Ganz v Childs & Ors

The Claimant, Morwenna Ganz, was born in Brazil on the 24 September 1985. Her mother, whose first language is Portuguese, is Brazilian by birth and her father is Welsh. Mr Ganz is now the Chief Executive Officer for Ingrain, a digital rock physics company. His work with Ingrain has taken him to various places in the world and the family currently live in Houston, Texas. At the time of the material events they were living in the UK in Teddington in what is now the London Borough of Richmond-on-Thames.

Apart from two or three matters in her medical history to which I will refer later (see paragraph 23-25 below) and apart from being (as is her father) asthmatic, by and in December 1999 she was an otherwise healthy 14-year old. Over a few days in mid-December she became unwell because, as it emerged in due course, she had developed mycoplasma pneumonia, a common form of community acquired bacterial pneumonia caused by infection with Mycoplasma pneumoniae, a very small bacterium.

When she was admitted to Kingston Hospital via its Accident and Emergency department at about 10.20 in the morning of 19 December she was very unwell. During that day her condition deteriorated further, she effectively lapsed into a coma, her neurological condition worsened and in consequence she sustained significant irreversible brain damage leading to permanent disability. She has retained normal intellectual functioning although communication is difficult, though not impossible. However, she requires constant care. She attended the trial, attended by her sister, and plainly listened carefully throughout.

Her case is that suitable treatment administered in time would have avoided this catastrophic result. It is said that her GP at what was then St Mark’s Road Surgery, Teddington (now the Thameside Medical Practice situated in High Street, Teddington), Dr Amanda Childs, and a full-time NHS GP who was a Director of the out-of-hours service called Harmoni, Dr John Lloyd, were negligent in not arranging for her earlier admission to hospital. It is also said that when finally admitted to hospital there were delays by the hospital staff in addressing her obviously serious and deteriorating condition such that the opportunity to save her from the neurological damage was lost.

Dr Childs denies any breach of duty. Dr Lloyd accepts that he should have visited Morwenna after contact had been made with the out-of-hours service in the early hours of 19 December. The likelihood is that, had he done so, he would have arranged for Morwenna’s admission to hospital earlier than in fact occurred. The hospital accepts that there were some delays in identifying her true condition and in instituting appropriate treatment: indeed the outcome was sufficiently concerning for an internal Incident Review Group to be set up shortly after the events in question because of a “[possible] delay in treatment”. (The documents relating to that review were disclosed to Morwenna’s advisers in April and May 2010.) However, all deny that any inadequacy or delay there may have been in dealing with her made any difference to the outcome or that she can prove, on the balance of probabilities, that any admitted or established breach of duty caused or contributed to her neurological damage.

The trial before me has been limited to the issues of breach of duty and causation.

Before turning to the background, it may be helpful to record in general terms what mycoplasma pneumonia involves.

In the chapter on Respiratory Disorders in 4th edition (1992) of the well-known textbook, Forfar & Arneil’s Textbook of Paediatrics, of which Professor Peter Helms (see paragraph 180 below) is a current editor, ‘pneumonia’ is described as follows:

“Pneumonia is an inflammatory disease of the alveoli and may involve one or more lobes or segments. The airways are often also involved. The classical presentation of the bacterial pneumonias, such as pneumococcal and tuberculous pneumonia, has become uncommon in developed countries and the radiological and pathological descriptive terms ‘lobar pneumonia’ and ‘broncho-pneumonia’ are used much less frequently. More usual is the clinical diagnosis of simply ‘pneumonia’ of known or unknown cause.”

Pneumonia typically involves ‘consolidation’ of the lung tissue, namely, the filling of the air sacs in the lungs (the alveoli) with fluid. A chest X-ray (usually abbreviated as ‘CXR’ in medical notes) will demonstrate the existence and extent of any consolidation.

In the broad sense, pneumonia interferes with the normal gas exchange processes whereby oxygen (O₂) is taken into the body and carbon dioxide (CO₂) removed.

In Forfar & Arneil, Mycoplasma pneumoniae was said to be “probably one of the most common pathogens in school children” and to account for “about 12% of pneumonia [in the early school years], rising to about 20% in older schoolchildren and over 30% in young adults.” In a later Chapter it was said that Mycoplasma pneumoniae “can ... cause encephalitis”.

In a passage from the NHS Direct website attached to the report of Dr Adrian Rogers (see paragraph 64) ‘Encephalitis’ is described in these terms:

“Encephalitis is inflammation (swelling) of the brain tissue. It is caused either by infection, usually viral, or by an auto-immune disease. An auto-immune disease is when your immune system tries to fight off infection but by mistake, attacks parts of your body at the same time.

Some people who have encephalitis are left with permanent brain damage. The type and degree of brain injury can vary.

In most cases, a viral infection does not lead to encephalitis; only extremely rarely does a virus directly attack the brain and cause Infectious Encephalitis.

Viruses may also directly attack the linings of the brain (meninges) and cause meningitis. Encephalitis is more serious than meningitis, because it affects the brain itself. If the meninges are inflamed as well as the brain, the condition is called meninga-encephalitis.

Encephalitis can affect anyone in any part of the world at any age but it is extremely rare, with approximately four in every one hundred thousand affected in the UK each year.

Encephalitis can happen suddenly and cause serious problems to the nervous system and the brain. Some viruses have the ability to affect nerves and damage the central nervous system. The central nervous system is made up of the brain, spinal cord and nerves within the skull and spine. The peripheral nervous system is a group of nerves that connects the brain and spinal cord to the rest of the body….”

In an article in ‘Clinical Infectious Diseases’ in June 2001 (which related to a series of cases in Toronto) it was said that “[acute] childhood encephalitis is a potentially devastating illness with an incidence of ~10.5 cases per 100,000 child-years in developed countries.” The same article confirms that Mycoplasma pneumoniae is one of the pathogens that cause encephalitis. In that series of 159 children with acute encephalitis, 31% showed evidence of Mycoplasma pneumoniae infection.

It is plain from the foregoing that the development of an acute encephalitis is rare (and Mycoplasma pneumoniae is only one of the pathogens that can cause it). Indeed, in his preliminary report, it is to be noted that Dr Rogers, who has been a GP for over 30 years, recalls seeing only one case of encephalitis in a teenager in that career.

Nonetheless, it is, of course, accepted that GPs generally would need to be alert to the possibility of the development of pneumonia in a child or teenager from whatever cause. Its development can lead to life-threatening consequences and it accepted that there is a risk of those consequences developing rapidly. Dr Rogers, in an unchallenged part of his evidence, said that “all GPs know that community-acquired pneumonia is unpredictable and can be rapidly progressive.”

Equally, of course, it is accepted that in a hospital setting there would, at the very least, be that general level of awareness of the risks associated with pneumonia in a child or teenager.

The period before admission to Kingston Hospital

Mr Ganz started working overseas immediately after graduating from university in the UK. As I have indicated, his work took him to a number of places. I imagine he met Mrs Ganz when working in Brazil. In addition to Morwenna they have two other children, another daughter born in 1988 and a son born in 1992. Following the arrival of the first two children, he and his wife decided they should settle in the UK and he asked for a position with Ingrain in the UK. That was achieved and they moved to Teddington in 1995.

Morwenna became registered as an NHS patient at the St Mark’s Road Surgery in December 1997 having been with another surgery since the family’s arrival in the UK in 1995.

Morwenna’s GP ‘Summary of Treatment Card’, completed at the GP surgery with which she had been registered before she became registered with the St Mark’s Road Surgery, included the following entry after recording that her immunisations were up-to-date:

“ ... Encephalitis

PMH (1) Hernia operation 85 bilateral

(2)

Asthma

(3)

Encephalitis Dec’ 86

(metabolic encephalopathy) full recovery.”

That entry related to some aspects of Morwenna’s medical history (including encephalopathy) to I which will refer to in more detail shortly (see paragraphs 23-25). An issue has arisen as to the extent to which that entry should have alerted the St Mark’s Road Surgery to that history. I will return to that issue in due course (see paragraphs 88-91). However, there is no other entry referring to this aspect of Morwenna’s medical history in any of the notes taken at the St Mark’s Road Surgery.

The records from the St Mark’s Road Surgery indicate that Morwenna was seen at the surgery on 18 December 1997 by the Practice Nurse who undertook the “new patient check”. That check indicates that reference was made to her asthma and to the bilateral hernia operation, although there is no reference to her previous encephalopathy. It appears that she was seen by Dr Childs a few days later about her asthma and perusal of her notes up to December 1999 indicates that on those occasions that she visited the surgery it was in relation to her asthma. Those records indicate that prior to the consultation that lies at the heart of the case against Dr Childs, Dr Childs had seen Morwenna on five previous occasions.

Mrs Ganz says that, having seen Dr Childs on several occasions, she gained the impression that Dr Childs thought that she was an “over fussy mother” which she (Mrs Ganz) found very irritating. She and her husband recalled that on one occasion Mr Ganz went to explain to Dr Childs why they might occasionally appear over anxious about Morwenna given her history (see paragraphs 23-25). Dr Childs does not recall this. She does, however, accept that she found Mrs Ganz to be “slightly more anxious than an average patient”, but she put this down to Mrs Ganz being “apparently used to private medical treatment in Brazil” such that she “expected more immediate routine treatment from the NHS and would on occasion challenge what was available in the UK as compared to what she was used to in Brazil.” Dr Childs said that these factors made her “more cautious than usual when dealing with [Morwenna’s] family.” I will return to this issue later (see paragraphs 74 and 78).

The past history of Morwenna that was, or may have been, relevant to the assessment of her condition in December 1999 is reflected, at least to some extent, in the notes referred to in paragraph 19 above and goes back to when she was about 15 months old in December 1986. The family was in Brazil when she developed a cold and a temperature. Mrs Ganz’s parents were looking after her at the time and became concerned that she was holding her hands and the lower part of her arms in an unusual way. They took her to hospital where, according to Mr and Mrs Ganz, she remained for two days during which time she had a CT scan and a lumbar puncture both of which were clear. They recall that her mobility was mildly affected, but within a week she was fine and after a couple of weeks she was back to normal. The doctors were unable to identify the cause of the problem.

When the family was next in the UK arrangements were made for her to be seen privately by Dr Edward Brett, a Consultant Neurologist at Great Ormond Street Hospital. As he said in his report after the consultation in August 1988, he had arranged for “a limited number of biochemical investigations which [gave] normal results”. He concluded that she had possibly experienced some form of encephalitis (“perhaps associated with a polyneuritis”), but was of the view that it was “unlikely that she [would] have any further problems.”

Morwenna’s parents were reassured by this and indeed there were no further problems until March 1991 when she was about 5½ years old. By then the family were in Houston, Texas. Mrs Ganz says that she suddenly became ill with cold symptoms and high temperatures for two days. She became floppy, needed support to walk and her speech became slurred, although she did not lose consciousness. She was examined by a paediatric neurologist, Dr Tina Narayan, in Houston. She said that Morwenna presented with the “picture of a congenital hypotonia which may be due to a static encephalopathy and be exacerbated during the times of intercurrent illness.” Apparently, she told Mrs Ganz that she thought it unlikely that Morwenna would be prone to such problems again, particularly once she had passed puberty. Both her parents confirmed that she recovered from this episode, that her speech returned to normal and that apart from usual childhood illnesses there were no further problems of this nature. However, because of the unusual reactions to illness that she had experienced in 1986 and 1991 they were very attentive to her health. It is that that Mr Ganz recalls trying to explain to Dr Childs on the occasion referred to in paragraph 22 above.

That brief history indicates what had gone before. The relevant history for the purposes of the present case begins on Friday 10 December 1999 when Morwenna’s mother took her to the surgery. She was seen by Dr Caroline Mitchell-Heggs whose note was in these terms:

“Unwell 2/7 [2 days] cold, cough, scratchy throat, shivery,  wheeze using more inhalers. Ears Ok.

O/E [on examination] well, chest – faint wheezes bases. RR [respiratory rate] 26, good A [air] entry. HS [heart sounds]. PF [peak flow] 210 (exp 410).

On easibreathe ventolin & becotide 2p bd – did 3 p bd y’day.

As PF half for prednisolone 30 mg od 3/7 5mg x 18

adult size avoid aspirin & ibuprofen. Steroid warning given verbally

& double becotide 4 p bd has enough inhalers.

Mr [medical review] next week or sooner sos.”

The effect of this appears to be that Dr Mitchell-Heggs prescribed Prednisolone (a steroid), advised doubling the dose of Becotide (used in connection with asthma) and avoiding taking aspirin and ibuprofen. She recommended a review during the following week or an earlier return if there was deterioration or something adverse occurred in the meantime.

Morwenna went to school on the Monday, Tuesday and Wednesday. In the afternoon of the Wednesday, 15 December 1999, Morwenna’s mother took her back to the surgery as advised by Dr Mitchell-Heggs and she was seen by Dr Helen Tilly who made the following record:

“R/V [review] much better.

Peak flow 360 L/min

Chest clear

Advised re becotide.”

This undoubtedly suggested that there had been an improvement and Mrs Ganz accepts that she told the doctor that Morwenna was much better “because at that stage she was”.

However, there was a development later that day which, all the experts accept, undoubtedly evidenced the onset of the mycoplasma pneumonia even if (which is not clear) the symptoms of the previous few days were not associated with that development. Contact was made with the surgery which suggested that the on-call doctor at Teddington Hospital should be contacted. Mr Ganz took Morwenna to the hospital where she was examined by the out-of-hours GP, Dr Chris Smith.

Dr Smith’s note recorded the following:

“Condition: Fever. Has just completed prednisolone course for asthma.

On examination: Well Dyspnoea Chest clear. PF 380 (= usual best)

Red fauces [throat]/ cervical nodes.

Treatment: Paracetamol. Maintain Becotide dose”

It is, of course, to be noted that no history of encephalopathy was recorded as having been given. By then, of course, as Mr Ganz said, almost ten years had passed without any further incident and he did not consider that there was a continuing problem.

On the following morning (Thursday 16 December) Morwenna was taken by Mrs Ganz to St Marks Road surgery (where she vomited whilst they were there) and was seen again by Dr Tilly whose notes record the following:

“Acute nausea & vomiting since yesterday.

Chesty.

O/E T = 38.1 Peak flow 210

Chesty: chest clear

Abdo soft. BS 

Chat with mum.

[diagnosis] viral gastro

Paracetamol supps 1½ 4 hrly

Advised re fluids

To have asthma puffers.”

During the afternoon, according to Mrs Ganz, Morwenna’s temperature was controlled to a degree by the Paracetamol and by the administration of some cool showers. She was drinking plenty of fluids but had little appetite.

The next day (Friday, 17 December) she was very weak and stayed in bed. Mrs Ganz said she was very thirsty, drinking lots of fluids, and her temperature was high. That evening she vomited again. Mr and Mrs Ganz were very worried and took her again to see the on-call GP at Teddington Hospital. At about 20.00 she was seen by Dr Penny Sowden. Her note was in the following terms:

“Fever & vomiting. 14/12/09 on oral steroids for 3A of asthma.

O/E BP: 1205 T: 37.6 PEFR has dropped to 280. Cough unproductive.

Says had double vision this afternoon, but not now. LAST paracetamol 5pm.

Ears, throat fine, chest clear.

Domperidone 10 mg tds (15)

Viral illness? Influenza, Epigastric tenderness 2 days, coughing.”

The prescription for Domperidone was a response to the nausea and vomiting.

Morwenna’s parents became sufficiently concerned about her overnight such that Mrs Ganz took her to the St Marks Road surgery the following morning and she was seen for the first time in this sequence of visits to the surgery by Dr Childs. Dr Childs saw Morwenna at about 10.00 am. It is her case (evidenced by the absence of any note to this effect) that she (Dr Childs) was unaware of the intervention of Dr Sowden the previous evening. Her note was as follows:

“18/12/99

(E)

Vomiting

back to school Monday OK

New problem from Wed night  40 temp

Vomited Wed → Thurs lunchtime

vomiting started again Fri evening x 1 this am prob 0 coffee grounds 0 diarrhoea 0 black

Fever never < 38.5

Becotide at 100 mcg IV bd

Breathing OK barely needing salbutamol.

Epigastric pain achy constant. Not relieved by vomiting

OE [on examination] T36.3 (after paracetamol)

Chest clear

PFR 320, tender,  guarding,  rebound, BS+

[diagram of abdomen with area of tenderness]

Imp need to exclude pneumonia

FBC ESR

CXR

Trial Asilone 5-10 mls qds

U/A – has period bld prot + nil else”

The note ‘(E)’ indicates this was a non-routine appointment and the diary entry shows it to have been scheduled as a 15-minute appointment.

A considerable debate has ensued about what lies behind the entry relating to the need to “exclude pneumonia”, the steps taken in relation to further investigations concerning pneumonia and the implications of this for an admission of Morwenna to hospital that Saturday. It is an issue to which I will have to return. However, I should for present purposes simply record the factual situation and what Dr Childs and Mrs Ganz have said about it.

As Dr Childs’ note indicated, she put in hand arrangements for obtaining a chest X-ray (‘CXR’) and a blood test to indicate the results of a full blood count (‘FBC’) and the erythrocyte sedimentation rate (‘ESR’), a test designed to show the presence or otherwise of inflammation which, as Dr Ross Russell (the paediatric intensivist called on behalf of the Third Defendant) explained, is elevated in infection (and a number of other inflammatory conditions). These tests were, however, to take place on Monday, 20 December, for reasons to which I will turn shortly. In terms of what Dr Childs did, she said this in her witness statement:

“ ... I planned a chest x-ray, on a private basis, at the New Victoria Hospital x-ray department to take place on Monday 20 December 1999. I also advised a full blood count and ESR to be undertaken on Monday 20 December 1999 at Kingston Hospital. At this time we were experiencing delays in the Consultant reporting of X-rays at Kingston Hospital, and this would have been worse in the lead up to Christmas. It is likely that this is why I referred her to a Private Hospital as the family had private insurance. The New Victoria routinely return results by fax in 24 (occasionally 48) hours.”

The X-ray request form prepared for the New Victoria hospital had the following written under the heading ‘Clinical Information’: “Asthma better - still cough & fever & gastritis generally.”

Dr Childs said in her witness statement that had she considered pneumonia “a probability” she would have referred Morwenna to hospital the same day or at the very least started antibiotics. On that approach, it follows that Dr Childs did not consider pneumonia as “probable”. In her oral evidence-in-chief she said that she considered pneumonia “very unlikely” as Morwenna had no chest symptoms on the day and had recovered from her previous chest problems. When asked by Mr David Pittaway QC (who represented the GPs) why she mentioned pneumonia at all, she said she was not sure, but that it may have been because of concerns brought up by Mrs Ganz. She did say, perhaps more strongly than in her witness statement, that if there had been a serious prospect of pneumonia she would have sent Morwenna to hospital. She explained that the only way to get an X-ray done was by “sending her in”. However, my understanding of her evidence was that she considered pneumonia to be so unlikely that admission that day was not justified. She did indicate in her witness statement that following her examination she had considered sending Morwenna to hospital, but it does not appear that this related to any thought of a real prospect of pneumonia. Her view was that the most likely diagnosis was a “viral illness with gastritis and/or a dyspeptic reaction to the oral steroids [Morwenna] had taken for her asthma.”

