Sumner v Royal Surrey County Hospital NHS Foundation Trust & Anor

This is a claim for clinical negligence arising from the admittedly inappropriate treatment of a patient with an unstable 3 column fracture of the spine which was initially misdiagnosed as stable.

In the early hours of the morning on Boxing Day 2010, the Claimant, Mrs Susan Sumner (then aged 68) fell down a flight of stairs at her daughter’s home in Surrey where she had been staying over the Christmas period. The notes taken by the paramedics state that she lost her balance and fell down 13+ steps head first, landing on her head. According to the notes taken at the time of her admission to the A&E department of the Royal Surrey County Hospital at 2.45 am, she fell “from top to bottom of the stairs whilst going up”. That is the only factual evidence before the court as to the mechanism of her fall. Although the fall was witnessed by her daughter Maureen Sumner-Smith, who gave evidence at the trial, she was asked no questions about it. Mrs Sumner herself has no recollection of the accident or its aftermath.

Mrs Sumner initially complained of pain in her neck and upper back, and what was recorded by the paramedics as pain in her left arm and left shoulder. When the ambulance arrived around 15 minutes after the accident, she had full mobility in all four limbs, no pins and needles, and no neurological deficit. However, in order to move her to the A&E department she was (correctly) long boarded, with a collar and head blocks in order to protect her spine in case she had suffered a spinal injury. When she arrived in A&E she was fully alert, and complaining of arm pain and pain in her right shoulder (which it later transpired came from a fracture to her humerus). She was examined by a doctor at 3.55am who recorded that she had pain in her neck and in her upper limbs, that she was “weak on hands”, and had pain in her shoulder (presumably the right, though it does not say which) and arms. The collar and blocks were on, but she was still moving her head and neck. Her legs were functioning normally (motor power 5/5 on the ASIA scale, which ranges from 0/5 (no power) to 5/5 (full power)).

Mrs Sumner was rolled over and the doctor examined her back; she complained of pain in the C5, 6 and 7 area. The doctor formed the view that she had suffered an injury to her cervical spine and drew a diagram illustrating the reduced power in her arms; upper limbs 4/5 bilateral, lower limbs 5/5. An X-ray and CT scan were requested. The CT scan was taken at around 6am. The report stated:

“The cervical lordosis is maintained. There is some degenerative change seen at C5/6 with loss of the disc space and anterior and posterior osteophytes. There is very minor anterior subluxation of C6 on C7 and note is made of a fracture through the facet joint and pars intra-articularis on the left at C7 and a fracture through the right foramen transverse area at the same level. There also appears to be subluxation at the C6/7 facet joint on the right.” (emphasis added).

Subluxation means a slippage out of position. It was common ground that the subluxation at the right facet joint noted on the right hand side in the final sentence of the report would have had no impact on the spinal cord.

Mrs Sumner was seen again by a doctor at 8am. She was recorded as mainly complaining of her right arm/elbow/wrist. The spinal fracture shown by the CT scan was noted. The records show she was complaining of a loss of sensation in the left arm. However muscle power was still assessed as grade 4/5 bilaterally, believed to be secondary to pain, with no lower limb symptoms. She was appropriately treated at that juncture, by being kept immobile in bed with the head collar and neck blocks, and her spine in line. The plan at that stage was to discuss her case with the neurology team at St George’s Hospital to determine if the C6/7 fracture was stable and whether it was necessary to operate. Such an operation is designed to hold the spine in place so as to ensure that it is kept in line and stable, to enable the fracture to heal without the danger of further trauma to the spinal cord being caused by movement. The most important factor which causes damage to a spinal cord after injury is lack of oxygen, because the central nervous neurones cannot survive on anything other than the oxygen supplied. Thus it is vital to protect against anything that might cause a further interruption to the oxygen supply.

The principles of sound management of spinal cord injuries are set out in the British Orthopaedic Association Guidelines published in January 2006, which were adopted in full by the National Spinal Cord Injury Strategy Board (“NSCISB”) in a paper entitled “The Initial Management of Adults with Spinal Cord Injuries” published on 18 May 2012. The NSCISB has since been replaced by a different body, but the Claimant’s spinal expert, Mr Gardner, explained that the new body consists of the same people, and it and its predecessor are part of the corpus in the English NHS which governs appropriate management of spinal cord injuries.

The Guidelines provide that at the site of cord injury there will be a zone of critical ischaemia. This zone may expand with poor oxygen saturation or poor perfusion. Acute spinal injury must be nursed flat, (emphasis as in the original). In the acute phase of spinal cord injury management, where the spine has not been stabilised, and it is necessary to move the patient, the patient should be log rolled (by five persons). That is how the First Defendant managed Mrs Sumner until the mistake was made of assuming that the fracture was stable, and mobilisation was permitted. The Guidelines make no distinction between the management of flexion injuries and hyperextension injuries. Hyperextension of the spine occurs when the head is thrown back; flexion is when it moves forward. The question whether Mrs Sumner’s injury was a flexion or hyperextension injury assumed a central importance in the course of the trial, for reasons that will become apparent.

At 5.30pm on 26 December, the neurology team at St George’s discussed Mrs Sumner’s case and noted that the fracture extended from the lamina into the facet. They concluded that the fracture was likely to be stable, and therefore it was decided to put her in a hard collar for six weeks and mobilise as pain allowed. That was an error: the fracture was unstable, and the conclusion that it was stable could not be safely drawn on the basis of the CT scan alone. She should have had an MRI scan. An unstable fracture should not be treated simply by putting the patient in a hard collar, because the collar still allows enough movement of the head and neck to cause damage to the spine.

On 27 December Mrs Sumner was admitted to the ward, where a risk assessment was completed by the orthopaedic physiotherapist at 1pm. The hard collar fitted by A&E was found to be fitting inadequately and was changed. Mrs Sumner had been complaining of intermittent sensations similar to electric shocks in the left upper arm, and difficulty in pressing the call bell, but no additional neurological symptoms were observed after the collar change. The physiotherapist noted that Mrs Sumner had been sitting up at 30 degrees in the morning. She was returned to flat bed rest. Prior to the collar change, the power in her upper limbs was tested; the left side was now much weaker (muscle power recorded at 2/5 and 3/5 at C6-C8) but the muscle power remained at 4/5 on the right. She also had reduced sensation in the C6/7 dermatome on the left (the same side as the fracture). Her lower limbs were still normal (5/5) at that stage. The physiotherapist noted a clinical impression of deteriorating neurology in the C6/C7 dermatome/myotomes since admission, queried why this should be, and indicated that there should be an urgent review by a senior orthopod prior to further mobilisation.

In the period from then up to and including 29 December, Mrs Sumner was kept flat and “log rolled” in accordance with the guidance. The neurological examination on the morning of 28 December has similar test results to that taken at 1pm the previous day in respect of the motor power in her arms: left 2/5, right 4/5. The ASIA chart taken in between those two readings, at 6 pm on 27 December, appears to indicate a considerable improvement in power in her left arm, but the most likely explanation for this is assessment error. Mr Gardner accepted that the recorded level of improvement was unlikely to have occurred in that short timescale.

Meanwhile, the neurosurgical registrar at St George’s had recommended a CT head scan to exclude any intracranial pathology, but reiterated that no surgical intervention was required for left radiculopathy and that the doctors should keep a watch for any further deterioration. The only symptoms of deterioration recorded in this period were a report by Mrs Sumner on 28 December that she now had difficulty pressing the call bell with her right hand as well as with the left; but the neurological examination following that report assessed the motor power on the right side (and indeed on the left) as being no different from the previous day.

On 29 December, a CT scan was carried out on Mrs Sumner’s thoracic spine, which was undamaged, and repeated X-rays of her shoulder. A possible fracture to the right humeral head was spotted. This was confirmed on further imaging as a minimally displaced fracture through the right neck of the humerus. This was appropriately treated by a right arm collar and cuff. (That fracture probably explained some of the pain and discomfort that she was suffering; she made a good recovery from it, and it caused no lasting disability). The record of the ward round at 1pm (written up at 3.30pm) shows no worsening of her neurology so far as the spinal injury was concerned. Indeed the ASIA chart shows an improvement to 3/5 on the left arm and restoration of full motor power to 5/5 on the right.

On 30 December Mrs Sumner was seen again by the physiotherapist in the morning. She had been suffering hallucinations overnight, and was confused on and off in the morning; it was decided to try and avoid giving her morphine. No attempt was made to mobilise her until a plan was in place. However at 4.15pm, the doctor instructed that she be tilted to 30 degrees from flat and mobilised as able with the physiotherapist the following morning.

On 31 December the confusion was continuing, and apparently getting worse. However, when Mrs Sumner was examined on the ward round at 9am there was no progression of her neurological signs – the results recorded on the ASIA chart are essentially the same as on the previous chart taken at 1pm on 29 December (3/5 on the left arm, 5/5 on the right) though the doctors were unable to take a reading at C7, which was refused because of pain. Later that morning, Mrs Sumner was mobilised out of bed. She complained of pins and needles throughout her left upper arm when seated. On neurological examination by the physiotherapist at 11am the neurology of her upper limbs on both sides was apparently getting worse. The ASIA chart shows Grade 3/5 power in the left arm at C6, but now 2/5 at C7 and C8. The power in the right arm had also deteriorated to 4/5 at C6, and 3/5 at C7 and C8. There was decreased sensation in the C6/C7 dermatome bilaterally, left worse than right. That record does not necessarily mean the decrease had occurred since the last examination, but simply that sensation was reduced in that area (as it had been for some days). The notes state “? Changing neurology as a result of mobilisation”. Thus the physiotherapist made a connection at the time between movement and deterioration in the patient’s neurology.

