he had been diagnosed with Noonan Syndrome in his childhood and that he had had a series of associated syndromal features and medical problems that included severe thoracic lordoscoliosis with restrictive lung disease. The latter condition was the basis for referral to Dr Gray. The main concern was a worsening of Mr Hobson's lordoscoliosis affecting his thoracic and upper lumbar spine with progressive deformity of his middle thoracic region and associated restrictive lung disease. Results of respiratory function at that time indicated a persistent restrictive pattern of lung disease with mild decrease and diffusing capacity with some responsiveness to bronchodilators. Mr Hobson had been on inhaled corticosteroids.
It is uncontroversial that Mr Hobson would benefit from deformity correction surgery of his lordoscoliosis in order to increase his lung capacity and prevent further deterioration of his lung disease and eventual cor pulmonale secondary to pulmonary hypertension. Mr Hobson reported that he was finding himself increasingly short of breath, particularly with exertion. These symptoms had become progressively worse over the preceding 12 months. Mr Hobson had no lower limb neurological symptoms and had good bowel and bladder control. In summary, Dr Gray noted that Mr Hobson had a significantly reduced vertebra-sternal distance due to his thoracic lordoscoliosis causing the pattern of restrictive airway disease.
Dr Gray discussed the option of surgical correction with Mr Hobson, including the combined anterior and posterior approaches in two stages, wedge osteotomies through the apex of his thoracic lordoscoliosis and subsequent posterior instrument fusion of his thoracic and upper lumbar spine. The first stage involved a thoracotomy with multiple anterior thoracic discectomies and wedge resections of the adjacent end plates in the form of a closing wedge osteotomy. That stage was planned in association with cardiothoracic surgeons and was to be performed by the RNSH cardiothoracic team. The second stage was the posterior instrumented fusion from T2 to L1, following the anterior release to correct the lordoscoliosis to a more normal kyphosis of the thoracic spine.
The anterior procedure was performed on 13 November 2009 by Dr Gray, Dr Cree and Dr Marshman. The surgery was uneventful and successful. Relevantly, Mr Hobson was found post-operatively to be neurologically intact.
The original plan was to perform the second operation after approximately ten days. However, on 15 November 2009 Mr Hobson was found to have extrinsic compression of his left main bronchus. His right upper lobe was normal and his right main bronchus was patent. Later that day Mr Hobson's left lobe was found to be collapsed further. The ICU was having trouble maintaining his oxygen saturation. Dr Gray said that the original plan of performing the second stage of the operation two weeks later was not practical due to the compression of the left main bronchus and the collapse of the left lung. Dr Gray formed the opinion that persisting with the original plan would place Mr Hobson's life at risk. The ICU staff asked for the second stage surgery to be brought forward.
Mr Hobson was reviewed on 17 November 2009. The obstruction of the left main bronchus and worsening respiratory function were matters of escalating concern. The anaesthetic and spinal teams decided to bring the surgery forward in order to create more space in the mediastinum and to relieve the extrinsic compression. This included arranging for spinal cord monitoring. The surgery commenced at 7.00pm. Dr Gray described what happened thereafter in the following terms:
"43. The procedure was performed by Dr Cree and myself with Dr Matthew Lyons (Registrar) assisting. The anaesthetists were Dr Sparks and Dr Wang. In relation to spinal cord monitoring, baseline spinal cord monitoring (motor evoked potentials) was obtained prior to the patient being positioned on the Jackson Table. The baselines were reported as being within normal limits and monitorable. Dr Lagopoulos set up the monitoring. This involved the connections, whilst the patient was supine, of probes into the patient's skull and lower limbs. I requested Dr Lagopoulos perform a run ('motor evoked potential') whilst he remained supine. Dr Lagopoulos attended to that request.
44. During the course of the surgery the patient, due to respiratory difficulties, was positioned prone on the Jackson Table. Dr Lagopoulos stated that the patient had normal motor evoked potential in both lower limbs.
45. The spine was exposed in a routine fashion through a midline posterior approach and pedicles were displayed between T2 and L2. I inserted pedicle screws into the left side between T7 and L2. Dr Cree attended to insertion of pedicle screws into the right side.
46. The patient, due to respiratory difficulties, had to be paralysed through the use of a muscle paralysing agent in order to be ventilated. vecuronium was used by the anaesthetic team to paralyse the patient. With the muscle paralysis, the patient's motor evoked potentials had become non-monitorable. Therefore further spinal monitoring was discontinued as the patient needed to be paralysed for the rest of the procedure to aid ventilation.
47. Dr Sparks informed those present of difficulties encountered by him including the ongoing reduction in oxygenation, hypotension, a decrease in end-tidal CO2 and an increase in PaCO2. He said words to the effect 'I'm having problems with ventilating…'. There was a collection of anaesthetic issues including hypoxia, hypotension, decreasing end-tidal CO2 and increasing PaCO2. Dr Cree said words to the effect 'Should we stop'. Dr Sparks indicated that the surgery could continue. Dr Sparks said words to the effect of 'no, keep going, I'll let you know'. Dr Sparks then shortly afterwards indicated that it would be necessary to cease the surgery. Dr Sparks said words to the effect 'I think we need to stop'. There was a collective discussion and decision to cease the surgery.
48. The surgery was abandoned and the wound was rapidly closed. The patient was repositioned to the supine position. There was significant hypertensive down time.
49. There was also significant reduction of SpO2 however, shortly thereafter the patient was placed supine and his cardiovascular status improved. There were concerns at the time that the patient may have suffered hypoxic brain injury due to the downtime of the cardiac arrest. The patient was taken to the ICU, intubated, ventilated and monitored.
50. Up until the point where the patient was paralysed Dr Lagopoulos kept the surgical team updated with regular feedback.
51. There was no neurophysiologist working in the theatre at the time with Dr Lagopoulos. It was not standard practice at the RNSH to have a neurophysiologist present.
52. As far as I was aware it was not the usual practice at RNSH to print out the monitoring tracing reports. As far as I am aware no records are generated by the monitoring technician. The technician may keep his own personal records.
53. A lengthy discussion was arranged with the patient's family, including his mother, father and sister. Dr Cree, Dr Sparks and myself were all involved in the conversation. Concerns were voiced regarding the possibility of hypoxic brain injury due to the prolonged period of hypoxia in the prone position. I noted that a combination of events at the procedure were hypotension, hypoxia and hypercapnia in the prone position."
Dr Gray was cross-examined about these recollections. This is referred to later in these reasons.
An MRI scan of Mr Hobson's thoracolumbar spine was performed the following day. That scan suggested anterior cord type syndrome of the thoracic spinal cord with signal change on the T2 weighted images in the anterior and middle part of the spinal cord. Post-operatively Mr Hobson had a complete neurological deficit of his lower limbs. The signal change was between T10 and T12 in the possible watershed area. Dr Gray thought that the changes were most likely secondary to an ischaemic event and other vascular ethology. No cord or thecal deformity was seen at or in the vicinity of the screws. All screws were in a good position. Dr Gray thought that Mr Hobson had suffered a hypotensive vascular injury to the lower part of his spinal cord.
The second stage of the originally planned surgery was successfully completed on 11 December 2009.
[5]
Dr Sparks' evidence
Dr Sparks' understanding of the need for Mr Hobson's surgery, and the two stage plan to effect it, was the same as that of Dr Gray.
On 17 November 2009, Dr Sparks was the Duty Director in charge of theatres for that day. He was contacted by either Dr Gray or his Registrar and told that the second stage of the surgery needed to be performed as soon as possible, "as the compression on the bronchus needs to be released". Dr Sparks formed the clear impression from that conversation that the operation needed to be performed within the next 24 hours. Dr Sparks was aware that the operation would be a very challenging procedure requiring an experienced anaesthetist.
Following the discussion with Dr Gray or his Registrar on 17 November 2009, Dr Sparks went to the ICU at about 12.30pm and spoke with the specialist on duty there. He did so in order to satisfy himself that the surgery was urgent and to assess Mr Hobson's clinical status from an anaesthetic perspective. Dr Sparks gained the impression that the ICU was having difficulty adequately ventilating Mr Hobson because of the compression of his left main bronchus. In practical terms, that meant that the left lung could not be ventilated or suctioned and that Mr Hobson had to remain intubated. Dr Sparks was concerned that Mr Hobson was developing pneumonia, which would be fatal if ventilation and suction of the left lung were not improved.
Dr Sparks returned to the ICU with Dr Barratt at around 2.40pm. Dr Barratt was a senior anaesthetist with experience in spine and thoracic anaesthesia. Dr Sparks wanted Dr Barratt to assist him to perform a bronchoscopy in order to assess Mr Hobson's left main bronchus. This was found to be compressed and stretched but permitted the insertion of the bronchoscope through the obstruction allowing measurement of the bronchus at about 5cm.
The surgery was re-scheduled to the evening of 17 November 2009 to facilitate the availability of the physician in charge of the spinal monitoring equipment. Dr Sparks volunteered to be the anaesthetist. He was in favour of the use of a double lumen tube so that Mr Hobson's left main bronchus could be splinted open, promoting ventilation of the left lung and improving oxygenation. Dr Sparks also expected that this would prevent air being trapped in the left lung, which might worsen during surgery in the prone position, and which in turn would increase pressure on Mr Hobson's heart and lungs.
Dr Sparks described what happened in the operation as follows:
"19 Mr Hobson was taken down to theatre at some time between 18:00 and 18:10 based upon the anaesthetic nursing notes.
20 According to the anaesthetic records vecuronium was administered by ICU by Dr Wang at around 18:00. Vecuronium was again administered at around 18:30 to enable the insertion of the double lumen tube. Vecuronium is a neuro-muscular blocking agent that, at the doses given, had a likely duration of 25-30 minutes.
21 With Mr Hobson still in a supine position, a 37 French gauge left double lumen tube was inserted over an exchange catheter.
22 Initially, I was concerned that the length of the bronchial lumen, 5cm, would not be long enough to pass through the compression of the left main bronchus which I had estimated at bronchoscopy to be 5cm in length.
23 After the double lumen tube was inserted the position was checked with a 10FG fibre optic bronchoscope and with alternate clamping, a typical CO2 waveform was seen for each lung. I remember that the bronchial lumen tube did not pass the narrowing completely, but I was able to advance far enough to splint open the left main bronchus which meant that Mr Hobson was effectively ventilated on the left for the first time in four days. I rechecked the position of the tube multiple times during the surgery and it remained in a good position.
24 There was a temporary reduction in oxygen saturation to 86% at 18:50 which coincided with the change to the double lumen tube. During the change to the double lumen tube there were a couple of minutes when no ventilation was occurring. This is normal and the patient's oxygen saturation recovered to 100% soon after.
25 …
26 A second radial line in the left hand was inserted which confirmed the accuracy of the first radial line inserted in the right hand. Arterial radial lines are used to measure blood pressure continuously and accurately. Both lines showed the same pressure wave form, a high systolic and low diastolic reading. Dr Wang and I then administered the anaesthetic agents Sevoflurane 1%, Remifentanyl 1-3ng/ml and Ketamine 10mg/hr. These anaesthetic drugs are compatible with spinal cord monitoring.
27 According to the anaesthetic record, Mr Hobson was turned over to the prone position sometime between 19:10 to 19:15. I said to the surgeons words to the effect: 'Can you minimise downward force on Mr Hobson's spine during the operation as it could cause cardiovascular compression'.
28 The reason why I asked the surgeons from refraining from pressing down was because I was conscious of Mr Hobson's CT aortic angiogram which showed bronchial compression and pulmonary artery compression. As a result of the pulmonary artery compression features on the aortic angiogram increased compression on Mr Hobson's pulmonary artery while in the prone position was possible.
29 When Mr Hobson was turned to the prone position there was a slight drop in blood pressure. This was corrected with Aramine (Metaraminol) 0.5mg. Mr Hobson's blood pressure subsequently remained fairly stable. I did not consider there was evidence of hypotension. The central venous pressure was around 32 and my goal was to keep it stable during the operation.
30 Between Mr Hobson being turned prone and the surgery starting, I checked the double lumen tube again, first by alternate clamping and then by examining it with a bronchoscope. I had to get down on the floor on my knees to check the scope. An appropriate CO2 waveform came from each lumen and the bronchoscope confirmed the correct positioning of the double lumen tube.
31 The medical records show the operation commenced at about 19:30 to 19:40.
32 The blood gas readings at 19:13 were: PO2 243 (90 to 95 normal parameters) and PO2 65 (35 to 40 normal parameters). A PCO2 reading of 65 was outside of normal parameters and in normal circumstances I would not anaesthetise such a patient, but the emergency nature of the situation meant I needed to accommodate the PCO2 level and did so by increasing ventilation in response. I assumed the PCO2 at 65 was a result of low minute volume, which is the reason why the ventilation was increased. I assumed the high reading of a PO2 at 243 was a result of Mr Hobson's left lung being oxygenated effectively for the first time in 4 days.
33 By around 20:30 the arterial blood CO2 level had risen from 64.7mmHg to 70.5mmHg. I could not detect any mechanical obstruction to ventilation but nevertheless I felt compelled to give muscle relaxant, vecuronium. I informed the surgeons of this course of action.
34 Vecuronium was administered at around 20:30 in response to the rising carbon dioxide level. It was given to allow us to attempt to improve ventilation. The O2 partial pressure remained high and the trend systolic blood pressure was normal to high. Because it was emergency surgery I had resolved in my mind that while the oxygenation and blood pressure were normal to high it was appropriate for the surgery to continue.
35 The arterial carbon dioxide levels continued to be elevated and I tried everything I could think of to identify the cause of the problem. I checked for mechanical problems with the ventilation. I increased the tidal volume, I undertook hand ventilation and I checked the position of the tube with the bronchoscope several times, but there was no mechanical problem with the double lumen tube or the breathing circuit.
36 I considered a pneumothorax and breath stacking in the left thorax. I tried to disconnect the left lung from ventilation and leave it open to air, but the blood gas results stayed much the same. The partial pressure oxygen (PO2) remained high.
37 The arterial carbon dioxide continued to be elevated and the expired waveform diminished. I tried hand ventilation and I got down on my knees on numerous occasions to check the tube with the bronchoscope again, but it was always in the correct position. I was comfortable that the double lumen tube was working properly.
38 Having excluded these reasons for the problem, I formed the opinion that the likely cause was cardiac and not the ventilation. I formed this opinion even though the systolic blood pressure was stable at about 150 systolic for most of the time. Each arterial line in the left and right hands measured the blood pressure continuously and recorded the same result.
39 I was conscious of Mr Hobson's history of previous ASD repair and pulmonary valvectomy in 1988; and a prior trans-thoracic echo showing raised pulmonary artery pressure. In addition there was the thoracic vertebral body compressing the left atrium all of which indicated that the patient's right ventricle had a high workload. I considered the use of cardiac inotrope but rejected it. With a typical systolic pressure of 140 to 150 during most of the surgery and obstruction to the right ventricle caused by bone I felt that inotropes would only precipitate right ventricular failure. In short I thought that inotropes were unlikely to assist or help the patient, rather they were more likely to harm him.
40 At about 20:50, I telephoned Dr Barratt and Dr Marshman, cardiothoracic surgeon, to discuss the circumstances, specifically the patient's low exhaled CO2 even though the blood pressure was high to normal and normal ventilation. Neither specialist could recommend anything that I had not already considered. In my telephone conversation with Dr Barratt, he said words to the effect: 'It must be due to 'dead space' and not a problem with ventilation'. Dr Marshman had nothing further to add.
41 By about 21:25, two hours into the procedure, the exhaled carbon dioxide expired waveform had diminished, which most likely meant that not enough blood was reaching the lungs. The CVP was 37 and I was concerned that the right ventricle was failing. I raised my concern with Drs Gray and Cree with words to the effect: 'hurry up as the patient's condition is deteriorating'. They responded by agreeing to operate faster in order to complete the operation as quickly as possible.
42 However, over the following minutes I became very concerned that Mr Hobson was about to suffer a cardiac arrest as his blood pressure dropped from the previous level of 150. I administered adrenaline and directed Dr Gray to stop the procedure immediately. Dr Gray closed up the wound as quickly as possible without completing the spine stabilisation, and Mr Hobson was turned to a supine position on the bed.
43 Once he was turned to a supine position, Mr Hobson's head was noted to be a purple colour, although within a relatively short space of time his carbon dioxide, blood pressure and CVP levels all returned to normal as did his colour without any other intervention.
44 I confirmed again that the tube position was normal and there was no sign of a pneumothorax. Dr Wang performed a trans-thoracic examination of the heart which confirmed that the left atrium was compressed by bone."
Dr Sparks was cross-examined about these recollections. This is also referred to later in these reasons.
Dr Sparks said that he visited Mr Hobson the day following the operation. He expected to be told that Mr Hobson had signs of permanent brain damage. However, he appeared not to have sustained any such damage. It became apparent later that day that Mr Hobson had an anterior spinal cord artery infarct that led to his paraplegia.
[6]
Dr Jon Westbrook
Dr Westbrook is a consultant anaesthetist and an Honorary Senior Clinical Lecturer at Oxford University. He provided a series of reports to Mr Hobson's solicitor.
In his first report dated 10 January 2012, Dr Westbrook commented upon the cause of Mr Hobson's paraplegia in the following terms:
"Throughout surgery there were episodes of reduced oxygenation, decrease blood pressure and falls in end-tidal carbon dioxide. There was later an episode of profound cardiovascular collapse associated with hypoxia and severe hypocarbia. Mr Hobson was appropriately resuscitated and a rapid decision made to abandon surgery. Despite this there was a period of several minutes when oxygen levels were very low and the blood pressure significantly below 100 mmHg systolic. It is this episode which is the probable cause of his paraplegia."
Dr Westbrook continued:
"It is unlikely that a similar episode of hypoxia and hypotension in isolation would have caused this degree of spinal-cord ischaemia in an otherwise well patient. However Mr Hobson's severe scoliosis and the major surgery he had already undergone will have made his cord very susceptible to further injury. As the surgery during the second operation had not reached the point of correcting the deformity (only a few screws had been placed at the time the surgery was stopped) it is unlikely that the surgery caused his spinal injury."
Dr Westbrook expressed his opinion in the first report as follows:
"Mr Hobson's case was always going to be very difficult with a significant potential mortality and high morbidity. It is likely that the spinal cord injury sustained was consequent upon the episode of hypoxia and hypotension experienced during the second operation.
…
I think that the anaesthetist should provide an explanation for his/her choice of a double lumen tube for the second operation as this probably contributed to the ventilator difficulties experienced. Consideration should also have been given to delaying the second operation once it was established that ventilation was difficult."
Dr Westbrook provided a supplemental report dated 21 October 2012. He expressed his conclusions in that report in these terms:
"7 The decision to perform Mr Hobson's second operation as an emergency on the evening of 17 November 2009 appears to be critical to this case and the adverse outcome. It meant that the anaesthetists had to persist with an anaesthetic technique that was not achieving optimal gas exchange and ultimately resulted in a significant period of hypoxia and hypotension. This appears to have been the cause of Mr Hobson's spinal injury. In addition the operation and the work up to it was commenced before spinal-cord monitoring was available. Although it arrived shortly after the start it was not possible to obtain baseline measurements. The monitoring was reported as abnormal throughout the case but this could have been due in part to the anaesthetic difficulties and the use of vecuronium making interpretation very difficult. It is likely that had spinal-cord monitoring been properly established in a timely manner that there would have been advanced warning to the clinicians that spinal cord perfusion was threatened particularly during the transient, earlier episodes of hypoxaemia.
8 Mr Hobson's spinal fusion was eventually performed on 11 December 2009. On that occasion his lungs were ventilated using a tracheostomy tube and he was successfully managed in the prone position. The delay imposed by the complications of 17 November 2009 demonstrates that the surgery could have waited on that date. This is however said with the benefit of hindsight.
9 On the balance of probabilities had Mr Hobson's operation not been done as an emergency on the 17 November 2009 he would not have suffered the cord injury that he sustained that day. The perceived emergency nature of the operation would appear to have caused the anaesthetists to persevere with a challenging anaesthetic procedure that led to difficulties and for the surgery to be done without adequate spinal-cord monitoring. In the absence of any threat to Mr Hobson's life or spinal cord whilst on the intensive care unit on 17 November 2009 the decision to perform emergency surgery needs to be justified."
[7]
Dr Michael A Johnson
Dr Johnson is an orthopaedic surgeon. He provided a series of expert medical reports. His most recent report is dated 9 August 2016. The following material is extracted from that report:
"I would note…that the decision that it was necessary to proceed with surgery to save Mr Hobson's life has subsequently been demonstrated to have been incorrect. The fact that Mr Hobson survived following the unsuccessful surgery on 17 November 2009, demonstrates that with very intensive and specialized peri-operative care his life could be preserved. This is in spite of the fact that following the operation on 17 November 2009 his overall condition will inevitably have been worse than prior to the surgical procedure.
I suspect that the decision to proceed with surgery was made in good faith but I think it highly unlikely there was a degree of urgency that made it impossible to delay the surgery until a time when spinal cord monitoring was available from the start of the procedure.
…
The appropriate action to take in the presence of absent [sic] spinal cord monitoring traces depends on the exact timing of when the monitoring difficulties occur.
I believe that the spinal cord monitoring should have been present from the start of the surgical procedure.
As I previously said the decision about whether to continue or cease surgery would have been dependent on the exact time at which the spinal cord monitoring disappeared. Unfortunately, that information does not seem to be available.
Whilst I do not believe that spinal cord monitoring is absolutely mandatory for all cases of spine deformity corrective surgery I think that in a case such as Mr Hobson's I would have insisted that spinal cord monitoring was available.
The decision about whether to proceed with surgery in the absence of spinal cord monitoring is very dependent upon whether satisfactory traces are obtainable from the start of the case.
The subsequent clinical course suggests that emergency surgery was actually not essential and that an alternative would have been ongoing intensive supportive medical care until Mr Hobson's overall clinical situation had substantially improved. Once this improvement had occurred then the second stage of surgery could have been performed at that time and I expect that if that had occurred the risk would have been less. It is of course easy to make these types of statements with hindsight."
[8]
Dr Peter D Heath
Dr Heath is a consultant in clinical neurophysiology. He provided a report dated 5 November 2012. He indicated that:
"Neurophysiological monitoring is used to provide early warning of disturbed spinal cord function during surgical correction of spinal deformities, when not otherwise clinically assessable, and which might lead to permanent spinal cord injury if not rapidly reversed.
Following results of multicentre studies in US and Europe in the early 1990s, in medically developed countries some form of monitoring in effect has become mandatory in situations, which involve significant risk of spinal cord injury. The spinal surgeon is responsible for assessing that risk and the selection of cases that require monitoring.
Where so indicated some form of monitoring should be used. However, techniques vary - some monitor the sensory tracts in the posterior part of the spinal cord - others monitor the more anterior motor tracts, as apparently was undertaken in [Mr Hobson's] case.
Importantly the use of spinal cord monitoring has been shown to reduce the risk of and severity of spinal cord injury."
Dr Heath expressed the opinion that the "attempted instrumented fusion on 17 November 2009 would have carried a significant risk of spinal cord injury and hence required monitoring". He indicated uncontroversially that the form of monitoring used in Mr Hobson's operation is "a well-established and sensitive technique" but that "its usage is compromised by the anaesthetic drugs used in this case - Sevoflurane and vecuronium". Dr Heath said that "these agents may preclude effective monitoring of spinal cord function using transcranial motor evoked potentials as a motor monitoring technique".
Dr Heath went on to express the following opinion:
"It is not possible to be certain when [Mr Hobson's] spinal cord injury occurred. It could have happened:
(i) During the operation, any time after induction of anaesthetic - the most risky time being during placement of pedicle screws in the region of the thoraco-lumbar junction.
(ii) During the major episode of cardio-vascular collapse which forced abandonment of the operation, or
(iii) During [Mr Hobson's] subsequent care whilst unconscious in intensive care.