The genesis of the idea for the X-rays and the blood test is a little difficult to unravel. In her witness statement (and repeated in her oral evidence) Mrs Ganz said that her friend, Mrs Jenny Provin, who was a trained nurse and, incidentally, at the time was a Booked Admissions Officer in the Chief Executive Officer’s office at Kingston Hospital, had suggested that if she was concerned she ought to ask for a blood test and a chest x-ray. Mrs Ganz’s evidence was that in the consultation with Dr Childs the initiative for this came from her (Mrs Ganz) as a result of this suggestion. Mrs Provin, who was not required by any of the defendants to attend trial and be cross-examined, did not mention this in her witness statement. Mrs Ganz’s account is that Dr Childs asked her if they had private health insurance because every GP’s surgery was allocated funds for X-rays and she did not want to waste funds that she did not consider necessary. In consequence she gave her the form for the X-ray to be performed privately at Victoria Hospital. She also said, according to Mrs Ganz, that this was because it would be quicker.

When Mrs Ganz was cross-examined Mr Pittaway put to her clearly that the suggestion for the blood test and X-rays was something Dr Childs raised with her and came from Dr Childs, not from Mrs Ganz. Mrs Ganz’s response was that she thought that it “came from both of us”. When Dr Childs gave evidence she said, in answer to the question of who raised the issue first, that she was not sure and that it could have been either of them. For reasons which will appear later (see paragraph 110) I do not think it is necessary to resolve what, if anything, remains of this issue of fact.

The positive suggestion is made by Dr Childs that she told Mrs Ganz that if there was any deterioration before Monday she should take Morwenna to the A & E Department. Mrs Ganz said that she did not recall that although she conceded that Dr Childs might have said it. I will return to this issue of fact later (see paragraphs 99-101), but it has to be said that the contemporaneous evidence that it was said is very weak and, if anything, supports the proposition that it was not said.

At all events, during the afternoon of the Saturday, according to Mr and Mrs Ganz, Morwenna became weaker. She became, they said, more lethargic, very thirsty, tired and weak. It was during the late afternoon that she had to be carried to the lavatory. She was, they said, “lucid but very light-headed.” Mr Ganz added that she was unable to stand up or walk unaided and complained of being very tired, but was not really able to sleep. There is no doubt that this general theme was passed on to Dr Lloyd in the conversation to which I will refer shortly (see paragraphs 48-52).

These concerns led to another approach by Morwenna’s parents to the out-of-hours service. Mr Ganz recalls that his wife first called a nurse at 22.30 -23.00. His recollection is that the nurse talked her through the symptoms and said it was flu. He recalls his wife ringing again after midnight at 01.00. Then there was then a delay before she spoke to Dr Lloyd. He was challenged by Mr Pittaway about this bearing in mind that it was not something mentioned in his witness statement. No record of an earlier call than one made at 02.45 has been disclosed by Harmoni, but the evidence did not demonstrate that a record would necessarily be retained of a telephone conversation with a nurse. It is to be noted that the transcript of the telephone conversation between Mrs Ganz and the doctor to which I will refer in paragraphs 48-52 below begins with the receptionist from NHS Direct saying to Mrs Ganz that there was a doctor on the line for her “for further advice”. I do not think anything particularly turns on this issue other than that if calls were made earlier it would support the growing anxiety that Mr and Mrs Ganz had for Morwenna as the Saturday afternoon and evening progressed and, if recorded and transcribed, would demonstrate precisely what Mr and Mrs Ganz were concerned about. I am inclined to think that Mr Ganz’s recollection is correct.

At all events, it is agreed that there was a telephone conversation between Dr Lloyd and Mrs Ganz at about 03.00 on 19 December. A transcript of the telephone conversation is available. The salient points of the conversation can be summarised in this way: Mrs Ganz told Dr Lloyd that Morwenna had a history of a “very high fever since Wednesday” and had seen “the GP and the emergency doctor almost every day” since then “because her fever does not go down”. She informed Dr Lloyd that she “[had] been taking paracetamol [suppositories] 500 mg - two of them - every four hours” but that her temperature “does not go down at all” despite this and also having given her cold showers. She explained that Morwenna had been “sick very much” on Wednesday, but this stopped Thursday morning although there was a further episode of sickness “on Friday evening and another one on Saturday morning.” She explained that Morwenna was “very lethargic” and, in answer to questions from Dr Lloyd, confirmed that there was no neck stiffness, headache, rash or photophobia although (after a little difficulty in choosing the right word because English is not her first language) she said that she had a staring “glassy” look. In answer to a question about having a cough or runny nose Mrs Ganz said Morwenna “did have a little bit of cough” which was “more than it was before”. She said that it was “not a dry cough but she [was] not putting anything out.” She said that Morwenna had stomach ache, that she had had “very bad vomiting” and that she had “hardly had anything to eat and drink from Wednesday onwards”. She said that she had that day drunk “about half a pint of coke” and “a pint and a bit of water” and that she had eaten an apple and a banana.

Mrs Ganz went on to explain that the “GP on Saturday morning ... [gave] her a form that if [Morwenna] is not better by Monday morning” to take a blood test, a chest x-ray and a urine test, but that she was to “contact a doctor” if she (Mrs Ganz) thought she was “getting worse”. Mrs Ganz added that her worry was “her lethargic way” and that she could not “stand up at all by herself” and that she could not “walk two steps”. She repeated that this was her concern. Dr Lloyd said that he thought they should wait to see how Morwenna was in the morning. If she was, as he put it, “on the mend” then the tests suggested by Dr Childs “[sound] like a good idea”, but if she “is still lousy tomorrow” then she should be taken to the Memorial Hospital in the morning. He said that if she “takes a turn for the worse tonight” that he was sitting in a car visiting patients and that he could come to see her although he did not think he could do more than what a doctor in the morning could do.

Mrs Ganz asked specifically whether it was normal “to be as lethargic as that” to which Dr Lloyd responded that a “nasty flu virus” (which is what it sounded like) running to a 6-7 day illness “with fever and lethargy and aches and pains is quite common.” He suggested that she should “not be too worried going by the length so far” but he said that he agreed with “your doctor that Monday would be the key day to see how things are coming along.” He added that “if things get worse we will see her any time”. He told her how to assess if she was dehydrated and said that he would be worried if her pulse was between 120-140. There was discussion about her asthma. He asked whether she was “breathing rapidly” to which Mrs Ganz replied that she was breathing “a little bit more than usual”, but she was not “wheezing”.

Mrs Ganz also said that Morwenna was “speaking very, very slowly” and attempted to give an explanation for the way she was speaking. She said her voice “gets very low”, starting with a “normal voice” and then going to a whisper.

Dr Lloyd at this point in the conversation said that everything sounded as if “your doctors have got it covered” and repeated the advice to which I referred in paragraph 49 above.

As I have indicated, it is accepted on Dr Lloyd’s behalf that he should have attended. If he had done so it is accepted that Morwenna would have been admitted to Kingston Hospital by about 05.00 or 06.00 that morning.

In view of the assertion that Mrs Ganz was an over-anxious parent at the time, I have to say that the content of the conversation as revealed in the transcript does not give any hint of that. It certainly highlights her anxieties - it would be odd if it had not done - but there is absolutely no hysterical or other “over-the-top” aspect to anything she said. It is also to be noted that Mrs Ganz made no reference to Morwenna’s previous episodes of encephalitis during this telephone conversation.

As it was, Mr and Mrs Ganz became increasingly concerned because Morwenna did not appear to be getting any better and they made contact again with the out-of-hours service. Mr Ganz recalls that his wife called the out-of-hours service again between 05.00 and 06.00 and indeed Mrs Ganz believes she telephoned earlier than the records show her call being made, namely, at 07.49. Again, nothing very much turns on this, but Mr and Mrs Ganz are clear in their recollection and I have no reason to doubt it. At all events, Dr Patricia Hurton arrived at 08.35 according to the note she made at the time and that accords with the recollections of Mr and Mrs Ganz.

Dr Hurton said that she had some recollection of the visit and that she recalled that Mrs Ganz was very anxious. I am sure that was so and no-one could possibly suggest that she had no reason to be anxious by then. Dr Hurton’s recollection is that she took a detailed history and conducted an examination whilst Morwenna remained in her bed.

Dr Hurton’s note was as follows:

“Metabolic problem, generally unwell

URTI [upper respiratory tract infection] last week treated with steroids as asthmatic was improving but over 4 days has deteriorated with high temp vomiting very weak. O/e tachycardic, pyrexial, flushed, tachypnoic, global weakness with reduced reflexes, chest clear, tender over liver and epigastric area, bm 6.1 mmols, no photophobia/ neck stiffness ? toxic ?cause note history of metabolic encephalitis ?recurrence refer paeds Kingston general.”

Her note confirms Mr Ganz’s recollection that he showed Dr Hurton the reports from Dr Brett and Dr Narayan and discussed these with her. He was concerned that something other than flu was affecting Morwenna and was worried there may be a connection between her previous problems and her current presentation.

Dr Hurton decided that Morwenna needed referral to hospital and arranged for an ambulance. The end time in the on-call sheet was noted as 09:22, a time which appears to coincide with Dr Hurton’s call to the ambulance service according to their records. The ambulance arrived at 09.32 and departed at 10.03.

Dr Hurton’s referral letter (only the first page of which has been disclosed with the result that the details of any abdominal examination, neurological examination and her impressions of possible causes for her symptoms are not available for consideration) was in the following terms:

“.. has been unwell for approx 8-9 days initially with a cough + temp + given oral steroids as her asthma was deteriorating - she seemed to imp [improve] mid week + went back to school but over last 3-4 days she has deteriorated with vomiting, weakness + malaise +++. o/e pyrexial pale ° cervical lymph throat red P [pulse] 110 min RR [respiration rate] 25-30 min º recession ... ºadded chest clear.”

She confirmed that the ‘+++’ went with the word ‘malaise’ to indicate that it was significant. Although she made no comment about it, the respiration rate was raised from normal (see paragraph 250 below).

Dr Hurton said in her evidence that pneumonia was not high on her list though she would not have ruled it out, but she was not concerned. It is, of course, the case that whatever view Dr Hurton had formed of the nature of Morwenna’s illness, her presentation was sufficiently serious for admission to hospital where it would be reviewed. To that extent there would not have been any particular concern on Dr Hurton’s part about making any particular diagnosis. The fact is that within 40 minutes or so of arriving in the Ganz household she had arranged for Morwenna to go to hospital in an ambulance. In those circumstances, I do not think that Dr Hurton’s view about the likelihood or otherwise of pneumonia at that time assists in determining whether Dr Childs’ thoughts about pneumonia the previous day should have been acted upon by arranging admission save to say that she (Dr Hurton) was unprepared to discount pneumonia completely, as indeed was the position with Dr Childs the day before.

The essential case against Dr Childs is that she ought to have arranged for Morwenna’s admission to hospital following the consultation on the morning of 18 December. I will examine the way that case is advanced in due course and identify the response to it. The case is supported by Dr Adrian Rogers and defended by Dr Gavin Young.

Dr Rogers has been in practice as a GP since 1976. His CV indicates that he has a wide experience of the issues confronting a GP, whether as a Principal in a GP practice (in his case in Exeter), a locum (both in Exeter and elsewhere in Devon) or in a number of “extra-mural” roles (e.g. advising the Civil Service or being a referee to a local crematorium). He has not been a Principal in a GP practice since 1996, but has continued his practice privately and as a locum since then. I imagine that a fair amount of his time in recent years has been spent giving opinions on cases as an expert witness. He states openly that 80% of his recent work has been on behalf of claimants and that 20% has been on behalf of defendants. He was articulate and clear in his assessment, though plainly embarrassed to have overlooked, when writing his substantive report, a factor that provides, he said, the effective “missing link” in the chain of reasoning of Dr Childs on 18 December that showed why she considered pneumonia to be a possible diagnosis. I will return to that below (see paragraph 107). His approach in this case to the issues was, as I perceived it, that a GP needs to err on the side of safety and make arrangements for a patient’s admission to hospital when there is the possibility of a serious condition even if not obviously diagnosable, most particularly so when a child is concerned.

Dr Young is of a similar generation to that of Dr Rogers. He has been a Principal in GP practice in Temple Sowerby, Cumbria since 1981. He has been a member of a number of important medical committees (including the Confidential Enquiry into Stillbirth and Deaths in Infancy) and has made a number of written contributions to the medical literature in the British Medical Journal and other places. He accepts that his principal interest is in maternity care. He has acted as an expert witness since 1996 and has provided approximately 50 reports per year. He indicates that he receives instructions from claimants, defendants and third party interests, though he has not given a breakdown of the relevant proportions. I sensed that he came from a robust school of thought that might be less disposed to decide on admission to hospital unless fully convinced that it was justified.

Both expert witnesses had wisdom that was of value for me to consider. However, neither had experience of practice in a London borough and neither would necessarily have had knowledge of the local factors that might drive consideration of the delicate issue of admission or non-admission of a patient in such an area with symptoms that are not easy to slot into an obvious diagnosis. It is no criticism of either of them that, from a court’s perspective, it is difficult to decide the common standards of the 35,000 or so GPs in the UK from what each had to say.

In view of some of the issues that fall for consideration in relation to breach of duty in this case (both in relation to Dr Childs and, at a later stage, in relation to Dr Driver), it is right to remind myself of how the evaluation of the evidence concerning breach of duty must be conducted. In the well-known case of Bolitho v City and Hackney Health Authority [1998] AC 232 the House of Lords considered that precise issue. Lord Browne-Wilkinson said this at p. 241:

“ ... in my view, the court is not bound to hold that a defendant doctor escapes liability for negligent treatment or diagnosis just because he leads evidence from a number of medical experts who are genuinely of opinion that the defendant’s treatment or diagnosis accorded with sound medical practice.”

And then, after referring to the test in Bolam v Friern Hospital Management Committee [1957] 1 WLR 583 and to observations of Lord Scarman in Maynard v West Midlands RHA, he continued thus:

“The use of these adjectives – responsible, reasonable and respectable – all show that the court has to be satisfied that the exponents of the body of opinion relied upon can demonstrate that such opinion has a logical basis. In particular in cases involving, as they so often do, the weighing of risks against benefits, the judge before accepting a body of opinion as being responsible, reasonable or respectable, will need to be satisfied that, in forming their views, the experts have directed their minds to the question of the comparative risks and benefits and have reached a defensible conclusion on the matter.

There are decisions which demonstrate that the judge is entitled to approach expert professional opinion on this basis. For example, in Hucks v Cole [1993] 4 Med.L.R. 393 (a case from 1968), a doctor failed to treat with penicillin a patient who was suffering from septic spots on her skin though he knew them to contain organisms capable of leading to puerperal fever. A number of distinguished doctors gave evidence that they wouldnot, in the circumstances, have treated with penicillin. The Court of Appeal C found the defendant to have been negligent. Sachs L.J. said, at p. 397:

“When the evidence shows that a lacuna in professional practice exists by which risks of grave danger are knowingly taken, then, however small the risk, the court must anxiously examine that lacuna-particularly if the risk can be easily and inexpensively avoided. If the court finds, on an analysis of the reasons given for not taking those precautions that, in the light of current professional knowledge, there is no proper basis for the lacuna, and that it is definitely not reasonable that those risks should have been taken, its function is to state that fact and where necessary to state that it constitutes negligence. In such a case the practice will no doubt thereafter be altered to the benefit of patients. On such occasions the fact that other practitioners would have done the same thing as the defendant practitioner is a very weighty matter to be put on the scales on his behalf; but it is not, as Mr. Webster readily conceded, conclusive. The court must be vigilant to see whether the reasons given for putting a patient at risk are valid in the light of any well-known advance in medical knowledge, or whether they stem from a residual adherence to out-of-date ideas.”

Again, in Edward Wong Finance Co. Ltd v. Johnson Stokes & Master [1984] A.C. 296, the defendant’s solicitors had conducted the completion of a mortgage transaction in “Hong Kong style” rather than in the old fashioned English style. Completion in Hong Kong style provides for money to be paid over against an undertaking by the solicitors for the borrowers subsequently to hand over the executed documents. This practice opened the gateway through which a dishonest solicitor for the borrower absconded with the loan money without providing the security documents for such loan. The Privy Council held that even though completion in Hong Kong style was almost universally adopted in Hong Kong and was therefore in accordance with a body of professional opinion there, the defendant’s solicitors were liable for negligence because there was an obvious risk which could have been guarded against. Thus, the body of professional opinion, though almost universally held, was not reasonable or responsible.

These decisions demonstrate that in cases of diagnosis and treatment there are cases where, despite a body of professional opinion sanctioning the defendant’s conduct, the defendant can properly be held liable for negligence .... In my judgment that is because, in some cases, it cannot be demonstrated to the judge^’s satisfaction that the body of opinion relied upon is reasonable or responsible. In the vast majority of cases the fact that distinguished experts in the field are of a particular opinion will demonstrate the reasonableness of that opinion. In particular, where there are questions of assessment of the relative risks and benefits of adopting a particular medical practice, a reasonable view necessarily presupposes that the relative risks and benefits have been weighed by the experts in forming their opinions. But if, in a rare case, it can be demonstrated that the professional opinion is not capable of withstanding logical analysis, the judge is entitled to hold that the body of opinion is not reasonable or responsible.

I emphasise that in my view it will very seldom be right for a judge to reach the conclusion that views genuinely held by a competent medical expert are unreasonable. The assessment of medical risks and benefits is a matter of clinical judgment which a judge would not normally be able to make without expert evidence. As the quotation from Lord Scarman makes clear, it would be wrong to allow such an assessment to deteriorate into seeking to persuade the judge to prefer one of two views both of which are capable of being logically supported. It is only where a judge can be satisfied that the body of expert opinion cannot be logically supported at all that such opinion will not provide the bench mark by reference to which the defendant’s conduct falls to be assessed.”

The reference to Lord Scarman referred to the words of Lord Scarman in Maynard v West Midlands RHA [1984] 1 WLR 634 where he said this at p. 639:

“ … I have to say that a judge’s ‘preference’ for one body of distinguished professional opinion to another also professionally distinguished is not sufficient to establish negligence in a practitioner whose actions have received the seal of approval of those whose opinions, truthfully expressed, honestly held, were not preferred. If this was the real reason for the judge’s finding, he erred in law even though elsewhere in his judgment he stated the law correctly. For in the realm of diagnosis and treatment negligence is not established by preferring one respectable body of professional opinion to another. Failure to exercise the ordinary skill of a doctor (in the appropriate speciality, if he be a specialist) is necessary.”

Plainly, I must apply that overall essential framework to the issues that I have to consider. There are one or two further observations of a general nature that need to be made.