The physiotherapist thought it inappropriate to continue with further rehabilitation at present, and decided to liaise with the orthopaedic team regarding possible neurological changes in the left upper arm when the patient was sitting up. If a patient with an unstable spinal cord injury sits up, this may cause “postural hypotension”, i.e. a lowering of their blood pressure, which may in turn disturb the circulation and cause spinal cord ischaemia. However, the charts show that Mrs Sumner’s blood pressure at that time was within a normal range. Mrs Sumner was returned to bed but left sitting up at an angle of 50 degrees, and reported a decrease in the pins and needles thereafter.

The physiotherapist reported her concerns to the registrar at 2.30pm, who advised a review by the on call registrar. When the doctors examined Mrs Sumner at 3.45pm they thought she looked hot and sweaty (it transpired that she had a chest infection, which later developed into pneumonia). She was still confused. At that point she was lying in bed at 40 degrees; she did not complain of pain or discomfort but said her left arm had been painful. Despite this, motor power in her upper limbs appeared to be deteriorating on both sides; she now had no power in her fingers on the left and very little power in her fingers on the right. However, there was still full power in her legs.

Apart from the diagnosis of the chest infection, nothing of note is recorded on 1 January 2011. Mrs Sumner remained confused but her son reported that she was more lucid. There were no tests of her motor power on that date. On 2 January, the physiotherapist recorded at 1100 that Mrs Sumner was in bed and poorly positioned (there is no description of how), although the hard collar was fitting appropriately. Mrs Sumner said that she felt “awful”, that she was unable to open her bowels (though it transpired that she had not done so since the accident), and that she could not move her right leg. This is the first record of any problems with her lower limbs. She was repositioned at an angle of 50 degrees (it appears that this was because of the chest infection), and complained of pain and pins and needles in her left arm during repositioning. There was again a record of decreased sensation at C6/7 bilaterally, left worse than right. There was no movement in the left hand and reduced movement in the right. The physiotherapist decided to liaise with the doctors prior to further mobilisation.

When the physiotherapist returned to see her at 3pm on 2 January, Mrs Sumner was drifting in and out of sleep. She reported that she was now unable to move both lower limbs. The physiotherapist had difficulty in assessing her lower limb neurology because Mrs Sumner was so sleepy. No sensory deficit was noted in the lower limbs. She was able to move her right ankle but not the left. At 4pm the on-call doctor was summoned to examine her. The notes record that the patient reported a loss of sensation and mobility to her legs “since last night.” She also complained of pins and needles in the left arm with rolling. The motor power to her legs was assessed at zero bilaterally, save for some distal power on the left. By this time she had also developed urinary retention.

Discussions about this situation with the surgeons at St George’s resulted in a recommendation to carry out a further CT of the cervical spine. The notes record that they “did not suggest any precautions for cervical spine”. They indicate that the doctors believed that she may have had a cardiovascular arrest or cord compression (indicating that they believed the likely cause of the degeneration in her muscle power to have been an interruption to the flow of oxygen). The first of these hypotheses was ruled out after a CT scan of the head. The further CT scan of the spine was reported as demonstrating a stable C6/C7 fracture. No new fractures were identified, and the overall cervical spinal alignment was unchanged. Of course, when she was positioned in the scanner, Mrs Sumner was lying spine in line. On receipt of the results, one of the doctors, Dr Saxena, still thought that the patient was likely to have a (spinal) cord compression, and that the CT of her neck needed to be reviewed.

The following morning, 3 January, Mrs Sumner was seen by the physiotherapist at 11.20am. She was still complaining of loss of movement in her legs. Essentially there was no change from the previous day. When the physiotherapist returned at 2.30pm, Mrs Sumner was in bed supine with her head at 90 degrees. The hard collar was fitting adequately and in a good position. There had been no medical review and no results from St George’s as yet. Her family became very concerned, and spoke to the senior house officer about the fact that she had no movement or sensation in her legs. Eventually, at 9.20pm, St George’s contacted the registrar on duty to say that Mrs Sumner was booked in for an MRI scan the following day. The registrar’s notes record slightly worsening neurology of the lower limbs, but much the same neurology in the upper limbs (though by now she had no movement in either hand).

On the morning of 4 January 2011 the physiotherapist spoke to a Dr Leong about a management plan whilst awaiting MRI in view of the further deterioration in neurology. He advised strict bed rest, flat lying and 5 person log-rolling. Although the physiotherapist explained that Mrs Sumner was at a high risk of respiratory deterioration whilst lying flat, the doctor said that a plan for Mrs Sumner would be established by the end of the day. His recommendations were passed on to the nursing and clinical staff on the ward.

The MRI scan revealed a significant unstable fracture. The notes state that the C7 fractures were better demonstrated on CT. However there was considerable oedema (swelling) surrounding the postural elements at C6/7 and high signal was also seen within the C6/7 disc, indicating anterior and middle column injury as well as the known posterior column disruption. In addition, at this level, there was a significant narrowing of the spinal canal with focal cervical cord oedema and a fragment of bone projected into the spinal canal on the left side. If a person suffers a trauma of any sort to the spine, and oedema is shown on the spinal cord on an MRI scan, then one would expect the patient to have neurological deficit, but as Mr Gardner explained, it is the injury that causes the oedema, not vice versa. One cannot draw a conclusion as to what the injury was merely from the presence of oedema, because one always sees swelling if there has been an injury.

The first entry on the medical records after the MRI results were verbally reported, which was made at 3.10 pm, describes “significant abnormality at C6/7 level” and states “oedema probably also signifies significant ligamentous injury”. The correct advice was given to take neuro precautions – immobilise and log roll. That advice was followed.

No complaint is made about Mrs Sumner’s treatment by the Defendants after the MRI scan was taken. Mrs Sumner was transferred to St George’s Hospital the same evening, where despite her chest infection she underwent surgery (posterior stabilisation at C6/7) in the course of the following day, 5 January. She was then transferred to the Intensive Care Unit to manage her pneumonia. Thereafter her condition slowly improved. On 29 January she was transferred to Kingston Hospital, where by all accounts she had a most unhappy experience, largely because her diabetes was poorly controlled. However on 4 March 2011 she was transferred to the National Spinal Injuries Centre (“NSIC”) at Stoke Mandeville. A further MRI scan was carried out on 7 March. It showed C6/C7 subluxation with canal narrowing. There is spinal compression, and a bit of disc protruding back into the cord. There were also indicators of a unifacet dislocation at C6/7 on the left hand side, which had not been seen on the pre-operative MRI image taken on 4 January.

A further surgical procedure was carried out at Stoke Mandeville on 15 March 2011 which involved anterior decompression of the disc between C6 and C7 with insertion of a plate and a cage. After rehabilitation (which was prolonged by the development of a deep vein thrombosis, leading to a prescription of warfarin) Mrs Sumner was discharged from the NSIC on 26 October 2011. Thereafter, her condition continued to improve.

It is common ground between the spinal experts that Mrs Sumner has made a good recovery. She has tetraparesis at the average to good end of the ASIA/Frankel D range, with the last normal sensory level being C7. That means that the large majority of her spinal cord is now functioning once more. Prior to the operation to stabilise her spine she was two grades worse, ASIA/Frankel B. The extent of her improvement was better than might have been expected at the time when she was tetraplegic. However she has still been left with significant permanent disabilities, and she needs the assistance of carers. Her mobility is impaired and she is catheterised. Although she can walk with the use of a stick, she uses both a manual and electric wheelchair to travel any significant distance. Her condition will deteriorate as she gets older and it is now common ground that she will need increased care in the last three years of her life. Her life expectancy is agreed to age 81 (she is now 72).

The Claimant’s case on liability is that there was a negligent failure to carry out an MRI scan by 27 December at the latest, or at any time prior to 4 January 2011. If Mrs Sumner had undergone an MRI scan by 27 December 2010 or thereafter, it would have shown that the fracture was unstable. She would and should have been immobilised and undergone emergency stabilisation of C6/7.

By a pre-action protocol letter of response from their solicitors dated 16 July 2012, the Defendants admitted that “there was a delay in diagnosing the unstable fracture and that this subsequently resulted in there being a delay in carrying out surgery to fix the spine. It is the Defendants’ case that the latest time that it was reasonable for surgery to have been carried out was 29 December [2010]” (the letter says 2011 but that is an obvious typing error). (“Admission 1”).

The letter went on to say this:

“It is further admitted that whilst the Claimant is likely to have been left with some neurological deficit in any event, on the balance of probabilities, had surgery taken place at the time that it should have the Claimant would have made a substantial recovery and regained her mobility” (“Admission 2”)

It continued:

“In the light of the admissions set out above the Defendants do not intend to dispute liability and will consent to Judgment being entered for damages to be assessed. The extent of the Claimant’s injury, loss and damage is not admitted and will need to be established by further investigations”. (Emphasis added).

By the time that letter was written, it was known that Mrs Sumner had already recovered and regained her mobility to the extent described in paragraph 26.

The claim form was issued on 22 March 2013 and the Particulars of Claim pleaded Admission 1 to the breach of duty (in paragraph 22). Under the heading “Causation and Injury” it was pleaded that if she had undergone timely stabilisation of the C6/7 fracture, Mrs Sumner would have been an in-patient for about 3 weeks and she would have retained normal power in both her legs and in her right upper arm; however there would have been some marginal residual weakness in her left upper limb which would have marginally restricted her activities of daily living. Her mobility would have been normal, as would her bladder and bowel function, and she would have been able to drive and live a normal life (paragraph 25).

