Hobson v Northern Sydney Local Health District

[2017] NSWSC 589

Supreme Court

New South Wales

• Amendment notes

Medium Neutral Citation:	Hobson v Northern Sydney Local Health District [2017] NSWSC 589
Hearing dates:	7–11, 14–17, 21–22 November 2016
Date of orders:	17 May 2017
Decision date:	17 May 2017
Jurisdiction:	Common Law
Before:	Harrison J
Decision:	Judgment for the plaintiff against the second and fourth defendants for $3,828,075 plus costs.
Catchwords:	NEGLIGENCE – medical negligence – where plaintiff with Noonan Syndrome rendered paraplegic in surgery to correct spinal deformity and associated respiratory difficulties – where plaintiff’s intraoperative condition deteriorated significantly – where operation halted but not before the plaintiff suffered a spinal stroke that led to paraplegia – whether operation should have been abandoned before this occurred – whether reasonable to continue with operation having regard to plaintiff’s pre-operative condition – whether operation should have been abandoned when spinal monitoring became ineffective following administration of vecuronium to assist ventilation
Legislation Cited:	Civil Liability Act 2002
Cases Cited:	Dobler v Halverson (2007) 70 NSWLR 151; [2007] NSWCA 335 Paul v Cooke [2013] NSWCA 311 Sydney South West Area Health Service v MD (2009) 260 ALR 702; [2009] NSWCA 343
Category:	Principal judgment
Parties:	Brendan Hobson (Plaintiff) Northern Sydney Local Health District (First Defendant) Dr Randolph Gray (Second Defendant) Dr Jim Lagopoulos (Third Defendant) Dr Christopher Sparks (Fourth Defendant)
Representation:	Counsel: P Menzies QC with R de Meyrick (Plaintiff) M K Scott (First Defendant) S A Woods with T Hackett (Second Defendant) M J Walsh SC (Third Defendant) K Burke (Fourth Defendant)   Solicitors: T D Kelly & Co (Plaintiff) Henry Davis York (First Defendant) Norton Rose Fulbright (Second Defendant) Meridian Lawyers (Third Defendant) Avant Law Pty Ltd (Fourth Defendant)
File Number(s):	2013/00080267
Publication restriction:	Nil

Judgment

1. 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.

2. 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.

3. 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.

4. 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.

5. 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.

7. Failing to carry out or cause to be carried out spinal cord monitoring effectively or at all.

8. Failing to pause or cease the surgery when either a baseline had not been achieved and/or the results were reported to be abnormal.

9. 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.

10. 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.

11. Continuing the surgery with Mr Hobson in the prone position.

12. Commencing the surgery before baseline spinal cord monitoring was established.

6. 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.

7. 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.

Spinal cord monitoring

8. 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.

9. 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.

10. 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.

11. 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.

12. 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.

13. 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.

Background

14. 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.

15. 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”.

16. 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.

Liability

Dr Gray’s evidence

17. 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.

18. 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.

19. 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.

20. 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.

21. 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.

22. 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.”

23. Dr Gray was cross-examined about these recollections. This is referred to later in these reasons.

24. 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.

25. The second stage of the originally planned surgery was successfully completed on 11 December 2009.

Dr Sparks’ evidence

26. 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.

27. 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.

28. 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.

29. 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.

30. 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.

31. 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.”

32. Dr Sparks was cross-examined about these recollections. This is also referred to later in these reasons.

33. 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.

Expert evidence – Mr Hobson

Dr Jon Westbrook

34. 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.

35. 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.”

36. 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.”

37. 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.”

38. 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.”

Dr Michael A Johnson

39. 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.”

Dr Peter D Heath

40. 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.”

41. 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”.

42. 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.”

43. 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.”

Dr Peter Richards

44. 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.”

Dr James Wilson-MacDonald

45. 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.”

46. 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.”

47. 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.”

48. 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.”

49. 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.”

50. 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.”

51. 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.”

52. 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.”

Dr Guy V Sawle

53. 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.”

54. 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.”

55. 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.

314. I consider that Mr Hobson’s calculations are realistic and reasonable. I propose to allow the sum of $900,090 that he claims.

Past treatment expenses

320. Damages under this head have been agreed at $200,000.

Future treatment expenses

321. Damages under this head have been agreed at $200,000.

Holiday care

322. 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.

323. 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.

324. 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.

325. 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.

Motor vehicle expenses

326. 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.

327. 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.

328. 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.

329. 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.

330. 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.

331. 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.

332. 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.

333. 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.

334. 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.

Equipment requirements

335. 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.

Building expenses and maintenance

336. 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.

Conclusions and orders

337. 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.

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Amendments

17 May 2017 - Correction of legal representatives

23 May 2017 - Correction of legal representatives

Decision last updated: 23 May 2017