However, the probable cause of the infarction of Mr Hobson's lower thoracic spinal cord was the major episode of cardio-vascular collapse, which occurred just before 21.30.
There is reason to suspect breach of duty in respect of:
(i) The lack of effective monitoring of spinal cord function that was employed during the operation of 17 September [sic, November] 2009 and
(ii) Proceeding with such surgery, blind to whether the spinal cord was functioning abnormally and hence vulnerable to injury if surgery proceeded.
It is established practice that a baseline should be obtained by the end of surgical exposure and certainly before instrumentation is commenced, so that any subsequent change in spinal cord function is detectable relative to an infarct reference. As such, in the absence [of] effective spinal cord monitoring, I would have expected surgery to have been halted and some alternative strategy for monitoring considered. Continuingly abnormal or ineffective monitoring would normally have informed stopping until an alternative form of effective monitoring was in place.
Whilst it is more within the expertise of specialist spinal surgeons it is my experience that, if no effective monitoring of spinal cord function is possible then it would be normal for surgery to be abandoned, unless it is argued that this was an emergency surgery to address pre-operative life-threatening cardio-respiratory problems.
Had surgery been abandoned at any time prior to the major cardiovascular collapse just before 21.30 I think it most probable that Mr Hobson would have avoided paraplegia."
Dr Heath also furnished a supplementary report dated 7 August 2016. Part of that report is as follows:
"In the present context of apparently ineffective motor monitoring it is my opinion that either the anaesthetic should have been changed to ensure effective monitoring (such as replacing Sevoflurane by an exclusively intravenous technique with Profanol and Remifentanil) or perhaps more practically mid-operation some form of effective sensory monitoring should have been established. Certainly some form of effective and reliable monitoring should have been established before giving the go-ahead for surgery to proceed."
[9]
Dr Peter Richards
Dr Richards is a consultant paediatric neurosurgeon. He provided a report dated 1 December 2012. Referring to Mr Hobson's second operation he commented in these terms:
"The operative procedure was intended to be carried [out] with the assistance from spinal cord function monitoring. However, the documentation suggests that this was never achieved and at no point was an appropriate spinal cord function trace obtained. The specialist expected to interpret the monitoring was not present at the start of the procedure and only entered the operating theatres to discover that spinal cord monitor function traces were absent. From a neurosurgical perspective I cannot see the point of planning to use monitoring and then proceeding without that monitoring available. Again, with regard to this specific case, this should be a matter for comment from a spinal orthopaedic surgeon who carries out scoliosis surgery.
There were clearly difficulties during the surgery with a number of episodes of profound hypotension. I would consider that it would have been one of these episodes of hypotension that led to the spinal cord ischaemia identified on MRI scanning that would have caused the paraplegia.
I consider it likely that had such hypotension been avoided the spinal cord ischaemia would not have occurred. Without the development of spinal cord ischaemia paraplegia would therefore have been avoided.
It should be for an anaesthetist and a spinal orthopaedic surgeon to comment as to when surgery should have been abandoned. The first indication of cardiovascular instability appears to have been at 19.17. The most profound episodes were later at 20.40 and 21.10. It cannot be determined which episode of hypotension caused the spinal cord infarction but I consider it likely that had the procedure been abandoned at the first indication of cardiovascular instability prior to the profound episodes of hypotension that spinal cord function would have been preserved and paraplegia avoided.
Given that if the neurophysiologist's recollection is accepted that there was no visible monitoring trace showing normal spinal cord function for the conditions, as well as cardiovascular instability, I am surprised that the operation was not abandoned at the first point of concern."
[10]
Dr James Wilson-MacDonald
Dr Wilson-MacDonald is a consultant orthopaedic surgeon at the John Radcliffe Hospital, Oxford & Nuffield Orthopaedic Centre, Oxford, England. Dr Wilson-MacDonald provided a series of reports for Mr Hobson's solicitors. His first report is dated 6 February 2013. Dr Wilson-MacDonald was provided with significant documentary and other material with the benefit of which he produced the following short description of the 17 November 2009 operation:
"[Mr Hobson] was placed prone on a Jackson table. The operation note records that spinal cord monitoring was used. In fact in the spinal cord monitoring report (Jim Lagopoulos 14/9/12) he records that he arrived at the Royal North Shore Hospital just after 6pm. The procedure was already underway. He was not able to carry out baseline spinal cord monitoring. It was not clear if this was due to the anaesthetic effect or the surgical intervention. Dr Gray was informed that the monitoring was abnormal. The patient was becoming increasingly unstable at this point in time due to the administration of muscle relaxants.
Dr Gray was told on multiple occasions that the spinal cord monitoring was abnormal. Mr Gray records a posterior mid line approach. Pedicles were displayed at T2-L2 and pedicle screws placed on the left. Screws were placed [at] T7-L2. There was an increase in the patient's PCO2 and the operation was abandoned due to poor metabolic state with clips to skin and Opsite. He was to be returned to theatre when appropriate.
Dr Westbrook records in his two medical reports the events which occurred in the peri-operative period. Dr Westbrook notes that during the surgery the CO2 was elevated, and he questions why a double lumen tube was used. Dr Westbrook questions why the surgery was carried out as an apparently urgent procedure out of hours."
Dr Wilson-MacDonald went on to express the following opinion:
"Out of hours surgery in this situation is full of difficulties. One of the difficulties is that the spinal cord monitoring technician was not present at the time that the surgery commenced. He was busy in another hospital, and presumably there was difficulty because the surgery was planned at very short notice. If it is accepted that the surgery was not extremely urgent, then there is no reason why the surgeon could not have waited until the spinal cord monitoring team were available, and the extreme urgency may have been unacceptable. The aetiology of the spinal cord injury is almost certainly vascular due to the previous anterior surgery with revision of the segmental vessels, and the severe hypoxia and hypotension which occurred at the time of the second operation. Mr Richards has alluded to this in his medical report, and undoubtedly the cord injury occurred because of severe vascular damage to the thoracic spinal cord with a typical anterior cord syndrome with loss of motor power but maintenance with sensory modalities. Had the hypoxia not occurred then the spinal cord injury would not have occurred. Almost certainly without the hypoxia the posterior instrumentation and fusion would have continued uneventfully, and the kyphosis produced would have probably taken the pressure off the left main bronchus by restoring a better kyphosis, and he would have avoided paraplegia. If the surgery had been stopped after the first severe episode of hypoxia [at 20.30], then the paraplegia would probably have been avoided."
Mr Hobson's solicitors subsequently provided Dr Wilson-MacDonald with some further information upon which they asked him to comment. He then provided a second report dated 3 October 2016. Some of what he considered included paragraph 41 of Dr Sparks' affidavit, reproduced earlier in these reasons at [31]. Dr Wilson-MacDonald commented upon this in the following terms:
"The patient was clearly in extremis by this point. The surgeons were in a very difficult position because their assumption was that if they did not correct the deformity the patient would die. This proved not to be the case. I note the anaesthetic joint experts have reached a conclusion about when surgery should have been discontinued. Dr Westbrook is of the opinion that surgery should have been abandoned no later than 20.37 given the evidence of his worsening metabolic state as evidenced by blood gas analysis demonstrating a sever acidosis. Dr Forrest is of the view that considering the surgery was potentially lifesaving at that time and was well advanced and the period of haemodynamic instability and desaturation were transient at 20.35 it was reason[able] to attempt to continue to improve [Mr Hobson's] ventilation and haemodynamic state. Dr Forrest however is of the view that at 21.30 it was clearly necessary to abandon surgery given the sudden severe respiratory and haemodynamic instability which suddenly occurred at that time."
Dr Wilson-MacDonald was asked a further series of questions. In answer to a question from Mr Hobson's solicitors whether there was any indication from the available material that the 17 November 2009 surgery "needed to be done to urgently at the time to [sic] save his life", he responded as follows:
"The patient was deteriorating. The continued inability to ventilate the left lung could have led to death. I note that Dr Westbrook is of the opinion that in light of the CT scan and the bronchoscopy findings it was reasonable to bring forward the planned second stage, but it did not need to take place that night and could have occurred within a time frame of 24 to 48 hours. Dr Forrest is of the opinion that it was reasonable to proceed with surgery given the deterioration which had occurred over the previous 12 hours with his worsening lung ventilation parameters. I note both the anaesthetic experts are of the view that [Mr Hobson's] respiratory condition was not severe enough to preclude surgery on 17 November 2009."
Dr Wilson-MacDonald was then asked whether there was any indication that the "operation performed on 17 November 2012 [sic, 2009] was urgent in terms of hours rather than days die [sic, due] to increasing difficulty of ventilating Mr Hobson in the ICU". He said this in response:
"If the assumption was that altering the shape of the upper chest would decompress the left main bronchus, then this was an emergency procedure. I would agree with Dr Westbrook that it was reasonable to bring forward the surgery, but there was no absolute indication to carry out the surgery as an emergency on the evening of 17 November 2012 [sic, 2009]. Surgery could have been carried out the following day without any increased risk."
The next question directed to Dr Wilson-MacDonald was whether, "in the absence of traces from the spinal cord monitoring [there] was a risk to Mr Hobson's life at the time such that continuing the surgery 'absent the monitoring' was reasonable". Dr Wilson-MacDonald said this:
"During the surgery Mr Hobson's life was at risk. This was the most important consideration. Under the circumstances given the assumption that the deformity surgery might decompress the left main bronchus, it was reasonable to proceed in the absence of monitoring."
Dr Wilson-MacDonald was then asked what should have been done if the spinal cord monitoring traces were abnormal or absent during the surgery. He said this:
"Given that the surgeons were assuming that they would save the patient's life by instrumenting the spine, under the circumstances it was reasonable to proceed without monitoring. However, I do note that monitoring was not available at the outset of the procedure, and thus it would be difficult for the surgeons to assess the importance of the changes of the spinal cord monitoring. The surgeon would have taken into account the abnormal spinal cord monitoring, and would have used this information to help him assess whether or not to continue with surgery, under the circumstances."
Finally for present purposes, Dr Wilson-MacDonald was asked what available alternatives there were to surgery at the time. He responded as follows:
"I have not seen a case where it has been suggested that surgical correction of a spinal deformity is likely to lead to reversal of a compressive thoracic lesion in the acute situation. This seems an extremely unusual decision. An alternative strategy would have been to wait and see if the patient's respiratory function could be improved with other measures. In the event the respiratory function appeared to improve spontaneously after the abandoned surgery."
[11]
Dr Guy V Sawle
Dr Sawle is a consultant neurologist. He provided a report dated 4 November 2012. By reference, among other things, to the intra-operative anaesthetic recordings, Dr Sawle expressed the view that three episodes of hypotension at approximately 19.40, 20.38 and 21.12 could be identified. With respect to these recordings, Dr Sawle said this:
"These episodes of hypotension will have put Mr Hobson's spinal cord blood supply at risk, but knowing as we do that he suffered a more profound cardiac event at 21.30, it seems more likely that the damage to his spinal cord all occurred at that time rather than at any of the earlier times when he was hypotensive."
Dr Sawle gave the following opinion about the significance of spinal cord monitoring in this case:
"Spinal cord monitoring
It is difficult to know what to make of the spinal cord monitoring undertaken in this case. If Dr Gray's recollection is correct and there was normal cord monitoring up to the point when vecuronium was given at 20.30 and the monitoring could not be continued thereafter, then clearly the spinal cord stroke occurred sometime after 20.20.
If it is the case that monitoring was never normal during the procedure then this cannot be interpreted unless it was normal before the surgery started. So Dr Lagopoulos' version of events which is that the monitoring signal was abnormal throughout but there was normal preoperative monitoring does not help establish the timing of the stroke.
Bearing in mind the known but unexplained area of gliosis in Mr Hobson's spinal cord and in the knowledge that a number of arteries supplying blood to Mr Hobson's spinal cord had been sacrificed in the first operation, I would have thought it vital to ensure that proper spinal cord monitoring was undertaken (and documented). This should have included proper baseline monitoring as well as careful monitoring during the procedure."
Dr Sawle's report then dealt with the topic of Mr Hobson's stroke in these terms:
"Avoiding the stroke
When surgery was discontinued and Mr Hobson was turned on to his back again it is said that his cardiorespiratory function returned to normal almost straightaway. I can see no reason to suppose that the same would not have happened if the operation had been stopped earlier.
Subject to anaesthetic analysis and comment on the intraoperative traces, the most severe event was the final cardiac event after which adrenalin was given.
Importantly, the brain and spinal cord are relatively resistant to the effects of hypoxia. So long as blood flow is maintained and the waste products of neural metabolism are being carried away, the brain and spinal cord can withstand quite long periods of pure hypoxia.
…
Hence, if Mr Hobson suffered several periods of relative hypoxia due to ventilation problems with preserved cord perfusion, and there were other times when his systolic blood pressure was low but then finally he suffered an episode of combined ventilation failure together with more prolonged and severe perfusion failure then the latter event is the event most likely to have precipitated the spinal cord stroke.
If the decision to halt the operation had been taken early enough for the surgeons to close the wound so that Mr Hobson could be turned supine prior to 21.30, then I believe that the episode of cardiac collapse which happened at that time would have been avoided and Mr Hobson would not have suffered the spinal cord stroke.
Whether it was reasonable to proceed with surgery without satisfactory spinal cord monitoring is a matter for surgical/ neurophysiological expertise to whom I defer. Meanwhile, my own view is that absent normal spinal cord monitoring signals, it was unwise to continue surgery in the face of recurrent episodes of systemic hypotension.
I say this because Mr Hobson was known to have an unexplained gliotic area in his spinal cord and it was known that a number of arteries supplying his anterior spinal cord had been sacrificed in the first operation. It was foreseeable that his thoracic spinal cord was at risk of infarction if he were to suffer a prolonged period of profound hypotension.
Absent normal spinal cord monitoring it was not possible to say that his spinal cord was not being damaged, although in fact (as explained above) I consider that the damage which occurred is much more likely to have happened as a result of the more serious cardiac event at 21.30 rather than the earlier episodes of hypotension."
[12]
Expert evidence - Northern Sydney Local Health District
Before it settled the proceedings with Mr Hobson, the first defendant relied upon the evidence of one expert witness. He gave evidence on the second day of the hearing. This is referred to below.
[13]
Dr Stephen McGregor Barratt
Dr Barratt swore an affidavit on 12 November 2015. It was relevantly in the following terms:
"2. I am a Staff Specialist at the Department of Anaesthesia and Pain Management at the Royal North Shore Hospital (the Hospital). I started working as a trainee anaesthetist in 1985 and became a consultant (specialist) in 1991. I have been working as a specialist anaesthetist for 22 years.
17 November 2009
3. Mr Hobson has Noonan Syndrome with thoracic lordosis. As a result, his breast bone was pushed against his spine which was restricting his lung capacity.
4. I understand that Mr Hobson underwent a thoracotomy at the Hospital on 13 November 2009. I was not involved in that surgery. Mr Hobson was supposed to undergo a second stage procedure (posterior thoracic lumbar fusion) about two weeks after the first surgery.
5. I first came across Mr Hobson at approximately 2.40pm on 17 November 2009 when Dr Christopher Sparks, VMO anaesthetist, asked me to consult the patient in the intensive care unit of the Hospital. Mr Hobson was not receiving adequate ventilation through a single lumen tube. His condition was deteriorating and the intensivists did not think that they were going to be able to continue ventilating him adequately to last until when the second stage surgery was to take place.
6. Dr Sparks and I performed a bronchoscopy to confirm the ICU consultant's view that Mr Hobson was becoming increasingly difficult to ventilate. We sedated Mr Hobson with anaesthesia to perform the bronchoscopy. I used a 15 French anaesthetic scope. Mr Hobson's trachea was deviated to the right however the left main bronchus was severely narrowed and effectively not functioning. It was difficult to ventilate him and a lot of pressure was being used to keep him ventilated.
7. The bronchoscopy demonstrated that Mr Hobson's ventilation was unstable. Concurrently, he was hypotensive. His condition was deteriorating and his anatomical structure needed to be fixed. Based on what I saw, I certainly agreed that waiting two weeks for the second operation was not appropriate.
8. I was aware of subsequent discussions between the ICU consultant and Dr Sparks at Mr Hobson's bedside that the second stage surgery possibly needed to be brought forward to that evening, pending discussions with the surgeons. I raised no objections to these deliberations.
9. Following the bronchoscopy, Dr Sparks and I went to discuss our observations with Mr Hobson's mother in the ICU waiting room. Dr Sparks did all of the talking. He explained the problem with ventilation and that Mr Hobson's surgery would probably need to be brought forward to that evening, though the final arrangements needed to be made (that is, further discussions with the surgeons). Dr Sparks discussed the risks extensively in view of his condition and this included the risk of death, difficulty with ventilation and hypotension, amongst others.
10. At about 9.30pm on 17 November 2009, I received a call from Dr Sparks whilst he was in the operating theatre with Mr Hobson. Dr Sparks was concerned about Mr Hobson's consistent hypotension and ventilation issues during the surgery. He explained that Mr Hobson's carbon dioxide levels were not decreasing which meant increased dead space.
11. Dr Sparks told me that Mr Hobson was in the prone position on a Jackson table during the surgery. In my view, if the breast plate of the Jackson Table was pressing on Mr Hobson, the cardiac compression would generate potential for hypotension.
12. Dr Sparks expressed his concern about a high arterial carbon dioxide at the time, I think he said approximately 65 mmHg. This is about 50% more than normal. This usually means inadequate ventilation and this issue had been excluded with multiple bronchoscopies, checking for breath stacking and pneumothorax. However, at the time Mr Hobson's end tidal carbon dioxide was only 30-25mmHg which means a significantly increased dead space ventilation. Inadequate ventilation on its own does not explain this. Therefore, I proposed to Dr Sparks that maybe a pulmonary artery was being compressed along with possible cardiac compression which would mean he would have a section of his lung which was being ventilated, but not perfused. The telephone call abruptly ended when Dr Sparks said 'I gotta go'.
13. I have seen this type of spinal surgery performed multiple times but I have never seen it performed on a patient with Noonan Syndrome."
In a footnote to his affidavit Dr Barratt explained that "dead space" refers to lung units that are being ventilated (from the ventilator and breathing tube) but not being perfused (not receiving blood from the heart). This manifests as an increased gap between the end tidal (breathing tube) carbon dioxide and arterial (blood) carbon dioxide. This is normally in the range of 5-10mmHg.
[14]
Dr Geoffrey Askin
Dr Askin is a spinal orthopaedic surgeon specialising in the management and surgical treatment of spinal deformity in both adults and children. He furnished a report on behalf of Dr Gray dated 13 March 2014. His opinion set forth in that report is as follows:
"This patient suffered significant co-morbidities, particularly regarding his respiratory function.
He had a major spine deformity which was contributing to his respiratory compromise and was progressive.
Surgical management of such a deformity is complex. In this case it was well planned with the procedure being discussed with Dr Gray's colleagues in Sydney.
The first stage anterior procedure was performed in conjunction with a cardiac surgeon and was seemingly technically carried out competently. Pre-operative angiography had also been performed to ensure that the major feeding vessels to the lower end of the spinal cord were preserved.
Post-operatively the patient continued to suffer deteriorating respiratory function and the planned second stage procedure was brought forward, this was presumably due to the thought that correcting the patient's thoracic lordosis would improve the space available for the heart and lung and the patient's respiratory compromise.
The plan to monitor the spinal cord with Motor Evoked Potentials and Sensory Evoked Potentials is considered mandatory for the spine deformity surgery. It was established once the patient was supine that there were satisfactory responses. The patient was positioned prone on the operating table for the second stage of the operation and again, prior to commencing the procedure, the responses were adequate.
The ability to ventilate the patient and maintain a satisfactory PCO2 and blood pressure was not possible with the patient in the prone position. It was therefore decided that the patient be drug paralysed (MEP recordings are only possible if the patient is not drug paralysed). Hence, the MEPs were no longer a viable source of monitoring.
Despite drug paralysing the patient, ventilation was still technically difficult and the patient's wellbeing continued to deteriorate. Eventually his PCO2 rose significantly and the blood pressure fell to the point where the patient had a cardiac arrest. The patient was taken off the operating table and turned supine, ventilation became much easier and blood pressure was restored as was the PCO2. However, the patient was unfortunately paralysed and this is presumably due to poor spinal cord perfusion at the time of the cardiac arrest. It was noted on the post-operative MRI scan that the lower end of the spinal cord was oedematous but without haemorrhage which would indicate that there was no damage to the spinal cord. This was in keeping with poor perfusion to the spinal cord.
Spinal cord monitoring is only useful if remedial action is possible in the event of deterioration of the monitoring signals. The aim is to reverse the underlying cause of loss of signal as soon as possible and minimise the risk of paralysis.
In this patient however it was not the surgical procedure per se that caused the spinal cord damage rather than the lack of blood supply to the spinal cord. MEP monitoring in this case would not have allowed remedial action given that the only remedial action that allowed the patient to restore blood pressure and PCO2 was to turn the patient supine. Having MEPs running during the time of the physiological crisis would not have expedited the termination of the procedure and changing the patient's position at all. Hence, the loss of MEPs would not have changed the outcome."
Dr Askin said that in his opinion Mr Hobson's general medical condition posed a significant risk in the correction of his complex spine deformity, which "definitely required surgery". He considered that Dr Gray acted in a manner that was competent in the current setting of spine deformity surgery in Australia.
[15]
Dr Mike Lambros
Dr Lambros is a consultant anaesthetist. He prepared a report for Dr Gray's solicitors dated 22 October 2016. He was asked a series of specific questions and offered the following presently relevant responses:
1. Mr Hobson's surgery and anaesthetic care were not compromised by the hour of the day.
2. Mr Hobson was preoperatively haemodynamically stable.
3. There was a definite downward trend in respiratory function but Mr Hobson's "respiratory condition was not severe enough to preclude surgery" (joint anaesthetic experts' opinion). Indeed, given the downward trend in the preceding hours, it may have been imprudent to wait further.
4. The decision to proceed was entirely reasonable, based upon the premise of a deteriorating (but still stable) patient, with the likely primary cause being that of extrinsic left main bronchial compression secondary to "marked AP narrowing of the thoracic cavity", which could not have been addressed with only supportive ICU management.
5. It was reasonable to use vecuronium during the surgery. The last dose was required because of Mr Hobson's parlous ventilation state and appears to have been necessary at the expense of losing spinal cord monitoring.
6. The anaesthetic technique used represented an appropriate standard of care where spinal cord monitoring was required with the exception of the administration of vecuronium which would have made monitoring meaningless for the duration of the action of the drug. There may have been sufficient recovery between the 18.30 dose and the 20.30 dose of neuromuscular function to provide a window of meaningful monitoring but not thereafter.
7. It is not 100 percent clear that Mr Hobson's condition from a respiratory functional point of view would have improved without surgery and anaesthesia on 17 November 2009. It would have been difficult to justify a wait and see approach.
[16]
Dr Bojidar Manasiev
Dr Manasiev is a specialist anaesthetist. He provided a report dated 26 October 2016. He gave his opinion in response to a series of questions set out in that report.
Dr Manasiev was asked whether Dr Gray should have advised that the surgery be halted. He responded at length by reference to various specified times during the course of the surgery. These have been discussed by other experts as well. At the risk of too much detail, it is instructive to record a selection of Dr Manasiev's views:
"18:50 - There is a temporary reduction in oxygen saturation. From Dr Sparks' affidavit this occurred at the time of changing the endotracheal tube from a single lumen tube. I would expect some degree of desaturation during this process where there is a temporary cessation in ventilation, particularly as the plaintiff had a compression on this left main bronchus and as such a reduction in lung reserve and oxygen store. The plaintiff's oxygenation responded appropriately once ventilated and saturations returned to normal. Under these circumstances there would be no reason for Dr Sparks or Dr Gray to advise halting the surgery.