In paragraph 26 of the Particulars of Claim, Admission 2 is set out and characterised as an admission of causation. In my judgment that characterisation is correct: on a natural reading of the letter of 16 July 2012, the Defendants were accepting that if she had been operated upon to stabilise her spine by 29 December, Mrs Sumner’s recovery would have been better than it turned out to be, although (as is common ground) she would have suffered some neurological deficit come what may. It is clear that they also accepted that she had suffered some further injury to her spine. She was put to proof of the extent of her injury, loss and damage, i.e. the extent to which her condition was made worse as a result of their admitted negligence.

If a defendant accepts liability in a negligence case, he must be accepting that some loss was caused by the negligence, because causation and loss are two of the four essential ingredients of the tort (the others being duty of care and breach of duty). Of course it remains for the claimant to prove the damage he or she alleges was suffered in consequence of the negligence, and to that extent the defendant may challenge whether a particular head of damage was caused (or materially contributed to) by the breach of duty. However if a defendant’s case is that despite the breach of duty the claimant has suffered no loss at all, but would have ended up in precisely the same state regardless, he should not be admitting liability, but rather, admitting the breach of duty and denying causation. That was not what the Defendants did in this case.

Mr Skelton submitted that liability was accepted in 2012 because at that stage the Defendants accepted that Mrs Sumner’s recovery must have been delayed to some extent by the delay in undergoing surgery. He said that she has made a substantial recovery and she has regained her mobility, and that is what admission 2 said she would have done if the surgery had been performed by 29 December. However that is not the natural interpretation of admission 2. If it had been the Defendants’ case at that time that if the operation had taken place earlier, Mrs Sumner would have recovered to precisely the same extent but sooner, the letter would have been expressed very differently, and admission 2 would not have been couched as an admission. An admission necessarily involves accepting as correct a state of affairs alleged by the opposing party that would otherwise have been contentious.

The Claimant’s solicitors, quite understandably, did not interpret the admission in the way that Mr Skelton submitted it should be interpreted. The Particulars of Claim go on to plead particulars of Mrs Sumner’s injuries, commencing with the general plea that as a result of the delayed management of her unifacet instability at C6/7 she suffered avoidable pain and deterioration in her neurological condition. No Defence was served, although in due course the Defendants served a Counter-Schedule. On 28 August 2013, judgment was entered for the Claimant with damages to be assessed, and interim damages of £60,000 were directed to be paid within 28 days. The Master’s order on entry of judgment records that the nature and extent of the Claimant’s injuries and provisional damages remained in dispute. The order does not record that causation is in issue, or that it is the defence case that no injury was suffered by reason of the failure to operate on her by 29 December.

Subsequently expert evidence was directed in respect of “condition, prognosis and quantification of damages”. Mr Skelton submitted that any practitioner in this field would understand that quantification of damages would include causation. That may well be right as a general proposition, but it begs the question whether, and if so to what extent, causation is a live issue between the parties or precluded by prior admissions or by the terms of the judgment.

It was against that background that spinal experts came to be instructed by both parties to examine Mrs Sumner. Both the experts are well qualified to express an opinion on the issues upon which they have been asked to assist the Court.

Mr Brian Gardner is a Fellow of the Royal College of Physicians both in London and Edinburgh. He is now an Emeritus Consultant in spinal cord injuries at the NSIC. In fact he was the treating Consultant at the time of Mrs Sumner’s admission to Stoke Mandeville in March 2011, though he retired in July that year. He was a consultant in spinal cord injuries at Stoke Mandeville from 1985-2011, acting as the Clinical Director of the NSIC from 1988-1999, and the Lead Clinician from 1999-2003. He has a neurosurgical background, but although he had a regular surgical list at the time when Mrs Sumner was admitted to the NSIC, he was not then a spinal surgeon but was predominantly dealing with pressure sores and neurological care. Since his retirement he has been in private practice for spinal cord injury patients. It was readily apparent that he is not out of touch with modern clinical practice or developments in his field of expertise.

Mr Gardner has held overseas lectureships or professorships or clinics in 10 different overseas jurisdictions ranging from the United States to China. He was Chairman of the British Association of Spinal Cord Injury Specialists from 2008-2011, and has done an extensive amount of teaching of medical students (undergraduate and postgraduate) and others within or connected with the medical profession. He was spinal tutor at the Department of Medical Education in NSIC from 1991-1998. He is a regular lecturer both to those within the medical profession and to lawyers. He has been working with the National Institute of Clinical Excellence since 2013 to establish guidelines on the management of spinal trauma, and has published over 100 publications, the vast majority of which relate to spinal injury.

The Defendant’s expert, Mr Firas Jamil, is a consultant spinal surgeon in the Mid Yorkshire NHS Trust. He deals with spinal trauma and also runs the Yorkshire Regional Spine Injuries Centre, which deals with people from the Yorkshire region with spinal cord injury. They have 120-130 patients a year, but he also receives all spinal trauma patients, with or without neurological deficit, from the Mid Yorkshire region. He is a senior lecturer at the University of Leeds teaching medical students and postgraduates about spinal trauma, and like Mr Gardner he has a background in neurosurgery. He is a Fellow of the Royal College of Surgeons in London and Edinburgh and has an MSc in surgery from University College London. His CV does not state how many publications he has published, but he states that most of them involve neurological trauma, including co-authoring two chapters in the latest edition of “The ABC of Spinal Cord Injury”.

Mr Gardner stated in his first report that he had been requested to comment on causation, condition and prognosis. Under the heading “Medical causation” he said that Mrs Sumner’s spinal cord function was mildly impaired when the admitted breach of duty occurred. The large majority of her spinal cord was still working normally. As a result of the admitted breach of duty her spinal cord suffered severe further damage, and the large majority of her spinal cord ceased to function. She has since improved, so that the large majority of her spinal cord is now functioning once more. The relative mildness of her initial spinal cord damage, the very severe damage that occurred, and the very good recovery in spite of this severe damage all point to her spinal cord being either normal or almost normal now, had the severe additional damage not occurred. Based upon what happened in her case, it is likely that the small minority of nerves that were not working normally at the time the breach of duty occurred would have recovered, probably fully. His conclusion was that if the breach of duty had not occurred she would probably now be in the same state as she was pre-injury. Mr Gardner did not elaborate upon how the “severe further damage” to the spine occurred, because that was not something that appeared to be in issue.

Mr Jamil stated that he was required to report on Mrs Sumner’s “pre-existing medical condition, the description of her current medical and physical functional status, and her prognosis”. However in his report, served on 25 July 2014, Mr Jamil expressed the opinion that “on balance, Mrs Sumner’s neurological deterioration had very little to do with her spinal instability and the way she was managed and more to do with the natural progression of her spinal cord damage as a result of secondary trauma related changes.” He said that regardless of any breach of duty or the timing of the surgery, Mrs Sumner would still have been left with a residual weakness in her upper limbs and suffered from bladder and bowel problems and residual disability in her neck “directly as a result of the trauma to the spinal cord caused by her fall” (Emphasis added). It was Mr Jamil’s view that there was little or no further damage to the spine and that Mrs Sumner’s neurological deterioration was a direct consequence of the original injury sustained in the fall.

Mr Jamil maintained his stance in the Joint Statement and in his evidence at trial, when he developed his reasoning in a way which was not set out in his Report or referred to in any detail in the Joint Statement. This meant that Mr Wilson-Smith had to recall Mr Gardner to give further evidence, and the evidence of both experts continued to develop right through to the end of the fourth day of trial.

It is Mr Jamil’s opinion that Mrs Sumner fell within the small minority of patients who would have suffered severe neurological degeneration regardless of whether her spine was kept stable or not, because she suffered from “central cord syndrome” (“CCS”). The characteristics of CCS are summarised in Kirshblum’s Spinal Cord Medicine (2^nd Edn 2011). It occurs when a person with a narrowed spinal canal, which could be due to spondylosis, suffers hyperextension of the spine which causes the osteophyte (the degenerative change) to hit the spinal cord powerfully. In such a case the stability or instability of the spine following the fall is irrelevant to the damage. The initial injury causes oedema which progressively worsens over a period of days or even weeks, with associated neurological deficit. Mr Jamil likened this in his oral evidence to a smouldering fire which gathers momentum and eventually ignites. There is little that can be done by way of treatment, save to let nature take its course, though steroids may be prescribed. The prognosis is generally favourable, with the lower extremities being the first to recover, though Dr Kirschblum’s writings indicate that there is often residual upper extremity motor weakness. Mr Jamil said that on average, 50 per cent of patients with an incomplete central cord injury could regain some function or return to some sort of functionality. Mrs Sumner fell within that group.

It is important to note that it was common ground between the experts that CCS would only have arisen in this case if the injury were a hyperextension injury. The suggestion that the injury was a hyperextension injury was made for the first time by Mr Jamil in the witness box.

I am in no doubt that the Defendants’ attempt to resile from their admission of causation arose as a direct consequence of these views expressed by their expert, which of course post-dated the admissions. It led to some argument at the start of the trial, with Mr Wilson-Smith QC contending that the permission of the Court was required to withdraw Admission 2, and Mr Skelton contending that he did not need permission because causation was always in issue, and that if the Claimant’s legal representatives believed the Defendants to be reneging on the admissions, the appropriate course would have been for them to have applied to strike out those parts of the Counter-Schedule that were said to be inconsistent with them.

