[2002] EWHC 1649 (Q.B.)
Case No: 97Q00195
 
IN THE HIGH COURT OF JUSTICE
QUEENS BENCH DIVISION

Royal Courts of Justice
Strand, London, WC2A 2LL

Date: 6th September 2002

Before :

THE HONOURABLE MR JUSTICE FIELD
- - - - - - - - - - - - - - - - - - - - -
Between :

	Alan Roy Dunk	Claimant	
	- and -		
	North Staffordshire Hospitals NHS Trust	Defendant	

- - - - - - - - - - - - - - - - - - - - -
- - - - - - - - - - - - - - - - - - - - -

Mr. Kieran Coonan Q.C. and Miss Tejina Mangat (instructed by Taylor, Simpson and Mosely) for the Claimant
Mr. Terence Coghlan Q.C. and Mr. Andrew Kennedy  (instructed by Reynolds Porter Chamberlain) for the Defendant

Hearing dates : 8th, 9th, 10th ,11th, 12th,15th,16th & 17th July 2002
- - - - - - - - - - - - - - - - - - - - -
Approved Judgment

I direct that pursuant to CPR PD 39A para 6.1 no official shorthand note shall be taken of this Judgment and that copies of this version as handed down may be treated as authentic.

.............................
Mr. Justice Field

Mr Justice Field:

Introduction

1.	On 5th May 1994 two ENT surgeons, Mr. William Vere Carlin and Mrs. Marcelle Macnamara carried out a tracheostomy on the claimant (“Mr. Dunk”) at Stoke City General Hospital (“Stoke”). A tracheostomy is an operation in which the windpipe is opened from the front of the neck so that air may obtain direct entrance to the lower air passages. The diagnosis made by Mr. Carlin and Mrs. Macnamara was that Mr. Dunk’s upper palate, tongue base and pharyngeal walls were collapsing into his upper airway when he was asleep on his back with the result that he was suffering from a condition known as obstructive sleep apnoea. Almost six years later he was examined by a Consultant ENT surgeon at the Royal National Throat, Nose & Ear Hospital, Mr. Paul O’Flynn, who, although he observed palatal flutter, found little if any sign of the collapsing structures that had been observed by Mr. Carlin and Mrs. Macnamara. Instead, he found that Mr. Dunk had an enlarged floppy epiglottis which was slamming over the opening of the larynx on inspiration. Mr. O’Flynn removed a section of Mr. Dunk’s epiglottis to prevent it from obstructing the windpipe and reversed the trachestomy.
2.	 Mr. Dunk alleges that his condition was misdiagnosed by Mr. Carlin and Mrs. Macnamara and that the tracheostomy they performed was unnecessary. In the alternative he asserts that the doctors in charge of him after the operation, who included Mr. Carlin and Mrs. Macnamara at Stoke and others at the General Hospital in Burton-on-Trent (“Burton”) negligently failed to reassess his condition either by causing a second nasendoscopy to be performed or by referring him for a second opinion.  If they had done so, he says, the alleged misdiagnosis would have been discovered and the tracheostomy reversed and an epiglottectomy done much earlier than eventually happened. Mr. Dunk avers that the tracheostomy ruined his life. He says that it was the cause of many infections and that it brought on serious psychological problems; it also made his pre-existing asthma much worse; not only was he unable to work before the tracheostomy was reversed but he will never be able to work again. He claims damages in the order of £717,800 from the defendant NHS Trust which at the relevant time employed Mr. Carlin, Mrs. Macnamara and the doctors at Burton into whose care he was transferred in April 1995. 
The factual background
3.	The story begins in 1992. Mr. Dunk, then aged 34 years, was working on off-shore oil rigs as a pipe fitter and was becoming very unpopular with his work mates on account of his very loud snoring.  On 20th March 1992 his GP, Dr. Farrell, referred him to Mr. De, a Consultant ENT surgeon at Burton, in respect of a recurrence of a nasal obstruction and loud snoring. Mr. De put Mr. Dunk’s name on the list for repeat submucous resection of the nasal septum.
4.	 In addition to snoring, Mr. Dunk was sleeping badly. He felt very lethargic and would wake swollen from the neck up with blue lips and blue under his eyes. He was finding it difficult to carry out his daily work and began to make silly mistakes. On 1st October 1992 his GP again referred him to Mr. De saying that his problem with his nose and throat “is getting an awful lot worse…. his snoring is becoming quite anti-social.”
5.	On 10th February 1993, Dr. Corlett, Staff Grade in ENT (Mr. De) at Burton wrote to a Burton Consultant Anaesthetist saying that Mr. Dunk was a prime candidate for a sleep study; he was a major snorer, was often tired next day and appeared to have apnoeic episodes i.e. episodes when he stopped breathing so that there was a marked fall in the level of oxygen entering the arterial blood stream. The letter went on: “His nose has satisfactory airways. He has a lot of floppy tissue around his posterior fossi” [i.e. the cavity at the back of the throat]. In May 1993 Mr. Dunk underwent a sleep study at Burton. Dr. Corlett concluded that he had an upper airway obstruction when he was lying on his back or stomach and recommended that he had  uvulopalatopharyngoplasty (“UPPP”) which involves trimming the soft palate. In the event, however, Dr. Corlett referred Mr. Dunk to Dr. Keith Prowse at Stoke. At the relevant time Dr. Prowse was a Consultant Physician whose main research interest was sleep disordered breathing and transnasal ventilation. In 1982 he established at Stoke the first laboratory for sleep and breathing disorders in England and Wales which became the Sleep Centre for the West Midlands Region of which he was Director. Dr. Prowse is eminent in the field of sleep apnoea. Before he retired earlier this year he saw between 1000 and 1200 patients a year for this condition. 
6.	Mr. Dunk’s referral to Dr. Prowse was a “tertiary referral”. It required special authorisation and had funding implications. Authorisation was given because of the seriousness of Mr. Dunk’s condition. Dr. Prowse arranged for Mr. Dunk to undergo two sleep studies on 16th and 17th March 1994. During these studies the oxygen saturation level of Mr. Dunk’s arterial blood was measured. On 16th March 1994 the maximum saturation level was 97% and the minimum level was 91%. Episodes in which the drop in the saturation level was 4% or more (“desaturations”) were recorded. On 16th March Mr. Dunk had 53 such episodes. A normal person has about 1 or 2 such episodes in a night. Mr. Dunk also had 94 hypopneas, i.e. occasions when he stopped or almost stopped breathing. It was Dr. Prowse’s evidence that the most important information provided by the sleep studies was the number of desaturations.
7.	During the second sleep study on 17th March 1994 an attempt was made to  provide Mr. Dunk with Continuous Positive Airways Pressure (“CPAP”). CPAP is the usual treatment for patients suffering from obstructive sleep apnoea. Obstructive sleep apnoea is caused by a loss of muscle tone in the palate, tongue base and the walls of the pharynx which causes these structures to fall back and obstruct the upper airway when the patient is asleep and lying on his back. The floppiness of the palate causes the palate to vibrate as air is breathed in and out. It is this which produces snoring. CPAP is the continuous delivery of air under pressure through the nose and mouth. Since the air is under pressure it opens up the airways and allows air to enter the windpipe (the trachea). It was described in evidence as an internal or pneumatic splint.  The regular use of CPAP (together with weight loss and reduction of alcohol consumption) often relieves obstructive sleep apnoea.
8.	The delivery of CPAP requires the patient to wear a mask through which air is blown into his nose and mouth. On 17th March 1994 Mr. Dunk had difficulty with the CPAP delivery. He found the mask to be claustrophobic and the inside of his nose swelled because he suffered from rhinitis, an inflammation of the mucous membrane of the nose. He said in evidence that he only tolerated the mask for 15 minutes. The surviving records do not show directly for how long CPAP was delivered to Mr. Dunk. However, the records include a trace drawn by the instrument measuring oxygen saturation. From this it can be seen that between midnight and 2.00 am there were no desaturations exceeding 4%. Throughout a sleep study at Stoke the patient is videotaped but the recordings are not kept longer than a few days. In making his assessment of Mr. Dunk’s condition, Dr. Prowse studied the video recordings of the sleep study and the trace record and also took into account an oral report from the supervising technician.
9.	When giving evidence Dr. Prowse clearly recalled on the basis of the video recording and the technician’s report that Mr. Dunk was asleep and wearing the mask and receiving CPAP between midnight and 2.00 am on 17th March 1994. I accept this evidence of Dr. Prowse who in my judgement was a careful and reliable witness. Mr. Dunk gave his evidence honestly but he has developed a great deal of anger and resentment over what he feels were serious shortcomings in the care he received at Stoke and Burton and this in my view has caused him in some instances to give unreliable evidence at the expense of the physicians and surgeons who treated him before he was referred to Mr. O’Flynn. In short, I conclude that Mr. Dunk is an unreliable historian when describing his treatment and his condition.
10.	During the 17th March 1994 sleep study the number of desaturations was 22; the maximum and minimum saturation levels were 91% and 78% respectively; and the number of hypopneas was 156.
11.	The following day  Dr. Prowse wrote to Mr. Corlett with his assessment of Mr. Dunk. He reported that the overnight sleep study confirmed severe obstructive sleep apnoea with numerous episodes of apnoea. There were frequent periods of arterial oxygen desaturation but in the main the oxygen level was in the range 80-90%. CPAP abolished the abnormalities but Mr. Dunk still had considerable difficulty in breathing because of his nose problems. There was no doubt that he had sleep apnoea syndrome and of such severity that nasal CPAP would usually be the treatment of choice. There was strong evidence that UPPP is effective in mild cases but in severe cases sleep apnoea almost always returns within about 12-18 months and it is then more difficult to treat with CPAP. Before CPAP could be used the nasal problems required action on the ENT front. If it could be helpful, Mr. Corlett could have a word with Mr. Carlin who worked closely with Dr. Prowse on snoring and CPAP problems. As soon as the nasal problem had cleared, Dr. Prowse would be happy to see Mr. Dunk again to review the use of CPAP.
12.	 It was suggested to Dr. Prowse in cross-examination that his conclusion that CPAP abolished the abnormalities was insupportable because in fact Mr. Dunk had only been able to tolerate the CPAP for a short time. However, as I have said, I accept Dr. Prowse’s evidence that he based his conclusion on the trace and the video recording and the technician’s report and that these latter two sources indicated that Mr. Dunk was asleep receiving CPAP between 12.00 midnight and 2.00am on 17th March 1994. Accordingly, I find that CPAP did indeed abolish the abnormalities which were the cause of Mr. Dunk’s severe obstructive sleep apnoea.
13.	On 29th March 1994 Mr. Carlin saw Mr. Dunk for the first time in his clinic and placed him on steroids to see if this would calm his nasal problems and so clear the way for CPAP treatment. Mr. Carlin did not suggest further nasal surgery since Mr. Dunk had already had four operations on his nose and he was still having problems. Mr. Carlin saw Mr. Dunk again on 11th April 1994. The steroids had not improved the nasal problem and Mr. Dunk was continuing to suffer greatly from obstructive sleep apnoea. Mr. Carlin therefore advised that Mr. Dunk undergo a nasendoscopy. This is a procedure in which the patient is sedated to mimic sleep and his upper airway and pharynx are examined using a flexible scope. A nasendoscopy would allow Mr. Carlin to see where the obstruction was which was causing the sleep apnoea. If the obstruction was at the palate level, he suggested that Mr. Dunk have UPPP. Mr. Carlin discussed the possibility of a tracheostomy with Mr. Dunk. He told him that if UPPP was not appropriate a tracheostomy would be likely to cure the obstructive sleep apnoea. The procedure was reversible and he hoped it would be temporary but he did not promise that it would resolve the obstruction causing the sleep apnoea. He explained how the procedure was carried out and what the after-care would be. Mr. Dunk denied that there was any such discussion with Mr. Carlin but I accept Mr. Carlin’s evidence about this without reservation.
14.	Mr. Dunk was accordingly booked in for a nasendoscopy and possible UPPP or, failing that, a tracheostomy. Before the procedure was carried out Mr. Carlin again talked to him at some length making sure that he was clear what was involved. I find that Mr. Dunk unequivocally consented not only to a nasendoscopy but also to UPPP or a tracheostomy depending on what Mr. Carlin thought was the better option once the causes of the obstruction had been seen through the endoscope. Mr. Dunk told Mr. Carlin that he would accept anything that would improve the quality of his life; if Mr. Carlin thought that a tracheostomy was the only option, he (Mr. Dunk) would accept the procedure.              