19:10 - There is a short period [of] desaturation and drop in blood pressure. From Dr Sparks' affidavit, this occurred at the time of transferring the plaintiff from the supine position to the prone position. There was a question by Dr Sparks whether the desaturation recorded may have been erroneously due to malposition of the pulse oximeter during the movement of the patient. This may be a completely warranted assumption as an arterial blood gas analysis at the time showed a p02 of 243 which does not correlate with desaturation.
The transient hypotension rapidly stabilised and maintained stable with the administration of Metaraminol. On that basis it would not have been warranted for Dr Sparks or Dr Gray to advise halting the surgery.
20:35 - there is a transient period of desaturation and relative hypotension, which from my understanding from the clinical notes and affidavits, was at the time of placement of a pedicle screw. It appears recognised that the downward pressure of the screw placement was affecting the respiratory and cardiovascular systems of the plaintiff. From Dr Sparks' Statement in Answer to Interrogatories, the hypotension resolves without any intervention. In my opinion, there are 3 reasons to justify not halting the operation at this time. First, there was a potentially identifiable and reversible cause of the hypotension and desaturation, in that of the downward pressure during screw insertion. Second, there was a quick resolution to normal values of blood pressure and saturation, presumably once the downward pressure was ceased. Third, the decision was balanced against the apparent necessity of the operation as a potential lifesaving technique. As such, it was not warranted by Dr Sparks or Dr Gray to halt the surgery at this time and would be considered widely accepted in Australia by peer professional opinion as competent medical practice to continue the surgery.
21:20 - although a drop in blood pressure to 90 mmHg on its own would not necessarily be a sufficient reason to halt the surgery, when coupled with a profound desaturation it becomes apparent that the patient is in imminent danger of a cardiac and respiratory arrest. Dr Sparks appropriately advises halting the surgery.
It is important to note that the management of the ventilator and cardiovascular parameters are primarily the responsibility of the anaesthetist. The anaesthetist would be the first to comment on difficulties in achieving adequate ventilation and perfusion of the vital organs and as such direct the surgeon if the surgery would need to be halted to effectively resuscitate the patient. It would not be the responsibility of the surgeon to halt the surgery on the basis of haemodynamic or respiratory difficulties unless there was a question of the management of those difficulties by the anaesthetist. In my opinion Dr Sparks' management would be considered widely accepted in Australia by peer professional opinion as competent medical practice in directing Dr Gray to proceed at times 18:50, 19:10; 20:35 and halt at 21:20. As such it would be considered competent medical practice by Dr Gray to heed Dr Sparks' direction and proceed with the surgery at times 18:50, 19:10 and 20:35 and halt the surgery at 21:20."
Dr Manasiev went on to offer the following conclusions:
"In my opinion, Dr Gray was not negligent in continuing the operation in the circumstances pleaded. As outlined…above, the management of the ventilator and cardiovascular parameters is the primary responsibility of the anaesthetist.
Dr Sparks' management of the plaintiff in regards to directing Dr Gray to continue the surgery at 18.50, 19.10 and 20.35 and halt the surgery at 21.20 would be considered widely accepted in Australia by peer professional opinion as competent medical practice, with reasoning for each specific time as outlined…above. As such it would be considered competent medical practice by Dr Gray to heed Dr Sparks' direction and proceed with the surgery at times 18.50, 19.10 and 20.35 and halt the surgery at 21.20."
[17]
Dr Peter Silbert
Dr Silbert is a neurologist. He is an expert in spinal cord monitoring. He provided a report dated 26 October 2016. He completed a fellowship at the Mayo Clinic where he gained experience in all areas of general neurology and neurophysiology including intraoperative monitoring of the brain and spinal cord.
Dr Silbert was asked whether, on the balance of probabilities, any, and if so which, of the types of spinal monitoring proposed by Mr Hobson, would have detected abnormalities in his spinal cord during the surgery. His answer was long but needs to be noted in full:
"Considering the anaesthetic events between 20.30 hours and 21.30 hours on 17 November 2009, based on the statement of 'assumptions for anaesthetic conclave', the hypotensive and hypoxic event of significance was primarily that at 21.25 hours. There is no indication from the anaesthetic conclave that the patient was significantly hypotensive prior to that.
It needs to be noted that there was no distraction of the cord occurring between 20.30 hours and 21.25 hours, and therefore any significant changes in the IOM would have more likely been on the basis of changes in blood pressure.
Changes before 2125 hrs:
Blood pressure changes may affect arterial supply to the spinal cord through the anterior spinal artery, however blood pressure changes also affect cerebral perfusion and affect the SSEPs [somatosensory-evoked potentials] and MEPs [motor-evoked potentials] at a cerebral level. It is therefore not possible to determine the level of causation for any change in an SSEP or MEP in the setting of significant hypotension.
It would seem from the anaesthetic conclave that those changes prior to 2125 hrs were very transient and not considered significant by the anaesthetic conclave. If motor-evoked potentials were being performed at that time, the response may have been that the MEP reduced in amplitude but this may have reflected a change in blood pressure effect on the cortex, the spinal cord or both.
Provided the MEP response returned after transient hypotension, the usual practice would have been to proceed with surgery, recognising that the purpose of surgery on this critically ill patient was to correct the scoliosis that was causing problems with his ventilation in ICU.
Assuming anaesthesia and temperature remained stable, changes in IOM before 2125hrs would have been reflective of the critically ill patient, and not maintaining an adequate blood pressure, as there was no distraction of the spinal cord occurring.
The preoperative MRI scans would suggest that the spinal cord was vulnerable as there was already an area of ischaemic change in the lower thoracic cord on the preoperative MRI scans. SSEPs through the posterior (dorsal) columns (and posterior spinal arteries) would have been slower to acquire information (as they require multiple stimuli), and would not have detected the transient changes in blood pressure between 20.30 and 21.25 hours, given that this is a chronic problem and collaterals and vascular changes would already have occurred.
MEPs for this procedure were direct cortical stimulation and recording in lower limb muscles. It was not possible to continue these once the patient required neuromuscular blockade for the respiratory ventilation difficulties, and we therefore need to hypothetically consider whether if an epidural electrode had been placed, further information could have been obtained.
MEPs recording a D-wave with the epidural electrode placed over the distal thoracic cord or conus may have recorded a D-wave, however as stated by Deletis.
'Another disadvantage of the D-wave monitoring method is that it cannot be applied during surgery on the spinal cord caudal to the Th10-11 spinal cord segments because there are not enough fast CT axons to generate a D-wave below that level with sufficient amplitude for monitoring.'
I do not believe that cranial stimulation with caudal recording over the conus through a D-wave would have detected any abnormality. It is an unreliable technique and not performed at that level of the spinal cord. Furthermore, it would have delayed the procedure significantly with the surgeon trying to position an epidural electrode in a critically ill patient in whom the anaesthetist is having significant difficulty with ventilation. The time to record a D-wave and setup intra-operatively with an epidural electrode in an ideal situation might be 5-7 minutes (after realisation there was a technical problem), but it would probably be a further 5 minutes before there was confidence in the response. There would therefore have been at least a 10 minute hiatus in surgery for that evaluation, recognising that as stated by Deletis, it cannot be relied upon.
I do not believe that peripheral stimulation of the tibial nerve and recording a D-wave cranial of the operative site could be relied upon, as in ischaemia, the tibial stimulation can pass up the posterior (dorsal) columns and that wave response may be recorded and confused with the motor response.
I do not believe that IOM of any sensory or neural pathways using distal and/or epidural electrodes would have detected significant abnormalities in Mr Hobson's spinal cord during the surgery prior to the cardiovascular collapse at 2125hrs.
IOM is a useful technique but it does have limitations. This was a critically ill patient in whom the anaesthetic/medical issues dominated the management of the patient. It was for that reason that neuromuscular blockade had to be given and that precluded continuation of MEPs.
Changes at 2125 hrs:
MEPs would have been lost at the time the patient became hypoxic and hypotensive at 21.25 hours, but at that time anaesthetic issues would have overridden any IOM recording or response. SSEPs would most likely have continued to be present if the posterior (dorsal) column circulation was adequate through the posterior spinal arteries."
Dr Silbert was also asked whether, on the balance of probabilities it is likely that spinal cord monitoring would have detected abnormality in Mr Hobson's spine prior to the collapse at about 21.30. He responded in the following terms:
"SSEPs would have been unlikely to detect any abnormality prior to 2125hrs.
MEPs recording at the muscle following cortical stimulation would have been precluded by the neuromuscular blockade after 2030hrs and prior to 2125hrs.
If it were not for the neuromuscular blockade, then MEPs would not be expected to have been abnormal in the absence of spinal distraction or any significant changes in blood pressure as from the anaesthetic conclave document, the only significant period of hypotension was at 2125hrs.
MEPs recording from an epidural electrode placed distally would have been technically difficult…and would not be considered a reliable or appropriate approach.
Peripheral tibial nerve stimulation MEPs with cranial epidural electrode recording are not recommended as posterior (dorsal) column impulses cannot be separated from the motor pathways.
In summary, I do not believe that SSEPs and MEPs would have detected significant spinal cord electrophysiological abnormalities prior to 2125hrs."
[18]
Associate Professor Mark Sheridan
Dr Sheridan is a neurosurgeon. He provided a very short report dated 7 November 2016. He said that it was not Dr Sparks' responsibility to decide the patient's positioning before or during surgery. That was the responsibility of the surgeon. He said that the use of a Jackson's table is standard care in managing patients having spinal surgery in the prone position. It decreases the cardiovascular effects of the procedure by allowing the abdomen to be decompressed and it minimizes the compressive effects on the chest.
Dr Sheridan also said that the decision to reposition a patient during surgery is a combined decision of the surgeon and the anaesthetist. In prone spine surgery, as in the case of Mr Hobson, a decision to reposition the patient from prone would have meant abandoning the operation. That is not a decision to be taken lightly or in the absence of quite extensive consultation and discussion. It would not be solely the decision of the anaesthetist.
Dr Sheridan also considered that the suggestion that Mr Hobson could have been repositioned during the course of surgery so as somehow to allow the surgery to continue is not practical. It is a decision that requires the surgery to be abandoned and the wound closed. It is never a simple matter and is limited to cases of emergency. Dr Sheridan said that, in an operation such as Mr Hobson's, where the original decision to operate was taken in order to save the patient's life, the concern would have been that he was going to die if the operation were abandoned.
[19]
Dr Paul Forrest
Dr Forrest is a specialist anaesthetist. He provided a report and two supplementary reports. The first is dated 26 October 2013. He considered that the cause of Mr Hobson's intraoperative collapse was acute right ventricular failure. He said that that would account for the high central venous pressure, low oxygen saturation and low blood pressure that occurred at about 21.30. It would also account for the large difference in the carbon dioxide level measured in Mr Hobson's blood and expired breath before then, and the congested "purple" appearance of his head when he was turned from prone to supine. Dr Forrest thought that Mr Hobson probably developed acute right ventricular failure because of predisposing factors and the use of the prone position for his surgery. The predisposing factors were his spinal deformity, which caused restrictive lung function, and his left lung collapse/infection due to bronchial compression. These factors would have caused the pulmonary arteries to constrict and thereby increase pulmonary vascular resistance. An increase in pulmonary vascular resistance can cause the right ventricle to dilate and may eventually decrease its capacity to pump blood. He said that the combination of increased pulmonary vascular resistance and decreased cardiac output causes the blood supply to the right ventricle to fall. When it falls below a critical level, acute, severe right ventricular failure can occur. Dr Forrest said, however, that it was not possible accurately to predict in an individual patient if or when this will occur.
Dr Forrest considered that it was appropriate and reasonable for Dr Sparks to direct Dr Gray to cease performing surgery when the systolic blood pressure dropped to 95. That was because at about that time (21.30) Mr Hobson had rapidly falling oxygen saturations to less than 80 percent, a high cardiovascular pressure and severe respiratory and metabolic derangement. This systolic level signalled the onset of critical haemodynamic deterioration, which would likely have progressed rapidly to refractory cardiac arrest if the surgery had not been abandoned at that time and Mr Hobson turned to the supine position. Dr Forrest said, therefore, that it was appropriate and reasonable for Dr Sparks to request that the surgery be abandoned at that time.
Dr Forrest considered that Dr Sparks provided a reasonable standard of anaesthetic management to Mr Hobson during the surgery. He reasoned as follows:
"Mr Hobson was a high-risk patient who required major emergency surgery at that time. He posed a very unusual and difficult anaesthetic challenge due to the significant compression of his left main bronchus by his spine and due to the requirement for prone positioning during surgery.
Dr Sparks was well aware of the complexity of the patient's pre-existing problems, having attended his preoperative bronchoscopy (with Dr Barratt) in the intensive care unit. From the preceding, the use of a DLT to manage the extrinsic compression of the bronchus was reasonable, and confirmation of its position by repeated bronchoscopy was appropriate.
The patient was appropriately monitored during the case, and the choice and dosages of anaesthetic drugs and intravenous fluids were also appropriate.
The main clinical dilemma in this case was whether surgery should have been allowed to continue given the difficulties in ventilating the patient that were encountered before the severe deterioration that occurred at 21:30h. As noted above, the patient had been difficult to ventilate prior to this time due to compression of his left main bronchus, which was exacerbated in the prone position. However, given that the patient's surgery was considered to be sufficiently urgent that it needed to be performed out-of-hours, and given also that his lung infection would not have been expected to resolve until the compression of his left main bronchus was relieved by surgery, it was reasonable to continue the anaesthetic at that time."
Dr Forrest considered that Dr Sparks' anaesthetic management of Mr Hobson was in accordance with widely accepted peer professional opinion in Australia as competent professional practice at the time the service was provided.
In his first supplementary report dated 11 September 2015, Dr Forrest expressed the opinion that Dr Sparks was not responsible for the performance or supervision of spinal cord monitoring for Mr Hobson's operation. He also considered that it was reasonable for Dr Sparks to have administered vecuronium at about 20.35 in an attempt to improve ventilation. He explained his opinion in the following terms:
"Vecuronium (a short acting muscle relaxant) is routinely administered to patient's having major surgery. The only reason that it was not given throughout Mr Hobson's surgery was because it would have interfered with his spinal cord monitoring and rendered it completely uninterpretable.
However, not giving Mr Hobson vecuronium also made him more difficult to ventilate, which was likely due to a combination of his bronchial compression, pre-existing pulmonary hypertension, presence of a double-lumen endotracheal tube and use of the prone position. Inadequate ventilation caused the carbon dioxide level in his blood to rise and increased his pulmonary vascular resistance. As outlined in my original report, this would have contributed to the development of cardiac decompensation due to acute right ventricular failure intraoperatively.
When Mr Hobson was showing signs of cardiac decompensation during his operation (at about 20:35), it would have become apparent to Dr Sparks that it was essential to improve Mr Hobson's ventilation by any means necessary. Because earlier attempts to do so had proved unsuccessful (including fibre-optic bronchoscopy to optimise the position of the double-lumen tube), the decision to administer vecuronium at that time was therefore reasonable and appropriate."
Finally, in his second supplementary report dated 31 October 2016, Dr Forrest was asked whether, by reference to the blood gas parameters at 20.21 and 20.37, the administration of vecuronium was a reasonable response to Mr Hobson's then current metabolic state. Dr Forrest considered that it was, for the following reasons:
"These blood gases revealed worsening metabolic acidosis between 20:21 and 20:37h. This was evidenced by: decreased pH (7.15 to 7.027), decreased base excess (-3.9 to 011.6 mmol/l) and increased lactate (6.0. to 8.2 mmol/l). This indicated that the patient's cardiac output was inadequate, which in this case was due to acute right ventricular failure.
These blood gases also revealed that the patient had persisting severe respiratory acidosis (pCO2 70.4 and 70.5mmHG). This would have contributed to the patient's right ventricular failure, because it would have significantly increased pulmonary vascular resistance. This is because increased carbon dioxide levels in the blood causes blood vessels in the lung to constrict, which in turn increases the work performed by the right ventricle to pump blood through the lungs.
Because the right ventricle is very sensitive to acutely elevated pulmonary vascular resistance, it is essential in patients with acute right ventricular failure to reduce blood carbon dioxide level to normal levels (about 40mmHg) is possible. The only practical way to do this in this case was to increase the level of lung ventilation.
Lung ventilation can be increased by increasing the volume of gas delivered by the ventilator, the respiratory rate, or both. However, increasing ventilation also increases the pressure inside the lungs (ventilation pressures), especially when lung compliance (change in lung volume /inflating pressure) is decreased, as was the case in this patient. In other words, a patient with poor lung compliance requires higher ventilating pressures than a patient with normal lung compliance to achieve the same increase in lung ventilation.
While increasing the level of ventilation decreases pulmonary vascular resistance (by decreasing carbon dioxide levels), this may not happen if high ventilating pressures are required to do so. This is because high ventilating pressures increase pulmonary vascular resistance due to compression of pulmonary blood vessels, which can exacerbate right ventricular dysfunction.
Muscle relaxants attenuate the increase in ventilation pressures that is required to increase the level of lung ventilation, by reducing the resistance to lung inflation caused by the muscles of the chest wall.
Hence given the presence of worsening metabolic acidosis between 20:21h and 20:37h due to right ventricular dysfunction, it was reasonable to administer vecuronium in an attempt to increase the level of lung ventilation."
[20]
The orthopaedic conclave
The orthopaedic conclave was attended by Drs Johnson, Askin and Wilson-MacDonald. Their joint report is dated 7 October 2016.
All doctors agreed that there was no orthopaedic imperative for the surgery to be performed urgently. Dr Wilson-MacDonald went further and suggested that there was in fact no medical reason at all for the surgery to be carried out when it was. All doctors agreed that the decision was based upon the advice from the intensive care team at the time. That decision was not to be criticised as the intensivists and anaesthetists agreed that Mr Hobson was fit to undergo the procedure.
All doctors agreed that the surgery should have ceased when the anaesthetists were unable to maintain the metabolic state in the form of satisfactory blood pressure and oxygenation. Dr Wilson-MacDonald noted that at 20.37, blood gas analysis demonstrated a deteriorating metabolic state following an episode of hypotension at 20.30 and considered that the surgery should have been discontinued very shortly thereafter. It was agreed among all doctors that at the time of the surgery the treating surgeons or physicians would not have been able to predict the respiratory outcome. They now have the benefit of hindsight. Dr Wilson-MacDonald and Dr Johnson were of the opinion that Mr Hobson would not have become a paraplegic if the surgery had not been carried out that evening.
Spinal cord monitoring was considered by all to be a necessary part of Mr Hobson's surgery. The doctors all agreed that in the absence of spinal cord monitoring, the surgery should not have commenced and should not have commenced until there were satisfactory motor and sensory evoked potentials. Spinal cord monitoring is not effective unless adequate baselines are obtained. Spinal cord monitoring should have been in place before the surgery commenced.
None of the doctors was able definitively to say whether surgery should be continued in circumstances where spinal cord monitoring, once commenced, fails to produce adequate traces. This would depend on the nature of the spinal cord trace abnormalities. The doctors considered that in this case, where the indications were primarily to preserve or improve Mr Hobson's respiratory function, serious consideration would have to be given to continuing the surgery. The doctors considered that if no baselines traces were obtained either before or during the surgery then in Mr Hobson's case the surgery should have continued. On the other hand, if baselines had been obtained but subsequently disappeared, the surgery should have been ceased.
There was agreement among all doctors that Mr Hobson became a paraplegic sometime after 20.30 when he became hypotensive for the first time. The surgery should have been abandoned when the anaesthetists were no longer able to maintain satisfactory cardio respiratory parameters.
[21]
The anaesthetic conclave
The anaesthetic conclave was attended by Drs Westbrook and Forrest. Their joint report is dated 12 September 2016.
Both doctors considered that it was reasonable to proceed with the surgery on 17 November 2009 and to bring it forward in light of the bronchoscopy findings. Mr Hobson's respiratory condition was not severe enough to preclude surgery. However, Dr Westbrook did not think that it was necessary to do so, and considered that it could have waited a further 24 to 48 hours.
Both doctors agreed that Mr Hobson's respiratory function would have improved had his surgery not been performed on 17 November 2009. That is because his lung function improved even though the surgery was not completed and his bronchial obstruction was not corrected. Both doctors agreed that Mr Hobson would probably not have become a paraplegic if the surgery had not been performed that evening, given his unexpected improvement in lung function and the subsequent uncomplicated completion of his spinal surgery.
Both doctors also agreed that a single lumen tube could have been used as an alternative to a double lumen tube, but would have carried the risk of ineffective ventilation of the left lung due to exacerbation of the left bronchial compression in the prone position.
Neither doctor was clear as to the cause of the oxygen desaturation at 20.35, but thought that it could have been related to checking Mr Hobson's double lumen tube position or simply increasing difficulty with ventilation. That is what necessitated the administration of muscle relaxants at around that time.
The significant point of disagreement between these doctors concerned the time at which surgery should have been abandoned. Dr Westbrook was of the view that in light of Mr Hobson's significantly worsening haemodynamic state at 20.35, surgery should have been abandoned within two more minutes. That was because of the concurrent evidence of Mr Hobson's worsening metabolic state evidenced by blood gas analysis indicating a severe acidosis. In contrast, Dr Forrest considered, given that Mr Hobson's surgery was thought to be potentially lifesaving at that time and was well advanced, and also given that the period of haemodynamic instability and desaturation was transient at 20.35, that it was reasonable to attempt to continue to improve Mr Hobson's ventilation and haemodynamic state. Dr Forrest was clearly of the opinion, however, that it was necessary to abandon the surgery at 21.30 given the severe respiratory and haemodynamic instability that suddenly occurred at that time.
Both doctors agreed that the administration of vecuronium was unexceptionable in the circumstances of this case.
Finally there was agreement between both doctors that the cause of Mr Hobson's spinal injury was most likely the result of an inadequate supply of oxygenated blood to his spinal cord at around 21.30. Mr Hobson's spinal cord was especially vulnerable to ischaemia because he had previously undergone ligation of the segmental spinal arteries during the first stage of the procedure, which may have reduced blood supply to his spinal cord. It was agreed that this most likely occurred during the cardiac and respiratory collapse that occurred around 21.30.
[22]
Mr Hobson
Mr Hobson accepted that the decision to bring the surgery forward was reasonable. He contended, however, that that did not inform the progress of the rest of the surgery and particularly whether it should have continued.
There was no evidence that the surgery was so urgent that Mr Hobson would die on the table if the surgery had been terminated sooner. As the defendants accept, Mr Hobson's blood oxygen and blood pressure were adequate and he was not in peril. There was therefore no reason to hurry to finish the job whilst blood pressure and oxygenation were within normal limits.
Mr Hobson contended that Dr Gray and Dr Sparks both understood that reliance on those two parameters was inappropriate. He referred to the following cross-examination of Dr Sparks:
"Q. As at 20.50, you knew, didn't you, that normal to high blood oxygen and blood pressure were not the answer to explaining the patient's deteriorating state?
A. So - yes."
However, the next answer should not be overlooked:
"Q. You're aware of that. So if that's right, those criteria are not appropriate to use as a measure of whether to persist in the surgery or abandon it, are they?
A. I disagree."
Dr Gray's evidence was to the following effect:
"Q. Doctor, the effect of the acidosis is it could lead to cardiac failure. That's right, isn't it?
A. Yes.
Q. That then could well cause spinal damage. That's right, isn't it?
A. Yes.
Q. So could I suggest to you this - leave aside whether you were told about it or not, the fact is had you known at that time, you would have stopped the surgery, wouldn't you?
A. Sir, with all due respect, it is not my role to stop the surgery based on medical parameters that are assessed by the anaesthetic team at the time."
Mr Hobson submitted, in circumstances where he began to have ventilation problems from the moment he was turned prone and began progressively to deteriorate due to his acidotic state, that by 20.37 at the latest, and probably much earlier, he was heading for an inevitable outcome, namely the spinal stroke that occurred at about 21.30.