Mr Skelton submitted that in any event, the Claimant’s legal team had had Mr Jamil’s report since July 2014 and Mr Gardner had recently produced a second expert report commenting upon Mr Jamil’s thesis as to the cause of Mrs Sumner’s deteriorating neurology in hospital, so there was no prejudice. Whilst it was true that Mr Gardner had produced such a report, he does not address CCS specifically in it (because Mr Jamil had not yet made it sufficiently clear that that was the foundation of his theory). Mr Gardner said in his second report, “there is no robust published evidence that shows that, in patients with an acute traumatic cervical spinal cord injury who are treated appropriately, such catastrophic deterioration occurs at this delayed stage after acute traumatic cervical spinal cord injury, other than if there is prolonged low blood pressure or a vertebral arterial injury. Neither of the latter applied in this case.” He referred in that report to the initial injury as “an unstable C6/7 flexion cervical spinal injury” and said that Mrs Sumner “sustained mild damage to her spinal cord at this time.”

In support of his submission that causation was a live issue, Mr Skelton referred to the case of Symes v St George’s Healthcare NHS Trust [2014] EWHC 2505 in which a decision of Master Roberts that judgment in default was to be regarded as conclusive on the issues of breach of duty and causation pleaded by the claimant in a clinical negligence case was overturned on appeal. Symes also concerned a delayed operation, in that case an urgent superficial parotidectomy on a lump on the claimant’s face which was suspected to be malignant. The claimant alleged that the delay resulted in metastasis of a tumour to his lungs and invasion of the facial nerve, meaning that by the time of diagnosis his lung cancer was inoperable and that he only had a short time to live.

The judge in that case, Mr Simon Picken QC, held that both he and the Master were bound by authority, in particular by the decision of the Court of Appeal in Lunnon v Singh [1999] CPLR 587, (following and approving its earlier decision in Turner v Toleman (1999) unreported, 15 January) to find that questions of causation in relation to the particular heads of loss claimed by the claimant remained open to the defendants at the damages hearing, notwithstanding that judgment on liability had been entered in default.

It is noteworthy that in Lunnon, when considering the effect of the default judgment, Clarke LJ (as he then was) cited with approval a passage in the judgment of Sir Richard Scott VC in Maes Finance Ltd and another v A Phillips & Co (1997) The Times, 25 March:

“The defendant cannot thereafter contend that his acts or omissions were not causative of any loss to the plaintiff [my emphasis]. But he may still be able to argue, on the assessment, that they were not causative of any particular items of alleged loss.”

Mr Picken QC expressly accepted in Symes at paragraph [58] that in all three of these earlier cases, Turner, Lunnon and Maes Finance, the defendants were precluded by the judgment from being able to argue that no loss at all was sustained, because that would be inconsistent with a judgment on liability. Beyond that, however, they were permitted to take issue with causation of specific heads of damage. Thus the court in each case drew precisely the same distinction that I have drawn above.

It is also worth noting that Lunnon and Symes were only concerned with the effect of a default judgment, and not with the extent or effect of a defendant’s express admissions. In Symes the defendants had admitted that the delay in operating caused some damage, but the claimant was put to strict proof of the nature and extent of damage, injury and loss said to arise from their admitted negligence. However, in contrast to this case, there was no express admission as to what would have happened had the patient undergone surgery at the recommended time instead of months later. There was a further significant difference, in that the claimant’s solicitors in the Symes case knew all along that the defendant intended running a causation case like that set out in their Counter-Schedule. Therefore, as the judge said, it was not some kind of unexpected ambush.

In principle defendants should not be permitted to run a positive case on causation that contradicts both their admission of liability and (more importantly) a judgment entered on liability by consent. I was therefore inclined to the view that it was not open to these Defendants to contend that the Claimant had suffered no loss at all. Nevertheless there was a potential for injustice if the deterioration in Mrs Sumner’s condition was indeed unrelated to the failure to stabilise her spine before 29 December 2010. It seemed to me that if that view had been expressed by their expert, perhaps unexpectedly, on review of the available evidence, it might be unfair to the Defendants if the issue could not be explored at trial. It appeared at that stage that the Claimant’s legal team and Mr Gardner had been able to answer Mr Jamil’s thesis (at least as it then appeared) and there was no apparent prejudice to them. It was not then anticipated that Mr Jamil would elaborate on his evidence in the way that he did. I therefore left over the question of whether permission should be granted, and heard the evidence of the two spinal experts de bene esse.

In the event, I reached the view that even if the Defendants had not made Admission 2, and had pleaded from the outset that the Claimant was unable to prove that their negligence caused her any loss, or that her current state of health would have been exactly the same if she had had the operation sooner, it would have made no difference to the outcome of the case. It has therefore been unnecessary for me to make any ruling on the admissions.

Mrs Sumner was widowed in 1998. She lived alone in a third-floor flat in Putney served by a single lift. She drove a Honda car, and was completely independent. She is an insulin-dependent diabetic but her diabetes was (and is) well-controlled. Her bladder and bowel functioning was normal. She had breast cancer in 2009 which was caught and treated at an early stage and which has not affected her life expectancy. She was (and is) on statin medication for cholesterol, and on medication for raised blood pressure, which keeps both conditions under control. She also takes a Vitamin D supplement.

Mrs Summer also suffered from age-related cervical spondylosis. This had caused progressively worsening pain in her left arm over a period of around six months in the summer of 2006, which became so bad that it disturbed her sleep. The pain radiated down in what the spinal and orthopaedic surgeon to whom she was initially referred described as “a very classical C6 dermatomal distribution”. His notes record that for about 60 per cent of the time she was in “absolute agony”. While she had no weakness, she had a very obvious stenosis at C5 on the left side. She underwent a foramenotomy for C6 radiculopathy by a neurosurgeon, Mr Johnstone, in February 2007, after which her evidence was that the pain disappeared (though the post-operative notes suggest that it had gone down to around 30% of the pre-operative level, which was easily tolerable, but the neurosurgeon was sure the symptoms would settle down over the coming weeks). Mrs Sumner told the court that it was like a miracle, and that she was so delighted that she could move her arm without any pain that she gave the surgeon a kiss when she came out of recovery.

I note from a letter from a Dr Phillips, an oncologist, relating to Mrs Sumner’s treatment for breast cancer, that in January 2010 she had a chest x-ray which confirmed “minor degenerative change in the left shoulder, and she has been having some pain in this area for the past three months radiating down the left arm”. This was three years after the foramenotomy, to which reference is expressly made in the letter. Thus there was a predisposition to pain in the left shoulder and radiating down her left arm which related to the spondylosis, and had nothing to do with the spinal injury suffered in the accident, let alone its treatment.

Mr Gardner readily accepted that the ongoing neck pain from which Mrs Sumner is now suffering was likely to be related to the injury she suffered in the fall, and not to the way in which it was treated by the Defendants, although he made the fair point that her spinal cord injury and reduced mobility makes that pain more difficult for her to deal with. Likewise, the stiffness that she experiences in both shoulders is something that she is likely to have suffered from in any event. The pain in her coccyx is also attributable to her fall rather than to her treatment.

In the early 1990s Mrs Sumner’s medical records show that she had a problem with epigastric pain and what was described as “fairly profuse vomiting”, which was episodic. She now has no recollection of this, which is understandable, as it occurred over 20 years ago. In March 1992 a GP, Dr Barnardo, recorded “intermittent attacks of lower abdominal discomfort, nausea and retching of uncertain causation”. Different medication was prescribed, which did not cure the problem, though it appears to have abated by the autumn of 1993.

The reason why this is significant is that there is a condition associated with diabetes called gastroparesis whose symptoms include nausea, vomiting, and abdominal bloating. Mrs Sumner developed all those symptoms after her spinal injury. There was associated weight loss. She saw a consultant gastroenterologist named Dr Emmanuel in 2012, who was fairly convinced that her symptoms were primarily related to diabetic gastroparesis. Dr Emmanuel had not seen the records pertaining to her episodic vomiting in the early 1990s and thought Mrs Sumner had suffered no complications from her diabetes earlier in her history. She may not have done - the cause of her nausea 20 years earlier remained uncertain, and gastroparesis was just one possibility that was considered. It was not diagnosed. In March 1993 a Dr Dayan, who was a senior registrar in the Department of Endocrinology at Charing Cross Hospital, wrote to Mrs Sumner’s GP about her episodic vomiting and expressed concern about her associated weight loss. He stated that “the pattern of vomiting seems typical of diabetic gastroparesis although surprising in view of lack of other complications.” He then refers to various stress factors that were affecting Mrs Sumner at the time, including the fact that her husband had been severely ill and undergone 10 operations, and said that he was sure that there was a psychogenic element to her vomiting.

In the absence of evidence from an expert endocrinologist or gastroenterologist it is impossible for the court to infer on the balance of probabilities that the gastroparesis with which Mrs Sumner has now been diagnosed by Dr Emmanuel was brought about by the Defendants’ negligence, regardless of whether that was what she was suffering from in the early 1990s or whether it was something else, as seems more likely in view of the fact that the symptoms disappeared for 20 years. The gastroparesis appears to be a complication arising from her diabetic condition, and whilst she may only have developed it after her fall, there is no evidence before the Court to indicate that she would not have developed it if she had had spine stabilising surgery by 29 December 2010.

The key question that the Court has to determine is what would have been the prognosis for Mrs Sumner if the unstable nature of the spinal fracture had been diagnosed in the first 72 hours, and she had undergone the stabilisation surgery by no later than 29 December 2010. It is for the Claimant to prove on the balance of probabilities that if she had undergone the operation then, she would not have suffered the marked neurological deterioration that occurred thereafter leading to tetraplegia, or alternatively, if there was more than one cause of the deterioration, that the failure to operate made a more than negligible contribution to it. The Defendant’s case is that an earlier operation would have made no difference.