15.	A nasendoscopy and tracheostomy were performed on Mr. Dunk by Mr. Carlin and Mrs. Macnamara on 5th May 1994. At this time the practice at Stoke was for a Senior House Officer (“SHO”) to obtain the consent of the patient to the contemplated procedure or procedures. The SHO would see what those procedures were from the notes and would specify them on a pro forma consent form He would then obtain the patient’s signature to the form. In Mr. Dunk’s case the SHO was a GP trainee who had little interest in surgery. She wrote on the consent form “? UPPP   EUA [i.e. examination under anaesthetic] of palate and nose.” There was no mention of a tracheostomy as there ought to have been. The normal practice was for the consent form to be  checked in the theatre by the surgeons before carrying out the operation. Unfortunately, this did not happen in Mr. Dunk’s case. Mr. Carlin and Mrs. Macnamara accepted that they should have looked at the form; if they had done so they would have noticed that it made no reference to a tracheostomy. This failure was an unfortunate lapse but, as I have held, Mr. Dunk had in fact unequivocally consented to a tracheostomy after Mr. Carlin had fully explained to him the procedure and its implications.
16.	Mr. Carlin was (and is) an experienced surgeon of considerable distinction. He had been appointed Consultant ENT Surgeon at Stoke in 1987 since when he had worked closely with Dr. Prowse. By May 1994 he had performed a great many nasendoscopies. Mrs. Macnamara is now a Consultant ENT Surgeon at Birmingham Heartlands Hospital. In May 1994 she was a senior ENT Registrar. Before coming to Stoke she had been a Registrar at the Royal National Throat Nose and Ear Hospital and had worked under Mr. Charles Croft, an eminent ENT Surgeon. Whilst at that hospital she had performed a considerable number of nasendoscopies. The first 10 to 20 were carried out under the direction of Mr. Croft; the remainder she did alone. 
17.	By the time Mr. Carlin and Mrs. Macnamara came to make their witness statements for the purpose of these proceedings, some seven years had gone by since they had operated on Mr. Dunk. Over that period they have each performed a great many operations, including many nasendosopies. It was not surprising then that they had little specific recall of the detail of the operation on Mr. Dunk. They were assisted by Mrs. Macnamara’s post operation note that she wrote very shortly after the operation. The relevant part of this note reads:
Sleep Nasendoscopy + Tracheostomy 
 Indicn:- Gross obstructive sleep apnoea with desaturation to 30-40% SaO2 
Sleep nasendoscopy  Gross complete obstruction at palatal & at tongue base level in normal supine position.
18.	The records show that at no time did Mr. Dunk suffer desaturation to 30 – 40% SaO2 whether during the operation or during the sleep studies. In the light of this Mrs. Macnamara thought that Mr. Carlin had probably told her during the pre-op discussion that Mr. Dunk’s desaturation level had reduced to around 70% SaO2 and that instead of writing “desaturation to 30-40% SaO2” she should have written “desaturation by 30-40% SaO2”. Mr. Carlin had no specific recollection of saying this but did not deny he might have done so. Since there is no basis for thinking that there was at any time desaturation to 30-40% and because Mrs. Macnamara struck me as being a reliable and straightforward witness, I conclude that Mr. Carlin did indeed tell her that there was desaturation during the sleep studies to around 70%SaO2 and that she wrote “to” when she should have written “by” in her note.
19.	It was Mrs. Macnamara who first looked down the endoscope into Mr. Dunk’s nose and throat. She then handed over to Mr. Carlin who repeated the procedure. In her note Mrs. Macnamara recorded the abnormalities that she and Mr. Carlin observed; she did not note the normal structures. She told me and I accept her evidence on this that not only did she observe that Mr. Dunk’s upper palate and tongue base were collapsing into his airway but she also observed that Mr.Dunk’s pharyngeal walls were prolapsing. She did not record this last feature because it was not the predominant feature. Mr. Carlin’s observations were the same. In evidence they used the expression “multi-segmental collapse” to describe what they saw.
20.	They had no specific recollection of moving the endoscope past the tongue base and into the larynx to look at that area, including the epiglottis, but both were adamant that this would have been in accordance with standard procedure and they were sure they followed the standard procedure. They said that if they had seen the epiglottis slamming over the opening of the larynx as was observed by Mr. O’Flynn they would have been bound to have noted such an abnormality. They saw no such thing and were therefore sure that Mr. Dunk’s epiglottis was not behaving abnormally when they carried out the nasendoscopy. 
21.	Both Mr. Carlin and Mrs. Macnamara said in evidence that if there is tongue base collapse room can be made for the endoscope to go into the larynx by moving the patient’s chin up and forward. There is also always available in the operating theatre a rigid endoscope that can be used to lift the tongue up and thereby gain access to the larynx. Mr. Carlin added that he always keeps the flexible endoscope in the throat as the patient is beginning to wake up. The tissues of the pharyngeal structures are sensitive to anaesthesia; the heavier the sedation the greater the degree of collapse. Thus as the sedation wears off the structures firm up permitting a view of the larynx, including the epiglottis. Although he had no specific memory of doing this when examining Mr. Dunk, he was sure that he would have done so because it was a standard procedure that he always carried out.
22.	Since structures in addition to the upper palate were collapsing Mr. Carlin and Mrs. Macnamara ruled out UPPP and performed a tracheostomy. This involved Mr. Dunk being given a general anaesthetic which required that he be intubated i.e. that a tube be passed into his lower airway to allow a gas (enflurane) to enter the lungs. Intubation was required because natural breathing ceases when a patient is under general anaesthetic. Mr. Carlin was sure that Mr. Dunk’s level of sedation would have been reduced to allow examination of the epiglottis before the general anaesthetic was administered for the tracheostomy.  
23.	Mr. Dunk said in evidence that when he came round from the operation he could not speak because he had not been given a speech valve and no-one explained what had happened; he thought his voice had gone for good. He said that he was not given a speech valve for two weeks because Mrs. Macnamara told him he could not have one. I reject this evidence. Whilst I am sure that Mr. Dunk found the tracheostomy strange and somewhat frightening in the first few days, I have no hesitation in accepting Mrs. Macnamara’s evidence that within a couple of days she had shown him how to speak by putting a finger over the hole in his neck. I also accept her evidence that Mr. Dunk had the support of the nursing staff.
24.	Mr. Dunk was discharged on 16th May 1994. He was still ill at ease with the tracheostomy but his sleep apnoea had improved dramatically. Three days later he was admitted to Burton for four days by Mr. De in respect of chest secretions and tracheostomy care. He was then admitted to Stoke under Dr. Prowse between the 14th to the 28th June 1994 for upper airway obstruction and acute asthma. During this admission he saw Mrs. Macnamara on 16th June whose note of the consultation shows that she was considering the possibility, albeit in the future, of decannulation i.e. the removal of the tracheostomy tube and the closure of the hole in the neck. Mrs. Macnamara saw Mr. Dunk again on 13th July 1994 after which she wrote to Dr. Prowse  saying that she felt fairly strongly that decannulation was not appropriate until there was objective evidence of improvement of obstructive sleep apnoea in the form of a full sleep study with the tracheostomy tube blocked off. She also queried the use of BIPAP (a variation of CPAP) with the tracheostomy in situ. Mr. Carlin also saw Mr. Dunk on 13th July. He suggested sleep studies with the tracheostomy blocked off.
25.	The hope at this stage was that Mr. Dunk’s multi-segmental collapse would become treatable with CPAP thereby allowing decannulation. However, following  an overnight oxygen study on 17th July 1994 Dr. Prowse wrote to Mr. Carlin saying that attempts had been made to carry out treatment with both CPAP and BIPAP but Mr. Dunk had not been able to tolerate any of the methods because of severe nasal symptoms. In Dr. Prowse’s view there was little option other than to leave Mr. Dunk with a permanent tracheostomy. By letter dated 11th August 1994 Dr. Prowse replied to Mrs. Macnamara’s letter of 13th July saying, inter alia, that the question was whether Mr. Dunk was left with a permanent tracheostomy or whether some attempt should be made at decannulation, which was where BIPAP came in. Dr. Prowse wrote that it was clear for reasons not fully understood that patients seem to tolerate the transfer from tracheostomy to BIPAP and thence to formal nasal ventilation or to CPAP better than the straight move from tracheostomy to CPAP. He concluded by expressing his concern at leaving a man of the age of Mr. Dunk  ( 36 years) with a long term tracheostomy.
26.	A short time later, following a visit from Mr. Dunk and his partner, Julie Slater, Dr. Prowse wrote by letter dated 15th August 1994 to Dr. Farrell, Mr. Dunk’s GP, with copies to those who had been treating Mr. Dunk at Stoke and Burton. Mr. Dunk was anxious to be rid of the tracheostomy as soon as possible and in his letter Dr. Prowse proposed a management plan as follows: (1) the tracheostomy would be left in place for at least a further 3-4 months to give time for it to settle and for Mr. Dunk’s sinuses and throat to improve; (2) in about March 1995, if the sinuses were clear, the next step would be to acclimatise Mr. Dunk to the nasal mask with the tracheostomy open to see if air flow induced blockage, rhinorrhea, or problems with sinusitis; (3) however, if such symptoms developed, Mr. Dunk would have to be left with a permanent tracheostomy; (4) if the sinus x-rays and nasal airflow were clear it would have to be weighed in the balance whether it was worth attempting decannulation under cover of BIPAP; factors which would need to be taken into account were the state of the tracheostomy itself, the benefit to the sleep apnoea and to the sinuses of keeping the tracheostomy, the disadvantage in relation to Mr. Dunk’s breathlessness and to respiratory tract mucus, and his general personality and psychiatric state. 
27.	Dr. Prowse was concerned about Mr. Dunk’s mental state. Mr. Dunk had a history of psychiatric problems and was reacting badly to the tracheostomy. Dr. Prowse therefore arranged for him to see a clinical psychologist. 
28.	Mr. Dunk saw Mrs. Macnamara  again on 31st August 1994. It seemed to her that he was managing his asthma well and also his anxiety problems. The tracheostomy looked fine and in particular was not causing any damage to the trachea. She thought that the problems of sorting out his nasal airway so that BIPAP and CPAP could be used were more complicated than Dr. Prowse had suggested in his recent letter. These problems had to be re-evaluated when Mr. Dunk came back in January 1995. They needed to be assessed and preferably sorted out prior to decannulation.
29.	On 16th November 1994, Mr. Dunk’s partner, Julie Slater, wrote a letter to Dr. Prowse telling him how worried she was about Mr. Dunk. She said the tube was blocked frequently; he was waking up at night with bad asthma; most days he seemed to be coughing up blood; he seemed to have had a few violent headaches; he had severe heart burn; and most days he bloated up; all this was having a drastic effect on their family life. She continued:
 We seem to have moved from 100% help to none. We feel very strongly that we have been abandoned and forgotten.