In the first place, as with any issue of breach of duty, it is very important not to assess the issue with the benefit of the wisdom of hindsight. This is particularly so in the case of a GP who sees many patients in a day or week, many of whom are complaining of the same or similar symptoms. It is very easy in those circumstances for the GP not to identify the one person whose underlying condition is in fact very serious, but whose clinical presentation is similar to countless others going through the surgery at the same time.

There is, equally, a balance to be struck between the duty of the GP to elicit a full and accurate history of the presenting complaint by asking appropriate questions and the role of the patient and his or her family in volunteering information that might not otherwise be immediately available to the GP, but which might be relevant to the diagnosis.

Prior to the material events in this case, Dr Childs had been in full time practice as a GP for about twelve years, doubtless with some time off when her two sons were born in 1991 and 1992 respectively. She would certainly by 1999 have been a GP with a good number of years experience and had been Principal in the practice since August 1987. The practice now has some 4000 registered patients and, as I understand it, at the time of the events with which this case is concerned there was another partner in the practice. However, it is clear that a number of locum doctors were employed at the time, two of whom saw Morwenna in the few days before she saw Dr Childs on Saturday, 18 December.

Dr Childs plainly found the trial a strain and indeed an upsetting experience. That was entirely to be expected given the serious consequence for Morwenna that are alleged to have been, at least in part, her responsibility for not admitting her to hospital on the Saturday. Furthermore, simply having her professional practice called into question will have constituted a strain, whether the allegations were or were not justified, the more so since the events occurred long ago.

There is one aspect of the background that I can deal with at the outset. I have already alluded to the fact that Dr Childs regarded Mrs Ganz as a parent who was more anxious than the average parent. Mrs Ganz saw it in starker terms than that although a review of her records indicates that Morwenna remained registered with Dr Childs (and there were continuing communications between Mrs Ganz and Dr Childs personally) until at least 18 months after the material events. I am not sure it would be appropriate to elevate this background factor to the status of a “personality clash”, but each will undoubtedly have found the attitude of the other more difficult to cope with than either would have wished. Whilst Mrs Ganz is undoubtedly and entirely understandably very distressed by what has happened to Morwenna and, as I shall indicate, as a result one or two areas of her evidence have probably been somewhat skewed by reason of that factor, it was obvious to me that she was speaking from the heart when she felt that Dr Childs was somewhat dismissive of her anxiety. It is always unfortunate if a patient should form that view of their doctor because it strikes at the heart of the trust and confidence that there has to be for the relationship to work properly. It is particularly unfortunate where the patient is a child who will not be able to control the dynamics of the relationship between his or her parent and his or her doctor.

There can be absolutely no doubt that Mrs Ganz was (and she and Mr Ganz were) entirely justified in being very concerned about Morwenna at the time: indeed it is a clear example of a situation where the sixth sense of a parent about their child’s wellbeing was right and, sadly, in the event was proved to have been right in the most tragic of circumstances. However, I am quite satisfied that Dr Childs did not let her view of Mrs Ganz interfere with her professional assessment of the situation. Had she done so, one might have expected to see a rather short note of the consultation and something of a “brush off” in her response to the visit. Her thorough note (which Dr Rogers has recognised was of good quality) does not convey any such message and, to be fair, Mrs Ganz does not suggest that Dr Childs’ attitude at the appointment was wholly dismissive although she sensed, she says, that Dr Childs thought she was making more of the situation than was justified. Obviously, she now thinks (and maybe felt at the time) that more could have been done, but, if that is so, it is, to my mind, more likely to have arisen from a misjudgement by Dr Childs about Morwenna’s true condition or about what ought to be done that day rather than through any personal antipathy or irritation on the part of Dr Childs towards Mrs Ganz. The fundamental question will be whether that misjudgement should be characterised as negligent.

All that having been said, however, I think there may be one feature of the attitude that each had to the other that may have had a bearing on one part of the history. Dr Childs is clear that Mrs Ganz did not mention the attendance of Morwenna at the out-of-hours service the night before the appointment on the Saturday morning: see paragraph 35-37 above. Whilst the fact that there was nothing about it in her note might not be wholly conclusive, I think it highly unlikely that Dr Childs would have failed to record this if she had been told about it. Unless she had been told about it, she would not have known about it because the report from Harmoni about it did not arrive at the surgery until it was sent by fax at 02.53 on 22 December, several days after the consultation on the Saturday morning.

Dr Childs has said that had she known about it, it would have prompted her to refer Morwenna to hospital on the Saturday. She said in her witness statement that this would not have been because of the information contained in the report, but simply on the basis of the fact of a further attendance within such a short timeframe would have heightened her level of concern. Although the disparity between what she said in the witness statement about this and what she said in her oral evidence was not examined during the trial, it is to be noted that in her evidence-in-chief she said that had she been told on the Saturday about the double vision that had occurred the previous day she would have performed a neurological examination and “almost certainly” admitted Morwenna to hospital. Given that, had she received the report from Harmoni by the time of the consultation on the Saturday morning, she would have seen the words “double vision this afternoon” recorded as part of the history, I am not entirely sure why she said in her witness statement that nothing in the report itself would have prompted referral to hospital. At all events, the case has proceeded on the basis that had Dr Childs known about the visit to Teddington the previous night and/or about the double vision, she would have admitted Morwenna on the Saturday. Although the case against Dr Childs was not pleaded on the basis that she should have referred Morwenna to hospital simply because of the report of double vision against the background of the rest of her presentation on the Saturday, I will approach my analysis on the basis that this does form a substantive allegation against her. Since Dr Childs seems to accept that it would have been necessary to admit Morwenna in this situation, I will assume that she accepts that it would have been negligent not to have done so had she known of the relevant factors.

I have to say that I think it is highly unlikely that Dr Childs, had she known of the double vision, would not have made a note of it in an otherwise generally full note. There would have been no reason to omit it and, if she was being cautious about matters, every reason to include it. In this particular respect, I do not think I can accept Mrs Ganz’s evidence that she mentioned the previous night’s consultation to Dr Childs at the consultation on the Saturday morning. This may have been because she assumed that a report would have been available to Dr Childs or, perhaps, because she was concerned (seeing Dr Childs) that Dr Childs would think that she had been running unnecessarily between doctors hoping for a response when it was unreasonable for her to expect one. At all events, I am not satisfied that Dr Childs was told about the previous night’s examination by Dr Sowden.

The other issue raised in this context is whether Dr Childs should, as Dr Rogers suggests, have begun the consultation by asking when Morwenna was last seen by a doctor or some other question that would have elicited the information about the previous night’s appointment with the out-of-hours doctor. Whilst I can understand that there may be circumstances in which this is an appropriate approach, I do not think it can be considered as a sufficiently mandatory requirement to render it negligent not to follow it in every case. It is largely a matter of personal style in the context of the particular patient concerned. I think that Dr Childs was entitled to assume that she would have been told everything about recent previous medical consultations by Mrs Ganz.

A prominent feature in the case against Dr Childs is the suggestion that she should have appreciated just how weak Morwenna was when she attended the surgery on the Saturday morning. The nature of this aspect of the case is reflected in the question posed to the GP experts and their answer:

If the Court accepts Mrs Ganz’s evidence that Morwenna needed assistance to walk into Dr Childs’ room, do you agree she should have been referred to hospital that day?

RESPONSE

The experts have agreed yes.

In her witness statement Mrs Ganz said this about Morwenna on the morning of 18 December:

“By this time Morwenna was so weak that she could not walk unassisted. I had to help her in and out of the car and hold her by the arm in order to help her maintain her balance as she walked into the doctor’s surgery.”

In her oral evidence she said Morwenna was “quite weak” but that “she could walk but needed some assistance.” She did not, she said, have very good balance and she had to hold her to make sure she could walk. She needed assistance getting out of the car. Mrs Ganz described how they waited in the waiting area before Dr Childs came to collect them. She confirmed that when they got up to follow Dr Childs to the surgery Morwenna was able to walk on her own although she had to help her. She did not recall Morwenna having difficulty getting on to the couch for the abdominal examination. When asked by Mr Simeon Maskrey QC, acting for Morwenna, whether it would have been apparent to Dr Childs that Morwenna needed assistance walking, her answer was “I would think so, yes.”

Recounting her evidence in this way, and bearing in mind that it was necessary for Morwenna to leave and then return to Dr Childs’ room to provide a urine specimen, I think Mrs Ganz (who I have no doubt at all is an entirely honest witness, even if her perception of events 10 years or so ago has been altered in some respects by the tragic perspective that subsequently ensued) was drawing back from positively asserting that Morwenna’s weakness was blindingly obvious to Dr Childs. The preponderance of the evidence, including that given by Mr Ganz, is that the significant weakness that affected Morwenna developed later in the day. It was later in the day that Mr Ganz had to carry Morwenna to the lavatory and, of course, it was during the telephone conversation with Dr Lloyd in the early hours of the following morning that Mrs Ganz told him that Morwenna could not “walk two steps” (see paragraph 49). There is no evidence that she said anything like that to Dr Childs and I do not think it was the case at that time on the Saturday morning. Undoubtedly, she had been able at 10.00 on the morning of the Saturday to get to and then in and out of the car, go into the surgery, engage in the examination and return home by car, getting in and out of it in the process. I have no difficulty in accepting that she was weak and, to a degree, unsteady, but I do not consider that the evidence supports the conclusion that this would have been so obvious to Dr Childs that it was negligent of her not to notice it and to act upon it. It has to be remembered, as I have already suggested, that, however it may have been achieved, Morwenna had been taken to the surgery: a home visit had not been requested.

For the reasons I have given, I do not think that Dr Childs’ decision not to admit Morwenna on the Saturday can be criticised on the grounds of a failure to have regard to the previous evening’s consultation with the out-of-hours doctor or on the basis of her failure to appreciate the severity of her weakness. So far as the latter is concerned, I do not think that the severity that was plainly manifest later in the day had become that great (and certainly not that obvious) by the time of the appointment in the morning.

However, there are two, more troubling, matters to which I must now turn. The first relates to the suggestion that Dr Childs failed to have regard to Morwenna’s previous encephalitis and encephalopathy. The second relates to the thought she gave on the Saturday to pneumonia being a possible cause of Morwenna’s presentation. I will consider each separately for present purposes.

The pleaded allegation against Dr Childs was that she failed to consider Morwenna’s “previous history of encephalitis in response to pyrexial and/or infective episodes”. That allegation met with a denial that the past history had been mentioned on 18 December, but that in any event Morwenna’s presentation was not suggestive of encephalitis. That position was, however, modified by Dr Child’s acceptance in her oral evidence that had she known of the history of encephalitis she would have asked questions that might have revealed neurological matters, including the double vision, which would have led to hospital admission.

There is no reference anywhere in the notes taken by any doctor (or indeed any nurse) at the St Marks Road Surgery to the previous history of encephalitis. The only note about it is the Summary of Treatment card from the previous GP practice: see paragraph 19.

Dr Childs’ evidence about the Summary of Treatment card is that at the time of the material events, on the assumption that the card had been received from the FHSA (theFamily Health Service Authority) by December 1999 (which, despite any delays there might have been, seems highly likely), it would have been placed at the back of the sequence of Lloyd George cards. In other words, it would not have been the first document seen by a doctor when Morwenna attended for an appointment and, accordingly, nothing about the previous history would necessarily have been flagged up immediately.

Standing back from any expert evidence about this practice, I am bound to say that it does not seem to me very logical not to have what are, in effect, bullet point features of a patient’s previous medical history right there staring at the GP at the moment he or she starts a consultation. Placing the document at the back of the bundle does not seem to make any real sense from the practical point of view.

Things have, of course, moved on since then and most GP practices will have fully computerised records which are doubtless designed to ensure that the GP will see some significant parts of the patient’s history as soon as reference is made to the electronic record. Obviously, however, the practice then cannot be judged by reference to present day standards. Furthermore, where the Summary of Treatment card is put is, perhaps, not to the point and practices could vary although Dr Rogers was of the view that it was “routine” to put it at the front of the bundle: the question is in what circumstances should a reasonably competent GP refer to such a card? Although Dr Rogers appeared to express the view that it should be consulted by a GP on every occasion, Dr Young was of the view that, whilst it was ideal for a GP to be acquainted with the Summary of Treatment card, it was not mandatory to look at it on every occasion.

On balance, I am not persuaded that Dr Childs was negligent in not looking specifically at the Summary of Treatment card. Since Morwenna’s presentation did not suggest anything neurological, it was understandable that she did not have a look at the history to see if there was anything to explain what might otherwise be inexplicable. Even if her index of suspicion in relation to pneumonia was high enough to warrant admission of Morwenna to hospital (see paragraphs 92-109), there would have been no reason to look at the previous history for further justification to do so.

I must now turn to the question of whether Dr Childs was in breach of duty by not admitting Morwenna to hospital on the Saturday in the light of suspicions that Morwenna may have had pneumonia. It is, of course, the case that Morwenna did have pneumonia at this time, but there is no way that Dr Childs could have been expected to know that and, as I have already said, it is important that her actions are not judged by reference to that subsequently-acquired knowledge. Nonetheless, the fact that Morwenna did in fact have pneumonia adds some credence to the suspicion to that effect (whatever its strength) that Dr Childs may have had.

Whilst the matter might be approached in a number of ways, there are, as it seems to me, two essential questions to consider: (a) at what level of suspicion concerning potential pneumonia in a 14-year old child should a reasonably competent GP admit the child to hospital for tests and (b) did the presentation of Morwenna on the Saturday morning cross the relevant threshold of suspicion?

For my part, I do not think that there can, in principle, be much doubt about the answer to the first question. Given what, on the evidence in this case, is the received wisdom of General Practitioners, namely, that pneumonia can give rise to life-threatening consequences and that its development can be unpredictable and rapidly progressive (see paragraph 15 above), the risk of not following up even a relatively minor suspicion in a child cannot be taken. Dr Rogers said that if a GP suspects that there might be pneumonia in an unwell child it is “almost mandatory” to follow it up immediately and, if possible, to exclude it from further consideration. Dr Young did not venture a view directly on this question, merely taking the position that Dr Childs was justified, in the circumstances, in not admitting Morwenna that day because her presentation (according to Dr Childs’ note) was not sufficiently indicative of pneumonia to warrant admission for further investigation that day. As I have observed previously, there has been no challenge to the proposition that pneumonia can develop rapidly, particularly in children.

Any weighing of the risks and benefits of investigating further if a suspicion of pneumonia exists must, as it seems to me, operate in favour of deciding to investigate further. If that can be achieved on an outpatient basis then, of course, that could be an appropriate avenue. But if the only way in which a relatively immediate chest X-ray can be obtained is by admitting the patient to hospital, then the GP would have to take that course.

As I have said, I do not think that Dr Young disagreed with that approach in principle even though he did not think it was necessary in this case. If he did disagree with it (and it was certainly not investigated fully with him), I would have had to have said that the approach would not have demonstrated the necessary weighing of the risks and benefits that a court would require to see before accepting it as a reasonable and responsible view: see paragraph 67 above. His assessment was that what presented itself to Dr Childs in terms of Morwenna’s symptoms on the Saturday morning was not sufficient to give rise either to any suspicion of pneumonia or certainly none that warranted immediate investigation. It is to that, essentially factual, issue that I must now turn.

As to that issue, in one sense the answer is provided by what Dr Childs recorded at the time, namely, that she did feel it was necessary to exclude pneumonia. Although she says now that it was not her view that pneumonia was at all likely, the fact is that at the conclusion of her examination and at the conclusion of her note she wrote an expression to the effect to which I have referred. She also did set in motion the steps needed to send Morwenna for the appropriate investigations. However, although it was not reflected in her note, it is common ground between her and Mrs Ganz that it was likely to be a further 48 hours before these tests were to be carried out although, according to Mrs Ganz, she did try to make arrangements for the chest X-ray at the Victoria Hospital on the Saturday. Dr Childs has given her reasons for that and Mrs Ganz has put forward her recollection: see paragraph 40-44 above.

Although Dr Childs put the word ‘pneumonia’ in her note, it does not appear on the X-ray request form and Mrs Ganz has not said that Dr Childs ever mentioned the possibility of pneumonia to her (and one would have expected Mrs Ganz to mention Dr Childs’ concern about this to Dr Lloyd in the early hours of the following morning and indeed to Dr Hurton, but no reference was made to it.) Mr Ganz was under the impression that Dr Childs still felt Morwenna had flu and, accordingly, any further deterioration would not require immediate admission to hospital. Dr Childs may, of course, have decided deliberately not to mention pneumonia to Mrs Ganz so as not to alarm her, but if pneumonia was even an outside chance, it does seem surprising that it was not mentioned or that very firm advice was given that if there was any further deterioration that day, Morwenna should be taken to hospital urgently. Dr Childs says, of course, that she told Mrs Ganz to take Morwenna to the Accident and Emergency Department if there was a deterioration. That advice is not recorded in the note and Mrs Ganz does not recall what was said: see paragraph 45 above.

As to that issue of fact, it seems to me that the contemporaneous evidence supports the view that Dr Childs did not make express reference to the A & E Department in her conversation with Mrs Ganz. First, as I have indicated, there was no note about this in Dr Childs’ note whereas, when it had been mentioned on a previous occasion, it was recorded: as recently as July that year, after there had been a meningitis scare at Morwenna’s school, Dr Childs saw Morwenna with her mother who was advised that, if the symptoms of viral meningitis that she then had got worse, she should go to “major casualty” and not to a minor injuries unit. Dr Childs accepted that it was generally her practice to record giving advice to go to A&E. Second, Mr and Mrs Ganz did not in fact take Morwenna to the Accident and Emergency Department even though she plainly deteriorated later that day. If only from the events of the previous July, they would have been aware of the A & E pathway, if I can so describe it. Third, when they contacted the out-of-hours doctor late that night or early the following morning (see paragraphs 47-52), Mrs Ganz merely referred to having been told to contact “a doctor” if Morwenna got worse. I think I must conclude, therefore, on the balance of probabilities, that Dr Childs did not advise that Morwenna should be taken to the A&E Department in the event of a further deterioration. I am inclined to think that her suggestion that she did say this is a rationalisation of what she now believes she ought to have done in the circumstances.

Having made that finding, I have to express some surprise that Dr Childs did not suggest that Morwenna should be taken to the A&E Department if there was a deterioration if she thought that there was even a faint possibility of pneumonia being the diagnosis. Whilst Dr Young may have a point when he says that the out-of-hours doctor was simply another route to hospital, advice to a parent of a child to go straight to the A&E Department in the event of a deterioration reflects a stronger level of concern. It also means that a GP has decided that any deterioration does demand the attention that can only be given in a hospital setting.