I start by assessing the reliability of the two spinal experts. This has to be judged not only on the manner in which they presented their evidence, but also on how their opinions fit with the inherent probabilities, the medical records, and any published literature on which they relied.

Mr Gardner was an impressive, manifestly impartial witness. Although he had been in charge of Mrs Sumner’s treatment on her admission to Stoke Mandeville, Mr Gardner has had no responsibility for her care since July 2011, and he was never retained as a liability expert. He made it clear that he would have accepted instructions to give expert evidence for the defence on quantum had he been asked to do so. He gave his evidence in a considered and measured manner, referred to literature in support of his opinions where such literature was available, gave explanations of why his views accorded with the physiology of the patient and her symptoms, and paid meticulous attention to the medical chronology and radiological evidence. The only material evidence he did fail to consider was the blood pressure charts, which eventually made it clear that postural hypotension was not a cause of the loss of muscle power to Mrs Sumner’s legs, but that was not a matter raised by Mr Jamil, but by Mr Skelton.

Mr Gardner was careful never to over-state his position. If a particular feature was neutral, or as consistent with Mr Jamil’s opinion as with his differing opinion, Mr Gardner said so without hesitation, and often without being asked. There were a number of instances of Mr Gardner making concessions which were unhelpful to the Claimant’s case, the most striking of which was his ready acceptance that if Mr Jamil’s theory about CCS were correct, Mrs Sumner would not have recovered any more quickly than she did even if she had undergone surgery a few days sooner.

I have no doubt that Mr Jamil’s views were honestly held and that he was doing his level best to assist the Court. However, he was far less reliable as a witness, largely because he was so wedded to his own opinion that he refused to acknowledge that he might be mistaken. This confidence that he was right and that anyone who disagreed with him was wrong pervaded his evidence, and there were occasions where in consequence he appeared to me to lack the necessary objectivity. For example, he refused to consider how his views might differ if the injury were a flexion injury, whereas Mr Gardner considered the question why Mrs Sumner’s condition deteriorated both on the hypothesis that it was a flexion injury and on the hypothesis that it was a hyperextension injury. Mr Gardner was prepared to accept that in the latter case, it was possible that the deterioration was indeed due to CCS, but he considered it was improbable for the reasons that he adumbrated.

When the BOA Guidelines put to him, Mr Jamil took issue with the emphasized statement that acute spinal injury must be nursed flat. To the extent that he was making the point that the Guidelines represent “best practice” and one has to make allowances for clinical judgment if the patient is experiencing extreme discomfort or becoming distressed in that position, or if the patient develops a respiratory problem, or if there are insurmountable resource difficulties, e.g. insufficient nursing staff to do the log rolling, his caveats were fair. What was far less impressive was his dismissive description of the BOA Guidelines as being produced by “just a group of people … most of [whom] have not even cared for spinal cord injury patients”. He said the study had not been commissioned by the Royal College of Surgeons or Department of Health, criticized the validity of the statistics referred to, and at one point said that he “disregarded it”. Mr Jamil seemed to have been unaware of the fact that the Guidelines were adopted, with some passages reproduced verbatim, by the NSCISB. When that was shown to him by Mr Wilson-Smith QC, Mr Jamil’s initial response was to point out that the author of the NSCISB paper was the chairman of the working party that had produced the BOA booklet.

Around half the patients that Mr Jamil sees have hyperextension injuries. He is of the view that in such a case it is acceptable practice to incline the bed slightly to make the patient more comfortable, and that a head collar is sufficient to protect against further potentially damaging movement even if the spine is unstable. Mr Gardner was visibly shocked by Mr Jamil’s assertion that a head collar would afford sufficient protection against movement where the spine was known to be unstable. Treating the patient with a head collar alone, whatever the type of injury, would be contrary to accepted standard practice.

Mr Gardner’s evidence was that if the patient had a stable fracture with minimal neurological deficit, it would be acceptable to raise them to 30 degrees, but unless there were some very pressing reasons to do it, it would be wrong in principle to treat a patient with an unstable fracture in that way (he used the word “awful”). He explained it in this way: the moment you cease to keep a person spine in line, you are permitting the spine to move in an uncontrolled manner, and whilst a collar will help with stability it will not suffice, because the patient can still move the neck to some extent and that can cause further damage. He pointed out that if a head collar were sufficient protection, it would be a huge waste of resources to carry out log rolling. In my judgment, it is one thing to say that in the real world one has to manage as best one can with inadequate human or other resources, and to deal with each patient as they present; it is quite another to deprecate the guidance as if it were a counsel of perfection dreamed up by theoreticians, serving no useful purpose, which appeared to be Mr Jamil’s approach.

Mr Jamil accepted that if the patient had a flexion injury it would “not be ideal” to treat them with just a collar, because then there would be a greater range of movement which could cause injury. He said that whilst the collar would protect by 65-70%, it would still allow enough movement to potentially cause further damage. However he said categorically that could not have happened in the present case. Such an injury would show up straight away because the spinal cord would be crushed and the patient would immediately become tetraplegic. However, he had never seen a patient in a head collar who had suffered tetraplegia as a result of movement, and he was unable to refer to any literature in support of his evidence that tetraplegia would be immediate.

Unlike Mr Gardner, Mr Jamil had not gone carefully through the medical notes and assessed whether there was any correlation of the deterioration in Mrs Sumner’s neurological condition with any specific events recorded in them, such as any movement that might have caused a further injury or loss of oxygen to the spinal neurones. Had he done so, he would have appreciated that both on 27 December and on 31 December 2010 the physiotherapist had expressly queried whether the noted neurological deterioration was linked to the patient’s prior mobilisation, and that after the initial left arm deterioration on 27 November until 11.00 on 31 December, Mrs Sumner’s muscle power in her upper limbs had appeared to be either stable or improving, depending on how much reliance can be placed on the ASIA charts including, most importantly, the assessment carried out at 9am on 31 December, shortly before she was mobilised out of bed. When he was taken through the notes by Mr Wilson-Smith and it was put to him that they showed a correlation between mobilisation and deterioration, Mr Jamil’s response was that correlation was not the same as causation. Whilst that is true, he was signally failing to engage with any material that might support a different conclusion from his own. When shown the physiotherapist’s concerns on 27 December that mobilisation might have brought on the deterioration, Mr Jamil was keen to criticize her for suggesting that the patient be returned to flat bed rest on the basis that this was outside her remit, but seemed disinterested in considering whether her concerns might be justified.

In his expert report Mr Jamil repeatedly asserted, with no evidential foundation, that Mrs Sumner had been “thrashing around”. He was unable to give any satisfactory explanation for this, though he apologised and withdrew those remarks when he gave his evidence in chief. It appears that he had drawn that conclusion purely from the fact that she was said to have been confused. This is indicative of a lack of care and attention to detail, in marked contrast to the approach of Mr Gardner.

It is true that at the time of her accident Mrs Sumner was 68 and already had problems due to cervical spondylosis, and so she fell within the category of patients who might be susceptible to CCS. In my judgment Mr Jamil jumped to a conclusion that this was a case of CCS because (a) she fell into that category, (b) there was a high level of oedema shown on the March 2011 MRI scans, despite the surgery two months earlier, and (c) she made a better than expected recovery. He also relied on the fact that the initial deterioration was in her hands and arms and progressed to the legs, bowels and bladder, which was consistent with her suffering damage to the central cord and, according to Mr Jamil, consistent with a natural progression caused by increased swelling. Having reached that conclusion, Mr Jamil refused to engage with the possibility that it might be wrong.

However Mr Jamil accepted that even if a patient presented with CCS, care would still have to be taken to manage an unstable spine to prevent further damage occurring from movement in that spine. It follows that even if there was an inevitable worsening in her neurological symptoms due to spreading oedema from the original trauma (which might have caused the initial deterioration in the left arm, for example), there could still have been a further deterioration caused by the movement of the unstable fracture at the site of injury.

It was common ground that if damage occurs in the cervical cord region and affects the inner grey matter of the spinal cord, the predominant injury is going to be to the arms, sensory and motor, and to the hands in particular. If the damage is to the outside of the spinal cord, then the arms would be affected to some extent but the damage would be predominantly to the lower limbs. However it is common ground that this was a three column fracture. Mr Gardner said that no conclusions could be drawn merely from the fact that the neurological symptoms began with the upper limbs. There was insufficient information in the records to suggest that there was a real problem with motor power in the hands, other than the mention of weakness there in the notes upon admission.

The published literature relied upon by Mr Gardner shows that spontaneous improvement is the norm in incomplete spinal cord injury cases when they are managed appropriately. The level of improvement of course depends on the nature and extent of the injury, and other factors such as the age of the patient. Spontaneous deterioration occurs in a very small minority of cases: on Mr Gardner’s evidence (supported by the literature) between 0.8% and 5%. Even Mr Jamil’s evidence on the statistical likelihood of spontaneous neurological deterioration put the likelihood of it happening at no more than 8.1%, and that was based on a paper by Tator and others in Canada relating to spontaneous deterioration occurring during traction. The authors of that paper said that information was not available regarding the severity of that deterioration and whether the deficits were temporary or permanent. Mrs Sumner did not undergo traction.