Whilst I can understand Ms. Slater’s concern and anxiety, I am bound to say that her suggestion that Dr. Prowse and his team had abandoned and forgotten her and Mr. Dunk was unjustified and unfair. Mr. Dunk had been admitted either to Stoke or Burton on four separate occasions for a total of over 30 days since the tracheostomy and additionally had been seen as an out-patient by each of Dr. Prowse and Mrs. Macnamara. 
30.	Dr. Prowse did not reply directly to Ms. Slater’s letter for fear of further misunderstandings, but he sent a copy of her letter to Mr. Carlin and Dr. Courthold, the clinical psychologist who had now taken on Mr. Dunk. In  his covering letter he addressed the problems of the blocking tracheostomy tube, the heartburn, the headaches and the bleeding. The final paragraph  reads:
I’m sorry that Mrs Dunk feels that we are not now supporting her because I think that is not true. We are in a position where I think there is little else we can do beyond the psychological support which Dr Courthold and his colleagues are now providing. The limitations and problems of a tracheostomy have been discussed with them many times and unfortunately it is very difficult for people to appreciate these in advance and not at all surprising that it puts on considerable stress. I do not know whether there are any specific support agencies locally which could help. 
31.	Between 22nd and 30th November 1994 Mr. Dunk was admitted to Stoke under Mr. Carlin for tracheitis, chest infection and exacerbation of asthma. On the first day of this admission he was examined by Mrs. Macnamara with an endoscope which was passed through the upper airway. She said in evidence that if Mr. Dunk’s epiglottis had been behaving as observed by Mr. O’Flynn she would have seen it, but it seems clear that Mr. Dunk had to be supine and asleep for his epiglottis to behave as it was observed to behave in 2000.
32.	On 6th December 1994 Mr. Dunk underwent an upper GI endoscopy to investigate his complaints of heart burn. The finding was: “There is grade 1 oesophagitis above a small hiatus hernia. No other lesion seen on this examination.” On 21st  December 1994 Mr. Dunk saw Mrs. Macnamara again, this time as an out patient. Flexible nasendosopy through the tracheostomy tube showed a normal trachea. It was decided that he would be reviewed in two months’ time.
33.	On 19th January 1995 Mr. Carlin saw Mr. Dunk as an out patient. He seemed quite well. Mr. Carlin decided to keep him under 4 monthly review. However, on 22nd February 1995, Mr. Dunk was admitted under Mr. Carlin’s care for four days with tracheitis. He was seen by Mrs. Macnamara on the first day of admission who noted that he had severe asthma, was coughing yellow sputum and was puffy in the face. Mrs. Macnamara saw him again on 7th March 1995  and reviewed him the following day. In a letter to Dr. Farrell (copied to Dr. Prowse) dated 13th March 1995 she reported that Mr. Dunk had complained of “his nose feeling red, hot and very sore”.
34.	By letter dated 28th March 1995 to Dr. Farrell, Dr. Prowse said that Mr. Dunk at present did not have any further appointment because his problem related to his tracheostomy which was within the province of Mr. Carlin. He would, however, be pleased to see him again if Dr. Farrell thought that appropriate. This was followed by a letter dated 6th April 1995 from Mr. Carlin to Dr. Farrell in which he asked that it be arranged for Mr. Dunk to see a chest physician at Burton since he was no longer on the books of the physicians at Stoke. Mr. Carlin said that he was looking after the tracheostomy which was not proving a big problem but he did not think that there was any real reason why someone at Burton such as Mr. Rockley should not look after Mr. Dunk’s tracheostomy. The concluding paragraph reads:
He [Mr. Dunk] once again brought up the question of his tracheostomy and whether this could eventually be reversed. I have severe doubts as to whether this is going to be possible and certainly at the moment would not be feasible. 
35.	Dr. Farrell then referred Mr. Dunk to Dr. Sheldon, a General Physician at Burton and to Mr. Rockley, a Consultant ENT Surgeon also at Burton at which point (apart from an admission of eight days under Mr. Carlin in June 1995 for tracheitis) Mr. Dunk ceased to be in the care of anybody at Stoke. Thereafter, until 2000, Mr. Dunk was treated at Burton and at Derby City General Hospital (from July 1998). He was treated for, inter alia, psychological problems, asthma, chest infections, tracheitis, and oesophagal reflux (i.e. acid coming up from the oesophagus). At some point after the tracheostomy either in 1994 or 1995, it is not clear precisely when, consideration was given to whether the obstructive sleep apnoea could be treated with surgery to the jaw and face but this was ruled out.
36.	By letter dated 10th June 1996 Dr. Farrell referred Mr. Dunk to Dr. Britton who was then Reader in Respiratory Medicine at Nottingham City Hospital. Dr. Britton saw Mr. Dunk and obtained a lengthy history from him. He wrote to Dr. Farrell on 18th July 1996 giving a preliminary view and  stating that he was going to get hold of Mr. Dunk’s notes from Stoke and Burton. Having obtained and considered the notes, he wrote to Dr. Farrell on 23rd August 1996. His conclusion was that there was little doubt about the diagnosis of obstructive apnoea and that the tracheostomy, at least as a temporary measure to see if it brought about improvement in symptoms, was a reasonable measure. In view of the difficulties experienced in trying CPAP therapy, it seemed appropriate for the tracheostomy to remain. Dr. Britton could see no reason why the problems of infection and suction could not be dealt with at home. Copies of both of Dr. Britton’s letters to Dr. Farrell were sent to Dr. Prowse. 
37.	Dr. Britton wrote to Mr. Dunk by letter dated 27th August 1996. The first paragraph reads:
Further to our consultation a few weeks ago I have now had a chance to look through your Stoke and Burton notes. I’m satisfied by the diagnosis of obstructive apnoea, and I understand that you had great difficulty dealing with the CPAP machines tried. In the circumstances a tracheostomy seems appropriate. I see no reason why with regular changing (once a month or thereabouts) combined with appropriate suction when necessary the tracheostomy shouldn’t (sic) be a problem. I don’t see evidence that intraveneous antibiotics are necessary or indeed are in your best interest.  
38.	On 1st May 1997 Mr. Dunk issued a generally endorsed writ signed by counsel (who did not represent him at trial) seeking damages against the defendant and Burton Hospitals NHS Trust for “personal injuries arising out of their management of his asthma and obstructive sleep apnoea  between 5th May 1994 and 1st May 1997.” I was told that this claim was founded on a Condition and Prognosis Report written by the same Mr. O’Flynn who operated on Mr. Dunk in 2000. That report simply sets out a very short history up to the tracheostomy and notes that Mr. Dunk has required hospital admissions for chest infections on a number of occasions. It then lists 9 additional problems that Mr. Dunk had as a result of the surgery such as the need for neck dressings, the deterioration of his asthma and the inability to work as an engineer. It provides no support at all for the claim signed by counsel.
39.	Mr. O’Flynn brought in a Mr. Bhik Kotecha, a Consultant ENT Surgeon, to produce a report on the sleep study investigations done at Stoke. On the basis of Mr. Dunk’s notes Mr.Kotecha felt able to say in a report dated 6th February 1998 that he did not feel that there was any evidence of significant obstructive sleep apnoea that had been documented objectively; there was no documentation of “sleep architecture” (eg EEG) and Mr. Kotecha was not aware of any clinical features of Mr. Dunk’s history which might suggest obstructive sleep apnoea. There followed a Statement of Claim based on this report which alleged that the sleep studies did not support a diagnosis of obstructive sleep apnoea; Mr. Dunk did not suffer from gross obstructive sleep apnoea; he did not consent to nor were there indications for an elective tracheostomy; and it was negligent not to have removed the tracheostomy since 5th May 1994. On 17th July 2000 this Statement of Claim was abandoned and replaced by an almost completely different pleading. 
40.	Towards the end of 1999, at the urging of Mr. Dunk and his solicitors, Dr. Bateman, Consultant Physician at the Derbyshire Royal Infirmary, agreed to refer Mr. Dunk to Mr. O’Flynn at the Royal National Throat, Nose and Ear Hospital in London. Mr. Dunk was admitted to this hospital on 19th January 2000 when he was seen by Mr. O’Flynn’s Registrar, Mr. Rea.  It was decided that there should be a sleep study with the tracheostomy tube blocked off the following night to be followed by a nasendoscopy the next morning. A nurse was asked to monitor half hourly the oxygen saturation level and pulse and for signs of respiratory distress. The nurse’s note records that the oxygen saturation was stable during the night and no signs of any respiratory distress/obstruction were noted. This is borne out by the contemporaneous observation chart which shows that Mr. Dunk’s oxygen saturation level fell within the 96% to 98% range throughout the study save for one occasion when it dropped to 93% at 3.30 am. Also, in a letter dated 24th January 2000 but apparently written or dictated on 21st January 2000, Mr. Rea said: “We capped off his tracheostomy and he seemed to sleep well with no desaturation.” 
41.	In evidence, Mr. O’Flynn said that in the morning of the 21st January Mr. Dunk told him that he had had a terrible night and had been awake throughout. Mr. Dunk put it differently when he gave evidence saying that he did not sleep very well that night. The nurse in question was one of three looking after a ward with 26 patients. She would therefore have had her hands full. On the other hand she had been given very specific instructions in respect of Mr. Dunk and thus I think considerable weight stands to be attached to her contemporaneous note. Weight also stands to be attached to the contemporaneous observation chart and to what Mr. Rea said in his letter. In the light of the nurse’s note, the observation chart and Mr. Rea’s letter I conclude that Mr. Dunk did indeed sleep that night, and slept pretty well with an oxygen saturation level that stayed within the 96% to 98% range, save for one occasion when it dropped to 93%.
42.	During the nasendoscopy carried out the following morning the tracheostomy tube was capped off.  As the anaesthesia deepened Mr. Dunk choked heavily and also snored. A floppy epiglottis was clearly seen folding back over the larynx and obstructing laryngeal airflow on inspiration, clearing on expiration.
43.	In the light of these observations it was decided to operate on Mr. Dunk’s epiglottis. First, however, his reflux problem had to be investigated because resectioning the epiglottis would give rise to a risk of acid being aspirated into the lungs. (The basic function of the epiglottis is to prevent material entering the larynx, and if a piece were removed this function would be impaired). Mr. Dunk was therefore referred to Professor Pounder, Professor of Medicine at the Royal Free Hospital who referred him on to Professor Winslet. On 29th March 2000 Professor Winslet successfully carried out a surgical anti-reflux repair through a mid-line abdominal incision.
44.	The reflux problem having been cured, Mr. O’Flynn assisted by Mr. Rea operated on Mr. Dunk on 28th April 2000. First they carried out a nasendoscopy and saw again the airway being obstructed by a bulky, floppy epiglottis. Mr. O’Flynn then removed a section of the epiglottis by laser excision. The removed section was retained for pathological examination. The nasendoscopy and the resectioning of the epiglottis were recorded on video tape, an edited version of which was shown to the court. 
45.	Mr. Dunk made a good recovery. On 26th May 2000, following an unsuccessful attempt seven days previously, the tracheostomy was closed by surgery. On 27th December 2001 he underwent a sleep study reported on by Professor Wedzicha. The report states:
Sleep study shows some sleep disturbance involving hypopneas at the start of the sleep study. The remainder of the study is within normal limits. There is not enough sleep disturbance to diagnose obstructive sleep apnoea. This degree of sleep disturbance should not cause daytime sleepiness.