According to Mr Hobson, continuation of the surgery in those circumstances, without spinal cord monitoring, could not be justified by the existence of an emergency because there is no evidence to support the proposition that cessation of the surgery before its completion was likely to result either in immediate death or death shortly thereafter. Continuing the surgery exposed Mr Hobson to that precise risk instead of alleviating it.
Mr Hobson reasoned by reference to the following facts that Dr Gray and Dr Sparks were in breach of the duty owed by them to him as professional medical practitioners.
Mr Hobson contended that the second stage of the surgery was not so urgent that it needed to proceed regardless of any risks to Mr Hobson's health that may have emerged or developed during the surgery. In this respect he relied upon Dr Westbrook's opinion in his 24 August 2016 report in these terms:
"Clarity is needed as to the exact reason that the surgery was expedited on the evening of 17 November 2009, as this is not clear from the medical records. Contemporaneous notes suggest that the clinical decision was to bring forward surgery to 18 November 2009 or 19 November 2009. Subsequent statements by the clinicians involved in Mr Hobson's care state that this was done on 17 November in order to save his life but this is not supported by the notes or the clinical condition. Professor Lagopoulos states that he was originally asked to provide spinal cord monitoring on 18 November but was not available…and so the surgery was scheduled for evening of 17 November. If the surgery were scheduled specifically to have the spinal cord monitoring available it would be surprising to then proceed without it effectively in place."
Dr Westbrook had previously offered the following opinion in his 14 November 2012 report:
"On the balance of probabilities had the surgery been abandoned before the start when the anaesthetic team were already in difficulty Mr Hobson would not have had the problems he had nor suffered his spinal cord injury. There was not sufficient surgical or medical indication to undertake the surgery that night with anything other than optimal ventilation and haemodynamics.
Furthermore the team embarked on surgery without establishing reliable spinal cord monitoring which was later further compromised by the use of muscle relaxants whilst the anaesthetic team tried to overcome ventilation problems. Mr Hobson's spinal cord perfusion had already been reduced by the ligation of the segmental arteries in the first operation and so spinal perfusion would have been critically important. Functional motor evoked potential monitoring (MEP) would have alerted the team that spinal cord function was compromised and enabled them to take corrective measures or abandon the surgery at an earlier stage. On the balance of probabilities functioning MEPs would have alerted the surgical team to impaired cord function and prompted them to take corrective measures to abandon surgery."
This needs to be compared with evidence given by Dr Gray as follows:
"Q. Do you agree that a continued inability to ventilate Mr Hobson's left lung could have led to his death?
A. Absolutely. That was our main concern that there's always a point of no return and you don't second guess that because once you reach that, taking him to theatre is of no use, and the overall opinion at the time by multiple medical experts is that we should do something before we reach that point."
The pre-anaesthetic assessment indicated that Mr Hobson had been suffering ventilation problems in ICU but was haemodynamically stable, with relatively normal blood pressure and blood oxygen. He was not then acidotic. That assessment indicated, however, that Mr Hobson had an extrinsic compression of his left main bronchus with left lung atelectasis, reduced ventricular compression and was difficult to ventilate. The plan was to release the extrinsic compression with spinal cord monitoring.
Vecuronium was administered at 18.00 in ICU and at 18.30 and 20.30 in theatre.
Having commenced the preliminary stages of the surgery, difficulties were encountered in satisfactorily ventilating Mr Hobson, commencing about 18.30 with particular difficulty achieving ventilation and metabolic parameters. These were described by Dr Westbrook in his 21 October 2012 report as follows:
"Having anaesthetised Mr Hobson, inserted the DLT and positioned the patient prone the team was still having difficulties ventilating his lungs. Airway pressures on the left side were high with low tidal volumes and he was receiving 100 percent oxygen and the arterial carbon dioxide level was significantly elevated. This had not been the case on the ICU prior to surgery. Despite these problems the team decided to proceed with the major surgery. The ventilation difficulties increased during the case with episodes of significant hypoxia and hypotension culminating in severe hypoxia and cardiovascular collapse necessitating urgent termination of surgery and return to the supine position. Mr Hobson was subsequently shown to be paraplegic."
It was Dr Westbrook's opinion that the surgery should have ceased at that point until satisfactory ventilation was achieved. However, satisfactory ventilation was never achieved during the surgery until Mr Hobson was turned supine at about 21.30. He had high CO2 levels from the moment he was turned prone.
Dr Lagopoulos arrived late and commenced monitoring when Mr Hobson was prone and surgery had commenced. He gave the following evidence in cross-examination:
"Q. Let me take you to your letters. Have you got them in front of you? You'll find them behind tab 4. Have them there?
A. Yes.
Q. Obviously you realise at the time that these were serious questions being asked by somebody who had an obvious interest in what your recollection was.
A. Yes.
Q. You were doing your best at the time to respond correctly.
A. Yes.
Q. You said in there - if you look at page 54 - in answer to question 8, 'When I arrived, the procedure was already underway and there was considerable activity within the theatre.' What was your recollection then, when you wrote that letter, of in what respect the procedure was already underway?
A. The patient was in the operating room.
Q. Can I suggest to you that he was in the operating table, on the Jackson table, prone.
A. Yes.
Q. That was your recollection then.
A. Yes.
Q. And it's your recollection now.
A. Yes.
Q. Because one of the things that you had to do was actually get under the drapes to connect your electrodes.
A. Yes.
Q. Having done that, you did a run.
A. Yes.
Q. Is that the word that everybody uses?
A. It's commonly used.
Q. You did the run and you informed Dr Gray that the spinal cord monitoring was abnormal, didn't you?
A. Yes.
Q. You told him it was abnormal, didn't you?
A. Yes.
Q. What you had observed at that time was that the signals were significantly depressed or absent altogether.
A. I'm not sure if I had significant, but they were decreased.
Q. If you have a look at your letter at page 56
A. I'm sorry, what point?
Q. Your answer to question 3 on the first page, end of the last sentence, 'I informed Dr Gray of the abnormal spinal cord signals, but I do not recall whether the signals were completely absent of significantly depressed.'
A. Correct
Q. In other words, there was something seriously going on.
A. No.
OBJECTION (WALSH). QUESTION ALLOWED
Q. They were either, at that point, significantly depressed or non-existent. Correct?
A. I think what I've written there was I do not recall whether they were significantly depressed.
Q. What you meant when you said 'I don't recall whether they were significantly depressed or absent' is 'I don't recall whether they were depressed, significantly depressed or absent.' Is that what you're saying?
A. No. That's not what I said.
Q. Then what are you saying?
A. In my line of work, significant basically means a statistic significance. So I used significantly, I guess, more stringently, than, I guess, you know, maybe a lay person might use. I didn't do any statistics on these signals. I had no way to know whether there was a statistically significant decrease in the signals. They were depressed, but I don't know whether they were significantly depressed.
Q. The important matter was, wasn't it, that if they were present at all, they provided a data point for comparison. Is that correct?
A. Yes.
Q. If they were significantly depressed, then that is a further piece of information that you would need to convey to the surgeon, wouldn't it?
A. Not necessarily.
Q. If they were absent, obviously that's another piece of information which needs to be conveyed to the surgeon.
A. Yes.
Q. For the simple reason that if they aren't there, you can't use them as a starting point.
A. Correct.
Q. Is that right?
A. Yes.
Q. In any event, you informed Dr Gray of something about, it would seem that there were some signals at that point.
A. Yes.
Q. Trying to express it neutrally.
A. Yes.
Q. And you then - and that they were, as you've said in answer to at page 54 and in your answer to the question, Dr Gray, the spinal chord monitoring was abnormal and you use the word abnormal.
A. Yes.
Q. You've told us that. Correct?
A. Yes.
Q. As time went on, on multiple occasions, you told Dr Gray that the monitoring was abnormal, didn't you?
A. No, I don't recall that."
Professor Lagopoulos indicated in his affidavit that the initial spinal cord traces were abnormal in that the "signal was slightly delayed and the amplitude was a little flat".
In the period of about 30 to 40 minutes before the administration of vecuronium at 20.30, the traces became "significantly abnormal" as reported by Dr Lagopoulos to Dr Gray on 5 or 6 occasions. These were clinically significant events.
At or about 20.30, Dr Lagopoulos informed Dr Gray that the traces had been lost. According to Dr Sparks, the traces were lost before the final administration of vecuronium as suggested by his evidence as follows:
"Q. My learned friend asked you a question, my learned friend Mr Walsh, who asked you a question about a comment by the monitor, by Dr Lagopoulos, that 'I have no traces'.
A. Yes.
Q. And you corrected what was being put to you as to the sequence of events as to how that arose. I didn't quite hear it. Would you please repeat it for me?
A. Okay. Sure. So, he said, 'I don't have any traces now', or something to that effect. And I said, 'I'm not surprised with the CO2 so high, and I need to give some muscle relaxant to try to bring down the carbon dioxide'.
Q. What did you understand then of the high level of CO2 had upon the appearance of traces?
A. That it would be difficult to get traces with the CO2 that high."
At or about 20.30, Dr Gray, via Dr Cree, instructed Dr Lagopoulos to discontinue his spinal cord monitoring. Dr Lagopoulos discontinued monitoring but remained in theatre until the procedure was abandoned at about 21.30.
The vecuronium given at 20.30 would have affected spinal cord monitoring for a period of about 30 minutes, and no more than 45 minutes. No further vecuronium or other muscle relaxant was administered after that. By 20.30 the surgery still had approximately three and a half to four hours to completion. Mr Hobson contended that had spinal cord monitoring been continued, there would probably have been monitorable traces by 21.15 at the latest.
Mr Hobson submitted that a motor evoked spinal cord monitor would probably have detected and given warning of any potential injury to the spinal cord caused by poor perfusion. He maintained that spinal cord monitoring of the kind applied in these circumstances was mandatory for surgery of this type. Mr Hobson referred to the report of the orthopaedic conclave that established agreement on the following matters. First, in the absence of spinal cord monitoring the surgery should not have commenced. Secondly, the surgery should not have commenced until there were satisfactory motor and sensory evoked potentials. Thirdly, spinal cord monitoring is not an effective tool unless adequate baselines are obtained.
The following questions and answers from the orthopaedic conclave report need to be recorded in full:
"12. If spinal cord monitoring, once commenced, does not produce adequate traces, then should the surgery be continued?
The experts agree it is very difficult to give a definitive answer without being aware of the spinal cord trace abnormalities.
In the circumstances of this patient, where the indications were primarily to preserve or improve the patient's respiratory functions, serious considerations to continue the operation would have to be made.
13. If there are no traces recorded, should the surgery continue?
The experts agree the answer to this question depends on whether or not baseline recordings were obtained.
If at no stage traces were obtained either prior to or during the surgery, given that the indication for surgery was appropriate, then the surgery would have continued.
If, however, baselines were obtained but subsequently disappeared, the surgery should have been ceased.
14. If spinal cord monitoring was not in place at the time of the commencement of the surgery, should the surgery have been commenced?
The experts agree the answer is no, spinal cord monitoring should have been in place before the surgery commenced.
15. If spinal cord monitoring was commenced but showed inadequate traces, should the surgery have continued?
See answer to question 12."
It was, however, Dr Gray's evidence that spinal cord monitoring was in place. This appears from the following evidence:
"HIS HONOUR. Would you have put knife to skin if spinal monitoring hadn't been in place?
A. No, your Honour."
Mr Hobson maintained that in proceeding with the surgery beyond 20.30 in the absence of spinal cord monitoring, each of Dr Sparks and Dr Gray was practising at a standard below that of a reasonably competent anaesthetist and surgeon, in Australia in November 2009.
Mr Hobson almost immediately developed acidosis when turned prone on the operating table. This state continued and progressively increased until he was turned supine. Acidosis results in an increasing risk of end organ ischaemia including spinal cord damage. This risk progressively increased as Mr Hobson's acidotic condition gradually deteriorated during the surgery.
The spinal cord stroke was an inevitable consequence of the continuing and progressively worsening acidotic condition resulting in poor perfusion caused by excessive carbon dioxide levels. Dr Gray and Dr Sparks both knew of this risk. However, Mr Hobson maintained that both doctors erroneously relied only or predominantly on the parameters of blood pressure and oxygenation to satisfy themselves that ventilation was at all times adequate. Such reliance, without taking into account the signs of acidosis, particularly the elevated CO2 levels, was inadequate to support a conclusion that ventilation was satisfactory. Such a failure was below the standard of care required of a reasonably competent anaesthetist and orthopaedic surgeon, performing spinal surgery in Australia in 2009. This submission needs to be understood, having regard to the following evidence. First, that given by Dr Forrest:
"BURKE: Yes. Dr Forrest, what do you say with respect to utilising the blood pressure and the oxygenation as the dynamic factors as a guide to determine whether to continue with the surgery or not.
WITNESS FORREST: Well, these are the parameters that are - that are used routinely in anaesthetic practice to - to guide our management and they're not the only factors that would determine how the surgery would be conducted. But in this particular case, they would be the - the main factors that would be used to determine whether surgery should continue or not."
Secondly, evidence given by Dr Askin:
"WALSH: That's the joint report. Dr Askin, I'll ask you. Page 119, the sentence under paragraph 4 that reads, 'The experts agree procedures should have ceased when the anaesthetists were unable to maintain the metabolic state, ie, satisfactory blood pressure and oxygenation.' In signing off on this document, Dr Askin, were you using the abbreviation 'ie' in the conventional sense of 'id est', 'that is' as the relevant considerations or were you meaning to write 'eg' 'for example'?
WITNESS ASKIN: I would have thought we could use it either way in that the metabolic state, be it the lactic acid or the PCO2, or the low PO2, and any other variable measured is in - closely interrelated to the blood pressure and oxygenation, so I suppose they're examples of the metabolic state rather than the sole metabolic state.
WALSH: Would you agree that they were the paramount considerations?
WITNESS ASKIN: No, they're the - they're - they would be ones that from an orthopaedic point of view, we would be more aware of, in other words, the anaesthetist would have let us know about the blood pressure and the, and the - or the PO2 arterial saturation of oxygen, because they're things that we commonly talk about. But other things like PCO2 and lactic acid and a whole lot of variable physiological parameters which would come under metabolic state, we wouldn't understand."
Thirdly, the evidence of Dr Westbrook:
"MENZIES: What did that inevitability arise? Or put another way, in as much as it was inevitable and you've already said the surgery should have been stopped, at what point then do you say the surgery should have been stopped?
WITNESS WESTBROOK: I - I mean I think at 2021 things were looking pretty grim but certainly at 2037 with a pH of seven and an increasing lactate I - it's my view that the surgery should have been abandoned at that point."
Fourthly, Dr Forrest:
"WITNESS FORREST: Well, with a benefit of hindsight I think you couldn't argue that would have been preferable to abandon the surgery earlier than - than - than at the time that it was abandoned. That's a retrospective interpretation of the events that the anaesthetist were faced with at the time. You've also got to bear in mind that the key imperative for performing this case out of hours in the first place was that the attending doctors felt that if they didn't operate, his respiratory state would continue to worsen because of the compression of his main stem bronchus. And there was a reasonable expectation, I think, that if surgery had not been successful or not been performed to alleviate that obstruction, that the patient would have died from contractible respiratory failure."
Finally, Mr Hobson referred to the terms of question and answer 4 in the orthopaedic conclave report:
"4. Once commenced, when should the surgery have ceased?
The experts agree that cardio respiratory problems arising in spinal surgery with the patient in the prone position occur infrequently but they have all experienced these problems necessitating the cessation of the operation.
The experts agree procedures should have ceased when the anaesthetists were unable to maintain the metabolic state, ie satisfactory blood pressure and oxygenation.
Dr Wilson-MacDonald notes that at 20.37 blood gas analysis demonstrated a deteriorating metabolic state following an episode of hypotension at 20.30. In his opinion surgery should have been discontinued shortly after this."
Mr Hobson was always going to be vulnerable to ischaemia during the second stage of the surgery due to the first stage surgery ligation of the segmental spinal arteries that necessarily reduced blood supply to the spinal cord. Mr Hobson submitted that neither Dr Sparks nor Dr Gray considered that vulnerability in deciding whether to continue or abandon the surgery. Dr Sparks said this:
"Q. Samples taken at 20.08 hours and 20.21 hours demonstrated a very high carbon dioxide level despite their attempts at pulmonary ventilation with a double lumen tube.
A. Yes.
Q. This was causing a significant respiratory acidosis.
A. Yes.
Q. What is a significant respiratory acidosis?
A. A high carbon dioxide makes the ph go lower.
Q. All attempts to improve the situation were proving to be unsuccessful?
A. Yes.
Q. There was also early evidence of an increasing lactate level suggesting inadequate organ perfusion.
A. Yes.
Q. Samples taken at 2037 and 2051 demonstrate significant further deterioration of all parameters such that the patient now had a profound respiratory and metabolic acidosis.
A. Yes, he had a - profound is a subjective term but, yes, he had a, yes, he had a definite metabolic and respiratory acidosis.
Q. Given that the anaesthetists had no clear means of reversing this and that seems to be the case, isn't it?
A. Correct.
Q. This was a deteriorating trend. Correct?
A. Yes. Yes.
Q. And should have been abandoned at this point and that is to say 20:37 or 20:51, the wound closed and the patient turned proven.
A. If it was an elective operation we would have abandoned it at about 19:30 or before we took him to theatre but if - if, as I believed it was an urgent operation to save his life, I felt compelled to go on while the oxygen and the blood pressure were normal to high."
Dr Gray's evidence was as follows:
"Q. The reason why adequate ventilation is important is that with inadequate ventilation, problems of various kinds may eventuate?
A. Yes.
Q. It was important, wasn't it, that appropriate perfusion, adequate perfusion, was occurring?
A. That's correct.
Q. Because with inadequate perfusion, there is a risk, isn't there, of damage to organs?
A. Yes.
Q. Just remind us of your understanding of what the word 'perfusion' means.
A. So the two factors that are most important and we were cognisant of were the mean arterial blood pressure and the oxygen saturation in the blood, both of which were normal until the milliseconds before there was an arrest."
Mr Hobson submitted that a failure to consider factors beyond oxygen saturation and blood pressure was indicative of a standard of medical practice below the standard required in Australia in November 2009 of a reasonably competent anaesthetist or orthopaedic surgeon, performing spinal surgery in the particular method adopted to treat Mr Hobson. He referred in particular to the evidence of Dr Barratt who Dr Sparks had called from the operating theatre for advice at a critical stage. This is referred to in detail later in these reasons.
Mr Hobson was in respiratory difficulty from the commencement of the surgery and the surgical team had trouble ventilating him throughout. His metabolic state, especially as reflected in his blood gasses, was also poor from the start and continually deteriorated during the surgery.
Blood gasses demonstrated a clear deterioration in Mr Hobson's metabolic state as the surgery progressed. Samples taken at 20.08 and 20.21 had by then already demonstrated a very high carbon dioxide level despite various attempts at pulmonary ventilation with a double lumen tube. This was causing significant respiratory acidosis. From the early stages of the surgery, blood gasses disclosed evidence of an increasing lactate level suggesting inadequate organ perfusion. Blood gas samples at 20.37 and 20.51 demonstrated significant further deterioration of all parameters.
A reasonably competent anaesthetist would have concluded that Mr Hobson was suffering a profound respiratory and metabolic acidosis. Both Dr Sparks and Dr Gray were aware of this dangerous downward spiral in Mr Hobson's metabolic state.
By 20.50 Dr Sparks had tried various means of reversing this deteriorating trend without success. In particular, maintenance of blood pressure and ventilation at reasonable levels after transient drops had failed to address Mr Hobson's dire and deteriorating metabolic state.
As noted above, Dr Sparks spoke to Dr Barratt over the telephone at 20.50 or thereabouts. Dr Barratt correctly suggested to Dr Sparks that the breastplate of the Jackson table may have been pressing on Mr Hobson, creating cardiac and pulmonary artery compression. This meant that a section of lung was being ventilated but not perfused. Dr Sparks agreed with this analysis. Mr Hobson submitted that a reasonably competent anaesthetist would have called a stop to the surgery by this time at the latest. Had the surgery been paused or halted at that, or any earlier time, and Mr Hobson turned supine, he would not have suffered spinal cord damage.
Dr Gray was aware, or should have been aware of Mr Hobson's metabolic deterioration. A reasonably competent spinal orthopaedic surgeon in November 2009 in Dr Gray's position should have ceased the surgery by 20.50 at the latest.
The blood gasses at 21.01 showed a further deterioration in Mr Hobson's metabolic state, such that eventual cardiovascular collapse was inevitable in the absence of corrective measures.
Dr Sparks called upon the surgeon to "hurry up" at around 21.25, which was about five minutes before the spinal cord stroke. Had the surgery been abandoned even as late as 21.25, and Mr Hobson's wound closed and turned supine, he would not have suffered spinal cord damage.
Between 21.26 and 21.30 Mr Hobson's cardiac, respiratory and metabolic status became critical due to a combination of mechanical, respiratory and cardiovascular factors. At or about that time Dr Sparks told or suggested to Dr Gray that the surgery should stop, and a team decision was made to cease the surgery.
In the minutes that followed, Mr Hobson was rapidly sewn up and returned to the supine position where his metabolic and respiratory state almost immediately recovered. Due to inadequate supply of oxygenated blood to his spinal cord at 21.30, he suffered an ischemic spinal cord stroke, which resulted in paraplegia.
[23]
Dr Gray
Dr Gray's contentions can be reduced to a series of propositions as follows:
1. Mr Hobson required the surgery that was performed.
2. Performance of the necessary surgery in a two stage process was uncontroversial.
3. Mr Hobson was adequately warned of all aspects of the proposed surgery and possible risks, including respiratory complications with prolonged ventilation, spinal cord injury causing paralysis and the possibility of abnormal vascular supply to the spinal cord, and the associated need for a pre-operative spinal cord angiogram.
4. The first stage of the surgical procedure was performed uneventfully.
5. The decision to bring the second stage of the surgery forward to 17 November 2009 was appropriate having regard to the opinion of the intensive care specialists that Mr Hobson's condition was critical, deteriorating and potentially life threatening.
6. The decision to continue with the surgery at 20.30 was proper and informed by the same factors that underpinned the original decision to bring the surgery forward.
7. Spinal cord monitoring was rendered ineffective by the administration of a muscle relaxant which became necessary having regard to Mr Hobson's critically deteriorating ventilation.
8. It was not a failure to conform to appropriate medical standards by not halting the surgery at some time before 21.25 because there were no indications for doing so before then.
9. There were no intraoperative indications that Mr Hobson had sustained a paralysing insult and his paraplegia was not detected until the day following the surgery.
10. Dr Gray acted at all times in a manner that was widely accepted by peer professional opinion as competent professional practice.
11. Mr Hobson's paraplegia was not caused by any breach of duty by Dr Gray.
12. Dr Gray is not liable for Mr Hobson's paraplegia because it was the result of the materialisation of an inherent risk of the surgery that could not be avoided by the exercise of reasonable care and skill.
[24]
Dr Sparks
In the context of Dr Sparks' understanding of the urgency of Mr Hobson's need for the surgery, and specifically the blood gas being taken more frequently than usual, he submitted that an inference is readily available that he had not excluded the metabolic blood gas results (Ph, base excess and lactate), but rather that he permissibly placed a different and greater weight upon the blood pressure and oxygen parameters.
Dr Sparks submitted that, in light of Dr Westbrook's evidence, Mr Hobson had not established that Dr Sparks was in error, or acted outside the relevant standard of care, by failing to ensure that the surgery was abandoned at 18.50, 19:10 or 20:30. As to the decision to proceed with the anaesthetic beyond 20.30, he submitted that the opinions of Dr Forrest in the joint report, and in his other reports, were supported by Dr Manasiev.