By contrast, in cases of missed unstable fractures, there is a greater likelihood of neurological deterioration. Mr Gardner relied upon an article entitled “Missed and Mismanaged Injuries of the Spinal Cord” by Poonnoose and others, published in the Journal of Trauma, Injury infection and Critical care, which showed that the diagnosis of unstable fracture was missed in 52 out of 569 spinal cord injury patients admitted into the Regional Spinal Cord Injury Unit in Sheffield over a period of 10 years from 1989. In 50% of those patients, the paper states there was neurological deterioration due to mismanagement. Mr Jamil was highly dismissive of this paper because it was not published in a specialist journal such as Spine, Spinal Cord, or Spinal Cord Medicine. He said it failed to explain what the alleged mismanagement was, or what criteria were used to produce the statistics, and that it was “poorly regarded”. Mr Jamil apparently overlooked the fact that the Poonnoose paper is quoted in the BOA booklet with apparent approval on internal page 4 under the heading “Think Spinal Injury”, a passage which is reproduced verbatim in the NSCISB paper. Therefore, although it is poorly regarded by him, those charged with giving guidance to clinicians in this field take a different view.

Statistically, therefore, it is more likely than not that Mrs Sumner’s condition would not have deteriorated to the extent of developing tetraplegia had she had an operation to stabilise the spine on or before 29 December.

There has to be a good reason why it is the received wisdom that patients with an acute spinal cord injury that is unstable should be kept flat with spine in line and log-rolled. That reason is plainly to avoid the risk of a further deterioration in their neurology due to further movement of the spine where it is unstable. It follows that if a patient with an undiagnosed unstable fracture is not managed in that way and their condition does deteriorate, then in the absence of an intervening factor such as a cardiac arrest, the likely explanation for that deterioration must be that the risk has eventuated and movement has caused further damage to the spine. It is not impossible, but far less likely, that the patient falls within the very small percentage of patients whose condition would have deteriorated come what may.

It is against that starting point that I have to evaluate the rival theories of causation. If the initial injury to the spine was a flexion injury, as Mr Gardner believed to be the case, then it is agreed that Mr Jamil’s thesis of CCS cannot be right, because it is common ground that that syndrome almost exclusively arises in hyperextension injuries. Mr Gardner said that he generally saw it in elderly patients who had fallen down and banged their foreheads. If it was a flexion injury, the further damage to the spine which caused the neurological deterioration resulting in loss of power to the lower limbs is therefore more likely than not to have been caused by further movement at or around the site of the initial injury.

If the initial injury was a hyperextension injury, then the fact that the profound deterioration in Mrs Sumner’s neurological condition followed almost immediately upon her mobilisation on 31 December 2010 has to have been pure coincidence if Mr Jamil’s thesis is right, and it would have occurred even if she had been kept spine in line throughout. Moreover, the apparent signs of improvement in her arms on both sides recorded in the ASIA charts not only on the afternoon of 29 December but also (to the extent that muscle power was able to be tested) at 9am on 31 December, which indicated a fully functional right arm, would have to be due to erroneous, but consistent, recording of muscle power by different doctors – Dr Jacob on 29 December, and Drs Buckle and Sharma on 31 December. Muscle power in that arm, which had been fine up till then, went down by two whole grades on the ASIA scale within a very short period on 31 December.

Mr Gardner explained that the movement required to produce further spinal cord damage can be relatively mild, and depends on the configuration of the injury. In this case there was a bony intrusion into the canal on the left. A drop in blood pressure on sitting could have caused further damage (though in this case there appears to have been no recorded drop in blood pressure during the key period leading to tetraplegia). Further neck flexion would narrow the spinal canal and potentially cause impingement on the cord.

When you get a fracture through the facet, as happened here, it is no longer held in place and it can therefore move forwards. The fracture can act like a dislocation, because it can move forward as a whole. On the other hand, if the facet is locked and stable, it cannot drift backwards and forwards. Mr Gardner demonstrated this with the aid of a spinal model, which showed that as the facet moved forward it rotated towards the side of the injury.

Mr Gardner’s evidence was that Mrs Sumner was managed inappropriately to different degrees at different times. At any time that the care was inappropriate she could have sustained minor or major incremental spinal cord damage – because she was not immobile. His best explanation for how the further damage occurred was that with forward movement, the fractured facet on the left was intruding intermittently into the canal, interrupting the blood supply to the spinal cord, probably intermittently impacting on the cord as well (especially if there was further neck flexion) and then returning into position when the patient returned to being spine in line, causing incremental damage which finally resulted in the damage causing loss of power to the lower limbs. This thesis applied regardless of whether the initial injury was a flexion or a hyperextension injury.

Since the movement required to produce serious injury could be disproportionately mild, especially with incremental damage, Mr Gardner rejected Mr Jamil’s objection that ischaemic damage sufficient to cause tetraplegia would have been clearly visible on the cord on the MRI scan. The only evidence that it would came from Mr Jamil, and I am not prepared to accept such an unequivocal assertion made by him if Mr Gardner, who I regarded as both more reliable and more objective, disagreed with it. As for the progression of the oedema shown on the MRI scans, Mr Gardner said it could be swelling due to such further incremental damage as he described; it could not be assumed that it was a progression of swelling due to CCS.

Mr Gardner relied on a paper by Xiong, entitled “Manipulation for cervical spinal dislocation under general anaesthesia” which shows that in the study that was carried out, unilateral facet dislocations resulted in no complete injuries, with the majority resulting in minimal impairment. This could be contrasted with Mr Jamil’s assertion, without any published literature to support it, that unilateral facet dislocation in flexion injuries results in 40% of patients becoming tetraplegic. Mr Gardner explained that on admission, Mrs Sumner fitted exactly into the category of unifacet dislocations which had minimal damage. The facet fracture that she suffered was identical to those considered by Xiong, except that it was not dislocated. It was fractured, but acting like a dislocation because it was unstable and could move forwards. Thus inappropriate movement forwards into the spinal canal would cause further incremental damage. He said that if the constant movement forward had happened in someone who had no neurology, it might not have hurt them, but in someone who had a delicate spinal cord, it would.

When it was suggested to Mr Gardner that it was implausible that the facet moved sufficiently forward to cause a sufficient degree of ischaemia to the spinal cord to cause tetraplegia, Mr Gardner disagreed. I found his explanation persuasive. Mr Skelton submitted that there was no published medical literature that ischaemia caused by this mechanism can cause tetraplegia. However, the absence of such literature is hardly surprising: gathering data would be difficult. Hopefully it would rarely be the case that an unstable fracture of this particular nature would be misdiagnosed in the first place and then mismanaged. That does not mean that Mr Gardner’s thesis is incorrect or medically implausible.

As for the point that Mrs Sumner would not have made the recovery that she did from tetraplegia, if it had been caused by further incremental damage to the spine, Mr Gardner said that one could not make that assumption; when a neurone is damaged such that it does not work then, whatever the cause of the damage, it either remains non-functional, it partially recovers or it fully recovers. One cannot draw assumptions about the likelihood of recovery from tetraplegia which occurs through degeneration in the condition of a patient with an incomplete injury, from studies relating to patients who initially present with complete injuries.

Mr Gardner’s view that the injury was a flexion injury was partly based on what he saw on the MRI scans and partly on a clinical deduction drawn from the fact that the accident had affected mostly one arm (the left) which he explained often happens when you get a unifacet dislocation, because it impacts or can cause a contrecoup impact of the spinal cord so you can get an injury predominant to one side (here, the left). When it was put to him in cross-examination that if Mrs Sumner fell head first, landing on her head, it was more likely than not to have caused a hyperextension injury, Mr Gardner disagreed. He explained that commonly a person with a hyperextension injury and an associated central cord lesion will have fallen striking their forehead, forcing their head backwards; but if you hit the back of the head, it is typically that blow which forces the head forward. If there is a degree of rotation, i.e. you hit one or other side of the head, it will then force it in that direction, which is why you will tend to get a unifacet dislocation as opposed to a dislocation on both sides.

Mr Gardner was taken to the notes made by the paramedics. He was not taken to the notes taken on Mrs Sumner’s admission to A&E, which record that she slipped and fell whilst ascending the stairs, so in order to have gone down head first and landed on her head, she must have fallen backwards. This means that the part of her head that she struck on impact at the bottom of the stairs would have been either the back or the side of it, not the front. The mechanism of her fall is therefore more likely to have caused a flexion injury than a hyperextension injury, just as Mr Gardner said.

Mr Jamil seemed to me to be alive to this problem, because at the end of his evidence in chief he volunteered a new theory that because there was no scalp laceration or “egg head”, and because she would have been relatively flaccid because she had consumed a quantity of alcohol, Mrs Sumner fell on her chin over her arm, which is what broke her right humerus, and this is what extended her neck. I did not find that explanation remotely persuasive; it appeared to me to be a very unlikely way for her to have landed if she fell backwards.

It was common ground between the experts that if the head is thrown back there may be no fracture to the spine at all. If there is one, the commonest fracture in Mr Gardner’s experience is to the spinous process. This happens when the two spinous processes, which are like the T of a T bone, and are almost parallel, come together, and one of them breaks. There was no such fracture here. However, Mr Gardner accepted that when the head is thrown back there could be a fracture to the lamina. Mr Jamil acknowledged that with hyperextension injuries you do not often see soft tissue disruption or a fracture in the place where it actually occurred in Mrs Sumner’s case. His explanation was that it was a severe form of hyperextension injury and said that the location of the fracture was inconsistent with it being a flexion injury, though I did not follow his reasoning as to why that was, and Mr Gardner disagreed, for the reasons that he gave.

Either type of injury could cause damage to the anterior longitudinal ligaments, although Mr Gardner said he would not expect to see it in a hyperextension injury, but would not be surprised to see it in a flexion injury. He very fairly accepted that damage to the anterior longitudinal ligament and posterial longitudinal ligament could be consistent with either a hyperextension or a flexion injury. Damage to both ligaments occurred in this case. With a flexion injury, both experts accepted there could be a fracture of the vertebrae because of the pressure on the front of the spine. Mr Jamil’s evidence was that this was “virtually inevitable” but there was no such fracture in Mrs Sumner’s case. However more commonly, according to Mr Gardner, depending on how the force is applied, there would be a dislocation or slipping forward of the facets, as happened here. Mr Gardner also drew support from the fact that there was damage to the facets on both sides, as mentioned in the report from the first CT scan, which he said was more likely to occur with a flexion injury.