Mr. Dunk’s case. 
46.	Mr. Dunk makes two broad, alternative claims which I shall call “the 1994 nasendoscopy claim” and “the post-operative care claim”.
         The 1994 nasendoscopy claim.
47.	Mr. Dunk alleges that his epiglottis was behaving on 5th May 1994 as it is seen to behave in the 2000 videotape and that it was this abnormality that was the cause of his obstructive sleep apnoea. He contends that Mr. Carlin and Mrs. Macnamara negligently failed to observe that his epiglottis was behaving in this abnormal way when they carried out the 1994 nasendoscopy and that as a result his tracheostomy was not medically justified and should not have been constructed. He contends that if his abnormally behaving epiglottis had been observed as he says it should have been, he would have had an epiglotectomy as he did in 2000 and this would have cured his condition and spared him all the consequences he suffered from the construction of the tracheostomy. 
The post-operative care claim
48.	In the alternative, Mr. Dunk asserts that his condition should have been re-assessed within a few months of the tracheostomy by the performance of a second nasendoscopy or by his being referred to another ENT surgeon for a second opinion. He contends that if such a re-assessment had been made this would have led to his having an epiglotectomy of the sort performed in 2000 which would have cured his condition and spared him the worst of the consequences he suffered from the tracheostomy.
The law
49.	As to whether there was a breach of duty I adopt the approach taken by Lord Scarman in Maynard v  W Midlands RIIA [1984] 1 WLR 634 at 638E:
A case which is based on an allegation that a fully considered decision of two consultants in the field of their special skill was negligent clearly presents certain difficulties of proof. It is not enough to show that there is a body of competent professional opinion which considers that their[s] was a wrong decision, if there also exists a body of professional opinion, equally competent, which supports the decision as reasonable in the circumstances. It is not enough to show that subsequent events show that the operation need never have been performed if at the time the decision to operate was taken it was reasonable in the sense that a responsible body of medical opinion would have accepted it as proper. I do not think that the words of Lord President Clyde in  Hunter v Handley [1955] SLT 213 at 217 can be bettered: “In the realm of diagnosis and treatment there is ample scope for genuine difference of opinion, and one man clearly is not negligent merely because his conclusion differs from that of professional men…The true test for establishing negligence in diagnosis or treatment on the part of a doctor is whether he has been proved to be guilty of such failure as no doctor of ordinary skill would be guilty of if acting with ordinary care.”
50.	In addition to proving negligence, a claimant must prove that the negligence caused the loss of which he complains. In other words in a medical negligence action the claimant must prove that had there been no negligence, the injury, loss and damage of which he complains would have been avoided or at least have been much less. Bolitho v City & Hackney Health Authority [1998] A.C. 232 establishes that where the alleged negligence was an omission (here, the alleged omission to observe and operate on an abnormally functioning epiglottis) a claimant may establish causation by proving either: (1) that no responsible body of the relevant type of clinician would have failed to have done the act which it is alleged should have been performed (here, the removal of a section of the epiglottis), or (2) that even if there is a responsible body of clinicians who would not have done so, the clinicians actually concerned would have done so, had they not missed that which they ought to have noticed.   
The issues.
51.	Mr. Dunk’s claims give rise to the following issues: 
(1) Was Mr. Dunk’s epiglottis behaving abnormally as seen in the 2000 videotape when Mr. Carlin and Mrs. Macnamara performed the nasendoscopy on 5th May 1994?  If the answer to (1) is “no”, Mr. Dunk’s nasendoscopy claim fails. 
(2) If the answer to (1) is “yes”, was the abnormally behaving epiglottis the cause of Mr. Dunk’s condition? If “no”, the 1994 nasaendoscopy claim fails. 
(3) If the answer to (2) is “yes”, would no responsible body of surgeons performing the nasendoscopy on 5th May 1994 have failed to have observed the abnormal functioning of the epiglottis? If “no”, the 1994 nasendoscopy claim fails. 
(4) If the answer to (3) is “yes”, would no responsible body of surgeons which had made this observation have failed to have given advice which would have led to Mr. Dunk having an epiglottectomy as performed by Mr. O’Flynn in 2000?
(5) If the answer to (4) is “no”, would Mr. Carlin, Mrs. Macnamara or Dr. Prowse have given advice which would have led to Mr. Dunk having an epiglotectomy as performed by Mr. O’Flynn in 2000? If “no”, the 1994 nasendoscopy claim fails. 
 (6) If the 1994 nasendoscopy claim fails, would no responsible body of doctors have failed to cause Mr. Dunk to have a second nasendoscopy or be referred for a second opinion before January 2000? If “no”, the post-operative care claim fails.
(7) If the answer to (6) is “yes”, would the result have been an epiglotectomy as performed by Mr. O’Flynn in 2000?
(8) If either the 1994 nasendoscopy or the post-operative care claim succeeds, what is the quantum of Mr. Dunk’s loss?