Whilst I regret having to say so, because I have no reason to think that ordinarily Dr Childs is not a highly competent and conscientious doctor, I do feel that there was some muddled thinking on her part on this particular occasion. Indeed I rather sensed that she realised this during cross-examination by Mr Maskrey and found the challenge uncomfortable. It does seem to me that she must have thought that, whilst unlikely, there was some chance that Morwenna had pneumonia otherwise there would have been no point in mentioning it in her note or seeking to exclude it from the differential diagnosis. In other words, given the uncertainties she entertained about the diagnosis, it was appropriate to exclude a potentially serious illness by the relevant tests. If there was some chance that Morwenna had pneumonia, it would be necessary to find out quickly because of the potentially rapid progression of the condition in a 14-year old child. Against that background, there could be no logical justification for delaying the relevant tests. If they proved negative, nothing would be lost and pneumonia would have been excluded. If the tests were positive, suitable treatment could be put in place quickly.

Although not asked the specific question, I am inclined to think that had Morwenna presented on a weekday with the symptoms she did after the several days of build-up to them, Dr Childs would have sent her off for a chest X-ray and the blood tests straightaway. It seems to me that the only reason for not sending her off on 18 December was that it was a Saturday and Dr Childs foresaw some possible delays in securing the necessary attention (see paragraph 40 above). Whilst one can sympathise with a GP who has local knowledge of the facilities available taking such a matter into account, I do not consider that such a consideration can possibly override the need to get a child into a system where the opportunity for appropriate investigation exists, particularly where the condition that might (even remotely) exist is one that could progress rapidly and lead to very serious consequences. Dr Rogers was of that view and it seems to me to be the only logical position to take. Dr Young did not address the issue specifically on the basis of whether a delay for 48 hours was justified because it was a weekend. He took the view that Morwenna’s presentation would not have led to him admitting her at all that day, presumably irrespective of whether it was a weekend or not.

Lest it be thought that I have marginalised the issue, I should deal with the question of Morwenna’s presentation on the Saturday morning. As will be apparent, my approach to the issue of fact that drives the answer to the second question posed in paragraph 94 above is that Dr Childs, who was then best placed in many respects to make the judgement, formed the view that, whatever was the true analysis of Morwenna’s presentation, it justified a decision demanding the “need to exclude pneumonia”. But for one fact that emerged somewhat late in the day, as I understood them, neither Dr Rogers nor Dr Young would have said that the presentation made pneumonia a likely diagnosis at that stage. Both in his preliminary and his final report, Dr Rogers had said that Dr Childs’ record made no reference to any neurological symptoms and, although it was said that there was a “need to exclude pneumonia”, his view was that “the clinical findings would not have made this a likely diagnosis”. That view was, as I understood him, shared by Dr Young.

What Dr Rogers said when he addressed the issues at the joint meeting of experts, was this:

Dr Rogers advises that the plan for a chest X-Ray and bloods to exclude pneumonia was entirely reasonable, but if such a diagnosis was seriously considered it needed to be established and treated carefully that day. He would have expected an adolescent suspected of having community acquired pneumonia and who was breathless to have been admitted to hospital.

A patient suspected of pneumonia and febrile at home but not necessarily breathless in whom a doctor is already considering admission, needs a paediatric assessment that day to refute or confirm the diagnosis.

Dr Childs wrote that she “needs to exclude pneumonia” and states that if she had seriously considered pneumonia she would have admitted Morwenna to hospital.

He added this:

Dr Rogers advises that it would have been the overall presentation of Morwenna that morning which should have resulted or not, in admission to hospital and it is not clear from Dr Childs record which of the symptoms described caused her to state that she “considered admitting to hospital”. This suggests to Dr Rogers that there may have been more to the presentation than recorded by Dr Childs and there was a half way house to be considered, ie. discussing the case with the on call team.

In other words, at that time, although he did not think that the clinical findings would have suggested a diagnosis of pneumonia, given that Dr Childs’ concern was that it might exist, she should have admitted Morwenna. He did say, however, that he wondered whether there was something else in her presentation that Dr Childs had not recorded.

I have already alluded (see paragraph 64) to a piece of evidence that was not highlighted by Dr Rogers, either in his preliminary report or his final report, that he now says does afford the link that he suggests was missing. It is right to say that Dr Childs’s note on the Lloyd George cards does not refer to a cough. There is little doubt that Morwenna did have a cough at least from the Thursday: see paragraphs 33, 35, 40 and 48 above. Indeed Dr Childs noted a cough on the X-ray request form (see paragraph 40 above), but failed to record it on the Lloyd George card. Dr Rogers says that if this feature had been added into the picture that he considered was conveyed by her notes on the Lloyd George card, it would make the suspicion of pneumonia obviously stronger and would have afforded the explanation for putting in hand the investigations that she arranged. He states openly that he had obviously known of the record of the cough, but had not made the connection to which I have referred. He was very apologetic about what he described as a “serious omission” on his part. He said that a high fever for 3-4 days (with a temperature never less than 38.5°C), plus a cough, plus epigastric pain, made a diagnosis of pneumonia much more likely – or, perhaps more accurately, one that did need excluding as a matter of priority.

Dr Young accepts that “ideally” the cough should have been recorded as part of Dr Childs’ note, but that it was not mandatory and, in any event, was consistent with Morwenna’s asthma at a time when her peak flow was reduced. He did not attach much significance to it. He says that, according to Dr Childs’ note, Morwenna’s chest was clear and that she had no difficulty breathing. Nonetheless, he did accept that Dr Childs’ may have had an impression of Morwenna’s presentation that gave her reason to consider admitting her to hospital. He was also of the view that, whether the question was the possibility of pneumonia or something else, if the decision to admit or not admit was “finely balanced”, then the GP should admit.

Although the issue of the cough was debated at some length, it was not something that, for example, made a failure positively to diagnose pneumonia wrong. All that it did, in Dr Rogers’ view, was to increase the index of suspicion that pneumonia might be the cause of Morwenna’s problems on 18 December. I do not, for my part, think that it necessarily makes a great deal of difference: if Dr Childs had in her mind (which it seems to me she plainly did) a possibility of pneumonia that was more than a merely fanciful possibility then, in accordance with the logic to which I referred in paragraph 95-97 above, it was incumbent on her to arrange for urgent investigation. That could only be achieved, according to her, by Morwenna’s admission to hospital that day.

It follows from this that, in my judgment, Dr Childs was in breach of duty to Morwenna in not making arrangements for her admission to hospital during the Saturday morning. I reach that conclusion with considerable reluctance (a) because I recognise how difficult it is generally for a GP in a 15-minute consultation in a list of others to identify a potentially serious case amongst those which are not and (b) there are many hallmarks of professionalism in Dr Childs’ contemporaneous records that demonstrate that she was taking care in her approach to the evaluation of Morwenna’s presentation. However, once the question of pneumonia raised itself in her mind, I cannot see how anything could have operated to prevent making arrangements for admission for a 14-year old girl who had by then been ill for several days. It was too much of a risk not to do so.

Had Morwenna been admitted to hospital, she would probably have arrived there by no later than midday. It is agreed that, subject to the effects of any treatment given to her once in hospital, the course of her illness would have been the same as the course it in fact followed. It follows from this that the deterioration that took place during the afternoon and evening of the Saturday and through until the Sunday morning would have been evident to the medical and nursing staff in the hospital.

I will return to the question of what would have happened had Morwenna been admitted by about midday on Saturday (and also had she been admitted by, say, 05.00–06.00 the following morning) when I have considered what happened at Kingston Hospital.

Kingston Hospital

The records indicate that Morwenna arrived in the A&E Department at Kingston Hospital at about 10.22 and was seen more or less immediately by the triage nurse, Nurse Zoee Theobald-Smith. The aim at the time was to complete the triagewithin 15 minutes and the recorded timings confirm that this was indeed achieved. In the circumstances, much of the history would have been given by Mr and Mrs Ganz.

Nurse Theobald-Smith’s note that records her presentation was in the following terms:

“Unwell since lastThursday — vomiting and temperature, saw GP → prednisolone → improved. Vomiting and temperature 40+ since Wednesday again → referred to paediatrics by GP. No vomiting since Saturday. Still [passing urine], drinking with small amount diet. Has her period. ° loose stools. Not able to mobilise unaided, pale, quiet, weak, lips dry, talking. ° wheeze, recession, [capillary refill time less than 2 seconds].

She took certain baseline measurements. Morwenna’s blood pressure was 126/76, pulse 130 beats per minute and respiratory rate (‘RR’) 38, somewhat higher than recorded about an hour or so earlier by Dr Hurton. Her temperature was 40.4°C and her oxygen saturation was 93%. Her blood sugar was 6.1. I will return to the significance of some of those readings later, but three other matters need to be noted about this examination.

First, in her first witness statement dated 30 April 2010 Nurse Theobald-Smith said that the triage would have been completed by about 10.57. However, the revelation to her subsequently of other documents (includingthe A&E Department computer record) has led her to the conclusion that she started it upon Morwenna’s arrival and that it took about 14 minutes - thus ending at 10.36.

Second, she gave Morwenna a triage category of “orange” and recorded “unwell →hot → orange” on the A&E records. The colour code reflected the urgency with which, in the triage nurse’s opinion, a patient should be seen by a doctor. According to Nurse Theobald-Smith, this meant that Morwenna should have been seen by a doctor within 10 minutes of the conclusion of the triage assessment although the Incident Review Group (see paragraph 5 above and 120 and 129-131 below) said that it meant “within 10 minutes of her arrival at hospital”. That view has not been maintained in these proceedings. However, there is no doubt that Nurse Theobald-Smith wanted her seen by a doctor, whilst not immediately, certainly relatively quickly. I will turn to this shortly (see paragraph 119 below).

Third, the triage assessment shows Morwenna’s Glasgow Coma Score (‘GCS’) was recorded as 15. I will say a little more about the significance of the Glasgow Coma Score below (see, e.g., paragraph 302), but a score of 15 is normal. However, it emerged that this entry was not made contemporaneously. It had not been made before Morwenna was transferred to Guy’s Hospital at about 17.30 because the copy of the notes sent to Guy’s did not contain the GCS score of 15. Nurse Theobald-Smith accepts that it was entered on the notes retained at Kingston at some stage before her shift ended at 19.30. Whilst there were, apparently, questions raised at certain stages in the preparation for trial about the accuracy of this assessment, it has been accepted as correct and everyone has proceeded on that basis. Nurse Theobald-Smith says that Morwenna was communicating, something confirmed by Mr Ganz who spoke in his witness statement of Morwenna expressing anxiety about being taken in an ambulance to hospital shortly before they left home.

It is at this point that the systems at Kingston Hospital started to break down. Although the triage assessment ended at about 10.36 and Morwenna should thus have been seen no later than 10.46, she was not seen by a doctor - Dr Anamika Kapse, then a Paediatric Senior House Officer (‘SHO’) - until about 11.00. When Dr Kapse arrived she was asked by Nurse Theobald-Smith to see another child before seeing Morwenna. The recollection of Mr and Mrs Ganz is that they were the only people in the department as far as they knew, although Nurse Theobald-Smith has said in her witness statements that it would have been busy at the time. In fact, as I understand it, the records show that there were five patients under the age of 18 in A&E at 10.22 that day. Whilst the department was not deserted, that rather confirms the recollection of Mr and Mrs Ganz and, of course, it is to be noted that Nurse Theobald-Smith was able to see Morwenna immediately upon her arrival. Nonetheless, it is common ground between Mr and Mrs Ganz and Dr Kapse that Dr Kapse asked if she could attend to another other child ahead of Morwenna and, whilst anxious about Morwenna, they say they assumed the hospital knew better and consequently agreed.

It is clear from the Incident Review Group report (see paragraph 5 above) that there were concerns about Dr Kapse’s actions during the relevant period. I will refer to those concerns below (see paragraph 130). However, it is not disputed that Dr Kapse carried out a full examination and recorded a detailed history which I should set out. Indeed it is right to record, given the other criticisms made of Dr Kapse’s actions, that her examination was plainly thorough and her notes were extensive. Her notes recorded the following: that the history of the presenting complaint was that Morwenna had been unwell from 11 days ago and had vomited twice 11 days ago producing fluid but no bile or blood and that from 11 days ago she had experienced an increased temperature of about 40^°C. This had been controlled with Paracetamol and the temperature had settled for four days. Ten days previously she had been taken to her GP where she had a decreased peak flow of 210 (360 being normal for her) and the GP prescribed Prednisolone for three days. Five days prior to her admission she went back to the GP and the peak flow was normal, but that evening she had an increased temperature of 40^°C. The emergency GP diagnosed a viral illness. Four days previously she started vomiting again, six or seven times, and three days previously she vomited once. Two days previously she had vomited again. She had no diarrhoea. For the last four days she had an increased temperature which had not been controlled with Paracetamol. She had had a cough for three days, but no shortness of breath, no rash, no photophobia and no neck stiffness. She had complained of double vision three days ago. She had right sided abdominal pain with no radiation for three days. The abdominal pain was constant and there appeared to be no precipitating factors and no relieving factors. Her period had started three days ago. She did not have a headache.

Dr Kapse’s notes record that she had decreased energy for three days and the previous day “could not sit up or walk [and was] unsteady on her feet.” She had a decreased appetite for five days and today had drunk two glasses of water, but had not had any solids. She had not lost any weight. Her notes then continued as follows:

“Brazil 15 months old - intercurrent illness, sick several months followed by severe ataxia. CT [illegible] serum amino acids, urine organic acid and ammonia normal. She subsequently had one more intercurrent infection at which time she became ataxic for a few days. [illegible] Seen Great Ormond Street - 2 years 10 months - cause unclear. Houston, 5% years - another episode unsteadiness of [illegible] + speech changes followed by physiotherapy 2 years. Follow up 1994 - Houston normal.”

Dr Kapse’s examination notes revealed the following:

“Lethargic, unable to sit up, difficulty opening eyes ... unable to stand up or sit up ...”

Her temperature was written as 30.4^°C but that was an error given that she had a temperature of 40.4^°C when she came into A&E. Her oxygen saturations were 93% on air. Her airway was patent. Her BM (which I take to be her blood glucose level) was 3.8. Her respiratory rate was 38 and her pulse was 130.

The physical examination confirmed that she was lethargic and unable to stand or sit up on her own. Her speech was intelligible. She had difficulty opening her eyes, but her pupils were equal and reacted to light. Her conclusion was noted as follows:

“Impression hypotonia exacerbated during intercurrent ...

? metabolic.

Plan [Full blood count] [urea and electrolytes] [liver function tests] [C reactive protein]

plasma amino and organic acids, urine organic acids, ammonia, lactate, [mid stream urine]

[To discuss with registrar]”

She did not record the GCS in her notes. However, in her statement prepared for the internal investigation she indicated that she felt Morwenna’s GCS was 12 out of 15. In cross-examination she said she formed that view at the end of the examination.

Dr Kapse believes that her examination took about 30 minutes. During a period when there was deterioration in Morwenna’s GCS score, it is obviously of concern that an examination should be so extended without any treatment being given. However, the actual period of time spent examining Morwenna is not criticised.

There is an issue about what Dr Kapse did in the period between the completion of her examination and the time that Dr Nicholas Driver, then a Specialist Registrar in Paediatricsat Kingston Hospital, arrived at 13.07. I will turn to that shortly (see paragraphs 135-137). However, one thing is clear: Dr Kapse undertook no recorded monitoring of Morwenna during that period and there were no records of any further examination of her by Dr Kapse or by anyone else until Nurse Theobald-Smith’s further intervention referred to in the next paragraph.

The only further observation recorded within that period was one recorded by Nurse Theobald-Smith at about 12.30 in the following terms:

Ҽ rash

Temperature 38.7°C

BM 3.7 MMOLS

Responds to pain

RR28”

She confirmed in her evidence that the note that Morwenna “responds to pain” is an indication that she had deteriorated from when she last assessed her. In a letter written on 20 December in the context of the Incident Review, Nurse Theobald-Smith indicated that during the period that Dr Kapse was seeing Morwenna (which Nurse Theobald-Smith suggested was from approximately 10.50 until 13.00), Morwenna “had deteriorated but no treatment was given”. She added that “[intravenous] access was not obtained or bloods taken”. She (Nurse Theobald-Smith) expressed concern that Morwenna was allowed to deteriorate during this period, a criticism that is reflected in the report of the Incident Review Group. Nurse Theobald-Smith said she suggested that she took a blood sample for analysis but that Dr Kapse declined: all she (Dr Kapse) wanted was a blood sugar reading. Nurse Theobald-Smith said in her letter that she could see that Morwenna had deteriorated so she rang the registrar as she knew that she “needed urgent treatment”. She agreed with the proposition that, following her return at 12.30, she was concerned by the delay there had been during which no registrar had attended and no treatment or investigations had taken place.

Given the debate that has taken place about blood gas levels, it is very unfortunate that no sample was taken during this period and indeed when Nurse Theobald-Smith suggested it. The Incident Review Group concluded that Dr Kapse should have arranged for intravenous access and blood for appropriate tests before Dr Driver arrived and that she should have conducted further examinations of Morwenna pending his arrival. I will return to this in due course (see paragraph 130 below). They could arguably have either substantiated or undermined, as the case may be, the causal mechanism based upon the existence of hypocapnia and hypoxia (see paragraph 224 et seq below). One factor I may have to consider is the extent to which it is legitimate for the Third Defendant to rely on the absence of blood gas readings to undermine this causal mechanism when their very absence arose from a breach of duty, if there was one.

That the Incident Review Group should express itself as it did is indicative of the view taken within the hospital and some evidence of the standard of care that might ordinarily have been expected in the circumstances. It cannot, of course, be determinative of the issue for the purposes of these proceedings. The view of Dr Harvey Marcovitch, the Consultant Paediatrician who gave evidence in support of Morwenna’s case, as reflected in the joint statement which forms part of his evidence, is that while she was waiting for a senior paediatrician to arrive, Dr Kapse should have kept Morwenna under observation, monitored her condition and commenced investigation and treatment. She should have obtained intravenous access for bloods and sent bloods and biochemistry for analysis. He was more specific in answer to another question about the need to take arterial blood gases though his answer reflected the then uncertainty about certain timings. He said this:

“Arterial blood gases would have been a useful investigation. They might have shown evidence of metabolic acidosis compatible with an underlying metabolic disorder. They should have been checked at the completion of Dr Kapse’s assessment at about 1130h or, if not done then, at the time at which her GCS fell below 12, likely to have been before 12.30h.”

It has, of course, been confirmed since then that the GCS score had fallen to 12 before 11.30 and not as late as 12.30.

Since Dr Ogilvie (the Consultant Paediatrician who reported for the Third Defendant) was not called to controvert the thrust of this evidence then, unless I was disposed to reject the evidence on the basis that it did not stand up to logical scrutiny, I would approach the case on the basis that it represented the received wisdom of the paediatric profession on what was required in the circumstances. Since it seems to me to be entirely logical and since Dr Marcovitch was, in my view and in any event, an extremely impressive and balanced witness who was an immensely experienced paediatrician, I have no difficulty at all in accepting the evidence.