So far as the MRI scans were concerned, the pre-operative MRI image shows the spine in alignment. However the post-operative MRI images of 4 March 2011 show that the spinal column at C6 and above has dislocated forwards because the fractured facet (on the left hand side) has been allowed to fall forward. Mr Gardner said that was consistent with a flexion injury. Although the post-operative images show that the spinal cord was being squeezed, the patient gradually improved after the operation. Mr Gardner said that this was because the spine was now fixed in position, which also fitted his theory as to how the damage occurred. Mr Gardner said that although the facet joint is not visible on the MRI scans, what is seen in the movement of the spine at C6 and C7 is exactly what you see in almost every case of a facet dislocation. Mr Jamil did not disagree with that proposition, but he said that the dislocation visible at C6 and C7 could be due to an over-correction in surgery. Although that was a perfectly fair point, and he could well be right, his evidence in this regard again displayed a lack of objectivity, because he refused to countenance the possibility that it could have been due to anything else.

In my judgment, on the balance of probabilities, the injury sustained by Mrs Sumner was a flexion injury for the reasons stated by Mr Gardner, whose evidence in this regard I prefer (even if the dislocation seen on the March 2011 MRI image is discounted as being the possible result of surgery). In any event, and regardless of the mechanism of her injury, she had mild neurological impairment on her admission to hospital. Up to 31 December only the left arm ever appeared to be getting worse. There was some history of problems with the left arm, and that was also the side of the fracture. However the first sign of significant deterioration in muscle power in that arm came after Mrs Sumner was mobilised out of bed on 27 December. After she was returned to flat bed rest, it remained stable and even showed signs of improvement.

The evidence in the medical notes points much more towards deterioration associated with movement/mobilisation rather than to a gradual downward progression associated with spreading oedema. The clinicians and the physiotherapists treating Mrs Sumner at the time when she became tetraplegic all believed that there had been an interruption to the oxygen supply from some new cause. The doctors mentioned spinal compression. They did not consider the possibility of injury through movement, presumably because they thought the spine was stable. None of them seems to have considered CCS. The physiotherapists, on the other hand, did query the correlation between mobilisation and neurological deterioration at the time. There was no reliable evidence of deterioration in her neurology whilst she was being kept spine in line. When she was kept flat she was either stable or improving. That also accords with the statistical probabilities.

At 0900 on 31 December 2010 Mrs Sumner appeared to be regaining strength in her upper arms, the muscle power in her right arm was back to normal (and had been for over a day) and there were no problems with her legs. There was a rapid loss in muscle power in the upper limbs after she was mobilised, consistent with further spinal damage. After that, and after the sudden deterioration in her condition, in marked contrast to what happened after her mobilisation on 27 December, Mrs Sumner was not kept flat with her spine in line. It is far more likely that her worsening neurology after she was mobilised on 31 December was due to further spinal injury caused by movement, as Mr Gardner believes, than to progression of the oedema caused by the initial trauma.

In my judgment, therefore, had she had an operation to stabilise her spine on or before 29 December, the anticipated prognosis for Mrs Sumner’s recovery would have been at least as good as her neurological condition at 72 hours post-accident, i.e. on that date. It is highly unlikely that her condition would have deteriorated after her spine was stable. The Claimant has proved causation on the balance of probabilities. Kirschblum suggests that an examination after 72 hours is a more reliable indicator of prognosis than examination upon admission. Mr Jamil did not disagree with that. I must take account of the pre-existing weakness on the left side due to the spondylosis, but in view of the good recovery that she did make from complete tetraplegia, I would expect that after the surgery Mrs Sumner would have continued to have full use of her legs and right arm and hand. There would have been some residual weakness in the left hand, possibly similar to its current condition. She would have had normal mobility and no impairment to her bladder or bowels.

Mrs Sumner has a number of significant permanent disabilities which I find, on the balance of probabilities, were caused by the failure to operate to stabilise her spine on or before 29 December 2010:

As I have already indicated, I am not persuaded that there is a causal link between the Defendants’ negligence and the development of gastroparesis. Her neck and coccyx pain are also due to the original injury and/or natural degeneration, but as Mr Gardner pointed out, pain management is easier when one is fully mobile.

General damages have been agreed at £135,000 inclusive of interest. So far as special damages are concerned, the parties have agreed the quantum on many of the items claimed; there are a few remaining matters in issue on which I have been invited to make a ruling in principle, and then Counsel have offered to carry out the final computations to put in the order. I was provided with a Scott Schedule which indicates the areas of disagreement.

According to Mrs Sumner-Smith, the level of family care provided to her mother prior to her admission to Stoke Mandeville was far greater than the care provided afterwards, which reduced to around 2 hours per week. The claim starts at 1 February 2011 (just under a month after the initial stabilisation operation) but Mrs Sumner would probably have required the second operation in any event and thus would have been in hospital for at least part of this period. Doing the best I can, I will allow 10 hours per week for the period from 1 February to 2 March 2011, and 2 hours per week for gratuitous family care during the remainder of Mrs Sumner’s period in Stoke Mandeville. I hope that the parties are going to be able to agree the figures for gratuitous family care from the end of March 2012, which I would reduce to 1½ hours per week. In terms of gratuitous family case management, which largely covers Maureen Sumner-Smith’s help with her mother’s finances, I shall allow the claim in full. The parties agree that the total is to be reduced by a 25% Housecroft discount.

Mrs Sumner has returned to, and stayed in her flat throughout. It is clear that she requires on-going care. On her initial discharge from Stoke Mandeville she engaged a specialist care agency, Active Assistance, to provide her with care. This is agreed to have been reasonable given that they specialise in caring for people with spinal injuries and Mrs Sumner was still recovering and required more assistance then. Subsequently as her condition improved, in October 2012 she moved to a private care regime which is provided by self-employed carers from South Africa who operate on a rota and who are managed by a lady named Pam. Mrs Sumner is very happy with that arrangement, although her daughter and some of the expert witnesses expressed some concern about it because of uncertainty as to how long it may be able to continue. I shall revert to that concern when assessing future care costs.

So far as past costs are concerned, I allow all the claimed costs for Active Assistance and for the care incurred and paid for since October 2012, in full, including the Bank Holiday double pay evidenced by the invoices. Accommodation is agreed at £9,480. So far as household expenses are concerned, clothing is agreed at £850. I accept the sum of £50 per week estimated by the Claimant for the carers’ food. The claim for heating costs relates to the estimated cost of the use of electric heaters to supplement the central heating. Since the heaters would only be used during the colder months of the year the Claimant’s estimate seems rather high. I will allow a total figure of £700.

In terms of travel and transport the cost of Mrs Sumner’s family’s travel to hospital and the carer’s use of public transport are agreed; the only contentious item is the taxi fares incurred for transport to and from physiotherapy sessions after the physiotherapist stopped visiting Mrs Sumner at home in mid-2012. On the basis that these are all supported by invoices, and would not have been incurred in any event, I see no reason to disallow them. I note that there is no evidence that Mrs Sumner would have managed to get to the hospital in Roehampton on public transport or that she could have been driven there instead. According to Mrs Sumner the intensive physiotherapy she received was responsible for the marked improvement in her physical condition.

On the evidence I heard, although a professional case manager was engaged to assist Mrs Sumner he did not do (or perhaps more fairly, was not permitted to do) as much as he might have done in that regard, save for the assistance he provided in the purchase of a new car. Most of the assistance she received that might have been provided by a case manager was provided by her two daughters, particularly Maureen, who gave particular help with matters such as her tax return. Mrs Sumner is mentally alert and capable of dealing with many matters herself, and she understandably prefers to keep matters such as her personal finances private. The claim for past professional case management has been reduced to the invoiced sum of £4,515.60. I consider a reasonable sum to be £2,000.

The pleaded claim for medical expenses is £3,404 and it is now said that this is an error and the real total should be £5,954 because some physiotherapy costs were overlooked in the calculations. It is claimed that Mrs Sumner has undergone hydrotherapy at a cost of £3,204. The Defendants’ physiotherapy expert Ms Edmundson supports a claim for three initial sessions and 50 group sessions per year at Parkside Hospital, and that was based on recommendations made by the Claimant’s physiotherapist, Ms Filson after June 2013 when Mrs Sumner had already been attending some hydrotherapy sessions, although not once a week. The cost estimated by Ms Edmundson for three further 1:1 sessions at £73 per session and 50 weekly group sessions at £15 per session, when rounded up, came to £969 (not £819 as stated by the Defendants). I have looked at the Claimant’s invoices said to fall under this category, only one of which specifically relates to a “hydroclass” and is for £16. The remaining invoices are for “physiotherapy” at what appears to be a cost of £26 per session (though they often involve 3 or 4 sessions per invoice). Some pre-date Ms Edmundson’s visit.

I am prepared to allow the weekly group sessions at £16 rather than £15, and the three 1:1 sessions at £73 each. It is difficult to assess how much to allow as a reasonable sum for hydrotherapy undertaken prior to June 2013 but I would have been willing to allow for another three 1:1 sessions at £73, bringing the total for hydrotherapy up to £1238.