The orthopaedic surgeons in their joint report in answer to question 18, concerning when the surgery should have ceased, indicated that it was when the anaesthetists reached the stage that they were unable to maintain satisfactory cardio respiratory parameters. Dr Sparks maintained that that point was not reached until immediately before the surgery was terminated in fact. The orthopaedic conclave report made no reference to the time the surgery should have ceased.
In all of his reports, Dr Westbrook provides no explanation as to what he says is the appropriate standard of care amongst anaesthetists with respect to when an anaesthetist should call a halt to surgery or why.
Dr Sparks contended that the evidence of Dr Forrest and Dr Manasiev, coupled with the orthopaedic surgeons' answer to question 18 in the joint conclave report, is preferable to that of Dr Westbrook.
[25]
The decision to operate
A convenient starting point is the decision to bring forward the second stage of the surgery to 17 November 2009.
Mr Hobson was reviewed by various medical practitioners on 17 November 2009. There was at this time an escalating concern about the obstruction and compression of his left main bronchus, his worsening respiratory function and difficulty ventilating him. The need to assist Mr Hobson to maintain adequate blood oxygen levels kept increasing. The surgery was brought forward as it was considered by the ICU team that it was urgent in terms of hours rather than days. There was a perceived need to create more space in the mediastinum in order to relieve the extrinsic compression of the left main bronchus. Dr Wilson-MacDonald confirmed the validity of the reasoning behind this plan.
On 17 November 2009 at about 10.20, Mr Hobson was seen by a dietician who noted, "Extrinsic compression L main bronchus. Note: planned for OT Wed/Thurs". At 11.00 he was seen by Drs Bennett and Penfold for the Acute Pain Program who noted, "? Further OT this week". Dr Matthews also saw Mr Hobson that day and noted "R/V Dr Gray (spinal surgeon)/Dr Sparks (anaesthetist). Will plan for second stage tomorrow at [about] 10.00".
Dr Sparks was contacted by Dr Gray and was informed that "the second stage of the operation needs to be performed as soon as possible, as the compression on the bronchus needs to be released". Dr Sparks formed the clear impression that the operation had to be done in the next 24 hours as ICU staff had been unable to extubate Mr Hobson. He then had moderately severe respiratory failure and was on a high level of increasing ventilator support. There was CT evidence of pulmonary consolidation in both lungs (developing pneumonia) and compression of the left main bronchus, which would be fatal if ventilation and suction of the left lung were not improved.
At 14.40 Dr Sparks returned to ICU with Dr Stephen Barratt, staff specialist anaesthetist, to perform a bronchoscopy for the purpose of satisfying himself of the need for the surgery to be brought forward and to assess Mr Hobson's clinical status from an anaesthetic perspective. The left main bronchus was compressed and stretched and the length of the bronchus was measured at about 5cm. Dr Barratt noted Mr Hobson's trachea was deviated to the right and the left main bronchus was severely narrowed and effectively not functioning. It was difficult to ventilate Mr Hobson and a lot of pressure was being used to achieve this.
Dr Sparks was satisfied that urgent surgery was required. He said that:
"After conversing with the ICU Specialist, I gained the impression that ICU were having difficulty adequately ventilating Mr Hobson because of the compression of the left main bronchus. In practical terms this meant that the left lung could not be ventilated or suctioned and Mr Hobson had to remain intubated. The medical records indicated that Mr Hobson was developing pneumonia, which would be fatal if ventilation and suction of the left lung was not improved."
Dr Sparks discussed the anaesthetic with Dr Barratt. They agreed that a double lumen tube would be required so that the left main bronchus could be splinted open during surgery. Dr Sparks approached Dr Barratt because of his extensive experience and knowledge. Dr Gray took on the role of attempting to co-ordinate and contact the surgical and anaesthetic teams.
The decision to perform the surgery on 17 November 2009 was made that afternoon. It was initially intended that the operation would take place at about 10.00 on 18 November 2009, but only if a team with sufficient experience to perform the surgery was available. During the process of coordinating the surgical and anaesthetic teams, it became apparent that at least two members of the intended team (Dr Cree and Dr Lagopoulos) were unavailable for the morning of 18 November 2009.
Mr Hobson has suggested that the urgency relating to the performance of the surgery on the evening of 17 November 2009 is mere confection. He alleges that planning to perform the operation throughout the evening of 17 November 2009 was in effect for the convenience of staff rather than for his benefit. Dr Gray does not assert that the operation could not have waited until 10.00 the next morning. What was problematic was that it was not possible to organize a team with sufficient skill to be able to perform what would undoubtedly be complex surgery. In particular, it was necessary to have Dr Cree, an experienced spinal surgeon who was involved in the first stage and who had seen Mr Hobson pre-operatively, as well as Dr Lagopoulos, the spinal cord monitor. Whilst an element of pragmatism was involved, it was an entirely appropriate arrangement designed to secure the best possible outcome for Mr Hobson. The expert evidence supports this proposition.
For example, Dr Johnson agreed that "putting together a team of two highly experienced spinal surgeons, a highly experienced anaesthetist, who was a senior member of the college of anaesthetists and a spinal cord monitor person was something that would have some logistical difficulties". He agreed that one would "perform the operation at that point in time when you could get that team together" and "plan the operation so that that team could be there". Dr Askin agreed.
The decision to bring the surgery forward to commence sometime after 18.00 on 17 November 2009 was the result of a consensus of the ICU Team, Dr Marshman (a cardiothoracic surgeon), and two senior members of the anaesthetic team in consultation with the surgical team. There were no dissenting views.
Dr Gray gave the following evidence about his views at the time:
"If you read the medical records commencing 15 November 2009 there is ample evidence to say that his condition progressively deteriorated over the next 24 to 48 hours requiring a cardiothoracic surgeon to come and review the patient, requiring two anaesthetists to come and review the patient, requiring Dr Sparks to come and do a bronchoscopy himself which is an extremely unusual situation and event to occur and requiring an urgent angiogram and a CT chest to be performed on the 17th… also the other parameters such as his PCO2, the ventilatory pressures, x-ray findings, his collapsed lung, and overall respiratory distress were all ample evidence and very concerning to us all that he was heading down a path of no return. And I think it would have been negligent to ignore those events and the way they progressed over those two days."
Dr Gray said that he "was very concerned by the opinions voiced by Dr Marshman and ICU team and the worsening clinical condition of Mr Hobson that it could only end up in a fatality".
Dr Sparks was of the belief that Mr Hobson needed life-saving surgery within 24 hours of when he and others met to discuss the patient at 14.00 on 17 November 2009.
Dr Sparks said in evidence that he would have refused to take Mr Hobson to theatre if it was merely elective surgery. Dr Sparks did more than simply accept that there was a need for urgency "because somebody else told [him] there was" and "[he] actually went up and examined the patient [himself] to satisfy [himself] that was true because it was such an important decision". Dr Sparks also said that "a risk of not doing the procedure exceeded the risk of going ahead with the procedure".
Dr Sparks considered that it was an emergency procedure and the consequence of the surgery not proceeding was Mr Hobson's likely death. He did not resist the suggestion that the surgery take place that evening.
Dr Sparks considered that Mr Hobson needed life-saving surgery within 24 hours of when they were together discussing his condition at 14.00 that afternoon. His explanation of the rationale for bringing the surgery forward was as follows. The ICU specialists wanted Mr Hobson operated on urgently because they were unhappy with his ventilation. He was developing pneumonia. The CT angiogram report from the Sunday clearly showed that Mr Hobson had a compressed bronchus and was developing pneumonia. Dr Sparks was aware that Dr Marshman said that he needed urgent surgery.
Dr Sparks had been told that Mr Hobson's left main bronchus was compressed and it was not possible to pass a fibre optic bronchoscope to identify what was going on. As already noted, Dr Sparks in fact satisfied himself that Mr Hobson truly had pneumonia, and that his bronchus was occluded. There was bloody sputum coming out from his left lung. In addition, the blood gas deterioration was severe. The case notes revealed clear evidence of problems with ventilation on the left side of the lung, and bloody pus being sucked out. Mr Hobson also had a fever.
In response to the proposition that Mr Hobson's lung function would have improved if he had been treated conventionally in ICU, Dr Sparks in cross-examination said that his respiratory function would improve without the operation but his cardiac function would not because the uncorrected cardiac compression would remain. It was Dr Sparks' opinion that "we always had to make this patient worse to make him better in the long term".
The decision to advance the second stage of the surgery in this case was in my opinion perfectly reasonable. As with several other aspects of what occurred on 17 November 2009, it is easy inadvertently to undertake an examination of the decisions that were made with the benefit of hindsight. Principal among those is the fact that, notwithstanding the catastrophic intraoperative events, and the fact that Mr Hobson's respiratory and cardiac restrictions were not surgically alleviated, he later recovered sufficiently to undergo the procedure shortly thereafter.
However, those attending Mr Hobson did not have the luxury of knowing what would later occur. The opinion that Mr Hobson was confronted with a potentially life threatening condition was not an isolated view at the time. Dr Sparks even went as far as to examine Mr Hobson physically in order to satisfy himself of the extent of the bronchial obstruction and the significance of his pneumonia. I am satisfied that both Dr Gray and Dr Sparks considered that there was a considerable risk that Mr Hobson might die if the surgery were not immediately performed. The fact that that decision appears now not to have been correct does not affect its reasonableness at the time it was made. The decision is not in my view one that can reasonably now be called into question.
I pause to observe that Mr Hobson challenges the correctness of the decision to operate because of what he contends is the irreconcilable tension between what was at the time considered to be lifesaving surgery on the one hand and the intraoperative decision to abandon it when Mr Hobson's condition deteriorated so significantly on the other hand. Mr Hobson in effect asks rhetorically how could it be sensible that the surgery was halted at a time when his condition was arguably considerably worse at 20.30 or 21.25 than it was in ICU when his very survival was the rationale for its commencement in the first place. In my view the answer lies in the fact that Mr Hobson's condition before the operation was at worst associated with the strong possibility of his death if the operation was not brought forward. In contrast, the situation as it developed during the operation suggested that by sometime between 20.30 and 21.25 the chance of Mr Hobson dying had been elevated to one approaching a probability, not to say a certainty, if the operation were not abandoned. In that sense the intraoperative decision to halt the surgery is not weakened by comparison with the original rationale for attempting it. The significant issue is whether the decision to abandon the procedure was made too late.
There is no evidence to suggest that the decision to proceed to surgery on the evening of 17 November 2009 was inappropriate. More significantly, there is no evidence to support the suggestion that anyone expected or even could have expected that Mr Hobson's condition would improve. Mr Hobson's concern that there is a tension between the two decisions necessarily requires evidence that Mr Hobson's remarkable post-operative recovery could have been expected. On the contrary, Dr Lambros described it as "a surprising improvement". He gave this evidence:
"Q. … On the balance of probabilities, it's more probable than not, isn't it, that he would have improved, without the surgery? I'm not asking you to say he would be cured, by any means; we're talking about improvement.
A. No, sure. For me, the difficulty in answering your question is that there was a mechanical blockage of the left main bronchus that, for some reason - and it was a surprising improvement in his respiratory condition post operatively - improved whether it was the minimal surgery or the interventions that took place during the aborted procedure. So for me it's difficult to reconcile the fact that there was a downward spiral in this patient's condition almost certainly related to the extrinsic compression, which is a mechanical thing not expected to be improved with intensive care management. For a patient who then does improve in intensive care, that's where the confusion in my answer would be. Did he recover? He did, but I feel that there may some impact by the manoeuvres that were carried out intraoperatively by the anaesthetic team and maybe even the surgery. There was some surgery done I understand."
As I have indicated, the decision to proceed with surgery on 17 November 2009 cannot be faulted.
[26]
Surgical progress until 20.30
The uncontested evidence reveals that Mr Hobson's spine was exposed in a routine fashion through a midline posterior approach and pedicles were displayed between T2 and L2. The pedicle screws were inserted into the left side between T7 and L2.
Mr Hobson experienced decreased oxygen saturations as follows. At 18.50 he suffered an acute reduction in oxygen saturation and end-tidal CO2 with pulse and blood pressure remaining stable. This was due to changing the single lumen tube. At 19.10 he sustained an acute reduction in oxygen saturation and end-tidal CO2 with reduction in blood pressure and sustained reduction in oxygen saturation due to turning him to the prone position. PO2 saturation readings were between 85 percent and 90 percent when he was turned prone. It is normal for the oximeter to be dislodged when rotating a patient to the prone position. However, an arterial blood gas taken at the time gave a PO2 of 243, which is not defined as hypoxia. At 19.10 there was a mild drop in blood pressure. Dr Sparks was aware of this from the CT aortic angiogram that showed bronchial compression and pulmonary artery compression, so that increased compression while in the prone position was possible. Dr Sparks spoke to the surgeons about minimizing downward pressure when inserting the screws as it could cause cardiovascular compression and they agreed to this. The evidence supports the contention that these events would not have caused any significantly abnormal monitoring results.
According to Dr Gray, Dr Lagopoulos was requested to do a run at various times and he reported that the monitoring was good. Dr Lagopoulos stated that Mr Hobson had normal MEPs in both lower limbs. At paragraph 21 of his affidavit dated 6 November 2016, Dr Lagopoulos stated:
"…during the surgery, the traces recorded were stable in that there was no significant deviation from the baseline trace obtained with [the plaintiff] in the prone position. Throughout the surgery, I informed the surgical team in words to the effect the traces were stable, or okay, or fine."
Dr Lagopoulos confirmed this version under cross-examination. He had previously written letters to Mr Hobson's solicitor. Those letters do not suggest that the monitoring changed over a period of time prior to its cessation.
Mr Hobson places particular reliance upon the evidence that Dr Lagopoulos informed Dr Gray of five or six occasions of clinically significant abnormalities in the traces at some time prior to 20.30. However, the evidence does not support the contention that those occasions occurred over an extended period of time. Moreover, Dr Lagopoulos explained the difference between the circumstances where the traces were abnormal and where they became significantly abnormal. He clarified that abnormal traces were in effect a reference to Mr Hobson's baseline signal and that the traces became significantly abnormal when they actually deviated from that. His construct of "significantly abnormal" was taken from the literature. He operated upon the basis that it was "a decrease in compound muscle action potential amplitude of more than 50 percent over a period of one minute".
Professor Silbert confirmed that the concept of "significant" was not limited to the loss of the response, but to a sustained loss of the response. He said that it was common to have a transiently abnormal motor evoked response during surgery, particularly using Dr Lagopoulos' definition of 50 percent. He considered that to be a "very sensitive measure of the change in MEP".
Dr Lagopoulos confirmed that until the time traces disappeared at 20.30, no "significantly abnormal" decrease in the relevant signal was detected. That was consistent with paragraph 13 of his first affidavit, in which he recounts events happening in a crisis and with great rapidity.
Dr Lagopoulos confirmed that, from the perspective of a neurophysiologist, there was no "clinically significant event" and he continued to inform the surgeons that the monitoring was satisfactory until "the point when the anaesthetic machines alarmed". Dr Lagopoulos denied that "there was something seriously going on" at that time.
Throughout the course of the operation up until the time when the anaesthetic machines alarmed, Dr Lagopoulos continued to inform the surgeons that the monitoring was "okay". Following the administration of vecuronium, Dr Lagopoulos was unable to detect any traces.
[27]
The surgery from 20.30 and the administration of vecuronium
The decision to bring the second stage of the surgery forward was due to the inevitable deterioration in Mr Hobson's condition. Dr Gray contended that the rationale for pressing on with the surgery at 20.30 was informed by the same clinical imperative.
In his evidence, Dr Gray summarised balancing the risks:
Q. Do you agree that a continued inability to ventilate Mr Hobson's left lung could have led to his death?
A. Absolutely. That was our main concern that there's always a point of no return and you don't second guess that because once you reach that, taking him to theatre is of no use, and the overall opinion at the time by multiple medical experts is that we should do something before we reach that point."
Dr Gray accepted the proposition that there were considerations pulling in two directions. The administration of the vecuronium was necessary to assist to resolve the respiratory compromise on the one hand but the spinal cord monitoring was unavailable during the time that it was operating on the other hand. This created a tension between two important aspects of the surgery. It was Dr Gray's clear understanding that the vecuronium would not dissipate as it did not operate in the short term but was essential to enable ventilation.
From Dr Gray's surgical point of view, Mr Hobson's blood pressure and oxygenation were normal. He considered that these were the two single most important factors relating to cord perfusion. As will be apparent, Mr Hobson is critical of what he would characterise as a negligent over-reliance on the importance of these factors as a basis for continuing the surgery.
Dr Forrest gave evidence regarding the impact of the pre-operative assessment of the critical need for the surgery, in the context of Mr Hobson's contention that he would not die on the operating table if the surgery had not been done at that time. He said:
"What the consequence would have been - and the expectation of the doctors looking after the patient at that time would have been - that because they hadn't corrected his underlying bronchial compression, that he would continue to have ongoing severe respiratory failure, which would ultimately be - would ultimately lead to his demise because the underlying cause had not been addressed."
Dr Forrest later confirmed his view:
"Well, I think, as I've said, that given the stakes that were thought to be involved at that time which would have been that if surgery was not completed that the patient would have died post operatively in intensive care from refractory respiratory failure that the decision to continue the case based on hemodynamic monitoring and saturation monitoring, blood pressure monitoring and making further attempts to improve the patient's ventilation were reasonable."
Dr Sparks considered that "in an elective operation, we would stop [the] surgery and we have done so in other cases. In an emergency operation, the cardiovascular and respiratory factors outweigh the spinal cord monitoring".
In response to the proposition that a simple alternative was to stop the surgery and turn the patient into the supine position, Dr Sparks indicated that it would not solve the problem, merely defer it, because the cardiac compression would still not have been corrected.
Dr Gray was asked why they could not have waited until the effect of the vecuronium dissipated:
"HIS HONOUR: There were imperatives pulling in two directions, weren't there, the administration of the vecuronium was necessary to assist to resolve the respiratory compromise on the one hand but the spinal cord monitoring was unavailable to you during the time that the vecuronium was operating so you had, effectively, a tension between two aspects of the surgery?
A. That's correct, your Honour.
MENZIES: There was no reason - could I suggest to you - why that tension could not have been resolved by waiting until the effect of the vecuronium dissipated, was there?
A. In my view, that would only delay it - the surgery - further because we were all very keen to correct this deformity without wasting too much time because the longer we had the patient prone, the more trouble Dr Sparks was getting into with his ventilation. So the vecuronium takes half an hour or sometimes longer and we didn't think - our clinical judgment at the time was that that was not a prudent path to follow."
Dr Gray indicated that reversing the effects of the vecuronium would defeat the whole purpose of giving it, supporting his belief that vecuronium was necessary until the conclusion of the surgery.
The loss of traces at 20.30 may have been due to administration of vecuronium at that time. However, in evidence Dr Sparks recollected that the sequence of events was in the reverse order:
Q. And you were aware that vecuronium can impede…potential spinal cord monitoring process, aren't you?
A. Absolutely, but I need to correct this. The sequence was the other way around. He said he had no traces and I said, 'I'm not surprised, the carbon dioxide is so high, and I need to give some muscle relaxant'."
It was Dr Gray's recollection that the traces were lost after the administration of vecuronium:
"A. My recollection is that when Dr Sparks was having difficulty with the ventilation of the patient, he did inform the surgical team that he may need to administer vecuronium in order to continue ventilating the patient. A collective decision or agreement was made at that point in time that that was necessary in order to improve the ventilation of the patient and it was inevitable that as a result of that, we would lose monitoring.
Q. What is your recollection with regard to the implementation of that decision to administer vecuronium, as to whether the traces were lost before or after the administration of vecuronium?
A. It was after the administration of vecuronium.
Q. You would therefore disagree with Dr Sparks' account that I read out to you, wouldn't you?
A. Yes."
I am unable from the available evidence to resolve this difference of recollection.
Dr Gray's evidence was that Dr Sparks informed the surgical team that he may need to administer vecuronium and that a collective decision was made at that point that it was necessary in order to improve Mr Hobson's ventilation. It was inevitable that as a result the monitoring would be lost. In any event, both Dr Sparks and Dr Gray were of the opinion that the priority to maintain Mr Hobson's respiratory health was more important than any competing considerations at that time. It will be apparent once again that Mr Hobson is severely critical of this approach and characterises it as a breach of the duty he was owed.
After Mr Hobson was paralysed with vecuronium, Dr Cree advised Dr Lagopoulos he could conclude his involvement in the surgery.
At 20.30, Dr Sparks administered vecuronium in an attempt to improve Mr Hobson's worsening ventilation. He formed the opinion that Mr Hobson's PaCO2 was very serious and believed that if 4mg of intravenous vecuronium was administered, it may bring his PaCO2 down. As it was an emergency procedure and a likely consequence of not proceeding with the surgery was death, Dr Sparks felt obliged to take this course.
By 20.30 the arterial blood CO2 level had risen from 64.7mmHg to 70.5mmHg. Dr Sparks was unable to detect any mechanical obstruction to ventilation but nevertheless gave vecuronium and informed the surgeons. Mr Hobson had to be paralysed through the use of a muscle paralysing agent in order to be ventilated.
Dr Gray confirmed that the loss of traces at about 20.30 did not mandate that the surgery be paused. This was because there was no need to look for a reason why the monitoring had ceased. It was clear, according to him, that there was a reason for the monitoring to have stopped that did not have a surgical cause.
Dr Gray confirmed the obvious proposition that whether surgery is stopped "depends on the circumstances of the surgery we are performing and the indications for performing that surgery". Dr Gray confirmed that the surgery was not an elective procedure.
Dr Gray indicated that he would not make a decision to cease surgery based upon medical parameters other than through taking the advice of his anaesthetic colleagues who were responsible for monitoring them.
At 20.35 Mr Hobson's blood pressure dropped transiently. Dr Sparks believed it was due to the surgeons using downward force to insert a pedicle screw. The blood pressure recovered before any intervention was required. At 20.45 there was one reading from the oximeter of 92 percent. Blood gas readings before and after were PO2 of 127 and 205, both of which did not indicate hypoxia.
On this topic, Dr Askin gave the following evidence:
"A: If you, the, it's ideal, and comforting for the surgeon, to know that the monitoring is working - generalising that is. In this case, where the imperative was to take the pressure off the patient's chest, bronchus, then losing the monitoring because the patient had to be muscle paralysed, is not ideal, but I would have continued the operation, because the end point was to be reconstructing the chest volume.
WOODS: And when you say you would have continued the operation, do you believe that many spine surgeons of good standing would have continued the operation as well.
A: If they were doing the operation to preserve a patient's lung function and it was predetermined before a patient went to theatre that that was the reason for doing it acutely, then I believe they would, yes."
In my view, the administration of vecuronium at 20.30 was reasonable in order to improve Mr Hobson's ventilation. It was a singularly uncontroversial procedure in the course of attempts to do so. The evidence does not in any event suggest that there was an available or viable alternative. If at 20.30 Mr Hobson's operation were to continue, it could not do so unless his ventilation was improved. Those performing the operation at that time were therefore confronted with a choice between stopping the surgery altogether in the face of Mr Hobson's ventilation and respiratory difficulties or continuing with the operation if those difficulties could be corrected. The administration of vecuronium would correct those difficulties. However, the significant compromise in those circumstances was that the spinal cord monitoring was immediately neutralised by its administration and any form of spinal insult that spinal cord monitoring might otherwise have been expected to highlight would remain dangerously undetected. In other words, Dr Gray and Dr Sparks were effectively trading off any concern they might have had that Mr Hobson may be neurologically compromised if the surgery proceeded in the absence of spinal cord monitoring against the possibility that he might die if the corrective surgery were discontinued.