 Was Mr. Dunk’s epiglottis behaving abnormally as seen in the 2000 videotape when Mr.Carlin and Mrs. Macnamara performed the nasendoscopy on 5th May 1994? 
52.	Leading Counsel for Mr. Dunk, Mr. Coonan Q.C., contended that the abnormal functioning of Mr. Dunk’s epiglottis as seen in the 2000 videotape was due to Mr. Dunk’s reflux problem which had existed since 1982. He submitted that since the abnormality unquestionably existed in 2000 and since the reflux problem had existed for 12 years come May 1994, it was to be inferred that Mr. Dunk’s epiglottis was functioning abnormally in 1994 as it was in 2000. In support of this contention Mr. Coonan Q.C. relied on the expert opinion of Professor Leslie Michaels, a distinguished histopathologist.
53.	 Professor Michaels was Head of the Department of Pathology at the Institute of Laryngology and Otology, London, from 1973 to 1990 and then became Professor Emeritus, University College London, and Honorary Consultant Pathologist, at the Royal National Throat Nose & Ear Hospital. Professor Michaels had examined histological sections of the removed portion of Mr. Dunk’s epiglottis. One of these sections contained two thin elongated slices which were vertical sagittal sections parallel to each other. The epiglottis is rooted in the tongue base and stands up more or less vertically. The side facing the back of the patient is the posterior (laryngeal) side. The side facing the front is the anterior (lingual) side. Professor Michaels was able to distinguish the posterior from the anterior surfaces of each slice. The material occupying most of the space in each slice was epiglottic cartilage. The anterior one half of the cartilage showed thickening of the perichondrium (the nourishing surface of the cartilage) by pale fibrous tissue. Beneath it, normal chondrocyte production by the perichondrium was greatly reduced, the cartilage had lost most of its chondrocytes (the living cells of normal cartilage) and most of its elastic fibres. On the other hand, the posterior one half of the epiglottic cartilage showed a normal perichondrium and normal numbers of chondrocytes and elastic fibres. Between the pathological anterior half and the normal posterior half of the epiglottic cartilage was a cyst-like space which Professor Michaels called a pseudocyst because, unlike a “true” cyst, it was not lined by epithelium. This pseudocyst measured 0.07cm x 0.5 cm on the longer, thinner section (1.5cm x 0.4cm) and 0.7cm x 0.2cm in the shorter wider section (1.2cm x 0.6cm). It was therefore about one third of the section.
54.	Professor Michaels had carried out a search of the relevant world literature and had  found no report of or reference to the serious pathological changes found in Mr. Dunk’s epiglottis. In his opinion these changes were caused by the reflux of gastric contents from which Mr. Dunk had suffered since 1982. Reflux of gastric contents results in the passage of highly acid material up the oesophagus where it pools in the pharynx. Mr. Dunk suffered no changes within the larynx because the epiglottis by reflex action closed over the larynx when reflux occurred. The acid therefore sat on the anterior surface of the epiglottis and insulted that surface but did not insult the posterior surface. In Professor Michaels’s view this would have happened many times over the years so that the epiglottis was frequently damaged, such damage extending to the closely underlying anterior perichondrium resulting in the disappearance of cartilage cells and elastic fibres and, because fluid was still emanating from the normal perichondrial capillaries of the posterior surface of the cartilage, in the production of the pseudocyst. In his opinion such changes would have been well established in May 1994.
55.	Professor Michaels rejected the opinion of one of the defendant’s experts, Mr. Bates, that after the tracheostomy there might have been simple degeneration of the tissues of the epiglottis or that the epiglottis had been damaged by being repeatedly sucked into the airway, because these theories did not explain why the anterior surface was damaged but not the posterior. Professor Michaels pointed out that a tracheostomy is situated on the laryngeal side and so if a tracheostomy were the cause of the damage one would expect the damage to be to the posterior surface of the epiglottis. Here, however, the damage was to the anterior surface. He also said that there was no evidence in the literature that a tracheostomy can affect the epiglottis even after prolonged intubation.
56.	The sections that Professor Michaels had examined showed no damage to the first two layers of the anterior part of the epithelium (the cellular layer forming the epidermis) and the connective tissue. It was put to him in cross- examination that this was inconsistent with the theory that the anterior surface had been insulted with acid for, if it had been, one would have expected to find damage to these two layers since they would have been nearest to the point of insult. Professor Michaels’s answer was that these layers had regenerated since the reflux problem had been cured at the end of March 2000: the gastro-intestinal tract has amazing powers of regeneration. He would only have expected to find scar tissue (and there was none) if the acid were powerful.
57.	Professor Michaels accepted that in many cases the cause of a cyst is unknown. He was confident that the enlargement of the epiglottis had been caused by the cyst but he was not so sure that it had also been caused by the fibrotic changes in the surface of the cartilage. He agreed that reflux is a common condition affecting about 25% of the population, 8% being badly affected. This being so it was put to him that if his view as to the cause of the floppiness of the epiglottis was correct it was extraordinary that there is no description in the literature of an epiglottis like that of Mr. Dunk. It was also suggested to him that his theory defied commonsense given that he himself had never come across an epiglottis like Mr. Dunk’s even though he had worked for years as a pathologist in ENT centres. In reply, Professor Michaels’s said that pathologists are very rarely asked to examine epiglottises since an epiglottis would only be examined post mortem if it were truly enormous and surgeons almost never require a biopsy of the epiglottis.
58.	In reply to Professor Michaels, the defendant called Dr. Peter Millard who has been a Consultant in Histopathology at the John Radcliffe Hospital, Oxford, since 1975. Dr. Millard said that the sections produced by Professor Michaels showed that the epidermis was not ulcerated and there was no fibrosis in the connective tissue separating the surface epidermis and the cartilage. Reflux produces ulceration and concurrent inflammation in the oesophagus and consequent fibrosis in the wall immediately adjacent to the surface epithelium. Thus, in Dr. Millard’s opinion, if the cause of the damage to the epiglottis had been reflux there would have been ulceration of the epidermis and fibrosis in the tissue beneath.
59.	When Dr. Millard was cross-examined there were put to him two photographs of slides that had not featured in Professor Michaels’s report but which he had produced since giving evidence. One slide was of a section of the anterior surface of Mr. Dunk’s epiglottis (“the Dunk section”) and the other was of a section of the anterior surface of a normal epiglottis (“the normal section”). Dr. Millard accepted that: (1) the epidermis in the Dunk section showed hypoplasia (thickening) whereas the epidermis in the normal section was of uniform thickness; (2) the connective tissue (the tissue next to the epidermis) in the Dunk section had been replaced by fibrous tissue whereas the connective tissue in the normal section was thin; and (3) there was abnormal cartilage around the cyst in the Dunk section whereas there was no cyst and no abnormal cartilage in the normal section. Dr. Millard agreed that the Dunk section showed longstanding damage both external and internal. However, he was still not prepared to accept that the damage was caused by reflux. It could equally in his view have been caused by the trauma of flopping or the release of something from the cyst. All three causes were consistent with what was seen in the photographs. In his view, since reflux is such a common problem, one would have expected to have come across an epiglottis like Mr. Dunk’s if reflux were the cause of the damage. Although the epiglottis is not looked at in autopsy, where there has been a laryngectomy a histopathologist would look at a section of the epiglottis. The rarity of the condition of Mr. Dunk’s epiglottis led Dr. Millard to conclude that bathing in acid was not the probable cause of the damage.
60.	On the question whether the abnormal functioning of Mr. Dunk’s epiglottis was caused by Mr. Dunk’s reflux problem, I prefer Professor Michaels’s evidence to that of Dr. Millard. Both are agreed that the damage to the epiglottis was long standing and by 2000 Mr. Dunk had been suffering from oesophagal reflux for 18 years. Further, the damage had been to the anterior side and not to the posterior side and I find Professor Michaels’s explanation for this – acid pooling in the pharynx on top of the epiglottis which has closed  on to the trachea by reflex action – convincing. It is true that reflux is a common complaint and the literature reveals no examples of an epiglottis like Mr. Dunk’s, but I conclude that the epiglottis is only rarely the subject of pathological examination. Accordingly, I find that the abnormal functioning of Mr. Dunk’s epiglottis observed in 2000 was caused by his reflux problem.
61.	The next question is whether that abnormal functioning was occurring in 1994? As I have already observed, Professor Michaels and Dr. Millard were agreed that the damage to Mr. Dunk’s epiglottis was longstanding. However, it does not necessarily follow that the damage was such in 1994 as to render the epiglottis so floppy that it slammed over the opening of the larynx on inspiration during sleep as it did in 2000. There is no evidence that the floppiness developed at an even pace over time. It is therefore possible that it was only some time after 1994 that the floppiness was such as to cause the slamming over the larynx. In this connection it should be remembered that in 2000 the pseudocyst was about one third the size of the section and thus it seems reasonable to infer that it made a major contribution to the epiglottis’s floppiness, but no one can say when the pseudocyst first appeared.
62.	If Mr. Dunk’s epiglottis was behaving in 1994 as it was in 2000, one would have expected this to be reflected in the results of the 17th March 1994 sleep study during which he was provided with CPAP. This is because if his epiglottis was floppy at this time one would expect the air blown into his airway through the CPAP mask to slam the epiglottis down over the trachea and cause a notable number of desaturations. However, as I have held, although Mr. Dunk was asleep and receiving CPAP from 12.00 midnight to 2.00 am on 17th/18th March 1994, he suffered no desaturations during this period. Indeed, as Dr. Prowse noted in his letter of 18th March 1994, whilst Mr. Dunk was able to tolerate CPAP, the abnormalities were abolished. Thus, far from supporting the contention that Mr. Dunk’s epiglottis was behaving in 1994 as it was behaving in 2000, the 17th March 1994 sleep study suggests that Mr. Dunk’s epiglottis was not flopping over the opening to the larynx when the 5th May 1994 nasendoscopy was performed.
63.	It also has to be borne in mind that both Mr. Carlin and Mrs. Macnamara were adamant that if Mr. Dunk’s epiglottis had been functioning on 5th May 1994 as seen in the videotape they would have observed and noted it. It was common ground that it was standard procedure to inspect all three relevant sites - the upper palate, the tongue base level and the larynx. It was also the unchallenged evidence of both Mr. Carlin and Mrs. Macnamara that if a patient’s tongue base is collapsing, the endoscope can be moved into the larynx by lifting the patient’s chin forward. Mr. Carlin also said (as I have recorded above) that it was his invariable practice to keep the endoscope in the throat whilst the patient was waking up so that if the palate and tongue base had collapsed under sedation he could see into the larynx. The defendant’s expert ENT surgeon, Mr. Grant Bates, confirmed that this was standard practice, as indeed did Mr. O’Flynn. Mr. Carlin was insistent that he would have adopted this practice in Mr. Dunk’s case even though he had found the state of the upper palate and tongue base to be such that he was going to perform a tracheostomy in any event. 
64.	It was put to both Mrs. Macnamara and Mr.Carlin that when they saw what appeared to be tongue base collapse they did not go on and look into the larynx because the nasendoscopy was being conducted to see if Mr. Dunk’s obstructive sleep apnoea was to be cured by UPPP or a tracheostomy and once they saw what appeared to be tongue base collapse they went straight on to perform the tracheostomy. Both denied that this is what happened. 
65.	It was also put to both surgeons that although the upper palate and tongue base appeared to be collapsing this did not reflect the reality of Mr. Dunk’s condition, which was that there was no true multi-segmental collapse but only a floppy epiglottis. To Mrs. Macnamara it was suggested that the appearance of tongue base involvement was due to the position of Mr. Dunk’s head but when Mr. Carlin came to be cross-examined a completely new line of attack was opened up. It was alleged that Mr. Dunk had not been sedated as he ought to have been to mimic sleep but had been given the (sedative) anaesthetic drugs recorded as having been used as a bolus dose and it was this that had induced the collapse of the structures which the surgeons observed. In the light of Mrs. Macnamara’s note, “Indicn:- Gross obstructive sleep apnoea with desaturation to 30-40% SaO2” it was put to Mr. Carlin that Mr. Dunk had indeed desaturated to 30%-40% during the operation and that Mr. Carlin had panicked and performed an emergency tracheostomy without ever getting to look in Mr. Dunk’s larynx.