When it comes to the physiotherapy, it is accepted in principle by the Defendants that some allowance should be made for physiotherapy to provide pain relief, but I have to bear in mind the fact that Mrs Sumner would have been in pain from her neck come what may. On the other hand, the Defendants’ figure of £1,200 only relates to the period from March 2014, which is too short. So far as dental hygiene is concerned, Mrs Sumner said she would have visited the hygienist in any event but not quite so often. I am not persuaded that it is reasonable to allow for an extra session every three months as claimed.

If I were to add £1238 for the hydrotherapy to £2,550 claimed for the physiotherapy sessions that would exceed the sum that is pleaded under this head. It seems to me that the fairest approach is to allow the Claimant £3,500 in total, a little more than she originally claimed, on the basis that there is sufficient evidence to support the reasonable expenditure of at least that sum, her actual expenditure has been higher, and no application has been made for permission to amend the Particulars of Claim.

In terms of past aids and equipment, although Mrs Sumner spent over £3,000 on a top of the range riser recliner chair, I accept the evidence of Mrs Ho that a reasonable sum for such a chair would have been in the order of £1,500. The remaining costs are agreed at £996. The parties have agreed the rate of interest on past losses at 1.02%.

For the future, there will have to be adaptations to the flat, among other things to allow greater accessibility to all the rooms using a wheelchair. The experts are agreed that some alterations will need to be made to the existing (sole) lift by putting in buttons that are more accessible at a cost of some £9,000. Mr Wethers, the Claimant’s expert on accommodation, drew some detailed plans to support his proposals. The Defendants’ expert, Mr Pile, agreed that this plan was reasonable, and in the end the issue between the parties turned on the reasonableness of the costing for Mr Wethers’ plan.

In general terms I considered the budget set by Mr Wethers for the works, bearing in mind that the flat is in London, where workmen’s costs are higher than elsewhere, was generally reasonable. Whilst it seemed to me that it ought to be possible to obtain a better idea of the cost of replacement windows from the local council’s preferred supplier, Govette, the estimate for such replacement seemed modest in the light of how much the samples cost.

There will be no need to replace the internal central heating, and I also felt that perhaps Mr Wethers had over-budgeted for the electrical work (which, as Mr Pile said, allowed for more than enough money to re-wire the entire flat), and for the cost of supervising the installation of specialist equipment given that the majority of this work will be undertaken by the occupational therapist. I will therefore allow a total of £250,000 for adaptations to the flat instead of the £283,706 budgeted for by Mr Wethers.

So far as the household costs are concerned, the Defendants are right in principle about there being no allowance for window cleaning which would be carried out anyway. Whilst I accept that Mrs Sumner is now more reliant on a mobile phone than she was prior to her accident, that may have been the case in any event; I shall allow half the sum claimed under this head (£180 per annum). Subject to those adjustments the Claimant’s figures are accepted.

In terms of travel and transport I allow the revised claim for the VW Caddy as calculated by the Claimant. Regardless of who does the driving, Mrs Sumner plainly needed a new car adapted to meet her needs; she could not fit the model recommended for her in the garage, but she appears to get by with the smaller car even though it will not accommodate her electric wheelchair.

So far as medical expenses are concerned, despite my general confidence in the opinions expressed by Mr Gardner, I consider that Mrs Sumner’s pain management can be reasonably dealt with on the NHS at Stoke Mandeville. It is reasonable in principle for her to have access to private treatment for her bladder and bowels, and the amount allowed by the joint expert Mr Reynard is agreed to be reasonable in those circumstances. The future physiotherapy and orthotic costs have now been agreed. I consider that Mrs Sumner should be allowed 20 sessions of OT at £120 per hour; as Mrs Ho said, that is a modest figure over the whole of her remaining lifetime.

So far as future care to the first periodical payment is concerned, I accept the Claimant’s revised figure for the current care regime to include the cost of food for the carers and the bank holiday supplement (£36,170). In terms of future commercial case management I am not persuaded by Mrs Sargent’s evidence that Mrs Sumner will need anything like 50 hours of such assistance per year. I will make an allowance for 26 hours per annum at the agreed hourly rate of £98 (the equivalent of an hour’s help per fortnight). The figure for travel will have to be adjusted accordingly. The parties should be able to work out the appropriate multiplier, which the Claimant has now reduced to 0.88.

For the period from 15 December 2015 to age 78 the parties have assumed a replacement of the current care regime with a commercial carer. I am far from convinced that will happen. I consider that it is far more likely that the existing arrangements will continue for the foreseeable future. They suit Mrs Sumner and I consider the anticipated problems over visas are unlikely to materialise. However, I agree that the contingency of a change in regime should be provided for. Mr Boyle has costed the matter on the basis of a non-specialist spinal care provider. Although in principle I agree that Mrs Sumner will not need an agency such as Active Assistance and it would be unreasonable to expect the Defendants to pay for care at their more expensive rates, his figures still seem to me to be on the low side. I would allow a weekly rate of £750 and the rates for food and travel claimed by the Claimant. I will allow the same provision for case management as before, namely, 26 hours per annum.

In terms of care for the final three years, there is not a great deal between the parties in terms of the enhanced care costs, the difference largely being based upon whether a specialist provider such as Active Assistance is engaged. Once again, I consider Mr Boyle’s rates are on the low side even though it would be inappropriate to engage Active Assistance; the costs of care are bound to increase over time. I shall allow £900 per week for the live in care and £600 for sleep in care, £50 per week for the carers’ food expenses, and £225 for agency break cover. It also seems prudent to make an allowance of £60 for travel expenses, as the Claimant has claimed. There may be a requirement for greater case management during this period and I shall provide for the 60 hours that Mrs Sargent recommends.

In terms of future equipment, agreement has been reached on many of the items claimed. As to the manual wheelchair, Mrs Ho has recommended a very lightweight model at a cost of £4,700. Mr Boyle’s recommended model, also lightweight, is said to be almost as light, but costs a fraction of the price. Mr Boyle has made no allowance for a replacement. I do not understand there to be anything inherently unsuitable about the model recommended by Mr Boyle other than the fact that it is (slightly) heavier, but the disparity in cost is enormous. Bearing in mind that Mrs Sumner will have a very good electric wheelchair, I shall allow the sum suggested by Mr Boyle, but also build in the cost of one replacement.

I also consider the Claimant is right in principle to allow for the cost of maintenance of equipment. I would be surprised if the electric wheelchair requires replacing in so short a time as 2 years; I should allow for replacement after three years. It is best to err on the side of caution in terms of the costs of recharging especially as electricity is not getting any cheaper, so I accept the Claimant’s estimated figure for that.

Although Mrs Sumner said that she would enjoy having a power scooter because she would be able to travel further in it, I do not consider it reasonable for the Defendants to have to pay for one. I have very considerable doubts as to whether Mrs Sumner would use it, and even if she did whether it would be safe for her to do so. In order to look to her left and right she would need to rotate her body from the waist because of stiffness in her shoulders. She no longer drives her car because she does not feel sufficiently confident to look right and left. In any event she needs to be accompanied by a carer when she goes out on a trip of any distance. In my judgment she should be able to manage well enough with the electric wheelchair and being taken out in the car if she needs to travel longer distances.

I accept the evidence of Mrs Ho that it would be reasonable for Mrs Sumner to replace her existing bed with a specialist profiling bed at a cost of £3,500. She spends a lot of time resting in bed and it is reasonable for her to have a bed which is comfortable and aethestically pleasing. However I am not persuaded that there is a need for a portable hoist to cater for the possibility of falls.

Although on her discharge from hospital and when she was feeling much more poorly, Mrs Sumner consented to her bathroom being turned into a wet room with only a shower (as she was not confident about getting into a bath even with a special chair lift provided by her local authority) she told me that she really misses having a bath. Mrs Ho accepted that she has no medical need for a bath, but felt that it would be therapeutic for her, and I agree that it might help to alleviate some of the stiffness and pain and fatigue from which she currently suffers. It would be reasonable for a suitable model of Gainsborough bath to be purchased which enables access by means of a chair or equivalent – a step-in bath may be unsuitable because of the length of time that Mrs Sumner would have to sit in it waiting for it to fill and then drain, not to mention the hazard created by the step itself.

I am persuaded that it would be reasonable for Mrs Sumner to purchase an après shower dryer for all the reasons given by Mrs Ho. However I agree with Mr Boyle that it is reasonable to expect Mrs Sumner to manage with a Mowbray toilet rather than the Clos-o-Mat model recommended by Mrs Ho. She has no apparent problem in using such a toilet at present, and whatever model is supplied, she will still have to cope with rails and have the same problems in balancing.

Finally, I turn to the contentious issue of future holidays. Mrs Sumner has a close connection with Brazil, where she lived for over 15 years and where many of her close friends still reside. Prior to her accident she was a regular traveller to that country, every two years or so, and she would dearly love to return there at least once more. I was satisfied on the medical evidence that it would be possible for Mrs Sumner to travel to Brazil and to manage the long-haul journey in safety on the plane if she travelled in business class with her carer; the journey would have to be carefully planned and, as Mrs Sargent said, the logistical problems are likely to arise more at either end than during the plane journey itself. I was also satisfied that Mrs Sumner really wants to go.

I did have some doubts as to whether she would ever pluck up the courage to make that journey, bearing in mind that she has had the financial resources to do so since she recovered to her current level of health and yet she has made no attempt to go. Indeed she told Mr Boyle last year that she doubted whether, realistically, she would ever venture the journey again. However, having taken Mrs Sumner’s evidence and that of her daughter into account, I take the view that an allowance should be made for one more trip, with a carer travelling in business class with her.

I believe that I have now dealt with all the contentious issues on the Claimant’s schedule. I therefore leave it to the good offices of Counsel to make the necessary calculations and provide the figures to go into the final order.