Mr Benjamin Browne QC and Mr Matthew Jackson have submitted that the question is not whether Dr. Kapse should have carried out further investigations in the period which she in fact spent waiting for Dr. Driver to attend, but whether she should have carried out further investigations in the space of time that it was her duty to seek advice from a more senior doctor. They suggest that the period of time in which that duty existed was relatively short and that the answer to the question posed is plainly “no”. They submit that this is what they term a Bolitho point. I regret to say that the subtlety of that argument has eluded me. If Dr Kapse, who was then a very junior and inexperienced house officer, was under a duty to call a more senior doctor for assistance (which she was and which she did), but equally was under a duty to do what was best for Morwenna whilst waiting for that senior doctor to arrive (which she was), then if there was a delay in the arrival of the senior doctor, it seems to me obvious that she should be taking positive steps that might assist in deciding on Morwenna’s future management once the senior doctor arrived. There is, to my mind, nothing more sophisticated in the issue than that. Ensuring the taking of bloods and sending them for urgent analysis was one positive step that could have been taken and the failure to do so at some point during this period was a breach of duty. It should not have been necessary, even for an inexperienced house officer, to have to await the suggestion to do so from a nurse.

Dr Kapse made her own representations to the Incident Review Group which included an assertion (a) that she remained with Morwenna throughout the whole period until Dr Driver arrived and (b) that Morwenna was “stable with [oxygen]”. The first assertion appears to have been supported by Nurse Theobald-Smith at the time, although the impression I gained when she gave her oral evidence was that she was less certain about it and indeed suggested she had no direct dealings with Morwenna after the initial triage until about 12.30. She certainly said nothing positive, either at the time or in her evidence, to support the proposition that Morwenna had been given oxygen at this stage. Indeed Dr Kapse herself was not very certain about it when giving evidence.

Although the Group commended Dr Kapse for staying with Morwenna, they had not in fact had any input from Mr and Mrs Ganz. They were both absolutely adamant that, once she had completed her examination, Dr Kapse left them and they and Morwenna were left on their own until Dr Driver arrived (Morwenna not having been given any oxygen in the meantime) save for the return of a nurse with some blankets they had requested for Morwenna who appeared to be cold. They say that Morwenna simply seemed to be asleep.

Whilst, of course, I recognise that recollections can be wrong after 11 years or so and they knew about what Dr Kapse had said for the first time some 10½ years after the event, Mr and Mrs Ganz were so clear about this that I do not think they could be wrong. One imagines that they have lived with the images of those few hours in particular for many years. Indeed it is a more plausible scenario than that of Dr Kapse simply sitting with Morwenna and her parents awaiting the arrival of Dr Driver whilst Morwenna was progressively going downhill. I prefer their evidence and find that Morwenna was not oxygenated or given any other treatment during the period before Dr Driver arrived. Had oxygen been given it is likely that her oxygen saturations would have been assessed periodically. They were not. Indeed I am unable to accept that Dr Kapse was with Morwenna and her parents throughout the whole of the period from the completion of her examination until 13.07. There were other patients in the department who will have required attention.

This brings me to the arrival of Dr Driver. If Dr Kapse’s account is correct, he was first bleeped between about 11.30 and 11.45. There was, she said, no response and she asked Nurse Theobald-Smith to try again shortly after that. Nurse Theobald-Smith did not refer to that occasion in her witness statement or her evidence and merely referred to the occasion when, having returned at 12.30, she realised that Morwenna needed urgent attention. She said that she made arrangements for the registrar to be telephoned whereupon Dr Driver arrived shortly thereafter. I think it highly likely (and I so find) that this was the first occasion that Nurse Theobald-Smith herself intervened to try to alert Dr Driver to the need for Morwenna to be seen.

Dr Driver’s contribution to the Incident Review Group’s investigation was somewhat anodyne and merely recited his findings, including his assessment of the GCS score as 7 (an assessment which is associated with someone in a coma and, as Dr Marcovitch put it, in a “life threatening” position and “on a knife edge”). The only emergency action he recorded in this contribution in the light of his findings was that he established venous access, took the bloods listed in the medical notes and started intravenous Cefotaxime (a broad spectrum antibiotic). He gave more details in his witness statement and described the relevant part of the sequence of events thus:

7.

I examined Morwenna and found that she had a patent airway, was breathing spontaneously with equal breath sounds and an intermittently fruity cough, but with no obvious vocal chest signs to review. She had adequate circulation but was mildly tachycardic at 128 with capillary refill time of three seconds. However, Morwenna was only responding to pain and was not able to talk, giving confused mumblings only. Her pupils were small, equal and reactive. She was tender on abdominal palpation in the epigastrium and would localise to this. Her generalised tone appeared to be low and mildly floppy, she had limb withdrawal to pain but no plantar responses and I was unable to elicit any deep tendon reflexes. I calculated her Glasgow Coma Scale to be 7 out of 15.

8.

My impression of Morwenna generated a differential diagnosis of encephalitis, meningitis or perhaps a stroke. She was, at that time, very unwell and I initiated resuscitative measures. Having established intravenous access, we took bloods for full blood count, erythrocyte sedimentation rate, urea and electrolytes, liver function, coagulation, blood cultures and blood sugar. I prescribed Cefotaxime and Acyclovir as antibiotic therapy and these were given to Morwenna intravenously.

That witness statement recorded that she was “very unwell” and that consequently he “initiated resuscitative measures”. When that witness statement was drawn up, he had not seen what Mr and Mrs Ganz said of their recollection of what had happened on his arrival. They both spoke in their witness statements of his reaction when he discovered Morwenna’s condition. Their recollection is that, once he had realised how serious her condition was, he called a crash team and arranged for an oxygen mask to be placed on her. They said that he appeared angry that he had not been called sooner and Mr Ganz described how, having shone a torch into Morwenna’s eyes, Dr Driver starting acting very quickly.

When he gave evidence Dr Driver accepted that he had detected no sense of urgency in the call to get him to the ward and was surprised by Morwenna’s condition. He accepted that it is likely that he was cross when he saw her condition. He agreed that when he made his assessment of her GCS score at 7 (or possibly 8) he did not know how long Morwenna had been in that state and over what period the score had reduced.

There is an issue about why, if his reaction to Morwenna’s condition was as I have indicated, he delayed involving an anaesthetist until he did. I will return to this below (see paragraphs 145-149). However, it was accepted on behalf of the Third Defendant in a letter written 5 days before the commencement of the trial that it acted in breach of duty “for failing to arrange for Dr Driver’s attendance earlier than in fact occurred.” This was further refined in the Opening Skeleton Argument on the basis that, because Dr Kapse failed to pursue the call to the registrar with the urgency that the situation demanded, there was an unjustified delay of one hour twenty minutes before Dr Driver arrived. This was the only period of negligent delay accepted at the outset of the trial to have occurred at Kingston Hospital. The argument is that Morwenna would have required the same investigations and treatments if Dr Driver had arrived sooner and those investigations and treatments would have taken at least as long to arrange as they in fact took. The concession at that stage of the case was that Dr Driver should have arrived to see Morwenna by no later than 11.47 and, accordingly, intubation should have taken place one hour twenty minutes earlier than it did. Given the contents of the report of the Incident Review Group (apparently discovered again only in April this year), the contents of the report prepared for the Third Defendant by Dr David Ogilvie (who, as I have said, in the event, was not called as a witness) and the contents of the joint statement between Dr Ogilvie and Dr Marcovitch, it is surprising that the full concession concerning the period of one hour twenty minutes was not made earlier than simply at the start of the case. At all events, it was, as I have said, made in the Opening Skeleton Argument and the period of one hour twenty minutes was extended by a further five minutes by the close of the case on the basis of an acceptance by the Third Defendant that Dr Kapse should have called Dr Driver five minutes before the end of her assessment and examination of Morwenna. I will have to consider in due course whether that concession is sufficient, but I merely record it for present purposes.

As I have indicated, Dr Driver assessed Morwenna’s GCS score at the time he examined her as 7. This was based on scores of 1 for eye opening, 4 for motor response (arm withdraws to pain) and 2 for verbal response (incomprehensible, consisting of moans and groans with no speech). Somewhat surprisingly, in his evidence he said he might have been wrong and that if she localised pain then this would have increased the score for motor response to 5. I say “somewhat surprisingly” because his notes were made very much at or about the time of his examination and one would have thought that reflected the reality of the assessment, and thus would be clearer and more accurate, than some later rationalisation. Given that Mrs Ganz has a recollection of him saying, when he realised the nature of Morwenna’s condition, that she was “nearly a 6”, it does seem that the assessment he made at the time was correct. Indeed, bearing in mind that Dr Evans assessed the GCS score at about 13.45 as 5, Mrs Ganz’s recollection would seem to have been accurate. At the end of the day, the difference is probably immaterial since Dr Marcovitch, whose view was not controverted by any other witness, said that “you know 8 is the real point of no return - you are going to intubate at 8.” However, Dr Driver’s comment when giving evidence may indicate an understandable subconscious desire on his part to suggest that things were not quite as bad as they truly were at that stage.

Dr Emma Evans (the Specialist Registrar in Anaesthetics) described her assessment at about 13.50 of the GCS score as arrived at by a ‘motor response’ score of 2 out of 6, a ‘verbal response’ score of 2 out of 5 and an ‘eyes opening’ score of 1 out of 4. She said that Morwenna had occasional decerebrate posturing of the left arm and both legs, but nothing in the right arm, which were abnormal movements to pain. She made incoherent mumblings and was not able to talk to her. Her eyes were shut and did not open. Dr Evans said that “[in] essence, Morwenna was responding to stimulus in a very abnormal way and I decided that she needed intervention to stabilise her condition.” Dr Evans’ notes were written at 16.10 and thus in retrospect.

I should turn to the issue of whether Dr Driver should, as is urged on behalf of Morwenna, have called for the assistance of the anaesthetic team earlier than he did so that intubation and ventilation could be put in place earlier than it was. The allegation was not pleaded specifically although it was probably embraced within the broad allegation of “[failing] … to intubate earlier.” However, the allegation appeared in Dr Marcovitch’s report, was discussed at the joint experts’ meeting and was debated during the trial. I do not think any prejudice flows from the fact that it was not pleaded specifically.

I should say immediately that the allegation (which may well be peripheral to the main issues in the case) was not advanced with any enthusiasm on Morwenna’s behalf. Mr Maskrey paid a handsome tribute to the exemplary actions of Dr Driver in all respects other than in this respect. Indeed I suspect that Morwenna and her family feel, possibly with justification, that but for Dr Driver’s rapid response to her condition on his arrival, she might have died or suffered even more extensive brain damage. Dr Marcovitch was himself very reluctant to criticise Dr Driver and one can well understand that reluctance.

The essence of the criticism made is reflected in Dr Marcovitch’s answer to a question posed for the joint experts’ meeting when he said this:

“There was a 36 minute interval between Dr Driver’s arrival at 13.07h and his call to anaesthetics at 13.43h. … this was an unacceptable delay. [Morwenna’s] need for intubation & resuscitation was clear and the anaesthetist should have been called while Dr Driver’s assessment proceeded.”

I have already referred to Dr Marcovitch’s opinion that a fall in GCS score to 8 (or, a fortiori, 7) dictates a decision for intubation. There may well be other, more immediately urgent, things to do, but putting in hand the availability of the anaesthetic team for the purpose of effecting the intubation was, in his view, mandatory. He said, when cross-examined by Mr Browne, that it takes no time at all to put in hand high flow oxygen, prescribe antibiotics, take bloods and secure an intravenous access, but all these things can be done whilst a call is put out to the anaesthetist to come as quickly as possible. Dr Driver had himself, when questioned about this, said that there may be reasons why the anaesthetist would draw back from intubation and that there were risks associated with the intubation process itself. Dr Marcovitch accepted that, but said that this was a matter for the anaesthetist to have engaged in; it was not a reason for not calling the anaesthetist as soon as the seriousness of the position (here evidenced by an assessed GCS score of 7) was realised. A competent registrar (which Dr Driver undoubtedly was) would have appreciated that very quickly, as indeed the evidence of Mr and Mrs Ganz demonstrated that he did.

I too am very reluctant to reach any decision which reflects adversely on Dr Driver’s actions in respect of Morwenna and the care given to her at the time. What he did was, in all other respects, exemplary, as Mr Maskrey conceded. Dr Driver is now a Consultant and I thought he was a very impressive witness who, I am wholly confident, gives first-class service to all his patients. The only part of his evidence that I did not find particularly convincing was his defence of not calling Dr Evans sooner. I am bound to say that the logic of the position seems obvious, albeit a logic that it is possible for the experts, and indeed the court, to consider and analyse in a measured way in the cold light of day when not faced with the kind of emergency that faced Dr Driver on the occasion in question. It is, of course, often the case that someone faced with an emergency is presented with a dilemma between taking two courses of action and in those circumstances it is normally inappropriate to question the taking of one course rather than the other which, in the event, proves to have been the wrong course. However, that was not really the case here. What was needed was an instruction to a nurse to call the anaesthetist immediately if making the call to the anaesthetist personally by Dr Driver was not feasible. That was not done and, regrettably, I can see no alternative but to characterise it as a breach of duty. In the overall scale of things, and indeed in the circumstances of this case, it was hardly the most egregious of breaches of duty and it may well have made no difference at all to the eventual outcome. But, ineluctably, I must conclude that it represented a breach.

The more important question, however, is probably what would have been required in terms of alerting an anaesthetist to the situation if Dr Driver had been called earlier, as plainly he should have been. I will deal with that in due course (see paragraph 314).

There is one issue of fact that it would be convenient for me to deal with at this point. Part of the case on causation advanced on Morwenna’s behalf is that she was hypocapnic for an extended period leading to cerebral vasoconstriction and reduced oxygen supply to the brain. That is said to be at least part of the mechanism that caused or materially contributed to her irreversible brain damage (see paragraph 177 et seq). Some significance in the analysis of Dr John Pappachan (see paragraphs 240-283 below), upon whose evidence reliance is placed for this purpose, is attached to an arterial PaCO₂ result obtained from a blood sample taken at 14.29. I will turn to that as a discrete issue at this stage.

The significance of the arterial PaCO₂ of 2.94 kPa at 14.29 was vigorously debated during the trial. The issue of fact that needs to be determined before considering that debate further relates to when, in relation to the manual ventilation administered by Dr Evans to Morwenna, the blood sample was taken for blood gas analysis and whether she had received any mechanical ventilation before it was taken. It is suggested on behalf of Morwenna that the result is reliable and assists in evidencing a prolonged period of hypocapnia (reduced levels of CO₂ in the blood). It is suggested on behalf of all defendants, and in particular on behalf of the Third Defendant, that the low reading is simply a reflection of the vigorous hand ventilation carried out by Dr Evans shortly before the sample was taken. Dr Ross Russell, the Third Defendant’s Paediatric Intensivist expert, considered that the only logical explanation for this low reading was that it was taken “immediately after intubation”.

Dr Evans did not herself use the word “vigorous” in relation to the manual ventilation, simply the word “nervous”. Although she had said nothing about it in her witness statement, she said, in answer to questions from Mr Pittaway, that she did not consider the result to reflect the true level of PCO₂ before manual ventilation took place. That, of course, is an expression of opinion from a witness whose presence in court was as a witness of fact.

Plainly, Dr Evans’ evidence on this issue of fact is the most important evidence available although it has, of course, been given many years after the event. In her witness statement, she had described the process that she adopted after Morwenna had been transferred to the Adult Resuscitation area for intubation. The area was apparently close to the Paediatric A&E Department. She said this in her witness statement:

“I then inserted a right radial arterial line and before intubation and whilst she was on her side, Morwenna vomited once, producing green bile. After this was cleared up Morwenna was given pre-oxygenation with 100% oxygen. I adopted standard pre-intubation technique and avoided Suxamethonium due to her congenital condition instead using Thiopentone 425mg and Fentanyl 100 micro grams. My technique involved rapid sequence induction with cricoid pressure using a size 7 cuffed oral endotracheal tube, tied 18cm at the lips. This was a grade 1 intubation being the most straightforward with an unobstructed view. Morwenna coughed on intubation and therefore I gave her 10mg Atracurium to try to prevent her from coughing and minimalise the risk of raised intracranial pressure. I gave her manual ventilation, squeezing a bag with 100% oxygen until she was transferred to an oxylog ventilator with a minute volume of 7 litres per minute.”

She then went on to say in the witness statement that the arterial blood gas timed at 14.29 “would have been taken just after Morwenna had been intubated.” She was questioned about this when she gave her evidence and an issue arose about precisely what she said. I told Counsel that, if necessary, I would listen to the recording of her evidence. I would merely record that for the purposes of preparing this judgment I have indeed done so and what follows is based upon listening again to her evidence.

She explained the sentence quoted in the first sentence of the preceding paragraph a little further in her evidence-in-chief when she clarified that Morwenna would not have been “bagged, masked and ventilated before she was intubated” because she had vomited. She explained that she (Dr Evans) would have pre-oxygenated Morwenna, performed a rapid sequence induction and then at that stage, after giving her appropriate drugs, would have intubated her. At that stage she would have hand ventilated her whilst she was intubated with a protected airway so that air would not be blown into the stomach, with the potential for regurgitation, then she would have set up the ventilator and would then have taken a blood gas. She was merely asked in examination-in-chief whether the sample for analysis would have been taken before or after the manual ventilation and she indicated that it would have taken place after the manual ventilation.

This was taken up in cross-examination by Mr Pittaway whose clients share the same interest in raising issues concerning causation as does the Third Defendant. Dr Evans described the pre-oxygenation process as involving in the first instance the fitting of a tight-fitting mask to achieve as high a level of oxygen as possible. She agreed that Morwenna would then have been transferred to the ventilator and then the blood gas would have been taken. Mr Pittaway invited her to confirm that the blood gases that she would have taken would have been taken “effectively immediately after Morwenna had been transferred to the ventilator”, which Dr Evans said was “correct”. He put to her that it followed that it would have been within a “very short time of being subjected to her manual ventilation” that the sample was taken. Dr Evans said that this was correct, but that it would not have been taken immediately, but “within ten minutes”. That answer, not volunteered before, suggested to me that she was uncomfortable with the suggestion that the sample was taken more or less instantaneously after Morwenna was placed on the ventilator, or that it was precisely correct to say that she had taken the sample “immediately after” intubation.

I think it is plain from what Dr Evans said (and I so find) that the sample would have been taken “within ten minutes” of the end of the period of manual ventilation. However, on the basis that there may have been up to ten minutes between the completion of the hand ventilation and the taking of the blood sample, then there would have been a period of mechanical ventilation in the meantime. That seems to be the logical conclusion to reach from what Dr Evans said. Unfortunately, the language previously used in the witness statement to describe what happened and the sequence in which events occurred was rather loose: it has been tightened during the process of questioning in court. It means that the sample taken may have been influenced to some extent by the manual ventilation to which Morwenna was exposed and also to an extent by the mechanical ventilation that would have been running for a period (not longer than ten minutes) between the end of the manual ventilation and the time when the sample was taken at 14.29. This overall timescale certainly seems to fit in with what Dr Evans (supported by the contemporaneous records) recalls of the events.