66.	These allegations were based on the thoughts of Mr. O’Flynn. They do not, however, appear in any of his pre-trial reports. I was told (and accept) that it was Mr. Carlin’s oral evidence that he would have left the scope in as Mr. Dunk woke up that started Mr. O’Flynn thinking in this direction. In the witness box Mr. O’Flynn said that he thought that the anaesthetist had misunderstood the position and had proceeded straight away to “shoot in” a general anaesthetic believing that the operation was simply a tracheostomy; Mrs. Macnamara and Mr. Carlin had not realised that the anaesthetist had made this mistake: there had been a muddle. Mr. O’Flynn attached weight to the fact that the anaesthetist had recorded the operation as being a tracheostomy and had ticked the “emergency” box on the pro forma. He could not think of any other mechanism that explained the fact that on 5th May 1994 Mr. Dunk’s tongue base was collapsing whereas when he was examined in 2000 there was no such collapse.
67.	Although it may have been Mr. Carlin’s evidence that prompted Mr. O’Flynn to go back over Mrs. Macnamara’s note and the anaesthetist’s record and so come up with his theories, he had had these documents when he wrote his Causation and Liability Report in October 2000 and the question why there was no tongue base collapse in 2000 when this had been observed in 1994 had been a question in the case ever since permission had been given to amend the Statement of Claim on 17th July 2000. When he was cross-examined and when the defendant’s expert Mr. Bates, gave evidence, it became clear that there were formidable difficulties with the suggestion that Mr. Dunk’s upper airway structures were seen to be collapsing through the endoscope because Mr. Dunk was then under or being given a general anaesthetic. In particular, it was pointed out that shortly after the administration of a bolus dose of anaesthetic, the anaesthetist would have had to put an endotracheal tube (“ETT”) into the windpipe thereby making an endoscopic examination by the surgeons impossible; and even before this, the anaesthetist would have had to put his own endoscope down Mr. Dunk’s throat to plot the course of the ETT. The amount of time for a nasal endoscopy to be performed would therefore have been very short and it would be extraordinary if the surgeons had treated their findings as authentic (as they did) once they had realised (as they must have done) that Mr. Dunk had been given a general anaesthetic from the outset.
68.	No doubt it was in the light of these difficulties that in his closing submissions Mr. Coonan Q.C. did not contend that Mr. Dunk had been given a general anaesthetic as suggested by Mr. O’Flynn but submitted instead that Mr. Dunk had simply been over-sedated: the anaesthetist had gone too far but had not set about administering a general anaesthetic. I have no doubt that Mr. Coonan was right not to rely on Mr. O’Flynn’s theories that Mr. Carlin had panicked and performed an emergency tracheostomy or that the anaesthetist had “shot” the anaesthetic into Mr. Dunk in the mistaken belief that the operation was not going to be a nasendoscopy with the possibility of a tracheostomy, but was going to be a tracheostomy tout court. In my judgement these theories were ill thought through and gave far too little weight to the competence and integrity of Mr. Carlin and Mrs. Macnamara and to Dr. Hindmarsh, the anaesthetist. Had they been relied on in closing I would have had no hesitation in rejecting them. Although I am sure that Mr. O’Flynn at all times tried to maintain the distance and objectivity appropriate for an expert witness, I fear he failed to do so when it came to his theories designed to explain how Mr. Carlin and Mrs. Macnamara had seen multi-segmental collapse and had not seen a floppy epiglottis. This was due, I think, to the fact that he had operated on Mr. Dunk, apparently successfully which had led him to embrace Mr. Dunk’s cause and thereby become too close to the issues in the case.
69.	Whether Mr. Dunk was over-sedated goes primarily to the question whether a floppy epiglottis was the principal cause of Mr. Dunk’s obstructive sleep apnoea in 1994 and not to whether Mr. Mr. Dunk’s epiglottis was behaving in 1994 as it was in 2000.  (If an abnormally functioning epiglottis was the principal cause of Mr. Dunk’s condition, the tracheostomy was unnecessary; if, however, multi-segmental collapse was the principal or a significant cause, the tracheostomy was medically justified). As to whether Mr. Dunk’s epiglottis was behaving on 5th May 1994 as it was in 2000, his alleged over-sedation is of only marginal relevance, for it is common ground that Mrs. Macnamara and Mr. Carlin saw the upper palate and the tongue base in a state of collapse. In respect of this question, the issue is not so much whether that collapse was caused by over-sedation but whether the surgeons looked at the third site - the larynx - for if they did they would have been bound to have seen the epiglottis flopping over the opening of the larynx if that is what it was doing.
70.	Neither Mr. Carlin nor Mrs. Macnamara could recall the operation on Mr. Dunk in specific detail, which was not surprising since it was carried out some 8 years ago and each of them would have performed a very large number of sleep nasendoscopies in the intervening period. Also, no one suggested that they were at fault in noting only the abnormalities they observed. Mr. Carlin was and is a well-known Consultant ENT Surgeon of considerable distinction and Mrs. Macnamara, whilst not so senior, was also a well-qualified ENT Senior Registrar who had been thoroughly trained in the nasendoscopy procedure. Both were impressive witnesses. In these circumstances I think that the case for saying that Mr. Dunk’s epiglottis was slamming down on the opening of his larynx on 5th May 1994 must be very carefully weighed before concluding that Mr. Carlin and Mrs. Macnamara departed from standard procedure and their own practice and thereby failed to observe an abnormality that they ought to have noted.
71.	 The parties’ expert physicians, Dr. Barnes for Mr. Dunk and Dr.Shneerson for the defendant, agreed pre-trial, “that in the light of Mr. Dunk’s clinical improvement after epiglottic surgery and the improvement of his sleep study it is likely that the main cause of his sleep apnoea before 5 May 1994 was his abnormal epiglottis.” 
72.	 In paragraph 16 of his Causation and Liability Report Mr. O’Flynn said:
I  have no reason to suppose that the basic anatomical shape of Mr. Dunk’s epiglottis changed in the intervening period [i.e.1994 to 2000] and the evidence from the sleep studies carried out in Stoke is that his sleep apnoea became worse when airway pressure was applied. This finding is in keeping with the epiglottis being pushed more firmly over his airway acting as a flap valve, and is confirmatory evidence that the cause of his obstructive sleep apnoea was his epiglottis.  
73.	Dr. Barnes is a Consultant Physician with the Royal London Hospitals Trust and Honorary Senior Lecturer at St. Bartholomew’s and the Royal London Hospital Medical College. In his evidence in chief he said that his agreement with Dr. Shneerson was not based primarily on the pathological evidence but on the fact it was too far-fetched to postulate that the cause of Mr. Dunk’s obstructive sleep apnoea (multi-segmental collapse) had spontaneously resolved between 1994 and 2000 and at the same time the epiglottis had grown but was not there in 1994.
74.	In his oral evidence Dr. Shneerson appeared to back away from his agreement with Dr. Barnes. He said that if Mr. Dunk’s epiglottis had been abnormal in 1994 it was not as abnormal as it was in 2000. In his opinion, if Mr. Dunk’s epiglottis had been closing over the opening of the larynx on inspiration in 1994 Mr. Dunk would not have been able to breathe during the 17th March 1994 sleep study. He said that the air delivered by CPAP is like a hammer. If Mr. Dunk’s epiglottis had been behaving in 1994 as it did in 2000 it would have been hammered down over the trachea making breathing impossible.
75.	In his closing submissions Leading Counsel for the defendant, Mr. Coghlan Q.C., submitted that when coming to their pre-trial agreement both Dr. Barnes and Dr. Shneerson had overlooked the fact that Mrs. Macnamara’s operation note makes it clear that the surgeons believed that the clinical pathology was multi-segmental collapse, a very well recognised cause of obstructive sleep apnoea, unlike a slamming epiglottis which had never before been identified in the literature as a possible cause of this condition. In other words, Dr. Barnes and Dr. Shneerson had failed to give proper weight to the fact that Mr. Carlin and Mrs. Macnamara were ENT surgeons of repute whose sleep nasendoscopy procedures conformed to generally accepted practice, including in particular an inspection of the larynx with access being obtained by moving the patient’s chin forward and by leaving the scope in whilst the patient wakes up.   I agree with Mr. Coghlan’s submission and would extend the observation to the reasoning of Mr. O’Flynn.
76.	Although I am satisfied that the abnormal functioning of Mr. Dunk’s epiglottis in 2000 was caused by his longstanding reflux problem, for the reasons I have given in paragraph 61 this does not necessarily mean that Mr. Dunk’s epiglottis was functioning in the same way in 1994. In my opinion, when weighed against the evidence of Mr. Carlin and Mrs. Macnamara, ENT surgeons of repute, and against the result of the 17th March 1994 sleep study, the evidence that the abnormal behaviour of Mr. Dunk’s epiglotttis in 2000 was caused by his longstanding reflux problem is insufficient to establish on the balance of probabilities that his epiglottis was behaving abnormally on  5th May 1994. Accordingly, I find that Mr. Dunk’s epiglottis was not functioning abnormally on 5th May 1994.
77.	It follows from this finding that Mr. Dunk’s 1994 nasendoscopy claim fails.  However, since doubts over Mr. Carlin’s and Mrs. Macnamara’s identification of the cause of Mr. Dunk’s condition have been raised by the contention that the collapse of the structures was not naturally-occurring but was caused by over-sedation, I think it is appropriate that I deal with this contention.
78.	In support of his submission that Mr. Dunk was over-sedated Mr. Coonan Q.C. relied on Mr. Carlin’s evidence that the level of anaesthetic was crucial: if too much is given, total collapse will occur. He also relied on the evidence that no tongue base collapse was observed in 2000 and none of the factors which normally cause resolution of obstructive sleep apnoea – weight loss and reduction of alcohol consumption - were in play here: Mr. Dunk had put on rather than lost weight and had never been a heavy drinker. As against this the evidence was that Dr. Hindmarsh was an experienced Consultant Anaesthetist who had been working with Mr. Carlin for 3 years prior to the operation performed on 5th May 1994. He was not called as a witness because by the time Mr. O’Flynn had set out his theories on over-anaesthetisation in his evidence in chief Dr. Hindmarsh was about to go on holiday to France. A statement made to the defendant’s solicitors by Dr. Hindmarsh on 12th July 2002 was, however, admitted under s.2 of the Civil Evidence Act 1995 in which he said that Midazolam was given over a period estimated to be 2 to 3 minutes to mimic sleeping/snoring and that then Propoful would have been administered to put the patient to sleep. Then Atracurium 30 mg was introduced for muscle paralysis for intubation. This was a controlled process and was specifically not an emergency situation. The anaesthetic agents were not administered as a bolus. Dr. Hindmarsh did not deal with the allegation that Mr. Dunk had merely been over-sedated. I conclude that this was because this allegation was not squarely put to Mr. Carlin or clearly postulated by Mr. O’Flynn from the witness box and therefore was not raised with Dr. Hindmarsh when his statement was taken.
79.	The two expert witnesses called by the defendant, Dr. Shneerson and Mr. Grant Bates, Consultant Otolaryngolist at the Radcliffe Infirmary, were each of the view that the collapse of the structures observed by Mr. Carlin and Mrs. Macnamara was naturally occurring and had resolved itself by the time Mr. Dunk was examined in 2000. Multi-segmental collapse is a classic presentation for causing obstructive sleep apnoea. In the view of Mr. Bates, the fact that Mr. Dunk was an “heroic” snorer in 1994 and had been observed by Dr. Corlett to have floppy tissue around the posterior fossi were strongly suggestive of multi-segmental collapse at that point in time. In the opinion of both experts the structures had regained muscle tone because the tracheostomy had relieved the structures from the vibration stress caused when air was inspired through the nose and mouth particularly when Mr. Dunk was asleep.  
80.	Both experts accepted that it is rare for a patient with obstructive sleep apnoea to be cured after undergoing a tracheostomy but there was a small number of cases known to them where after a period of time the collapse of the structures had resolved. This was also the evidence of Mrs. Macnamara and Mr. Carlin. 