It is not in issue that Mr Hobson had not sustained the neurological injury of which he now complains by 20.30. Cessation of the operation then would have meant that he would not have suffered from paraplegia and the operation to correct his spinal deformity could have proceeded at a later time. Mr Hobson's paraplegia was sustained after 20.30 and before 21.25, or what amounts to the same thing, before the operation was finally abandoned. The significant question is whether the decision to proceed at that time was wrong. The answer to that question is partially informed by an understanding of what properly functioning spinal cord monitoring after 20.30 might have been expected to show.
[28]
What might functioning spinal cord monitoring after 20.30 have been expected to show?
When cross-examined on this topic, Dr Westbrook gave the following evidence:
"WOODS: Is it within your expertise to answer this question; given the parameters measured by motor evoked potentials, you'd agree that motor evoked potentials, if being performed at that time - leaving aside the vecuronium - would not have shown any damage to the spinal cord?
WESTBROOK: I can't - I'm not sure I can comment specifically about that kind of transient change. I think I would - the particular complication for this gentleman was the fact that he'd already had his - the perfusion to his cord reduced by the first operation, so I think it was more vulnerable to ischemia than a normal spinal cord would have been.
…
WOODS: More vulnerable to, but that means when an event occurred at 21.25 or thereabouts, that would have been the first indication that spinal cord monitoring could possibly have picked up. That's correct, isn't it?
WITNESS WESTBROOK: Yep. I think that's quite possible insofar as the
motor evoked potentials are, by definition, an episodic test which the neuro physiologists does periodically. It's not - it's not like somatosensory evoked potentials, which are a continuous monitor. So if the - if the test run wasn't done by the neuro physiologist to coincide, then it would be missed."
This evidence has to be compared with the opinion of Dr Silbert that is extracted at some length earlier in these reasons to much the same effect.
Drs Heath and Sawle spoke of this in their concurrent evidence as follows:
"MENZIES: Okay. Thank you. Just one final thing, which I ask first of Dr Heath, and invite either of the other doctors comment. Let it be assumed that there is some event occurring which may cause damage to the spinal cord, which may be picked up the monitor. Is there a range of time before which the damage irretrievably occurs, or do the two events occur at the same time. Or put it another way, if one sees change, which requires, let us assume that the surgeon be told and the surgery stops, is there some time before that change results in inevitable damage? Are you able to comment upon that, Dr Heath?
WITNESS HEATH: It - would it be variable? It depends on the severity of the insult, but if it was a severe insult, I would - my estimate from, sort of, animal studies would be about ten minutes, I guess. You've got a window of opportunity, once the monitoring event occurs, to actually correct whatever there is - the disturbance that's causing it. So, I mean, there's no exact figure, but you
MENZIES: Yes.
WITNESS HEATH: I would say around ten minutes, you've got actually correct things, but we always say that after a hypoxic event, for instance, you've got about four or five minutes for the brain, and you probably - that's similar for other organs, if it's a complete cardiac arrest and no perfusion. So that's the severest possibility, but in general - maybe ten minutes, but you - there could be a window between five and 15, 20, I guess. 15 - I wouldn't go as far as 20. It's an estimate.
MENZIES: Thank you. Is that uncontentious I ask Dr Sawle.
WITNESS SAWLE: Again, specifically in terms of spinal cord monitoring I can't answer that, but from the time when blood pressure drops precipitously, for example, then that will certainly be the case that there's a number of minutes of opportunity."
Dr Gray argued in these circumstances that there would have been no time, from the point of view of motor evoked response monitoring, to respond to the cardiovascular collapse as there would have been no warning of Mr Hobson's impending collapse. Nothing could have been detected until the vecuronium ceased to compromise the spinal cord monitoring. In the present case, the cardiovascular collapse would have supervened before that had occurred. This is in my opinion an inevitable conclusion having regard to the opinions of Drs Lambros, Silbert and Askin.
[29]
The surgery is abandoned
Dr Sparks gave the following evidence in cross-examination:
"Q. And what was the discussion, if any, which took place before or about the time of the cessation of the surgery between you and the surgeon?
A. I don't remember exactly. But the first thing we wanted to ascertain was whether he had any brain or major organ damage.
Q. Stop there. Before then, at the time when you said they'd have to stop, was there any discussion about that event occurring or did it just happen?
A. I said 'You've got to stop as fast as possible' and they did. There was nothing to discuss, they didn't disagree with me."
Dr Sparks had earlier given this evidence:
"Q. If then the surgery was necessary to proceed, because if the alternative was that he was going to die…
A. Yes.
Q. … then why did it stop ever?
A. I was having difficulties with the anaesthetic and I made a decision that whilst the systolic blood pressure and the oxygen were normal to high, I would continue. If that changed, then I was obliged to stop because it was impossible to continue. Those are the two things that you can't - if they become abnormal, the oxygen or the low blood pressure, the patient will definitely suffer permanent damage. The other factors you can survive and get through and still have a normal outcome. They were the two I decided would be my criteria for stopping the operation.
…
Q. Those were risks, were they not?
A. It's a risk in every case of every patient I've ever looked after.
Q. Had those risks not - to use his Honour's expression - come home, you would have proceeded. Is that right?
A. Yes, that was my decision.
Q. No doubt that was your decision, but if they were always risks which could come home, then why did you consent to the operation in the first place?
A. Because I believed it to be urgent. A risk of not doing the procedure exceeded the risk of going ahead with the procedure.
Q. If those risks did come home, the urgency was still there. Correct?
A. (No verbal reply)
Q. You're nodding, but we…
A. Yes.
Q. Do you agree with that proposition?
A. Yes.
Q. Well, why did you stop?
A. Well, I just said that when I agreed to do the - go ahead with the procedure, the risk of not going ahead exceeded the risk of going ahead and at that moment when the blood pressure and the oxygen dropped, that changed. The risk of proceeding exceeded the risk of not proceeding.
Q. You say that that risk, that balance, if you like, was apparent at about 21.25?
A. The crossover point where - yes, 21.25. It might have been 24, it might have been 26, but yes."
Dr Westbrook and Dr Forrest agreed at the anaesthetic conclave that at about 21.20 there was a sudden reduction in oxygen saturation. The cause of relative bradycardia following the episode of hypotension was unclear but may have been due to a combination of patient and surgical factors. However, at the time, Mr Hobson's oxygenation was adequate.
At 21.24 the PO2 levels fell, Mr Hobson was bradycardic at 5bpm, hypotensive at 70/40 and had very low-end tidal CO2 level. Dr Sparks considered the drop in exhaled CO2 and blood pressure to be serious. About 2-3 minutes later (at about 21.28) Dr Sparks asked the surgeons to stop operating immediately and close.
At 21.25 Mr Hobson's blood pressure and his PaCO2 dropped. Dr Sparks considered the drops in exhaled CO2 and blood pressure to be significant. He administered adrenaline. At 21.30 Mr Hobson's PaCO2 dropped co-incidentally at the time the surgeons were told to cease operating.
Dr Sparks informed those present of a collection of anaesthetic difficulties he was encountering, including the ongoing reduction in oxygenation, hypotension, a decrease in end-tidal CO2 and an increase in PaCO2. He said words to the effect "I'm having problems with ventilating".
By about 21.25, the exhaled carbon dioxide expired waveform had diminished, the cardiovascular pressure was 37 and Dr Sparks was concerned that the right ventricle was failing. According to Dr Gray, Dr Sparks raised his concerns with the others saying words to the effect of "hurry up as the patient's condition is deteriorating". Dr Sparks gave this evidence:
"Q. At some point you said to the surgeons, 'Please hurry up.
A. Yes.
Q. When did that occur?
A. I'd like to check my notes, but it would have been after 21.20, possibly after 21.25. Is that enough? Is that a sufficient answer?"
Dr Sparks was cross-examined to the following effect:
"Q. The members of the surgical team were, I think, Dr Gray and Dr Cree and a Dr Lyons. Is that correct?
A. Yes.
Q. And the members of the anaesthetic team were Dr Sparks and Dr Wang?
A. Yes.
Q. The decision to stop the surgery at about 21.30 on 17 November 2009 was made by the process of discussion amongst the members of the surgical and the anaesthetic team. Isn't that correct?
A. Yes, but I think it was really my decision.
Q. Thank you. However, there was consultation between the two?
A. There was no disagreement when I told them what I thought.
Q. You'd agree that that was appropriate that those individuals made that decision?
A. That they concurred with my decision?
Q. Yes.
A. Yes."
At 21.30 it was clearly necessary to abandon the surgery given the severe respiratory and haemodynamic instability that suddenly occurred. As indicated, Dr Sparks had administered adrenaline and directed Dr Gray to stop the procedure immediately. The surgery was abandoned and the wound was rapidly closed. Mr Hobson was turned to the supine position. His cardiovascular status improved. There were concerns at the time that he may have suffered hypoxic brain injury due to the downtime of the cardiac arrest. He was taken to the ICU, intubated, ventilated and monitored.
Dr Westbrook and Dr Forrest agreed at the anaesthetic conclave that during the process of instrumentation of the right side, between 21.26 and 21.30, Mr Hobson's cardiac, respiratory and metabolic status became critical due to a combination of mechanical, respiratory and cardiovascular factors. These included obstruction of his major blood vessels in the chest, worsening ventilation due to his prone position, underlying lung disease, spinal manipulation, bronchial obstruction and low cardiac output due to acute right heart failure.
According to the orthopaedic conclave in answer to question 18, the surgery should have been halted when the anaesthetists reached the stage that they were unable to maintain the metabolic state, meaning satisfactory blood pressure and oxygenation and satisfactory cardio respiratory parameters. This occurred at 21.30 when Mr Hobson suddenly became hypoxic and hypotensive. That is when the surgery was halted in fact. Question 18 anticipates both the anaesthetic events and the spinal cord monitoring events. It was only when Dr Sparks made the call that the surgery was halted.
The decision about whether to stop the surgery at any particular time was a decision that had to be made by both the surgical and anaesthetic teams. The decision-making procedure involved the surgeons being aware of surgical issues, and the anaesthetists being aware of anaesthetic issues. Both teams were acutely aware of the pre-existing reasons for the operation being performed when it was. Dr Sparks stated that the decision to stop the surgery at 21.30 was his. This meant that he was the person who was aware of the anaesthetic issues that would have informed a decision by the surgeons and the anaesthetists operating together about what to do. Up until shortly before the cessation of the surgery, Dr Sparks had not informed the surgeons that he was having any difficulty with hypotension. It was only when significant issues arose after 21.20 that Dr Sparks informed the surgeons of the difficulties. Minutes after that Dr Sparks indicated that the surgery should stop:
"Q. So when you said, 'Please hurry up,' what did you mean?
A. I don't know, but I was worried about the patient.
Q. Then minutes later, you said, 'Stop.' Correct?
A. Yes. So I decided that whilst the oxygen was satisfactory and the blood pressure was near to normal that I would continue with this operation. When that ceased to be at that time, that's when I told them to stop."
In response to the suggestion that Dr Gray should have stopped the surgery, turned Mr Hobson over and waited to see what happened, assuming he knew there were "problems" or difficulties with the spinal cord monitoring, Dr Johnson did not agree with immediately stopping the surgery:
"MENZIES: Well, if you can just deal with it on a higher level of generality and ignore the fact what became known after the collapse, that was he was turned over and vital signs returned. Leave aside for the moment what the anaesthetist might have said to the surgeon. If the surgeon perceived that there was a difficulty with monitoring or the like, what would, in the general course, a surgeon be likely to do at that point? What Doctor Johnson is saying, 'Well, if I knew that there were problems', let's not deal with them in detail, 'I'd stop the surgery, turn the patient over and see what happened', that's correct isn't it, Doctor?
WITNESS JOHNSON: Well first of all, you go through a checklist such as Dr Askin has said, that you check aren't anaesthetic correctable factors, that there aren't technical problems related to the spinal cord monitoring itself. So if you believe that the change is a true change, then you do as Dr Askin says, you've got to assess 'Well, do I think this is a true change? And I think when have the co-existence of a significant anaesthetic problem, I think it is likely to be a true change in the spinal cord monitoring."
Dr Johnson continued as follows:
"MENZIES: So, Dr, you're the surgeon in the theatre, you're told that which I've just outlined by the anaesthetist, what would that tell you, Dr Johnson of (a) would you perceive that as a problem and (b) having done so, what, if anything, would you do about it?
WITNESS JOHNSON: First of all, I'm not an anaesthetist, and the people that I work with for this type of surgery are the same type of people that I have all along, and they're people who are very experienced in this, giving anaesthetics for this type of problem. And we have an understanding that we reinforce, that if the anaesthetist is unhappy, that they cannot adequately anesthetise the patient, we will stop. And so if the - and our anaesthetists say that, they say, 'This is - I can't, the anaesthetic is not going well, we should stop.' And that's what we do."
Dr Johnson later gave this evidence:
"WOODS: If you're under the belief that there is a significant chance of death, you would continue with the surgery?
WITNESS JOHNSON: It would have to be - it would have to be fairly significant. It - because as I said, it's a very unusual clinical scenario, I - I personally have never come across it.
WOODS: So it was a decision that had to be made by the team that is one that is outside your practice, outside your experience.
WITNESS JOHNSON: Yes, it's outside my - outside my practice. But as, you know, if of course the - the chance of the patient dying is 90 percent if you don't do the surgery, that's a totally different scenario to if the chance of the patient dying is 20 percent if you don't do the surgery."
The conclave of orthopaedic experts agreed the surgery should have ceased when the anaesthetists were unable to maintain the metabolic state. Dr Wilson-MacDonald considered that the surgery should have ceased shortly after 20.37 when blood gas analysis demonstrated a deteriorating metabolic state.
Regardless of what Dr Wilson-MacDonald opined in relation to anaesthetic considerations, the joint report, at answer 18, makes it clear that the surgeon is in the hands of the anaesthetist in relation to anaesthetic issues. Dr Forrest considered, in the context of Mr Hobson's deteriorating condition and the prevailing circumstances, that it was reasonable to continue the surgery. In his 26 October 2013 report he said:
"However, given that the patient's surgery needed to be performed out-of-hours, and given also that his lung infection would not have been expected to resolve until the compression of his left main bronchus was relieved by surgery, it was reasonable to continue the anaesthetic at that time."
It will be recalled that Dr Manasiev gave a summary of the overwhelming factors in favour of continuing the surgery at 20.30 in the context of Mr Hobson's deteriorating condition. There was a potentially identifiable and reversible cause of the hypotension and desaturation. There was a quick resolution to normal values of blood pressure and saturation. The decision was balanced against the apparent necessity of the operation as a potential lifesaving technique. In those circumstances, Dr Manasiev considered that Dr Sparks and Dr Gray were warranted in not halting the surgery at that time and would be considered by widely accepted Australian peer professional opinion to have conformed to competent medical practice by continuing with the surgery.
In my opinion, the decision to continue the surgery at and from 20.30 was reasonable.
[30]
Findings
I consider that it is possible to find the following matters upon the balance of probabilities.
First, the original decision to bring the surgery forward to 17 November 2017 cannot be criticised. Mr Hobson was considered by all accounts to be in extremis. He had or was quickly developing a serious lung infection. His left main bronchus was narrowed and was almost completely occluded. The double lumen tube was operating to splint it open, without which Mr Hobson's left lung could not have been ventilated. The consensus at the time was that Mr Hobson might die if the situation were not urgently corrected. The decision to operate was made in that context. That decision was reasonable. I consider that it is prudent to make this finding even though it was indicated on the last day of the hearing that Mr Hobson no longer pressed the proposition that the surgery should not have commenced. I note Dr Westbrook's opinion is to the contrary.
Secondly, the decision to continue with the operation at and beyond 20.30 was perfectly reasonable. There were no anaesthetic or surgical indications at that time that the surgery should have then been abandoned. Mr Hobson's ventilation improved with the administration of vecuronium to the point that continuation of the surgery was warranted.
Thirdly, (and subject to point sixthly below), the absence of effective (or indeed any) spinal cord monitoring after 20.30 is ultimately of no direct significance, as Mr Hobson's ventilation was critical and took precedence over the need to maintain it. Once it is accepted that the decision to proceed after 20.30 was reasonable, there was in the particular circumstances as they presented at the time no useful place for spinal cord monitoring. The attending doctors were faced with the choice of stopping or continuing at 20.30. There was no possibility of continuing after 20.30 without the administration of vecuronium, which neutralised the effectiveness of spinal cord monitoring. The administration of vecuronium in Mr Hobson's particular respiratory circumstances was unexceptionable.
Fourthly, Mr Hobson had not suffered any catastrophic intraoperative event leading to his spinal damage and paraplegia at any time before 20.30. The most likely time frame within which that event occurred is between 21.20 and 21.30.
Fifthly, even if there was arguably no single unambiguous indication for stopping the surgery before the decision to do so was made, there were several factors which together certainly gave that indication. As Mr Hobson emphasises, the evidence of Dr Barratt, who was after all the expert to whom Dr Sparks turned when his options appeared to be evaporating, emphasises the importance of heeding several factors in combination. It is reasonably clear that Dr Barratt's telephone input inspired the events that followed it. The attending doctors undoubtedly had access to several significant indicators of Mr Hobson's condition, even if none taken alone pointed only in one direction. The combination of these factors provided a different perspective. The earlier indications available from Mr Hobson's vital signs appeared to be that any deteriorations that were observed, in particular, episodes of hypoxia and hypotension occurring at or about 18.50, 19.10 and up until about 20.35, some of which were severe, were transient and recoverable but not such as to indicate that continuing with the surgery could not be justified. Up until about 20.35, Dr Gray and Dr Sparks were, in effect, permissibly taking an expectant approach, in the absence of material that indicated only one possible course of action. That position changed very shortly thereafter.
This finding requires some elaboration.
The contention that the surgery should have been stopped sooner appears to have initially arisen from Dr Westbrook's first report in which he refers to the elevated PCO2 of 64mmHg. He continued in these terms:
"The PaCO2 is significantly elevated and suggests inadequate ventilation. Consideration to defer surgery could have been made at this time. As the patient was haemodynamically stable at this time decision was taken to proceed with surgery. Throughout surgery there were episodes of reduced oxygenation, decrease blood pressure and falls in end-tidal carbon dioxide. There was later an episode of profound cardiovascular collapse associated with hypoxia and severe hypocarbia. Mr Hobson was appropriately resuscitated and a rapid decision made to abandon surgery. Despite this there was a period of several minutes when the oxygen levels were very low and the blood pressure significantly below 100mmHg systolic. It is this episode which is the probable cause of his paraplegia."
In his 24 August 2016 report, Dr Westbrook said this:
"It was the correct decision to abandon the surgery following the episode of severe collapse. There were opportunities earlier in the procedure when the anaesthetic team was struggling to achieve ventilation and oxygenation and effective spinal cord monitoring was not in place for the team to discuss discontinuing the surgery."
Earlier in the same report, Dr Westbrook offered the following analysis:
"A PCO2 of 65 is significantly above normal limits and well above that which was achieved on the ICU. The clear difficulties in achieving adequate ventilation due to this patient's distorted anatomy and prone position were the cause of this inadequate ventilation. However despite the efforts of the anaesthetic team the high CO2 was not successfully reduced and later in the anaesthetic reached extremely high levels (110mmHg). Furthermore whilst blood oxygen levels were satisfactory at the start of the procedure this was only being achieved with 100% oxygen (c.f. 60% on ICU). Therefore at the outset of this long and difficult operation the anaesthetist already had to use maximal ventilation and inspired oxygen concentration. This lack of reserve is reflected in the subsequent episodes of severe hypoxia and hypercarbia. Again it appears that the decision to persist under such circumstances was driven by the erroneous view that the surgery was lifesaving."
In cross-examination, Dr Westbrook conceded that the episodes of oxygen desaturation and low blood pressure at 18.50, 19.10 and 20.35 were of a transient nature, although the latter episode was against a background of deteriorating acid base. He conceded that there was no basis to stop the surgery at 18.50 or 19.10. Dr Westbrook agreed that when there was a drop in the blood pressure and oxygen desaturation at 20.35, both parameters were recoverable and quickly resolved. He also agreed that Mr Hobson was haemodynamically stable until 21.20, apart from the transient episodes referred to above.
However, Dr Westbrook did not agree that it was reasonable for Dr Sparks to use the blood pressure and oxygen parameters as his dynamic guide for continuing with the surgery until 21.20. In essence, he maintained his position as identified in the anaesthetic conclave report, that the surgery should have been abandoned no later than 20.37.
By contrast, Dr Forrest in oral evidence expressed the opinion that the parameters of blood pressure and oxygen were routine parameters for the management of these types of cases, and that it was reasonable to continue to make further efforts to alleviate Mr Hobson's respiratory and metabolic acidosis. In the anaesthetic conclave report, Dr Forrest expressed the opinion that because Mr Hobson's surgery was considered potentially lifesaving, and given that the periods of haemodynamic instability were of a transient nature, it was reasonable to continue to attempt to improve Mr Hobson's ventilation and haemodynamic state, until the sudden, severe respiratory and haemodynamic instability that occurred at around 21.30.
Dr Manasiev in both his report and in cross-examination expressed the opinion that these drops in blood pressure and oxygen were transient in nature, and that there were explanations for each event. He considered that it was appropriate to continue the surgery after each event at 18.50, 19.10 and 20.35.
Dr Sparks' evidence was that he was having difficulties with the anaesthetic and that he made a decision that, whilst the systolic blood pressure and the oxygen were normal to high, he would continue. If that changed he was obliged to stop. He said that in the presence of abnormal oxygen levels or low blood pressure the patient will definitely suffer permanent damage. He chose these factors as his criteria for stopping the operation.
As set out earlier in these reasons, Dr Sparks reasoned with respect to those two dynamic parameters that "the risk of not going ahead exceeded the risk of going ahead and at that moment when the blood pressure and the oxygen dropped, that changed. The risk of proceeding exceeded the risk of not proceeding".
Dr Forrest's evidence was to the effect that looking prospectively at the management of Mr Hobson's anaesthetic, the doctors treating him had a belief that if the surgery was not completed there was a risk that he might die post-operatively from "refractory respiratory failure". It was for this reason that he expressed the opinion that it was reasonable to continue the surgery using the haemodynamic and saturation monitoring and make further attempts to improve Mr Hobson's ventilation.
In cross-examination, Dr Manasiev said that the factors that would inform competent professional practice, with respect to anaesthetists and the continuance or otherwise of a surgery, were "the whole gamut of all the haemodynamic parameters" affecting a patient. He said that predominant among these were blood pressure and saturation, which indicate how the organs are being perfused. He conceded that other factors could not be excluded, but that different parameters would be differently weighted in terms of indicators of a patient's stability.
Dr Sparks understood that Mr Hobson's need for surgery was urgent. He examined him and formed that view for himself. Dr Westbrook's opinion that that view was "erroneous" is necessarily second hand and retrospective. Both Dr Westbrook and Dr Forrest in their joint report expressed the opinion that it was reasonable for the surgery to commence. I am however not satisfied that either Dr Gray or Dr Sparks conformed to the relevant standard of care in failing to halt surgery before 21.25.
As I have earlier noted, the orthopaedic surgeons in their joint report indicated that the surgery should have ceased "when the anaesthetists reached the stage that they were unable to maintain satisfactory cardio respiratory parameters". The orthopaedic surgeons made no precise reference to a time when the surgery should have ceased. Satisfactory cardio respiratory parameters were not being maintained by 20.30.
In my opinion, the evidence of Dr Barratt is critical in this respect. At the risk once again of including too much material, I consider that Dr Barratt's evidence in cross-examination is extremely instructive and is as follows:
"Q. Doctor, I want to take up a couple of matters in your affidavit, if I may.
A. Yes.
Q. At paragraph 10, you refer to receiving a call from Dr Sparks. You nominate a time at 9.30. What was that based upon? Do you have a note of it or a record or is it just your approximation?
A. The phone is opposite the oven and I just noticed the oven clock, it being about 9.30 when the DECT phone went off.
Q. You say that Dr Sparks was concerned about Mr Hobson's consistent hypertension and ventilation issues during the surgery?