I am not sure that any of the experts addressed this blood gas result precisely on the basis of that finding though it seems to me to be somewhat nearer to what Dr Pappachan assumed had happened than what Dr Ross Russell had assumed judging (a) by Dr Pappachan’s general analysis of the situation and (b) by answers he gave to Mr Browne in cross-examination when he recalled his understanding of what Dr Evans had said in her evidence (and, of course, before the opportunity to clarify her evidence existed). When asked by Mr Browne about the third point he had made in response to Dr Ross Russell’s arguments at the joint meeting (see numbered paragraph 3 under paragraph 253 below), where he had referred to “artificial ventilation with modest minute ventilation” having preceded the blood gas that gave rise to the 2.94 kPa result, he said that Dr Evans had said that the hand-bagging of Morwenna had finished and that she had been put on a ventilator before the blood gas was taken. His position, as I understood it, amongst other things, was that the further away from the episode of hand-bagging (which he did not see as needing to be “vigorous” in any event), the less effect such an episode would have on the CO₂ content of the blood. He was challenged about this later in his cross-examination and repeated his belief that Dr Evans had acknowledged that the blood gas had been taken after Morwenna had been put on the mechanical ventilator and added, from his perspective as an experienced anaesthetist, that this would be normal practice. Dr Ross Russell, though a very experienced paediatric intensivist, is not himself an anaesthetist (although he does intubate and ventilate patients). At all events, there was no challenge to Dr Pappachan’s assertion.

I will return to the significance of this issue later (see paragraph 277 et seq), but I am satisfied that there was a relatively short period of mechanical ventilation before the blood gas was taken: it was not longer than 10 minutes and must have had some impact on the blood taken for sampling purposes at 14.29.

Since Dr Ogilvie has not been called to give evidence, the essentially uncontested evidence of Dr Marcovitch sets the scene for what would have happened had Morwenna been admitted on 18 December and had received care and attention to the requisite standard. Dr Driver was asked questions about this the answers to which offer some illumination on what would probably have occurred, but his evidence does not alter materially Dr Marcovitch’s view. He accepted that a “senior paediatrician” (not necessarily a Consultant) would have wanted her to be the subject of close monitoring. He also accepted that the senior paediatrician would have been looking at her clinical condition and background and would have placed a high priority on ensuring that there was no deterioration in her conscious level. Professor Fenella Kirkham and Dr Neil Thomas also contributed to this debate and I will refer to those contributions below (see paragraph 165)

Obviously, to some extent what would have happened would have depended upon her presentation on admission and as the afternoon and evening progressed. As I have already observed (see paragraph 111), her increasing weakness and lethargy would, for example, have become apparent during this time.

Dr Marcovitch’s views can be summarised thus: Morwenna would have been admitted under the care of a Consultant Paediatrician and her past medical history of encephalitis with intercurrent illness would have been elicited. I would add that I am sure Mr and Mrs Ganz would have volunteered the reports of Dr Brett and Dr Narayan at that stage as they did the following morning with Dr Hurton and at Kingston Hospital. Dr Marcovitch was of the opinion that her fever, hypotonia (decreased muscle tone) and tachypnoea (increased breathing rate), coupled with likely hypocapnia on blood gas analysis and her past history should have led to a senior paediatrician reviewing her. He considered that the likely outcome of such a review would have been a presumptive diagnosis of a pre-existing metabolic disorder revealed by acute infection (as initially suspected by Dr Kapse the next day) and that this should have led to discussion with a metabolic specialist at a tertiary centre.

So far as her management was concerned, Dr Marcovitch was of the view that the frequency of observation would have been determined by the clinical assessment on admission. If there were concerns about her general condition, hourly observations (of temperature, pulse, respiration, oxygen saturation) would have been performed. If she was considered stable, then four-hourly observations would have been performed. A full blood count, a c-reactive protein (CRP) test, a routine biochemical profile, blood culture and chest X-ray would have been carried out on admission. (It would, of course, have been the case that Dr Childs’ request for admission would have raised the question of pneumonia and for a chest X-ray.) The chest X-ray is likely even then (given that the chest X-ray taken on 19 December showed right upper and middle lobe consolidation) to have demonstrated pneumonia. That would have led to the administration of intravenous fluids and antibiotics (probably Amoxycillin and/or Erythromycin) and if oxygen saturation fell, the administration of oxygen. A blood gas was indicated in the presence of tachypnoea - rapid breathing - as it might have represented a metabolic acidosis. Neurological observations would have been indicated if the GCS became abnormal. (Given that the GCS was still normal the following morning, it is unlikely that any neurological investigations would have been warranted on that account alone.)

Professor Kirkham expressed the view in her report that if Morwenna “had been admitted 24 hours earlier … the hypoxia, very low carbon dioxide and very high temperature is (sic) likely to have been avoided and she would not have developed the very severe … disorder” she did.

Dr Marcovitch’s position is that at the time Morwenna deteriorated significantly (namely, the following morning) she would have been in hospital, would already have received appropriate supportive treatment and would have had a treatment plan approved by her consultant in association with an expert in metabolic disease. If the supportive measures had not by then arrested the deterioration in her condition, the opportunity for a more rapid response to any acute and severe deterioration the following day existed.

Dr Driver indicated that had Morwenna been admitted on 18 December and, whatever antibiotics might have been administered in the meantime, weakness and reduced reflexes were observed at about 08.00 to 09.00 the following morning, monitoring would have been intensified. He confirmed that as soon as there was a reduction in her conscious level, alarm bells would have rung bearing in mind that what can happen thereafter can be unpredictable and rapid. He said that uppermost in his mind, had he been called, would have been to stop the conscious level falling and to reverse any such fall if possible. That would include giving her oxygen.

At the end of the day, the question is what would have constituted reasonable care and reasonable investigation in the circumstances. The uncontested evidence of Dr Marcovitch must represent the foundation for any decision that needs to be made in this context.

Dr Marcovitch was of the view that the same arrangements as those applicable if Morwenna had been admitted the previous day would have obtained.

Again, whilst Dr Driver gave some insight into what, practically speaking, would have occurred in this situation, the test is what would have constituted reasonable care and investigation in the circumstances.

There would, in my judgment, have been a heightened level of concern about Morwenna’s condition that should have led to close monitoring of her condition with appropriate checks being done on an hourly basis (see paragraph 164 above). It is, perhaps, unlikely that contact would have been made with a tertiary unit that early in the morning, but a general sense of the need for close monitoring would have arisen.

It must be borne in mind that by then Morwenna would have been showing an increased respiratory rate, would have been displaying considerable lethargy and would not, for example, have been able to get to the WC unaided. She would have had a high temperature. Again, there would undoubtedly have been an awareness then of Morwenna’s long term history that would have set up concerns about what the true cause of her problem was.

As will appear in due course, this is not a case (unlike many in the birth asphyxia area) where minutes are likely to have mattered (see paragraph 304 et seq below) and absolutely precise timings are less material than in other cases. Notwithstanding this, a fair part of the submissions on the part of Third Defendant has been directed to some fairly precise timings and indeed Mr Maskrey has contended also for some precise timings. I will deal with that later, but for the present will reflect on what it would have been reasonable for Dr Driver to do had he arrived, as I shall suggest would have been reasonable, by between 11.20 and 11.30.

Dr Marcovitch was invited to say whether, if Dr Driver had arrived within a few minutes of the examination by Dr Kapse and found that the GCS had indeed fallen to 12, immediate intubation would be mandated. By the time of that arrival he said that he would have expected Dr Kapse to have given oxygen and started the process for an intravenous line and for blood taking. His response to the question was that a fall to 12 was indicative of “early signs of trouble” and in those circumstances a rush to intubation is unnecessary. At that stage a calm and cool assessment of what is the cause of the trouble is needed and setting in place steps to mitigate what is going on as far as possible. The deterioration may not continue and, as Dr Marcovitch put it, “you have time on your side for a bit”. Identifying the cause of the trouble would involve sending bloods for urgent analysis. At that stage there would be concerns about possible meningitis or viral encephalitis so that appropriate antibiotic and anti-viral drugs would need to be got ready. The essential exercise would be to try to keep Morwenna’s biochemical and oxygen state stabilised until definitive action in the form of intubation and ventilation took place if it became necessary.

It is, I think, fair to say that the onus on Dr Driver in this situation to alert the anaesthetic team would not have been as great as it was when he arrived at 1.07 (see paragraphs 145-149). Dr Marcovitch was of the view (which I accept) that the anaesthetic team should have been alerted in this situation, but I do not think it could be said to have represented a breach of duty for 15 minutes or so to elapse before they arrived. An assessment would then take place and the likelihood is that what would at that stage have been a precautionary intubation would have taken place.

I will return to this scenario in due course (see paragraphs 314-315).

Having considered the issues of breach of duty, whether as admitted or as found, and having addressed what should have happened (and when) had Morwenna received timely and proper care, I must turn to the question of causation. As I indicated at the outset (see paragraph 5), Drs Childs and Lloyd and Kingston Hospital all say that, whatever deficiencies there may have been in their dealings with Morwenna, the outcome would have been the same in any event or, alternatively, that Morwenna cannot prove that proper care would have made any difference.

It is, of course, never an attractive submission to make when there have been deficiencies in standard care (in this case, including the giving of oxygen when it ought to have been given), but the law is clear that a sufficient causal link must be established between any admitted or established breach of duty and the damage or injury sustained.

The lead in seeking to undermine the case on causation presented on Morwenna’s behalf has been taken by the Third Defendant, though the First and Second Defendants maintain broadly the same position. I note that Dr Charles Essex, a Consultant Neurodevelopmental Paediatrician, who prepared a report for the First and Second Defendants (which was to the effect that earlier treatment would have made no difference) and participated in the joint meeting of experts, but who appeared to say one or two things that were in some respects more supportive than destructive of Morwenna’s case on causation, was not in the event called to give evidence. I must, of course, deal with the case on the basis of the evidence called.

There has been considerable debate about the mechanism for Morwenna’s permanent brain damage. This debate has arisen because of the different potential for treatment of the two principal candidates for causation as advanced on behalf of Morwenna and by the defendants respectively. The defendants contend that Morwenna, who was shown in fact to have been suffering from mycoplasma pneumonia, succumbed to mycoplasma pneumonia encephalitis (‘MPE’) and that this was the most likely cause of her permanent brain damage. In relation to the development of MPE it cannot be shown, beyond the bounds of a mere possibility, that the early administration of an appropriate antibiotic would have affected the development of the pneumonia and the encephalitis. In relation to that matter I should record that following the evidence of Professor Helms Mr Maskrey realistically conceded that if the court found that MPE was the cause (or even a contributory cause) of Morwenna’s brain damage, it could not be demonstrated that a failure to administer erythromycin would have had any impact on the development of that condition. It would almost universally have been regarded as the antibiotic treatment of choice at the time and it would probably have been negligent not to administer it. However, since no controlled trials would have been ethically possible, it could never be demonstrated to a sufficiently high level of satisfaction for a causal link to be established between a failure to administer erythromycin and the development of MPE. If, of course, MPE is not to be regarded as a likely cause of Morwenna’s brain damage, the issue disappears from the case in any event. I will deal with this at paragraphs 202-220 below. It is, however, likely that the administration of erythromycin would have had a beneficial effect on Morwenna’s pneumonia.

It is, however, contended on behalf of Morwenna that this was not the cause of her brain damage and that the more likely cause was, in broad terms, oxygen deprivation of the relevant part of her brain arising from the condition she was in when she arrived in hospital and which went uncorrected for too long. It is, of course, permanent and irreversible brain damage that is the focus of the consideration in this case. It is well-known that reduced oxygenation of brain cells can in some circumstances lead to neurological deficit, but a recoverable deficit. What is important in this case is to identify if possible when the brain damage Morwenna suffered became irreversible and, of course, to ask and endeavour to answer the question whether any steps that ought reasonably to have been taken prior to the time would have prevented the damage becoming irreversible. Identifying the mechanism of the injury is an important starting point in dealing with those issues.

I will explain each of the mechanisms contended for more fully in due course (see paragraphs 202 et seq). However, a number of things are common ground and form the backdrop to the debate about the mechanism of the damage:

In the first place, it is accepted that the disability that afflicts Morwenna is consistent with damage to the basal ganglia. The basal ganglia exist in a region at the base of the brain and comprise a collection of nuclei in four distinct groups. It is an important area of the brain which controls a number of functions, including motor control. Dr Neil Thomas, the Consultant Paediatric Neurologist called on behalf of the Third Defendant, has described the basal ganglia as comprising one of “the most metabolically active parts of the brain”, a view accepted by Dr Pappachan and by Professor Kirkham. In other words, the basal ganglia are oxygen dependent. Professor Kirkham explained that the basal ganglia, whilst generally well supplied with oxygen, are vulnerable to changes in blood supply, particularly in the small vessels that are near to what are known as the “watershed areas”, namely, the peripheral areas of the blood supply to the brain. The other consequence of the normal high metabolic activity of the basal ganglia is that at high temperatures the metabolic state will increase – in other words, there will be an increased demand for oxygenated blood.

Second, is common ground between the neuroradiologists who have been instructed by the parties that there is in fact no radiological evidence of damage to the basal ganglia. However, it is also accepted that clinical basal ganglia damage can occur without radiological evidence of such damage.

Third, it is accepted that there is some evidence of cerebral volume loss in the magnetic resonance brain imaging from 24 December 1999 to 11 January 2001 and two of the neuroradiologists consider that the loss of volume is likely to have occurred after December 1999 whereas the other considers the evidence equivocal.

Fourth, all the neuroradiologists have positively rejected the suggestion that if Morwenna had suffered brain damaging hypoxia or hypocarbia (which is the same as hypocapnia) on 19 December then features associated with hypoxia or hypocarbia would probably have been demonstrated on imaging performed that day or subsequently.

Fifth, two of the neuroradiologists are of the view that the imaging showed no lesions that were specific for hypoxic ischaemic injury, but in their opinion there had been a diffuse cerebral insult which resulted in the global cerebral atrophy that was revealed and which could have been caused by hypoxic ischaemia among other aetiologies. The third neuroradiologist agreed that hypoxia can be a cause of cortical atrophy, but that it was a non-specific finding for which there are other causes.

Sixth, two of the neuroradiologists agreed that the changes in brain volume shown on the imaging were in keeping with an acute event in December 1999. The third agreed that the changes could have been in keeping with an acute event, although there were other potential causes and, in any event, the changes may be considered by a body of radiologists to be within normal limits.

Given the wide measure of agreement between the neuroradiologists, sensibly none was called to give evidence. The differences between them appear marginal. The balance of the neuroradiological view seems to be that the changes seen are at least consistent with having been the result of an acute event on 19 December 1999 and do not rule out (but equally do not positively evidence) a hypoxic ischaemic insult.

There was further agreement between the neuroradiologists that the radiological appearances do not assist in determining whether any damage that was caused on 19 December 1999, if it was, was more likely to be consistent with hypoxic damage or encephalitis (including mycoplasmic encephalitis).

An issue has arisen between other experts as to whether the presence or absence of radiological changes makes one type of damage more likely than the other. That is a matter I will address later when the issue arises, but it is not directly affected by the views of the neuroradiologists on the imaging in this case.

I propose to turn to the competing arguments about causation, but before I do so I need to deal with an issue concerning, in particular, the professional credibility of two witnesses called on behalf of Morwenna, Dr John Pappachan and Professor Fenella Kirkham.

Dr Pappachan was subjected to a vigorous cross-examination by Mr Browne with barely concealed (indeed in a number of respects, openly made) suggestions of partiality, lack of objectivity and a failure to adhere to the requirements of the CPR in relation to his report. Mr Browne continued this attack in his closing submissions, suggesting that Dr Pappachan was not a responsible, dispassionate expert, that his report was “patently misleading” in a number of respects and that he was an “evasive and unsatisfactory” witness. It was suggested that his approach was inconsistent with “ordinary principles of physiology”.

The attack on Professor Kirkham was somewhat more restrained, but nonetheless included the suggestion that she had come up with a new theory of causation in the witness box and that her response to certain medical records “happened to suit her case”.

Whilst the close testing of an expert’s view in difficult and controversial areas is entirely to be expected and indeed the norm in all clinical negligence cases, suggestions of this kind can be counter-productive because, amongst other things, it may result in a forceful and convincing refutation of the points put to the witness.

Before dealing with each of these areas of criticism, there are a few observations I would make about this case generally. First, some experts on each side (and indeed including a witness of fact, Dr Driver, for the Third Defendant) produced additional literature upon which reliance was placed at or shortly before the trial. Because all parties were represented by experienced Leading Counsel and because all the relevant experts were available to be consulted, I took a reasonably benevolent view of this because, in a difficult and sensitive case like this, the court needs the fullest assistance it can get. However, that approach did have the disadvantage that some areas of the literature had not been considered in full by the relevant expert and, more importantly, had not been the subject of discussion between them at the relevant joint meeting of experts. Secondly, I did form the impression that there were some areas upon which witnesses were cross-examined about important aspects of their opinion where the issues could (and should) have, at least in the first place, been ventilated during the discussion at the relevant joint meeting. Experts do, however, feel constrained by the questions posed to them and going beyond those bounds (even if expressly encouraged by the preamble to the agenda) is often regarded as straying into forbidden territory. Third, whilst I have not gone back to check the detail, I am sure that every expert had said something in a report, or in an answer to a question posed for a joint meeting, that was, on further reflection, not as clear as it might have been or gave the wrong emphasis from their perspective. Furthermore, experts do, in my experience, often expect the readers of their reports and of their answers to questions posed (those readers being principally the lawyers, albeit assisted by the experts instructed) to understand clearly the nuances of what they say (and in some cases, the underlying physiology and pathaphysiology of what they are talking about) when, in truth, that is not the case. None of this makes any particular expert partisan, dishonest or whatever other epithet might be chosen. In this case, I did not form the view that any expert was telling me something that he or she did not believe was correct. I thought all were trying to assist me in what, on any view, is a difficult case to unravel: I can understand why views may differ. Ultimately, of course, I have to make the judgment calls.

Since Dr Pappachan and Professor Kirkham seemed to attract more attention than other experts in regard to criticisms from the Third Defendant, I will, accordingly, say something about the impression I formed of each of them as a witness. I will deal with the more difficult issue of where their views lead later.