81.	In light of (1) the fact that Dr. Hindmarsh is and was an experienced anaesthetist who had worked with Mr. Carlin doing sleep nasendoscopies for 3 years prior to May 1994; (2) the evidence of Dr. Shneerson and Mr. Bates, particularly the latter, giving their reasons for concluding that the multi-segmental collapse observed by Mr. Carlin and Mrs. Macnamara had resolved following the tracheostomy; (3) the evidence of Mr. Carlin and Mrs. Macnamara; and (4) the fact that the allegation of over-sedation came very late in the day with the result that Dr. Hindmarsh was not called to answer the claimant’s allegations, I decline to infer from the fact that there was no apparent tongue base collapse in 2000 that Mr. Dunk was over-sedated on 5th May 1994. Accordingly, I find on the evidence that the conclusion reached by Mr. Carlin and Mrs. Macnamara that Mr. Dunk’s severe obstructive sleep apnoea was caused by multi-segmental collapse was not negligently made and that therefore the tracheostomy performed on Mr. Dunk was medically justified.
Would no responsible body of doctors have failed to cause Mr. Dunk to have a second nasendoscopy or be referred for a second opinion before January 2000? 
82.	As I have said, Mr. Dunk alleges that the doctors who treated him at Stoke and Burton after the tracheostomy should have re-assessed his condition. He says that they should have had another nasendoscopy carried out or sent him for a second opinion either of which would have shown that his condition was caused by a floppy epiglottis and not multi-segmental collapse; he would then have had the epiglotectomy he eventually had in 2000 and thus would have been spared the consequences of having to endure a tracheostomy for over five years.
83.	Mr. Dunk’s principal case was that he should have been given another nasendoscopy or referred for a second opinion before May 1995 when he was transferred back to Burton. The time at which (if at all) there should have been another nasendoscopy or referral for a second opinion prior to January 2000 is important, for on the evidence it is apparent that after three to four years the main consequences of the tracheostomy suffered by Mr. Dunk, in particular the permanent deterioration of his asthma and the resultant inability to return to work, would have already been incurred. Thus, unless Mr. Dunk can show that he should have been given another nasendoscopy or sent for a second opinion within a year or so of 5th May 1994 he will have substantial difficulty in proving that the alleged failure to re-assess his condition caused him the damage for which he seeks compensation. No doubt it was primarily because of this that Mr. Coonan Q.C. concentrated on the period to May 1995, as well possibly as wishing to focus on the care given to Mr. Dunk by the doctors at Stoke who had diagnosed obstructive sleep apnoea and multi-segmental collapse and had performed the tracheostomy. 
84.	There is no doubt that from a time shortly after 5th May 1994 Mr. Dunk was raising the question whether his tracheostomy could be reversed. Within a short time he began to develop chest infections and tracheitis and was having increasingly serious psychological problems. On occasions he also had trouble with mucous excretions and coughing up blood. Mr. Coonan Q.C. conceded that it was appropriate to wait for a few months to see if Mr. Dunk’s problem with CPAP could be overcome, because CPAP was the standard treatment for obstructive apnoea. In August 1994 Dr. Prowse had proposed that if Mr. Dunk’s sinuses were clear he should in March 1995 be acclimatised to the CPAP mask to see if airflow induced blockage, rhinnorea or problems with sinusitis. Somewhat later Mrs. Macnamara had proposed that Mr. Dunk’s nasal airway problem should be assessed in January 1995. There was, however, no reassessment the following January. On 21st December 1994 Mrs. Macnamara saw Mr. Dunk as an out-patient and decided to review him in two months’ time and then Mr. Carlin saw him on 19th January 1995 (again as an out-patient) and put him on 4 monthly review. Shortly thereafter he was admitted for four days under Mr. Carlin for tracheitis and when seen by Mrs. Macnamara on 7th March 1995 his nose was “feeling red, hot and very sore”. Then in April 1995 Mr. Carlin wrote to Mr. Rockley at Burton suggesting that he be referred back to Burton because the continuing problems were problems with managing the tracheostomy.
85.	It is clear on the evidence that Dr. Prowse and Mr. Carlin and Mrs. Macnamara all gave continuing and anxious consideration to whether Mr. Dunk’s desire to have the tracheostomy reversed could be met. Their hope was that Mr. Dunk’s problems with CPAP could be overcome which would lead to a resolution of the multi-segmental collapse and eventual decannulation. However, in the period Mr. Dunk was in their care there were no clinical indications pointing to the need for another sleep endoscopy. They thought that they had obtained a sufficient explanation of the problem. Thus, whenever Mr. Dunk raised the question of reversing the tracheostomy with Mr. Carlin, Mr. Carlin would say that a reversal would bring back the obstructive sleep apnoea, at which point Mr. Dunk would drop the issue. Moreover, the tracheostomy had cured Mr. Dunk of his severe sleep apnoea; what he was suffering from after 5th May 1994 was something different: the management of the tracheostomy and consequential infections and psychological problems.
86.	In my opinion, the question of post-operative care has to be assessed on the basis that the first nasendoscopy had been competently conducted so that the doctors at Stoke were entitled to believe that multi-segmental collapse was the cause of Mr. Dunk’s obstructive sleep apnoea. The issue therefore is, given this premise, would every responsible body of doctors have provided Mr. Dunk with another sleep endoscopy or sent for a second opinion before April/May 1995 or at any rate within three to four years of May 1994? 
87.	Mr. Dunk relied on the expert opinion of Mr. O’Flynn who, in his Causation and Liability Report, said that the doctors at Stoke should have referred Mr. Dunk to appropriate specialists when they were unable to help him. In his oral evidence he expressed the view that whilst it was reasonable to wait six months, thereafter it was imperative that another sleep endoscopy be performed. 
88.	The defendant relied on the expert opinions of Dr. Shneerson and Mr. Bates. Dr. Shneerson said in his report that when Mr. Carlin wrote to Mr. Rockley suggesting that he supervised Mr. Dunk’s further care, he made it clear that this further care was only for supervision of the tracheostomy itself; Mr. Carlin did not expect Mr. Rockley to make further decisions about the closure of the tracheostomy or provision of alternative types of traetment for his sleep apnoeas. Mr. Rockley then passed Mr. Dunk on to Mr. De who had seen him before the tracheostomy. In Dr. Shneerson’s opinion, “these arrangements were satisfactory and there was no failure to provide a reasonable standard of care in transferring the ongoing supervision of [Mr. Dunk’s] tracheostomy to the ENT Department at Burton Hospital.” In his oral evidence Dr. Shneerson said that before an invasive procedure was carried out one must think the procedure will give treatment value. In his opinion there was no reason to think that following the 16th and 17th March 1994 sleep studies and the May 1994 nasendoscopy anything different would be found if a second nasendoscopy was performed. There was no clinical feature to suggest that the cause of Mr. Dunk’s condition had changed. However, Dr. Shneerson accepted that he would have been concerned that a man of 36 years had a tracheostomy which appeared to be permanent. Pre-trial, Dr. Shneerson and Mr. Bates were asked:
Is it usual treatment for moderate sleep apnoeas (like Mr. Dunk’s) to be managed by a tracheostomy for life without further investigation?   
            The reply (which turned out to be Dr.Shneerson’s not Mr. Bates’s) was:
It is unusual for sleep apnoeas to be managed by a tracheostomy unless other treatments have failed, or been shown to be impractical. Further investigation would be indicated if a new factor contributing to the apnoeas was suspected, if one of the contributing factors, such as obesity had resolved, if the tracheostomy was causing severe problems, or if an alternative such as nasal CPAP was a feasible option.
In his oral evidence Dr. Shneerson said that the longer the tracheostomy was in place and the more severe the problems it was causing the stronger was the case for doing a second nasendoscopy. Having regard to Mr. Dunk’s post-operative record, he would have referred him to a surgeon to have another look in 1997 or 1998.
89.	In his pre-trial report Mr. Bates said under the heading Post Nasendoscopy:
It is to be noted that Mr. Dunk appeared to be a lot better with a tracheostomy and his sleep apnoea seems to have been cured. I note that Mr. Carlin did keep Dr. Prowse informed of the developments. While tracheostomy seems to have cured the sleep apnoea it seems reasonable to have left the tracheostomy tube in place. It was known, and I am sure it was made clear to Mr. Dunk, that if conditions changed then the tracheostomy tube could have been removed.
Tracheostomy is a recognised treatment for severe sleep apnoea and is employed when the options are limited; for example the inability to apply CPAP as a treatment. This seems to have been the case in Mr. Dunk’s case and it is to be noted that the tracheostomy did successfully treat his sleep apnoea.
90.	In his oral evidence Mr. Bates said that he thought it completely reasonable for Mr. Dunk to be referred back to Mr. Rockley in April 1995. Mr. Rockley was fully competent and Mr. Dunk had been referred to Stoke on a tertiary referral that had funding implications. Mr. Bates also said that he disagreed with the second sentence of the reply to question 10 that had been posed pre-trial. Dr. Shneerson had said this; he had not. Although it was very unfortunate that Mr. Dunk had a lot of problems with his tracheostomy, he (Mr. Bates) saw no evidence of a disaster. In the period before the transfer to Burton all the doctors were thinking what could be done to decannulate Mr. Dunk. Once Mr. Dunk was referred back to Burton, the channels of communication were left open. In Mr. Bates’s view there was nothing lacking in the management of Mr. Dunk even though Mr. Dunk was not reviewed in January 1995 as Mrs. Macnamara had proposed.
91.	Whether a second opinion should have been sought or another nasendoscopy performed where there were no clinical indications that the diagnosis was wrong but there were serious problems, arising from the tracheostomy, was a  matter of clinical judgement. On the evidence I have heard I am quite satisfied that the judgement exercised by the doctors at Stoke down to the time that Mr. Dunk was transferred to Burton was not a negligent judgement. Whilst one or two responsible doctors might have caused a second nasendoscopy to be performed or sent Mr. Dunk for a second opinion, in my judgement, many others would not have.
92.	As to the period after the transfer back to Burton, I think that the doctors at Stoke were only under a duty to review Mr. Dunk and refer him for a second opinion if he was referred back to them. Even if this is not right I am not persuaded that every responsible body of doctors would have called for a second opinion or procured a second nasendoscopy before around 1998, a point in time by which Mr. Dunk would anyway have suffered the consequences of the tracheostomy for which he seeks damages. I base this conclusion on the evidence of Dr. Shneerson and Mr. Bates and also on the fact that Mr. Dunk’s case was in fact referred by his GP to Dr. Britton, then Reader in Respiratory Medecine at Nottingham City Hospital, who expressed the view that there was little doubt about the diagnosis of obstructive sleep apnoea and in view of the difficulties in trying CPAP, it was appropriate for the tracheostomy to remain. Dr. Barnes, who gave no opinion on Mr. Dunk’s post-operative care, said that in his view Dr. Britton was only giving an opinion on Mr. Dunk’s recurrent infections and worsening asthma but I do not accept this. To my mind it is quite clear that Dr. Britton was being asked to give and gave a second opinion on whether the tracheostomy should be reversed or should remain. I have also taken note that Mr. O’Flynn himself seems not to have recommended and certainly did not procure a second nasendoscopy for Mr. Dunk when he examined him for the purposes of his Condition and Prognosis Report in April 1997. 
Conclusion
93.	For the reasons given above Mr. Dunk’s claims in this action fail. His allegations focussed on the care he received at Stoke. In my judgement, Dr. Prowse, Mr. Carlin and Mrs. Macnamara were at all times conscientiously concerned about his condition and provided a level of care about which no just criticism can be made. I can also see no basis on the evidence before me for concluding that the care Mr. Dunk received at Burton fell below acceptable professional standards.
94.	Relying, inter alia, on the results of the sleep study done on 20th January 2000 when the tracheostomy tube was blocked off and Mr. Dunk experienced only one material desaturation, Mr. Bates was of the opinion that Mr. Dunk was no longer suffering from obstructive sleep apnoea when he was operated on by Mr. O’Flynn on 28th April 2000. I found Mr. Bates’s evidence on this question persuasive but it is unnecessary for me to express a decided opinion on it and I decline to do so. Suffice it to say that Mr. Dunk is now cured of the obstructive sleep apnoea from which he was suffering in 1994 and his tracheostomy was successfully reversed on 26th May 2000.  The psychiatrists who reported on him to the court expressed the view that his psychological state would improve once the litigation was over. In the event, his claims have failed but it is to be hoped that nonetheless he will now be able to put the past behind him and re-build his life.