A. Yes. He was very concerned.
Q. Apart from being concerned, can you help us with how he expressed that, what he was concerned about?
A. His speech was very pressured. He had multiple manoeuvres trying to suction the airway, bronchoscope the airway, check for breath stacking, checking for pneumothorax which is all critical events.
Q. You said something was pressured. His?
A. He was quite - his speech was quite pressured. He was - I could sense he was quite stressed for Chris.
Q. He talked about his carbon dioxide levels not decreasing which meant increased dead space. Now, is that what he said or is that what you interpreted?
A. That's what I interpreted.
Q. Then you discussed his position on the Jackson table and you suggested that if the breast plate of the Jackson table was pressing on Mr Hobson, the cardiac compression would generate potential for hypertension?
A. Yes, yes, it would.
Q. How does that occur?
A. If it's pressing on the main arteries coming out of the heart, the blood pressure will - can potentially fall basically.
Q. If that occurs, what's the downside risk of that occurring?
A. There might be critical organs which don't get perfused adequately.
Q. He also expressed concern about a high arterial carbon dioxide content.
A. Yes.
Q. What is the significance of a high arterial carbon dioxide?
A. Normally, that means you are not ventilating properly which is why they suction the airway, put a bronchoscope down the airway to check and did all those manoeuvres to check for ventilation.
Q. Is this correct? That what had happened, as you understood it, Dr Sparks had carried out all the tests or checks, if you like, to see that everything was connected up and mechanically all was okay?
A. Yes. He'd conducted all that and he was happy with it but he still could not explain the problem.
Q. So your response was that probably, or maybe, a pulmonary artery was compressed along with possible cardiac compressions, it means his lung was being ventilated but not perfused?
A. That is exactly correct.
Q. What is ventilated but not perfused mean?
A. It means that there is inability to eliminate carbon dioxide from the lung because there's no blood going through the alveolus and all this air is just coming into the lung and can't take the carbon dioxide out so the carbon dioxide is going to build up.
Q. And the consequence of that is what?
A. A carbon dioxide level of 65 is not a problem physiologically but for that to happen, you have to be pressing on a pulmonary artery in such a significant way that it's going to impede cardiac output and organ perfusion.
Q. And the consequence of that is what?
HIS HONOUR: If uncorrected you mean?
MENZIES
Q. If uncorrected?
A. Critical end organ ischemia.
Q. Critical?
A. End organ perfusion or inadequate perfusion to an organ, damage, organ damage.
Q. And the consequence of that in a longer term sense if these organs are damaged was what?
A. Well, a low cardiac output state could damage the brain, the spinal cord, the kidneys, or the liver, for instance, potentially.
Q. Now, you've said that you've seen a spinal surgery of this type many times, but not with a patient with Noonan Syndrome.
A. That is correct.
Q. Can I suggest something to you and ask you to agree or disagree with this? What was happening with respect to this particular surgical approach was that it seemed as if a technique to solve a chronic problem was attempting to be adopted to solve an acute problem.
A. Can you rephrase that? I'm not sure if I really understand.
Q. The idea of the surgery would seem to be to correct his scoliosis.
A. Yes.
Q. Which was going to provide a long term benefit for him.
A. Yes.
Q. And the mechanism was that approach. And that was, in other words, a resolution of the chronic problem. That is to say, his scoliosis and the like.
A. Yes, yep.
Q. But the approach of going to surgery then was, really, to deal with what was perceived to be an acute problem. That is to say, his breathing difficulties at the time.
A. Yes, that was the reason.
Q. Is that fair
A. It was an acute problem, there was an acute problem with his breathing at the time.
Q. Now, just going back to the timing. And you've told us how you recall that. Let me suggest to you that these events occurred quite a bit earlier than 9.30
A. Yeah.
Q. but around 8.50, about 40 minutes before. What do you say about that?
A. The phone call, or
Q. The phone call, yes.
A. That could be correct. My recollection is from what I remembered at the time, yeah.
Q. Doctor Sparks told you that the various metabolic indicators were critical.
A. Yes, yes.
Q. Despite, apparently, adequate blood pressure and blood oxygen levels. That was one of his dilemmas, wasn't it?
A. Yes, yep.
Q. Then in those circumstances, it really wasn't appropriate, was it, to look at the blood pressure and blood oxygen levels alone when making a decision whether to persist or abandon surgery?
A. I agree with that statement." [Emphasis added]
It is important not to lose sight of the fact that Dr Sparks and Dr Gray were confronted with what was patently a distressing and fraught intraoperative emergency. It is difficult to over-emphasise just how awful it must have been at that time for all concerned. It is clear that Dr Sparks had attempted all of the anaesthetic manoeuvres in his armoury to correct the problem without apparent success. Criticism of these doctors in those circumstances may seem harsh. However, it is not in question that stopping the surgery when no obvious answer to the problems confronting the doctors was presenting itself would have avoided the damage. We know with hindsight that postural adjustment from prone to supine produced immediate resolution of these problems. That was something which in my opinion Dr Sparks and Dr Gray should have foreseen and acted upon. Failure to do so amounted to a want of reasonable care. It was in my view not appropriate to take the risk that something that could not be explained would or might somehow spontaneously resolve or improve. It is no answer to insist that the surgery was lifesaving in circumstances where Mr Hobson's respiratory difficulties at or after 20.30 had deteriorated below his pre-operative condition in ICU.
Sixthly, there was a need to be particularly mindful of the consequences for Mr Hobson of his rapidly deteriorating ventilation by reason of the fact that spinal cord monitoring was absent or effectively neutralised. For present purposes it does not matter which it is. Indeed, I accept the opinion of Dr Silbert that he did not believe that SSEPs and MEPs would have detected significant spinal cord electrophysiological abnormalities prior to 21.25. In that sense I am not satisfied that the absence of spinal cord monitoring for whatever reason properly informs or supports a finding of negligence by either defendant. Its absence or ineffectiveness was a fact of life in the operating theatre at 20.30 and at the very point at which Dr Sparks telephoned Dr Barratt. It was however to my mind a critically significant factor that not only enlivened, but in fact heightened, the need to act conservatively and to proceed expeditiously. It told against the appropriateness of taking an expectant approach when the solution to Mr Hobson's difficulties had not emerged or was not understood.
Seventhly, and with respect to the previous finding, opinions such as that expressed by Dr Sawle, that if the decision to halt the operation had been taken early enough for the surgeons to close the wound, so that Mr Hobson could be turned supine prior to 21.30, the episode of cardiac collapse and spinal cord stroke at that time would have been avoided, do not appear to be controversial. At one level such opinions are afflicted with hindsight, and are no more than self-evident statements about timing: they say nothing about the propriety or otherwise of continuing with the operation after 20.30 or 20.37. They do not amount to a statement of opinion that the earlier hypoxic or hypotensive events mandated an earlier cessation of the surgery. Dr Sawle's opinion was only that the damage sustained by Mr Hobson was much more likely to have happened as a result of the more serious cardiac event at 21.30 than the earlier episodes of hypotension. To similar effect, it was Dr Wilson-MacDonald's opinion that if the surgery had been stopped after the first severe episode of hypoxia [at 20.30], then the paraplegia would probably have been avoided. As I have noted, however, so much appears entirely uncontroversial.
Finally, I do not consider that it was inappropriate for the surgery to have proceeded when it did, having regard to Mr Hobson's existing gliosis on his spinal cord and the reduction of the number of arteries supplying blood to his spinal cord following the first stage of the surgery on 13 November 2009. For a start, the effects of the first stage of the surgery were always going to be part of the surgical equation in the second stage. The two stage approach has never been criticised. Moreover, the factors that warranted the advancement of the second stage of the surgery necessarily included a consideration of immutable historical factors such as Mr Hobson's pre-morbid condition over which Dr Gray and Dr Sparks had no control and which could not be changed. I have previously rejected Dr Westbrook's opinion that the view held by Dr Gray and Dr Sparks, that the proposed surgery was considered to be lifesaving, was erroneous.
[31]
Civil Liability Act 2002 - s 5I
Section 5I of the Act is in the following terms:
"5I No liability for materialisation of inherent risk
(1) A person is not liable in negligence for harm suffered by another person as a result of the materialisation of an inherent risk.
(2) An 'inherent risk' is a risk of something occurring that cannot be avoided by the exercise of reasonable care and skill.
(3) This section does not operate to exclude liability in connection with a duty to warn of a risk."
In Paul v Cooke [2013] NSWCA 311, Leeming JA at [52]-[56] offered the following considerations:
"[52] In my opinion, the appropriate starting point in this appeal is s 5I, which is in these terms…
[53] If a case can conveniently be decided under s 5I, it should be. The language of s 5I reflects the elements of liability which the plaintiff needs to establish. That is why it is framed in terms of the broader causal language of 'as a result of', reflecting the language of s 5A(1) rather than of s 5D(1), and why its opening words are 'A person is not liable in negligence'. That is reinforced by s 5I(3), which carves out from the operation of the section 'to exclude liability' a class of liability connected with a duty to warn. Section 5I does not deny s 5D causation; rather it answers the implicit question posed by the 'claim' contemplated by s 5A(1) negatively: the defendant is not liable for that claim for damages for harm resulting from negligence.
[54] The reasons for my view that s 5I should be applied if it is available are as follows. First, once s 5I is engaged, there is no liability for a failure to exercise reasonable care and skill. The entire inquiry under Part 1A comes to an end.
[55] Secondly, s 5I is unyieldingly prescriptive. In contrast, the confining element in s 5D(1) of 'scope of liability' is burdened with evaluative and contestable elements: the 'appropriate' extension of scope of liability, and 'whether or not and why responsibility for the harm should be imposed'. Whenever a trial or an appeal is determined by reference to s 5D, it is necessary to address those contestable issues, which reflect what McHugh J called the 'common experience of the relevant community': Dovuro Pty Ltd v Wilkins [2003] HCA 51; (2003) 215 CLR 317 at [34], applied by Campbell JA in Lym International Pty Ltd v Marcolongo [2011] NSWCA 303 at [252]-[253]…
[56] Thirdly, it can never be 'appropriate' pursuant to s 5D(1)(b) to extend scope of liability to circumstances excluded by s 5I (or any other of the express exclusions in Part 1A). That is so because, although little guidance is given as to what are the 'relevant things' in s 5D(4) which inform what is appropriate, one such thing must surely be a provision in the self-same Part of the Act which negates liability in the first place."
In my opinion, this case cannot be conveniently decided under this section. In my view, having regard to the considerable evidence marshalled by all parties, the second stage of Mr Hobson's surgery was not attended by an inherent risk that he might suffer a cardiovascular collapse and vascular disturbance causing lower motor neurone injury, such as his anterior spinal artery syndrome, arising out of the circumstances as they occurred. Mr Hobson had a pre-surgical anatomical vulnerability to spinal cord stroke and the effects of hypotension. However, the damage sustained by Mr Hobson was not the materialisation of a risk that was inherent in undergoing posterior instrumented thoracolumbar surgery having regard to his medical condition at the time.
Mr Hobson's medical condition included the following:
1. He suffered from Noonan Syndrome which in his case included a significant lordoscoliosis and associated compromised respiratory function.
2. He had a pre-existing gliosis within his spinal cord at T11/12.
3. He came to the surgery on 17 November 2009 following the necessary division of his intercostal arteries on 13 November 2009.
4. He had sustained a post-operative compression of the left main bronchus as well as significant cardiovascular compression following that first stage of the surgery.
5. He suffered from a deterioration of respiratory function following the first surgery and had developed pneumonia and a collapsed left lung.
Added to these matters was the fact that the second stage of the surgery necessitated a posterior approach requiring that it be performed with Mr Hobson in the prone position. That posture exposed him to the prospect, but not the inevitability, of further cardiopulmonary compression.
However, Mr Hobson's paraplegia could in the circumstances have been avoided by the exercise of reasonable care and skill. Neurological injury, including paralysis, was an inherent risk of the surgery. A negligent failure to abandon the surgery, meaning a failure to exercise reasonable care and skill, before his paraplegia developed was not.
[32]
Civil Liability Act 2002 - s 5O
Section 5O of the Act is in the following terms:
"5O Standard of care for professionals
(1) A person practising a profession ('a professional') does not incur a liability in negligence arising from the provision of a professional service if it is established that the professional acted in a manner that (at the time the service was provided) was widely accepted in Australia by peer professional opinion as competent professional practice.
(2) However, peer professional opinion cannot be relied on for the purposes of this section if the court considers that the opinion is irrational.
(3) The fact that there are differing peer professional opinions widely accepted in Australia concerning a matter does not prevent any one or more (or all) of those opinions being relied on for the purposes of this section.
(4) Peer professional opinion does not have to be universally accepted to be considered widely accepted."
None of the experts in conclave was referred to or asked to comment upon the question of whether or not Dr Gray or Dr Sparks, in providing their relevant professional service, acted in a manner that (at the time the service was provided) was widely accepted in Australia by peer professional opinion as competent professional practice.
On the third day of the hearing I asked Mr Woods of counsel for Dr Gray the following question to which he gave the recorded response:
"HIS HONOUR: Just out of interest, is it pleaded by the defendants that there's a s 5O point that proceeding with the surgery in the absence of spinal monitoring upon a patient whose respiratory condition mandated the use of a paralysing agent, but having regard to the masking effect that that might have on damage to the spinal column, was accepted practice?
WOODS: That's not pleaded specifically, your Honour, but that is dealt with, for example, by Mr Wilson-MacDonald who confirms that it was appropriate to continue in those circumstances."
On the sixth day of the hearing, Dr Manasiev was asked in cross-examination whether Dr Gray was negligent in continuing the operation in the circumstances pleaded. Dr Manasiev confirmed what he said in his report, that it would be considered competent medical practice by Dr Gray to heed Dr Sparks' direction and proceed with the surgery at 18.50, 19.10 and 20.35 and to halt the surgery at 21.20.
Dr Forrest considered that Dr Sparks' anaesthetic management of Mr Hobson was in accordance with widely accepted peer professional opinion in Australia as competent professional practice at the time the service was provided.
As far as I have been able to determine, the evidence about these matters is otherwise completely silent. I have not been able to locate any evidence upon which Mr Hobson proposed to rely from a suitably qualified medical expert that suggested that Dr Manasiev or Dr Forrest should not be accepted. Nowhere in the submissions made on Mr Hobson's behalf is the issue of s 5O even referred to or discussed. Written submissions provided by Dr Gray and Dr Sparks both elaborated upon s 5O, reliance upon which each doctor specifically pleaded. Mr Woods of counsel for Dr Gray also made a brief oral reference to the provision.
Dr Gray and Dr Sparks bear the onus of establishing a defence under s 5O of the Act: Dobler v Halverson (2007) 70 NSWLR 151; [2007] NSWCA 335 at [54]-[61]; Sydney South West Area Health Service v MD (2009) 260 ALR 702; [2009] NSWCA 343 at [21].
As I have previously observed, Dr Manasiev considered that Dr Sparks and Dr Gray were warranted in not halting the surgery before they did and would be considered by widely accepted Australian peer professional opinion to have conformed to competent medical practice by doing so. For the reasons I have given concerning the defendants' negligence, I reject that view.
[33]
Causation
I have concluded that Dr Gray and Dr Sparks were both negligent. I take it to be uncontroversial that Mr Hobson's paraplegia occurred after 21.15 and before 21.30. It follows that if either doctor caused or permitted the operation to continue when the exercise of reasonable care and skill would have indicated and led to the conclusion that it be abandoned by 21.15 at the latest, the damage suffered by Mr Hobson would clearly not have been sustained. That damage was caused by the breach of duty consisting in persisting with the operation when it should have been abandoned. But for the operation continuing past 21.15, Mr Hobson would not have become a paraplegic.
[34]
Conclusions on liability
Mr Hobson's blood gasses demonstrated a clear deterioration in his metabolic state as the surgery progressed. Samples taken at 20.08 and 20.21 demonstrated a very high carbon dioxide level despite various attempts at pulmonary ventilation with a double lumen tube. This was causing significant respiratory acidosis. There were also several episodes of hypotension and reduction in blood oxygenation during the surgery.
From the early stages of the surgery, blood gasses disclosed evidence of an increasing lactate level suggesting inadequate organ perfusion. Blood gas samples at 20.37 and 20.51 indicated significant further deterioration of all parameters demonstrating to Dr Sparks a profound respiratory and metabolic distress. Dr Sparks was aware of this dangerous downward spiral in Mr Hobson's metabolic state. By 20.50 he had tried various means of reversing this deteriorating trend without success. In particular, maintenance of blood pressure and ventilation at reasonable levels after transient drops had failed to address Mr Hobson's dire and deteriorating condition.
Dr Barrett correctly opined that the breast plate of the Jackson table was pressing on Mr Hobson creating cardiac compression and pulmonary artery compression, so that a section of lung was being ventilated but not perfused.
Dr Sparks was negligent in not advising that surgery should have been abandoned no later than approximately 21.00. He was alive to Mr Hobson's metabolic deterioration which would have caused a reasonably competent anaesthetist to call a stop to the surgery. Had the surgery been paused or halted at that time, and Mr Hobson turned supine, he would not have suffered spinal cord damage.
Dr Gray was also negligent for not ceasing surgery at that time. He was being alerted to the problems encountered by Dr Sparks and had the ultimate say in whether to continue or not. He was aware of Mr Hobson's metabolic deterioration which would have caused a reasonably competent orthopaedic surgeon to call a stop to the surgery. I reject the proposition, if Dr Gray advances it, that he was in all respects dependent and reliant upon Dr Sparks concerning Mr Hobson's condition or that the decision about whether to proceed with the surgery or abandon it was, or should have been, that of Dr Sparks alone.
As the conclaves concluded, due to inadequate supply of oxygenated blood to Mr Hobson's spinal cord at 21.30, he suffered an ischaemic spinal cord stroke that resulted in paraplegia.
In my opinion, Dr Gray and Dr Sparks each breached their duty to Mr Hobson by failing to terminate, or to recommend or advise the termination of the surgery on 17 November 2009 following earlier episodes of hypoxia and hypotension (occurring at or about 18.50, 19.10, and 20.35) in the face of related complications reported in the anaesthetic record after approximately 20.37 that evening. They failed at the very least to provide a proper standard of care by not immediately terminating the operation after the completion of Dr Sparks' telephone call with Dr Barratt in the face of the abnormalities shown on the anaesthetic record and with Mr Hobson evidently in uncorrectable respiratory and cardiovascular difficulties for as long as he remained in the prone position.
I also consider that, whether it was or was not below an appropriate standard of care for the operation to proceed without the advantage of spinal cord monitoring, it is presently irrelevant. In this respect I limit my comments to a finding that, because Mr Hobson's respiratory difficulties required the administration of vecuronium, the surgery should have been terminated when it became apparent that no reliable indications of the integrity of Mr Hobson's spinal cord health would be available due to the masking effect of that drug upon informative traces. I have earlier expressed the view, which I maintain, that the absence of spinal cord monitoring, for whatever reason, should have heightened the doctors' need for caution when proceeding without it. I am not satisfied, however, as a matter of causation that Mr Hobson has established that spinal cord monitoring, if operating effectively following Dr Sparks' conversation with Dr Barratt, would have provided a sufficiently timely warning to avoid the damage that occurred. As Dr Lambros opined, there may have been sufficient recovery between the 18.30 dose of vecuronium and the 20.30 dose of neuromuscular function to provide a window of meaningful monitoring, but not thereafter. To like effect, Dr Silbert considered that SSEPs and MEPs would not have detected significant spinal cord electrophysiological abnormalities prior to 21.25.
In this same respect I repeat and specifically accept what Dr Askin had to say on this topic as follows:
"Spinal cord monitoring is only useful if remedial action is possible in the event of deterioration of the monitoring signals. The aim is to reverse the underlying cause of loss of signal as soon as possible and minimise the risk of paralysis.
In this patient however it was not the surgical procedure per se that caused the spinal cord damage rather than the lack of blood supply to the spinal cord. MEP monitoring in this case would not have allowed remedial action given that the only remedial action that allowed the patient to restore blood pressure and PCO2 was to turn the patient supine. Having MEPs running during the time of the physiological crisis would not have expedited the termination of the procedure and changing the patient's position at all. Hence, the loss of MEPs would not have changed the outcome." [Emphasis added]
It follows, having regard to the foregoing, that there should be judgment for Mr Hobson against Dr Gray and Dr Sparks.
[35]
Life expectancy
Mr Hobson was born in February 1985. He was injured on 17 November 2009. For ease of calculation I propose to treat Mr Hobson as being 32 years old precisely. The difference between that age and his actual age in years and months is arithmetically inconsequential for the purposes of calculating damages.
At the conclave of experts on damages, Dr Helprin and Associate Professor Adams agreed that Mr Hobson had a pre-surgical life expectancy of only five years because of his restrictive lung disease and pulmonary hypertension. That somewhat grave prognosis was significantly altered by the corrective surgery performed by the defendants. Each of these experts also agreed that Mr Hobson's life expectancy would have been 85 percent of the normal expected years for his age if the corrective surgery had been successful: his life expectancy would have been reduced by 15 percent due to his pre-existing Noonan Syndrome and related complications. Both doctors agreed that Mr Hobson's present (post-surgical) life expectancy is reduced by 25 percent of the years that would have now normally remained, had he not suffered from Noonan Syndrome and had he not become paraplegic.
Limited to the issue of Noonan Syndrome on life expectancy, Associate Professor Adams offered the following view:
"I think that the impact of Noonan's syndrome itself would reduce Mr Hobson's life expectancy of 78 years by around 30 percent or a life expectancy of around 55 years. This is due to the wide range of factors including potential for malignancy, need for further cardiac interventions, bleeding problems, urinary tract problems and other organ dysfunction."
On the issue of restrictive lung disease, he said this:
"In addition Mr Hobson has the problem of restrictive lung disease and spinal/chest deformity of a degree not common in Noonan's syndrome. This poses a large risk of worsening cardiorespiratory function and development of Cor Pulmonale which has an extremely poor prognosis. I think that the progression of his restrictive lung disease to his level is more likely than not to occur within the next 10 to 15 years and is likely to have a survival of 2 to 5 years…"
Combining these considerations, Associate Professor Adams concluded:
"Putting these two factors together I think that Mr Hobson's life expectancy would be somewhere in the range of 45 to 50 years of age."
Associate Professor Yeo additionally considers that Mr Hobson's paraplegia will reduce his life expectancy:
"On the balance of probabilities, the patient will have the additional risk of complications from his paraplegia and I would therefore apply a further 10 percent discount for these anticipated additional problems to Professor Adams' estimate.
If, as calculated by Professor Adams, Mr Hobson has an expected lifetime of 20 further years, then I would reduce that estimate by 10 percent making my estimate now of this life expectancy 18 further years".
Dr Dalton also considered that Mr Hobson's life expectancy has been reduced by his comorbidities:
"[L]ife expectancy is probably reduced by about 10 years on the basis that he is essentially a T10 paraplegic. I believe that his life expectancy is further reduced because of the other medical conditions which exist in this case due to the increased risk of respiratory failure and other cardiopulmonary complications…
The main factor influencing his life expectancy that has arisen directly as a result of the spinal cord injury is the increased risk of urinary tract infection and renal complications. There is a small increased risk of septicaemia secondary to skin and soft tissue infection were he to develop pressure sores. Patients who have suffered spinal cord injury are at greater risk of respiratory infections leading to pneumonia and presumably this risk is greater in Mr [Hobson]'s case because of his co-existing kyphoscoliosis and longstanding respiratory lung disease."
Dr Flecknoe-Brown additionally considered the impact of Mr Hobson's platelet dysfunction on his life expectancy:
"A mild platelet dysfunction such as this would have only a slight impact on Mr Hobson's life expectancy. If he were to fall and bump his head severely as he ages, he may develop an intracranial haemorrhage. Other haemorrhagic complications such as gastrointestinal haemorrhage relating to peptic ulcer are also possible. I would estimate that the direct effect of the platelet dysfunction on Mr Hobson's life expectancy would be an average reduction of five years or less on his life expectancy."