I will deal with Professor Kirkham first. Her CV demonstrates that she is a highly qualified and highly distinguished paediatric neurologist who has been a Consultant for about 20 years with clinical experience at Great Ormond Street Hospital and Southampton General Hospital. She was a senior lecturer in Paediatric Neurology at the Institute of Child Health for approximately 16 years prior to her appointment as Professor of Paediatric Neurology at the Institute in October 2006. Her written contributions to medical literature, both in textbook form and article form, is very extensive and her particular research interest has been in the detection and prevention of brain damage in acutely sick children. Her recent Doctor of Medicine thesis at the University of Cambridge was entitled ‘Cerebral Haemodynamics in Normal Subjects and Children in Coma’. She was eminently well-qualified to offer an opinion on relevant issues in this case. So far as her presentation as a witness was concerned, I thought she was authoritative when she felt she could be, cautious when she felt she had to be and entirely thoughtful and well-balanced in her approach. She was, in my view, an extremely impressive witness upon whom I felt I could place reliance. I detected no basis for thinking that she was partisan or that she was attaching herself to some document or piece of information “because it suited her case” nor, as Mr Pittaway suggested at some point in his cross-examination, that she had just said something because she had heard Mr Maskrey say something. The suggestion of a “new theory” being put forward in the witness box was, in my view, entirely misconceived.

Dr Pappachan is some 11 years or so younger than Professor Kirkham. His initial medical education was at Downing College, Cambridge, and he then moved to London and completed his clinical training at St. Thomas’s Hospital. Anaesthetics have been his speciality and he was appointed at the age of 33 to his first substantive consultant post in Adult Intensive Care Medicine and Anaesthesia in Southampton. He held that post until 2003 when he was appointed as Consultant in Paediatric Intensive Care Medicine and Anaesthesia, also in Southampton. It was doubtless there that he met Professor Kirkham and indeed they have collaborated on certain written contributions to medical literature (as indeed have Professor Kirkham and Dr Thomas). Dr Pappachan is plainly much less experienced as an expert witness than probably any other expert witness in the case, but nonetheless I have no reason to believe that he is not a very able clinician who has relevant experience and expertise to be able to assist the court: indeed, as I shall indicate below, Dr Ross Russell confirmed that assessment himself. Dr Pappachan was, I think, genuinely surprised by the nature of the attack upon him: he had almost certainly thought that he and Dr Ross Russell, his effective counterpart in the case, had discussed the areas of difference between them and thus he knew the issues that would confront him. However, he was presented with questions in cross-examination on issues that had not been ventilated at the joint meeting of experts and also had to field at short notice some written material that had previously not been disclosed. If there was any hesitation in some of his answers (something that was not wholly unique to him amongst the expert witnesses in the case), it was, in my judgment, because of that rather than any intention on his part to be evasive. Given that he had disclosed, as part of the literature prior to the trial, an article that might arguably have undermined a particular position he took in his report by reference to another article, it is very difficult to see how he could legitimately be described as “partisan”, lacking in objectivity or in breach of his obligations under the CPR. His opinions and conclusions were, of course, legitimate targets for scrutiny (as were those of all other experts in the case), but I did not think that the criticisms of his approach to the case were justified. Dr Ross Russell said that Dr Pappachan was a “scientific colleague and very good paediatrician”. Against that background, it is surprising that such a sustained attack upon his professional integrity was made.

As far as I am concerned, all the experts started (and indeed remain) on an equal footing so far as essential credibility is concerned. However, I still have to determine where, having regard to all the evidence and to what, I trust, is judicial commonsense, the various strands of this evidence lead in what Professor Kirkham said, despite Mr Browne’s invitation to her to confirm that this was a straightforward case from her point of view, was a very difficult case.

I should turn now to the competing arguments on their merits. It seems to me that the starting point is to decide whether Dr Thomas is right that MPE either is, on the balance of probabilities, the true explanation for Morwenna’s brain damage or whether it is simply one of a number of credible non-negligently caused possibilities that cannot fairly be discounted in a way that results in Morwenna not having proved her case to the requisite standard according to the law: cf. Wilsher v Essex Area Health Authority [1988] AC 1074.

Dr Thomas has said that he believes that Morwenna’s “neurological injuries were the result of an encephalopathy caused by Mycoplasma pneumoniae” and that “her outcome was the consequence of Mycoplasma pneumoniae encephalitis”.

For the purpose of analysing whether, on the totality of the evidence, I can accept this opinion as reflecting a finding of fact on the balance of probabilities, it is important to see the process of reasoning that led Dr Thomas to this view.

In his report, which contains a detailed analysis of the clinical history and of the investigation to which Morwenna has been subjected over the years, Dr Thomas asked himself a number of questions and endeavoured to answer them. He concluded (undoubtedly correctly) that no-one had yet made a unifying diagnosis and indeed he was unable to arrive at one himself.

He went on to assess the important issue of whether Morwenna has an underlying propensity to neurological disease and, of course, drew attention to the childhood episodes to which I referred in paragraphs 23-25 above. He addressed the issue of what the pathological basis for such an underlying illness might be, which he classified as either metabolic or para- or post-infectious causes. The two paragraphs of his report that deal with his analysis of metabolic causes were as follows:

117.

Potential metabolic causes for her neurological illnesses have been sought exhaustively and the existence of such a disorder in Morwenna has not been confirmed. In general, all such conditions involve abnormalities of metabolic pathways, usually due to enzyme deficiencies, which, when the pathway is stressed by the demands of intercurrent illness, fail leading to cellular energy failure, circumstances to which neurones are exquisitely sensitive. For example, medium-chain acyl CoA dehydrogenase deficiency, a fat oxidation defect, is compatible with a normal existence but under circumstances of intercurrent illness may lead to hypoglycaemia, hyperammonaemia, lactic acidaemia, as well as a characteristic dicarboxylic aciduria. This condition has been excluded in Morwenna by exhaustive testing, as have all other easily recognisable metabolic disorders.

118.

Mitochondrial disorders also lead to cellular energy failure, often precipitated by intercurrent illnesses. This group of conditions has also been sought by a range of investigations, all of which remain unsupportive of such a diagnosis. However, testing for mitochondrial diseases is complex and, even in 2009, it is difficult to make a definitive biochemical and genetic diagnosis in every case. While there is no clear supportive evidence that Morwenna has such a condition, a mitochondrial disorder remains, in my view, the most likely metabolic condition to underlie all her neurological deteriorations.

He then went on to consider para- and post-infectious encephalopathies and concluded that there was no evidence that Morwenna had been affected by those conditions. He then referred to the evidence that Morwenna did have mycoplasma pneumonia and then described the neurological sequelae that had been associated with that infection, including encephalitis, meningoencephalitis and polyradiculitis. He said that “the pathogenesis of encephalopathy associated with infection is unknown”. He referred to one other potential candidate for diagnosis in Morwenna’s case, namely, infantile striatal necrosis. His opinion was set out in the following paragraphs:

128.

I am unable to offer a view as to whether Morwenna had an underlying propensity to develop neurological deficits: there are points both for and against such a suggestion.

129.

If she did, I am of the opinion that she has an, as yet, unrecognised metabolic abnormality such as a mitochondrial defect which decompensated as a consequence of Mycoplasma pneumoniae infection.

130.

If she did not, I am of the view that her outcome was the consequence of Mycoplasma pneumoniae encephalitis, with her course being similar to that of patient 3 in the series reported by myself and colleagues in 1993 ….

…

132.

If she had an underlying metabolic abnormality, her blood sugar during this illness was normal; there was no evidence that she was significantly hypoxic, either from the blood gas measurements at the time or from the outcome seen on her brain imaging.

…

134.

I believe that Morwenna’s neurological injuries were the result of an encephalopathy caused by Mycoplasma pneumoniae; I cannot determine whether she had an underlying propensity to neurological illness which made such an outcome more likely ….

The reference to a series of cases in 1993 is a reference to an article entitled ‘Mycoplasma pneumoniae infection and neurological disease’ (Arch Dis Child 1993; 60: 573-576) to which further reference is made below.

It does appear that his final opinion, as expressed in his paragraph 134, is that the damage caused to Morwenna arose from an encephalopathy caused by mycoplasma pneumonia and that he was unable to say whether there was “an underlying propensity to neurological illness which made such an outcome more likely”.

Perhaps not surprisingly, what appears to have been a clearly expressed opinion in the final sentence of paragraph 118 of his report was seized upon by Mr Maskrey in cross-examination and Dr Thomas was asked when he had downgraded a mitochondrial disorder from a probability to a possibility. His answer was that this was “probably during the expert’s meeting”. A mitochondrial disorder means that the mitochondria, which are small structures responsible for producing the energy that a cell needs to function, are working less efficiently than they should.

The relevant parts of the Minute of the Joint Meeting (which apparently took place over the telephone, lasted some 3 hours and, of course, included Dr Essex) concerning a possible mitochondrial disorder are as follows:

5.

Is C’s clinical condition and distribution of brain injury on the neuroimaging after 19 December 1999 consistent with:

(a)

Mycoplasma pneumoniaeencephalitis? A: The experts agree that this is possible but it is unusual to have such profound disability in the context of Mycoplasma pneumoniae encephalitis with normal brain imaging

(b)

Infantile striatal necrosis? A: No evidence but most unusual to have normal brain imaging with infantile striatal necrosis

(c)

Mitochondrial disorder? A: No evidence but most unusual to have normal brain imaging with mitochondrial disorder

(d)

…

(e)

A channelopathy? A: Very unlikely but we cannot exclude the possibility that the Claimant has an as yet undescribed channelopathy.

6.

If C has an underlying mitochondrial disorder … would this make her more susceptible to cellular loss in the presence of intercurrent illness?

A: If the court were to find that the likely diagnosis was a mitochondrial disorder, she would have been more susceptible to cellular loss in the presence of intercurrent illness ….

I think that if Dr Thomas had changed the emphasis of his view about mitochondria, it was not apparent from these answers; but equally, the questions were not posed in a way that would necessarily have led to this changed emphasis being revealed. Professor Kirkham indicated in her evidence that the experts focused on the lawyers’ questions. I have no recent experience of the way preparations for meetings of experts are made, but I have little doubt that the expectation of the parties’ legal teams is that the experts will not stray too far off the path mapped out in the questions posed (see paragraph 196).

Despite having agreed with Mr Maskrey initially that he had changed his view, during a later part of his cross-examination and in re-examination by Mr Browne he said that, so far as his report was concerned, he thought he had been saying that he did not know whether Morwenna had an underlying mitochondrial disorder.

In the light of the answer to Question 6 on the agenda for the meeting (see paragraph 210 above), the likely presence of a mitochondrial disorder would offer some assistance to the case advanced on Morwenna’s behalf, namely, that a diminished oxygen supply to her basal ganglia that itself was afflicted by a mitochondrial disorder would mean that the likelihood of damage being caused would have been greater because of that underlying disorder.

The question of the possible existence of a mitochondrial disorder is, in one sense, peripheral to Dr Thomas’ own thesis that Morwenna’s disability arose from mycoplasma encephalitis because, if his thesis is right, the existence of the mitochondrial defect would not necessarily have made any difference to the outcome. It is a defect that would only make worse the effect of a reduced oxygen supply to the basal ganglia. It is, as I have said, of relevance to the case presented on behalf of Morwenna and the suggestion is made by Mr Maskrey that Dr Thomas has downgraded his assessment of the likelihood of mitochondria because of this.

I would have been concerned had I thought that was the case. However, I think that the most that Dr Thomas might be accused of is being a little ambiguous in his report about the status he gave the possibility of a mitochondrial defect. He said very clearly, and does not, as I understand him, resile from it, that Morwenna’s clinical history does positively suggest that she has an underlying condition which may predispose her to neurological impairment. The issue, as yet unresolved from the medical point of view, is what that underlying condition is. I propose to return to this later if I come to the conclusion that MPE must, on the balance of probabilities, be excluded as a sole candidate for the cause of Morwenna’s damage.

The backdrop to Dr Thomas’ opinion that MPE is the likely cause is that he could not identify “a significant hypoxic event” during Morwenna’s presentation at Kingston Hospital and he did not consider the mechanism of the cerebral injury to her suggested on her behalf to be plausible, whether based upon hypocapnia or a combination of hypocapnia and hypoxia. He appears to have attached significance to the fact that there was no neuro-imaging evidence of a hypoxic insult. As indicated above, he considered there were parallels between one of the cases in his 1993 series and Morwenna’s case.

The issue relating to that patient was considered at the joint meeting. The patient was a 5-year old girl whose clinical presentation was MPE who was left with a marked spastic quadriplegia and intellectual impairment whose CT scan three weeks into the illness showed marked cerebral atrophy.

At the joint meeting Dr Thomas recognised that this patient was not a perfect match for Morwenna, but that, in his view, there were some common features between the two cases and MPE has a wide range of outcomes. Professor Kirkham, however, pointed to the significant neuro-imaging changes shown in relation to this patient which Morwenna does not have. She said at the meeting that she had been unable to find cases reported in the literature of severe disability, including dystonia, after MPE without neuro-imaging changes being evident. When she gave her evidence she said that it is something about which she had thought very carefully, but was of the view that MPE did not fit with Morwenna’s case. She said that it was unusual to have a severe dystonic disorder (as Morwenna has) without imaging changes. Dr Thomas accepted that there are no published papers that show a normal scan where there has been a severe outcome and did not go on to speak of clinical experience that suggested such cases exist. He also recognised that in most cases someone who develops a post-infection encephalopathy recovers completely. And, of course, he accepted that the mere fact that Morwenna had an infection and pneumonia did not mean that she necessarily would go on to develop an encephalitis. As he said, the vast majority do not. (That would seem to be consistent with the statistics to which I referred in paragraph 13 above.) When an encephalitis occurs, Dr Thomas considered that any brain damage that might be occasioned would result from an inflammatory process and accepted, in principle, that the effect of that on its own might be to reduce cerebral blood flow but was unable to say whether this would result in the patient being poorly perfused or hypoxic. He could not indicate the nature of the mechanism by which inflammation could cause brain damage in this situation, repeating that this is an unknown area.

Dr Thomas did accept that when he prepared his report he had assumed that Morwenna’s vital signs had been monitored throughout the morning. It is, on any view, clear that this was not so: the GCS assessments were patchy and unrecorded contemporaneously and measurements such as oxygen saturations were not undertaken. Against that background, he accepted that his opinion that there was no hypoxia-induced damage was dependent on the neuroradiological appearances. He accepted also that the degree of global atrophy identified by two of the neuroradiologists (see paragraph 187 above) was indicative of a systemic process rather than of a focal insult and conceded that one possible cause of this was hypoperfusion and hypoxia. It appears that he effectively agreed with Professor Kirkham that the slight global atrophy identified by the neuroradiologists was consistent with hypoxic damage. However, he also questioned how, if there was neuroradiological evidence of global damage, there was no neuroradiological evidence of damage to the basal ganglia – a point, incidentally, not referred to in his report or the subject of discussion at the joint meeting of experts. Nonetheless, that does seem to be capable of happening given the views of the neuroradiologists. He suggested, however, that inflammation itself can give rise to neuronal cell loss and thus a global atrophy. I do not believe Professor Kirkham was asked about this particular matter and, accordingly, I do not have her view about it.

If one leaves to one side, for present purposes, Dr Thomas’ opinion that the process by which Dr Pappachan suggests that hypocapnia caused damage in this case was impossible from the physiological point of view (a central tenet of Dr Ross Russell’s opinion), on analysis, the process of his reasoning that leads to the conclusion that MPE caused the brain damage is somewhat fragile. My task, of course, is to look at Dr Thomas’ evidence in the context of all the other expert evidence, and indeed the whole of the evidence in the case, to see whether I should conclude, on the balance of probabilities, that MPE was the cause of Morwenna’s brain damage – in other words, to the exclusion of any other cause or mechanism. I do not think that I can so conclude. It would, statistically, be a rare occurrence in any event, but the pointers upon which Dr Thomas relies do not seem to me to add up to a conclusion that MPE probably caused Morwenna’s brain damage. In my view, the same analysis would lead to the conclusion that, on the balance of probabilities, MPE did not operate as a contributory factor either to the brain damage. The existence of MPE as such has not been demonstrated and, accordingly, it cannot be said to have any contributory influence. If that conclusion was wrong and it was thought that MPE did, on the balance of probabilities, play some material part in the process that led to the brain damage then, since it will constitute a non-negligent contributory factor, the question might arise as to the effect that it may have on the causation case made on Morwenna’s behalf. I will turn to that issue later, should it arise.

Before moving to the important issue of whether the causation case advanced on Morwenna’s behalf can be sustained, I should address briefly the contention that there is an unidentified mechanism that caused the injury. If, of course, I reject the mechanism advanced on behalf of Morwenna and can find no other mechanism, then the logic is that the mechanism of injury, so far as the court is concerned, has not been identified. However, the purpose of addressing the issue now is simply to deal with the observation made on behalf of all defendants, namely, that over the years a number of distinguished and experienced teams of clinicians, including Professor Lin and his team at Guy’s Hospital, have never really got to the bottom of what the underlying diagnosis for Morwenna is.

It is undoubtedly the case that various clinicians have sought to explain the background to the acquisition by Morwenna of her disability and have failed as yet to arrive at a satisfactory solution. It is, however, to be observed (as Professor Kirkham suggested) that not all those who have looked into the background will necessarily have had all the information that is available to the court and will, in any event, not necessarily have approached the issue in the same way that the court does. It is also to be noted, as I think all the appropriate experts in this case accept, that some features of medical and scientific knowledge have moved on over the last ten years or so and, accordingly, it is too simplistic to say that merely because conclusions were not reached ten years ago means that no view could now be formed if the issue was revisited. But there seems to me to be another, more fundamental, point about this argument: the court is not acting in the same way that a clinician would be acting in seeking to determine a diagnosis. Clinicians will be influenced, at least to some extent, in endeavouring to reach a concluded view by the usually accepted confidence limits applicable in scientific analysis. Whilst the court does not, of course, ignore those matters, the threshold for accepting that a factual issue is established is less rigorous than is required by such an analysis – and indeed the experts are usually (as indeed they were in this case) reminded before they discuss matters that they should bear in mind the Court’s “balance of probabilities” test. To that extent the analytical processes involved are different. Obviously, what emerged from the clinical investigations at the time is something upon which the experts in the case are entitled to draw for the purposes of expressing their opinions.

For my part, whilst I am mindful of the fact that no proper and accepted diagnosis has yet been established, I do not consider that it means that I should be deterred from making such findings as I can on the evidence about how Morwenna’s brain damage was probably caused - provided, of course, that my conclusion is supported by the evidence I accept, both medical and factual.

At the outset of the trial Mr Browne characterised the causation case advanced on Morwenna’s behalf as involving a “controversial theory” and Mr Pittaway characterised it as “novel”.

Given that this, as Professor Kirkham said, is a very unusual case, it is likely that any suggestion as to causation that is not agreed will prove to be both “controversial” and probably “novel”. If no identical or similar case has been reported in the medical literature, it is likely that those seeking to provide an answer will look to arguably parallel situations. Furthermore, a court is in the position of being able to stand back from the minutiae of the sophisticated and intricate medical and scientific arguments and look at the broader picture. Whilst it is important not to take too simplistic an approach, inferences can sometimes be drawn from the wider picture.