Mr Hobson relies primarily on Dr Helprin. Dr Collins offers an opinion that to some extent aligns with the defendants' experts:
"There is little evidence in the literature to suggest that the life expectancy of an individual is reduced by the diagnosis of Noonan syndrome per se…Mr Hobson's own life expectancy is likely to be reduced by his medical comorbidities of severe chest deformity and restrictive lung disease, which if untreated would have increased his risk of right sided heart failure…In addition, Mr Hobson now has a lower limb paraplegia which is likely to reduce his life expectancy."
As Dr Yeo observed, one can search the literature and not find a Noonan Syndrome survivor over the age of 61. Dr Adams' original calculations produced a life expectancy to age 55 years. Mr Hobson contends for a life expectancy to age 71. The defendants conceded that a compromise was justified on the evidence.
As I have noted, Mr Hobson is now 32 years of age. Despite his critical condition in the ICU prior to his operation, and notwithstanding the considerable intraoperative cardiovascular and respiratory assaults upon him, he quite remarkably survived. Although my ability to make findings of a technical medical nature based upon observations of Mr Hobson in the courtroom setting is necessarily constrained, he rather impressed me as a particularly resilient individual. His experiences in the operating theatre and since have tended to confirm that impression. Moreover, in the particular events that have occurred, Mr Hobson is likely from now on and for the rest of his life to receive close and constant expert medical attention of the highest order. These factors combine in my view to support a finding, admittedly somewhat impressionistic, of a future life expectancy of 30 years or to the age of 62.
[36]
Non-economic loss
Mr Hobson's original assessment of his own non-economic loss was 85 percent of a most extreme case pursuant to s 16 of the Civil Liability Act. His current contention is that he is now entitled to damages for non-economic loss calculated as 100 percent of a most extreme case.
Mr Hobson is significantly disabled. His life expectancy has been relevantly reduced by the effects upon him of his paraplegia. He was formerly active within the confining limits of his respiratory restrictions and associated consequences of his Noonan Syndrome. Even so, he might reasonably have expected to enjoy a considerably enhanced and improved lifestyle and physical existence following corrective surgery if his paraplegia had not intervened. His non-economic loss is therefore permanent and severe.
I do not consider that Mr Hobson's loss equates to a most extreme case. It is however my opinion that his original assessment of 85 percent was entirely accurate. It is regrettably possible to imagine cases more extreme than that of Mr Hobson. He should be awarded damages of $514,500 under this head at that rate.
[37]
Economic loss - generally
The defendants argued as follows.
Dr Dalton considered the position if Mr Hobson's injuries had not been sustained:
"In my opinion it is unlikely that Mr Hobson would have been able to work as a veterinary nurse under this scenario without physical restrictions. That is to say, he would have been able to work as a veterinary nurse caring for small animals but he would have struggled to lift, carry and manage larger animals.
Presuming he had completed his studies at Richmond TAFE then he would have been able to work full-time as a veterinary nurse but with physical restrictions due to his reduced capacity for lifting, carrying, manual handling and also his reduced exercise tolerance. I also believe that over the course of time his ability to work in such a role would have gradually diminished due to complications arising from his severe kyphoscoliosis and restrictive lung disease."
Dr Dalton additionally considered that had the injury not occurred, this would have "increased his prospects of finding work as a veterinary nurse, albeit on suitable duties, or alternative employment of a semi-sedentary nature". As a consequence of Mr Hobson's paraplegia, Dr Dalton was of the following opinion:
"This would limit his prospects of finding work on the open labour market given that he is now best suited to clerical, administrative or other sedentary type work. He would also need a workplace which is wheelchair accessible and his prospects for finding work on the open labour market are reduced as a result of his paraplegia."
Associate Professor Yeo offered a similar analysis:
"Mr Hobson has limited potential for employment in open industry but has demonstrated his interest to complete his studies as a veterinary nurse. I understand this course will be completed at the end of 2013 and I would then expect the patient to seek employment over a further six months to twelve months and then hopefully be successful in obtaining part-time employment for up to thirty hours per week until the necessity for him to retire earlier than usual at the age of fifty years. This retirement will become necessary because of the patient's paraplegia necessitating the use of the wheelchair and the inevitable complications of advancing years which increase his proneness to arthritis with painful shoulders and diminishing agility which is already limited by his permanent paraplegia."
Ms Hardy offered a similar opinion:
"Mr Hobson has demonstrated his commitment to gaining employment by undertaking a two-day per week volunteer position since his injury. In the absence of his injury, it is assumed he would have completed his vet nursing qualification and commenced employment as a vet nurse in either a part-time or full-time capacity. As a result of his injury there are some aspects of vet nursing that he is unable to perform and workplace access issues. His need for a wheelchair reduced the number of potential employment options due to the need for a wheelchair accessible veterinary clinic, which will make it more difficult to gain employment than it would have been in the absence of a spinal cord injury."
With respect to alternative employment, Ms Hardy considered that:
"Mr Hobson would be capable of undertaking work that involves being seated at a desk, using phones, computers, and/or engaging with people should he be willing to undertake further job training. He is limited in the type of environments he can access in a wheelchair. He will require significant assistance to locate a supportive employer who is willing to give him an opportunity. An employment support service that has experience in placing people with spinal cord injury into jobs would be necessary…Should Mr Hobson gain paid employment I believe it is more probable than not, that this would constitute part-time employment of 20-30 hours per week."
The defendants submitted that there is a significant prospect that Mr Hobson's earning capacity would have been considerably diminished even if the surgery had proceeded without incident. Dr Cree considered that, even with successful surgery, veterinary nursing may have been beyond his capabilities. In the damages conclave report all experts deferred to the opinion of Dr Dalton in respect of Mr Hobson's employment prospects and loss of earning capacity.
[38]
Past economic loss
Mr Hobson was not employed at the time leading up to his operation, but was in receipt of a disability support pension. He had previously worked for a short period between 9 August 2008 and 1 October 2008 as a veterinary nurse at the Greater Western Veterinary Hospital and received net wages during that period of $160 net. He otherwise worked in a voluntary capacity doing that kind of work. Mr Hobson claims past economic loss upon the assumption that he would have commenced full time work as a veterinary nurse on about 1 January 2011. It is agreed that an arithmetical calculation of award wages in that role for the period from 1 January 2011 until 17 November 2016 is $210,000.
The defendant's contend that Mr Hobson's capacity for work would have been reduced by reason of his Noonan Syndrome. Specifically, although not exclusively, they submitted that his ability to deal with animals would have been limited to small animals, thus restricting either his employability in general or his utility as a full time employee in particular. So far as the evidence reveals it, neither Mr Hobson's work record on the one hand nor his true capacities in the workplace on the other hand has been well illuminated. Any fair determination of Mr Hobson's pre-injury earning capacity is therefore a matter that eludes any obviously supportable calculation.
Mr Hobson's claim after a deduction of ten percent for vicissitudes is $190,000. The arithmetic supporting this claim is accepted by the defendants. The defendants have indicated a preparedness to allow the sum of $150,000 without reference to an arithmetical framework. Doing the best I can I consider that Mr Hobson had a work capacity that could have been exploited in some form of appropriate work. I do not consider that his capacity should be measured only by the prospect that he could have obtained or retained work in his preferred field. I think that a net sum of $175,000 fairly represents Mr Hobson's past economic loss.
[39]
Past loss of superannuation
Mr Hobson's loss under this head amounts to $175,000 x 11.5 percent or $20,125.
[40]
Future economic loss
Mr Hobson's future working life does not automatically correspond to his life expectancy, even though in my opinion his life expectancy is less than what might be considered as an ordinary or usual retirement age. Indeed, Mr Hobson specifically concedes that he would be unlikely to work beyond the age of 60 years. In my opinion, that concession is overly generous to Mr Hobson. Although the difference may seem small, I would not expect Mr Hobson to be able to work productively much, if at all, beyond the age of 50 years. That is because the collocation of factors that are likely to combine to reduce his life expectancy could not realistically be expected to fall in simultaneously at the age of 62 years. Factors identified by the evidence, such as the potential for malignancy, cardiac interventions, bleeding problems, urinary tract infections and related problems, as well as organ dysfunction, are likely to affect Mr Hobson at different times and in differing degrees of seriousness. Added to these factors are Mr Hobson's underlying restrictive lung disease and spinal deformity. The defendants have contended that these things would have operated progressively so as to reduce Mr Hobson's employability, rendering him on their assessment unemployable beyond the age of 45 or 50 years.
I consider that range to be too pessimistic. I agree that these factors are likely to become patent progressively rather than simultaneously. I do not consider that they will operate in combination finally to render Mr Hobson unemployable until approximately 10 years before his statistically anticipated death. In my view Mr Hobson is likely to remain employed in one form or another until the age of 52 years, or another 20 years in round terms.
Mr Hobson and the defendants have all proceeded upon the assumption that a net weekly sum of $725 is an appropriate base figure for calculation purposes, representing net weekly earnings of a level 4 veterinary nurse under the Animal Care and Veterinary Services Award 2010. Applying a five percent discount rate multiplier of 666.4 over 20 years at $725 per week produces an amount of $483,140.
Mr Hobson contends that a discount for vicissitudes of 15 percent should apply to that sum. The defendants on the other hand suggest that a discount in the order of 30 percent should apply. That is said to be because Mr Hobson may not be able to perform all of the duties of a level 4 veterinary nurse and may suffer from an inability to compete on the open labour market by reason of his underlying Noonan Syndrome. In my opinion the negative effects of any additional factors applying in Mr Hobson's case have already been factored into my conclusion that he will not work until his expected date of death but will in all likelihood be forced to leave the work force at the age of 52 years. Any extra discount for the vicissitudes to which the defendants draw attention would in my view be a species of unfair double counting.
I consider that Mr Hobson is entitled to damages for future economic loss in the amount of $410,670.
[41]
Future loss of superannuation
Mr Hobson's loss under this head amounts to $410,670 x 11.5 percent or $47,225.
[42]
Domestic care generally
The defendants proffered the following matters for consideration.
Dr Dalton said this:
"At the current time Mr [Hobson] is independent with all aspects of self-care. He is able to access shopping centres but needs assistance with transport or would need to use a home delivery service or online shopping. He requires assistance with housework, cleaning, home maintenance and gardening. In his current accommodation he relies on gratuitous assistance from his family but without that he would require 4 hrs assistance a week for housework and general cleaning…
He currently does not require any personal assistance as he is managing his bladder and bowel care independently. His requirements for domestic assistance, gardening and home maintenance will depend on his living arrangements. Given his independence in transfers he does not require assistance with community access and in his case there are no requirements for child-care services. The allowance for home nursing and respite care does not apply at this point in time. There should be some allowance for hospitalisation in the future should he develop any complications related to his neurogenic bladder and bowel. This is clearly difficult to quantify but there should be some allowance for the fact that Mr Hobson may require hospitalisation from time to time. A reasonable estimate would be to allow for one week of hospitalisation every four years. This includes estimated future costs for home nursing."
Ms Hardy calculated domestic assistance for Mr Hobson at 3 hours per week, garden maintenance at 1 hour per week and handyman services at 12 hours per year. This does not include allowance for daily assistance with meal preparation since Mr Hobson would have some capacity to undertake this for himself provided he had a fully wheelchair accessible kitchen. Allowance for assistance with transport is not included, on the assumption that provisions are made for Mr Hobson to gain his driver's licence and have access to a hand controlled vehicle and wheelchair hoist when required.
Ms Hardy additionally considered that:
"Some allowance for provision of attendant care services may be reasonable and necessary in the future. Allowance for an additional 3 hours assistance per day for a period of 6 weeks following injury or significant illness resulting in Mr Hobson being temporarily unable to care for himself is reasonable and may be necessary on 2-3 occasions."
In the joint conclave report on damages, Dr Dalton's view was that Mr Hobson required 10 hours of care per week. Despite his more generous assessment (21 hours per week and 28 hours after 50 years of age) Professor Yeo ultimately conceded in evidence that Mr Hobson only requires two to three hours per week for domestic cleaning, could order groceries online and up until the age of 50 would be able to attend, in large measure, to many of the tasks in respect of which domestic assistance and personal care is claimed.
Given the opinions of Dr Dalton in accordance with the Lifetime Care and Support Scheme Guideline, and the pragmatic concessions by Professor Yeo, the defendants submitted that Mr Hobson's claims were unreasonable. In the context of the assessments by the rehabilitation physicians and occupational therapists of the actual need for domestic assistance in his circumstances, a reasonable compromise would be to award 14 hours per week for domestic assistance up to and beyond age 50. That analysis is said to be designed to take into account Mr Hobson's variable needs as he ages. An alternative approach would be to allow ten hours up to age 50, and, say 18 hours thereafter. These allowances accommodate at least partly Mr Hobson's additional needs for holidays and the like.
[43]
Past domestic care
Mr Hobson claims 40 hours of gratuitous domestic assistance and personal care per week from the date of his admission to Ryde Rehabilitation Hospital in February 2010 until the present time. That claim amounts in total to some $325,000 as at the end of 2016. The defendants concede the arithmetical foundation for that calculation. However, the claim has necessarily to be modified in the light of the evidence of Siobhan Hobson, Mr Hobson's sister, which was in these terms:
"Q. Your catalogue of assistance doesn't deal with how many hours a week you're involved in those various tasks.
A. Yeah.
Q. You specify at E, twice a week taking your brother to his place of voluntary work and return. Just that alone, how much time does that take you?
A. Probably, like - I take him, I come back and then I pick him up when he rings, so maybe four hours all up.
Q. Each time?
A. Well, that's to go get, to take him, come home and then in the evening come pick him up.
Q. And is that once or twice?
A. Twice a week.
Q. And so we're clear about that, does that mean that at least eight hours are spent doing that?
A. Correct.
Q. Are you able to give an estimate of overall how much time you would spend a week on these various tasks that you've nominated?
A. 20 or more, maybe."
The defendants concede that Mr Hobson required domestic assistance following his discharge from Ryde Rehabilitation Hospital on 31 May 2010 until the date of my assessment. The defendants do not concede that Mr Hobson required 40 hours of assistance over that time. The defendants submit that an average of 20 hours per week through the relevant period would be appropriate. They contend that a sum of $185,250 would be a proper sum under this head of damages, once again up until the end of 2016.
Calculation of hours required or provided for domestic assistance in cases such as this is notoriously unscientific and draws upon usually undocumented recollections of people whose principal concern is understandably the provision of appropriate care and assistance rather than the recording of how long it took to provide it. Ms Hobson's assessment of "20 or more, maybe" is a perfect example of an honest recollection, the accuracy of which cannot ever confidently be tested.
It is in my opinion a mistake to underestimate the challenges for someone such as Mr Hobson, who is rendered a paraplegic, and who is required to come to terms with the mental and physical consequences of that dreadful discovery. Accommodating to life with such a significant disability is too easily discounted as an everyday vicissitude in the life of the injured person. In my opinion, it is not a mistake to err on the side of overstating, rather than understating, the hours of assistance that Mr Hobson required following his discharge from rehabilitation. His sister was very conservative in her evidence in my assessment and played down what the true difficulties probably were.
In my opinion Mr Hobson is properly compensated by a sum calculated upon the basis of 30 hours per week of domestic assistance during the period to May 2017. That produces a sum of approximately $285,000 in round figures, which I propose to allow.
[44]
Nursing care after age 40
Mr Hobson claims nursing consultation and treatment at the rate of two hours per week after the age of 40 years at $81.88 per hour. It is not apparently contested that this is supported by the findings of the experts in conclave. The sum of $163.76 per week deferred for 8 years until the age of 40 years on a life multiplier of 822 to age 62 years (M476.5) is $78,030.
[45]
Domestic assistance up to age 62
The members of the expert damages conclave agreed that after the age of 50 years Mr Hobson would likely require attendant care of two hours per day. That could be provided by a trained nursing aid or a personal care worker. Dr Dalton was of the view that ten hours of domestic assistance per week would be required, based on the upper level of recommended domestic assistance in the guidelines referred to in his report. Dr Yeo considered that Mr Hobson would require 21 hours of domestic assistance per week and four hours per day after the age of 50 years. Dr Dalton considered that provision of one to two hours per week of handyman assistance was reasonable. That level of assistance would necessarily be a function of Mr Hobson's particular living arrangements from time to time. Dr Yeo was of the opinion that Mr Hobson would require three hours per week of handyman assistance until the age of 50 years and four hours thereafter.
Mr Hobson claimed 21 hours of domestic assistance per week at $45 per hour and three hours per week of handyman and gardening maintenance at $50 per hour or a total of $1,095 per week. At that weekly cost to age 62 years, at a 30 year multiplier of 822, a total amount of $900,090 is produced.
The defendants emphasised that Mr Hobson would benefit from the proposed housing modifications. On that basis they were prepared to concede 14 hours per week of assistance as a compromise. At a weekly cost of $376 to age 50 years, at an 18 year multiplier of 625, a total amount of $235,000 is produced. The defendants also accepted that Mr Hobson will require, in addition to agreed building maintenance costs, one to two hours per week of handyman assistance. At $75 per week, a sum of $46,875 is produced. These two amounts total $281,875.
After the age of 50 years, the defendants contend that Mr Hobson will require 18 hours of domestic assistance per week together with 2 hours per day of attendant care as well as 1.5 hours per week of handyman assistance. The defendants contended that Mr Hobson was entitled to 12 years at these rates until age 62 years appropriately deferred.
I feel compelled to resort to what I consider to be a common sense understanding and appreciation of the nature and extent of the difficulties confronting an individual who has lost the use of his or her legs at the age of 30 years or so. The apparently dispassionate and empirical analyses of these difficulties does not often or always in my opinion pay sufficient regard to the monumental adjustments in life that such unfortunately afflicted individuals are forced to make, not to say endure. The suggestion that three hours per day of assistance for Mr Hobson is on the generous side, even taking into account modifications to his home environment, seems to me to ignore the realities of life. By analogy with the time it takes to care for an infant, a disabled and paraplegic adult would in my view conservatively attract the need for at least 21 hours per week of domestic assistance. Having regard to the view I have taken, there does not appear to me to be any practical reason to distinguish or differentiate between the periods up to Mr Hobson's 50th birthday and beyond it.
I consider that Mr Hobson's calculations are realistic and reasonable. I propose to allow the sum of $900,090 that he claims.
[46]
Past treatment expenses
Damages under this head have been agreed at $200,000.
[47]
Future treatment expenses
Damages under this head have been agreed at $200,000.
[48]
Holiday care
Mr Hobson claims annual holiday care of 24-hourly assistance per day for three weeks at a total annual cost of $23,930, together with the sum per annum of $10,000 additional travel and accommodation costs for the carer. That is said to produce a total discounted sum over Mr Hobson's 30 year expected life at the rate of $652.50 per week of $536,355.
The defendants contest this claim in significant respects. They accept that Mr Hobson may require some assistance with holiday travel. However, as he aged he would have required similar assistance in any event as a result of the ongoing and progressive effects of Noonan Syndrome. It is submitted that it would be likely in such circumstances that Mr Hobson would have had reduced travel opportunities as a result of his condition and what would have been his limited financial resources having regard to his pre-morbid occupational prospects. The defendants proposed a cushion in the amount of $10,000 per annum covering the costs of the carer on either a gratuitous or commercial basis and including the carer's additional travel and accommodation expenses, as well as any additional costs incurred by Mr Hobson such as business class airfares. That approach produces a sum of $158,000.
In my opinion, a reasonable approach lies somewhere in between these two approaches. Allowance has already been made for Mr Hobson's future domestic and nursing assistance. Mr Hobson's approach makes no allowance for the double counting of that head of damages for the annual periods when he is on vacation. The real prospects are that Mr Hobson would not have been able to afford annual vacations away from home that required even modest financial expenditure. That prospect is also likely to have been affected by his progressing Noonan Syndrome symptoms on the one hand with a corresponding disinclination to travel far from home, as he became significantly more severely affected as he approached the age of 62, on the other hand.
As with any calculation of this type, significant assumptions resting on what are very often frail foundations have necessarily to be made. I prefer the defendants' approach but I consider that their annual allowance is too niggardly. I would allow a buffer of $20,000 per annum, producing over 30 years a discounted total of $316,150.
[49]
Motor vehicle expenses
Mr Hobson claims capital motor vehicle costs of $32,600 together with replacement costs of $68,220 and running costs of $190,900 totalling $291,730.
The defendants contend that there is a conceptual error in Mr Hobson's base calculations. He claims both capital and running costs. The amounts claimed for running costs are based upon the NRMA Car Operating Cost Calculators for Toyota Corolla and Chrysler Grand Voyager. The NRMA document provides an average whole of life weekly cost based on new to five year private operating cost in cents per kilometres and dollars per week travelling 15,000 kilometres per annum. The whole of life cost includes the purchase price and takes into account depreciation and the value of the vehicle upon resale. In those circumstances Mr Hobson's calculations contain significant double counting. Moreover, Mr Hobson has no need for an electric wheelchair at the present and would therefore not need the Chrysler Voyager until much later in life. In those circumstances any allowance for such a vehicle in the future would need to be appropriately discounted.
The defendants contend that Mr Hobson is likely to require a suitably modified vehicle with hand controls. The discounted capital and maintenance costs associated with those modifications are approximately $4,500.
The defendants accept that Mr Hobson does require a larger than average vehicle and accept that such vehicles cost more to purchase and to run. They estimate these extra costs at $50 per week. Over the plaintiff's lifetime to 62 years, that cost would amount to $41,100.
The defendants also accept that at some point Mr Hobson may require a mechanical lifter to facilitate the placement of his wheelchair components into the vehicle. They estimate that the need for that equipment would not arise until about the age of 40 years, or eight years from now. The cost of the lifter is $17,000 approximately, deferred for eight years, which produces a capital cost of $11,510.
The defendants submit that by no earlier than around the age of 50, Mr Hobson will require a motorised wheelchair or the equivalent. Accepting that the cost of vehicle modification to accommodate such a wheelchair is $31,500, then the deferred cost to age 50 is $13,105.
These sums total $70,115. Taking into account annualised replacement costs or the prospect that Mr Hobson may choose to continue his current arrangements relying on family and friends or take a combination of gratuitous assistance and taxis, at the estimated sum of $123 per week, amounting to $101,105 over his lifetime, the defendants propose a buffer under this head of loss in the amount of $125,000.
I accept that there are errors in Mr Hobson's calculations of the type pointed out by the defendants. Having had the opportunity to observe Mr Hobson in the witness box, however, I consider that he remains a relatively young man of quite some modest resolve and independence. If driving a modified vehicle that would provide him with the greatest degree of independence were an available option, I consider that he would adopt that course.
Doing the best I can, I consider that Mr Hobson is entitled to damages as a buffer under this head of loss in the sum of $240,000.
[50]
Equipment requirements
The parties are effectively agreed upon damages under this head, being only $30,000 apart on their competing assessments. I propose to allow the sum of $145,000 as the mid-point between the parties' respective contentions.
[51]
Building expenses and maintenance
Damages under this head have been agreed at $249,105. Running and maintenance costs have been agreed at $57.40 per week. Calculation of that weekly sum over Mr Hobson's 30 year life expectancy produces a figure of $47,182. I allow the total sum of $296,285 under this head.
[52]
Conclusions and orders
Upon the basis of my findings and calculations, there should be judgment for Mr Hobson against the second and fourth defendants for $3,828,075 plus costs. Allowing for the prospect of arithmetical error, I will invite the parties within seven days to draw any such error or other like concern to my attention before my orders are made final.
[53]
Amendments
17 May 2017 - Correction of legal representatives
23 May 2017 - Correction of legal representatives
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Decision last updated: 23 May 2017