In their helpful and detailed written Closing Submissions Mr Browne and Mr Jackson suggest that Morwenna’s causation experts have put forward three different theories: hypocapnia, leading to cerebral vasoconstriction leading in turn to hypoxic ischaemic insult; “free standing” hypoxia; and a combination of hypocapnia and free-standing hypoxia. It is suggested that the “free standing” hypoxia theory was advanced for the first time by Professor Kirkham when she gave her evidence. I may have missed the subtlety of the argument, but it seemed to me that Professor Kirkham’s report made it entirely clear what was being suggested. She said that Morwenna’s “severe movement disorder” –

“… is likely to have come about as a result of a combination of hypoxia (a low oxygen level), hypocapnia (a low blood carbon dioxide level) leading to global cerebral ischaemia (low blood flow to the brain) and a very high temperature which will have increased the metabolic demand of the brain. This meant that the low blood flow was not adequate for the metabolic demand, both globally leading to the cerebral atrophy and the cognitive difficulties, and specifically in the basal ganglia, which have a very high metabolic demand, leading to the choreoathetosis.”

This has been contrasted with her response to a question posed on the basis that “[if] the court accepts C’s case that brain injury was caused by a prolonged period of hypocapnia causing cerebral vasoconstriction” could it have been avoided or ameliorated by intubation and ventilation, and if the answer was ‘yes’, “what is the latest time by which intubation and ventilation would have had to be achieved to avoid lasting brain damage in this case?”. Professor Kirkham answered thus:

“[Should] the court accept that brain injury was caused by a prolonged period of hypocapnia causing cerebral vasoconstriction, which she thinks is the most likely explanation, to prevent the majority of the brain damage, she thinks that the Claimant should have been intubated before her Glasgow coma score deteriorated from 12 (intubation not mandatory but close watch for deterioration essential) to 7 (intubation mandatory). The Glasgow coma score was 12 at 1130 and may have been 7 by 1230 but was not formally documented as 7 until 1307 at the earliest (when Dr Driver arrived) so intubation should have occurred between 1130 and 1230.” (Emphasis added.)

She had previously answered the question, based upon the same premise, whether this could have been avoided or ameliorated by giving oxygen therapy on or soon after arrival in the hospital with the answer:

“[Yes] because (a) the drive to hyperventilation and therefore the hypocapnia would have been less and (b) the brain damaging effect of reduction of cerebral blood flow and therefore oxygen delivery with hypocapnia would have been ameliorated by a 7% increase in oxygen delivery in parallel with a 7% increase in oxygen saturation to 100%.”

Furthermore, a later question asked whether the experts were agreed as to “whether earlier assessment and/or resuscitation following admission at 10.20 on Sunday 19 December 1999 would have avoided an acute deterioration in her consciousness” and her answer was this:

“[Earlier] assessment and/or resuscitation following admission at 10.20 on Sunday 19 December 1999 would have avoided an acute deterioration in her consciousness if the Claimant had been given oxygen because the length of time of exposure to hypoxia and hypocapnia would have been reduced.”

It is plain that at least part of the mechanism advanced was associated with the suggestion that there was “a prolonged period of hypocapnia causing cerebral vasoconstriction”, a suggestion to which Dr Pappachan’s report and evidence was directed.

When she gave her evidence Professor Kirkham explained that her view was that the brain damage was a combination of the hypoxia and what she described as the hypocapnic response. In other words, as she put it, the over-breathing (i.e. raised respiratory rate) was in part related to the hypoxia in an attempt to maintain the oxygen saturation which then led to hypocapnia in an acute situation. The basis for her belief that there was hypoxia present was the one pulse oximetry reading of 93% which she indicated was at the lowest range for a child, and even lower than the lowest saturation seen in a child who is a asleep and has a respiratory problem. She said that, on the balance of probabilities, Morwenna became hypoxic in the period between the pulse oximetry test and when Dr Driver arrived some considerable while later and, if the 93% saturation was maintained during this period, particularly given that Morwenna was sick and that this was an acute situation, she felt that the hypoxia thus arising would have contributed to Morwenna’s brain damage. It would have been, as I understood her, an added component to the effect of the hyperventilation leading to hypocapnia and the consequent reduced cerebral blood flow. This seems to me to be substantially, if not entirely, consistent with the quotation from her report to which I referred in paragraph 226 above.

Dr Pappachan’s approach, however, focused substantially, if not exclusively, upon the hypocapnia. As indicated in paragraph 151 above, hypocapnia is the expression used to describe reduced carbon dioxide (CO2) levels in the blood. The relevance of this is that it is common ground that hypocapnia can give rise to cerebral vasoconstriction (the narrowing of the blood vessels in the brain) which itself causes a reduction in cerebral blood flow and, consequently, hypoperfusion (under-perfusion) of the nerve cells in the brain with oxygenated blood. That can cause cell damage and eventual cell death particularly, it is to be presumed, in areas of the brain where the vulnerability to such damage is the greatest. It is self-evident that the existence of hypocapnia could, if sufficiently sustained, give rise to brain damage. In his report Dr Pappachan spelt out the consequences of this in these words:

“Assuming Morwenna’s basal ganglia were particularly vulnerable, that brain metabolic rate would have been increased significantly by her pyrexia AND that cerebral blood flow would have been severely limited by her hyperventilation and low levels of carbon dioxide in her arterial circulation all of the factors leading to a hypoxic ischaemic insult existed.”

It follows equally that if hypocapnia acted in some way that was additional, or complementary, to hypoxia caused by some other process or by an interaction of the two, the two could act cumulatively to cause brain damage. It is, of course, well understood that hypoxia can itself cause cell damage or death. As I have indicated, the focus of Dr Pappachan’s analysis was upon the hypocapnia although he suggested it could go on to cause what he described as a “hypoxic ischaemic insult”. Professor Kirkham’s approach embraced both hypoxia and hypocapnia.

I will return to the suggestion that the case presented has shifted significantly shortly, but I should record one other suggestion made by Mr Browne, namely, that Professor Kirkham declined to support Dr Pappachan’s hypocapnia theory. It is correct that she deferred to him on his “physiological construct” approach, but I think it is wrong to say, if it is being suggested, that she did not support the proposition that there was hypocapnia during the relevant period. So much is evident from what I have recorded of her evidence so far. However, it is right to record also that she added further support to the contention that hypocapnia could have played a part in the mechanism of injury by reference to literature she produced.

She had said very clearly in her report that low blood CO2 levels are a factor in (i) generalised brain damage and (ii) choreoathetosis secondary to basal ganglia damage. She relied upon two papers, both written in the context of cardio-pulmonary bypass which, she said, was a good model for basal ganglia injury without neuro-imaging changes. The two papers were Nevin and Others in 1987 and Curless and Others in 1997. The former contained this passage in its introduction:

“Up to 80% of patients undergoing coronary artery bypass surgery show diffuse cerebral impairment in the immediate post operative period. In most cases this seems to resolve completely although up to one third of cases may still have a significant deficit at one year post operatively. Even though this cognitive loss may not be immediately obvious on routine clinical examination, it can have a devastating effect on physical and psychological wellbeing. Two major factors have so far been implicated on the aetiology of this diffuse form of neuro-psychometric deficit – namely, micro-embolism and cerebral hypoperfusion.”

“Cerebral hypoperfusion” is a consequence of cerebral vasoconstriction which, as already indicated, is itself a consequence of hypocapnia.

The second paper related to three young patients who developed severe choreoathetosis (a movement disorder associated with basal ganglia dysfunction) following cardio-pulmonary bypass surgery where the authors postulated hypocapnia-induced cerebral vasoconstriction as a contributory factor to the ischaemic damage caused (of which there was no neurological evidence). There was no other indication of hypoxia or ischaemia. All the patients had hypocapnia and respiratory alkalosis during the re-warming period after surgery. Professor Kirkham thought that this group, albeit a small one, represented a reasonable group by which to assess the mechanism of injury in Morwenna’s case.

It was suggested to her in cross-examination that the hypocapnia seen in each of these patients was considerably more severe than anything that could be said to have occurred in Morwenna’s case. However, she said (and it was not subsequently challenged by Dr Thomas) that she could not be sure that the authors of the article had corrected the PaCO2 readings for temperature – and, of course, body temperature is lowered considerably for the purposes of this surgery. She did say that the Curless paper does explain, or at least evidences, selective damage to the basal ganglia arising from what might otherwise be thought to be a generalised reduction in blood flow and/or properly oxygenated blood through the brain. Dr Thomas said that he did not regard the Curless paper as providing a suitable model for Morwenna’s case and produced a paper by Medlock and Others, published in 1993, dealing with other children who had undergone cardio-pulmonary bypass and had developed choreoathetoid movements subsequently. He relied upon that paper to some extent to suggest that there were other factors that might impact upon the development of choreoathetosis rather than hypocapnia. Professor Kirkham’s response was that, in the series of patients concerned, no PaCO2 measurements were taken at all and consequently no conclusions about the possible influence of hypocapnia could be drawn from this series. Dr Thomas said that he found it difficult to accept that ischaemia and hypoxia would not affect the rest of the brain rather than simply the basal ganglia.

I have made reference to these matters simply to demonstrate that Professor Kirkham did positively address the issue of hypocapnia in her report and, as it seems to me, it has always formed a part of the picture that she had in mind about the way in which the injury to Morwenna was occasioned. I will return to the significance or otherwise of her view when I have looked at the rest of the evidence concerning hypocapnia.

At all events, for my part, whilst (as with a number of experts in the case) the words and expressions used to convey the meaning of what Professor Kirkham and Dr Pappachan had in mind has altered, I have not detected a substantial basis for saying that there has been a significant change in the way in which the case on causation is advanced on Morwenna’s behalf. Every aspect of it has been tested and some complex medical issues have been joined. But the essential mechanism suggested for how the damage occurred has, to my mind, remained the same throughout: at a crucial time and for a crucial period too little oxygen got to her basal ganglia, probably by the combined impact or effect of hypoxia and hypocapnia.

It is Dr Pappachan’s opinion, based upon calculations derived from the very limited observations of Morwenna on the day in question and from material in the medical literature, that her arterial CO2 tension (PaCO2) was “below the normal range … from the time of her admission to Kingston Hospital when she was fully conscious to the time she was intubated at 14.29 when she was comatose”. He added this strongly expressed opinion to that general opinion in these terms:

“It is ... physiologically impossible for [Morwenna’s] arterial partial pressure of carbon dioxide to have been above 2.94 KPa [kilopascals] at any time between the time of admission (10.22) and the time of her intubation (approximately 14.29). This was a period of 4 hours and 7 minutes and this conclusion is based upon the several unrelated threads of evidence…:

i.

Clinical observations made

ii.

Proven respiratory physiological principles

iii.

Accepted age related normal ranges for tidal volume, respiratory rate and arterial partial pressures for carbon dioxide.”

As will become apparent, that conclusion is challenged fundamentally by Dr Ross Russell on behalf of the Third Defendant and Dr Thomas has added his voice in support of Dr Ross Russell. I will deal with the challenge after having set out Dr Pappachan’s approach.

Much, of course, for this purpose depends on being able to calculate the level of CO2 in the blood at relevant times. The essential physiology is thatblood which passes through the lungs becomes oxygenated by air drawn into the lungs while carbon dioxide moves out of the blood into the lungs and is expelled when air is expelled from the lungs. The most relevant test for determining the levels of oxygen and carbon dioxide in blood that is used in the body to maintain the essential integrity of the tissues of the body is an arterial blood gas. The arteries are blood vessels that carry blood away from the heart and arterial blood is blood that when it leaves the lungs should be appropriately balanced in relation to oxygen and carbon dioxide.

How did Dr Pappachan arrive at the conclusion to which I referred in paragraph 241 above? As will be apparent from what I am about to record, because of the lack of proper monitoring of Morwenna during the period of a couple of hours or so on the morning of 19 December (see paragraphs 130-131), the objective evidence upon which to make appropriate calculations is, on any view, more sparse than it should be. I will return to this feature later (see paragraph 309). I will be referring to the specific blood gas results upon which Dr Pappachan based his conclusion shortly. However, in order to put the whole argument into context, I have collected together what appears to me to be the other results and the other evidence which arguably have an impact on this particular debate. I have done so by adapting slightly the table of results which was helpfully included in the Third Defendant’s Closing Submissions prepared by Mr Browne and Mr Jackson. My version of that table appears as an Appendix to this judgment.

In order to address the issue of what Morwenna’s likely arterial partial pressure of carbon dioxide (PaCO₂)was between her admission to Kingston (at 10.22) and the second arterial blood gas performed at 15.19 (and thus after intubation and ventilation), Dr Pappachan set out to determine (a) what Morwenna’s PaCO₂ wouldhave been if she had had “normal physiology” and (b) what it was likely to have been in the context of what he characterised as her “abnormal physiology” on the day in question, namely, her “significantly increased respiratory rate of 38 from 10.22 … until 14.29”. I understand that he would add her raised temperature at admission as a further feature of her “abnormal physiology”.

He drew attention in his report (prepared before the evidence was heard, of course) to the fact that the only three known variables which were measured were -

The pH is, of course, a measure of the acidity/alkalinity of the blood. The normal pH of blood is 7.35–7.45 which makes it slightly alkaline. When blood has a pH below 7.35 it is usually regarded as too acidic and blood with a pH above 7.45 as too alkaline.

By reference to a long-standing paper (‘Arterial blood gases and acid base in normal children’, Cassels DE, Morse M. Paediatrics 1950; 6: 557-572), Dr Pappachan said that the normal range for arterialPaCO₂ in the age group of which Morwenna was a member was 4.61-5.92 kPa.

In relation to that matter, when he and Dr Ross Russell discussed matters the following was stated in relation to whether they could agree on “the normal range of CO₂ in the arterial circulation in a 14 year old girl”:

“There are a number of ‘normal’ ranges published, but the figures used in Dr Pappachan’s report (4.61 - 5.92 kPa) are acceptable.”

Although it did not figure in the discussions between Dr Pappachan and Dr Ross Russell, I do not understand it to be disputed that, as Dr Pappachan said in his report, the normal range for respiratory rate in this age group is 12 – 20 breaths per minute.

Before setting out the calculation made by Dr Pappachan, it is necessary to record the definition of one expression that figures in this context, namely, ‘minute volume’. This is the volume of air inhaled into and exhaled from a person’s lungs in one minute.

The way he approached the conclusion to which I referred in paragraph 241 above was set out as follows in his report:

“(a)

The expiratory minute volume [V_E] is defined by the volume of gas that is exhaled per minute. It is equivalent to the volume of gas exhaled with each breath (the tidal volume [V_T]) multiplied by the respiratory rate.

(b)

There is an inversely proportional relationship between V_E and the arterial PaCO₂. Thus the higher the minute volume, the lower the PaCO₂.

(c)

The median tidal volume [V_T] for a 14 year old child is 7 ml/kg and the normal range for respiratory rate is between 11 and 20 breaths per minute.

(d)

Thus Morwenna, [who] weighed 58 Kg would be expected to have a minute volume [V_E] of between 4.8 and 8.1 litres per minute.

(e)

At the lower value for V_E (4.8 L/minute) one can assume Morwenna’s PaCO₂ would be approximately 5.92 kPa and at the higher level of 8.1 L/minute one can assume Morwenna’s PaCO₂ would be approximately 4.61 kPa.

(f)

Morwenna actually had a respiratory rate of 38 and thus a V_E of 15.4 L.

(g)

Using these data and a validated equation presented in a paper by Wexler… in which the new value of PaCO₂ can be related to any change in observed minute ventilation [V_E] and the initial PaCO₂ one can estimate what Morwenna’s arterial PaCO₂ would have been before she was ventilated.

(h)

Using this reasoning I am confident that Morwenna’s arterial PaCO₂ between her admission to Kingston Hospital and the time that she was anaesthetised and ventilated was very low (between 1.43 and 3.13 KPa).”

The reference to Wexler was a reference to an article by Wexler and others entitled ‘A simple formula for adjusting arterial carbon dioxide tension’ published in July 1981 in the Canadian Anaesthetic Journal.

This approach, which only has Morwenna’s weight, age and respiratory rate on admission fed into it, was described by Dr Pappachan as his “physiological construct”.

I would observe that on reading this part of his report (and simply stopping at the point where the extract finishes) it would appear that Dr Pappachan had assumed a respiratory rate of 38 breaths per minute throughout the whole period under review – in other words, from admission to intubation. Interestingly, although he raised a number of matters concerning Dr Pappachan’s calculation, this assumption was not a matter raised specifically by Dr Ross Russell at the joint meeting (see paragraphs 262-263 below) and the first time it emerged as a contentious issue was when Mr Browne cross-examined Dr Pappachan. I will return to it in due course (see paragraph 265-267).

Dr Pappachan and Dr Ross Russell did agree that ‘hyperventilation’ in this context referred to an increase in minute ventilation, that the CO₂ level is inversely related to the alveolar ventilation and that changes in the tidal volume will affect the alveolar ventilation at a given minute ventilation.

Before dealing with Dr Ross Russell’s response to this part of Dr Pappachan’s analysis, I should refer to another feature of Dr Pappachan’s overall analysis which derives from the venous blood gas taken before ventilation at 13.44 (wrongly noted as 13.55 in his report) and the manner in which the results of venous blood gases can be converted to an equivalent arterial PaCO_2.

Dr Pappachan’s argument, based upon the venous blood gas and its conversion to an arterial PaCO_2, ran as follows:

(a)

Venous values for CO₂ although useful for trend analysis can differ significantly from arterial values limiting their utility when making clinical decisions….

(b)

The arterial PaCO₂ is almost 1 kPa lower than the venous value at normal temperature.

(c)

For every 0.5 degree Celsius rise in temperature the metabolic rate rises by about 7%, tissue carbon dioxide production increases and the difference between arterial and venous PCO₂ will widen.

(d)

Morwenna had a temperature of 38.4, her metabolic rate will have been increased by about 20% and the arterio- venous PCO₂ difference must therefore have been significantly greater than the 1 kPa observed when the body temperature is normal.

(e)

Thus the venous PvCO₂ of 5.11 kPa must represent an arterial PaCO₂ of less than 4 kPa.

Two matters arise from this description of his analysis. First, the issue of how to calculate the arterio-venous (‘AV’) PCO₂ difference in a particular situation. Second, an understanding of the significance of an arterial PaCO₂ of less than 4 kPa.

As to the first issue, Dr Pappachan relied on a paper by Rang and others entitled ‘Can peripheral venous blood gases replace arterial blood gases in emergency department patients?’, published in January 2002 in the Canadian Journal of Emergency Medicine. On the basis of that paper (which related to the analysis of venous and arterial blood gases of 218 unwell patients whose ages ranged from 15 to 90) Dr Pappachan demonstrated that in unwell conscious patients there was usually a 0.8 kPa difference between the venous and arterial PCO₂, the arterial value being the lesser value. In addition he drew attention to a paper by d’Hollander and others, published in 1984 also in Canada, which related to a series of 35 patients who were under general anaesthetic where the difference was nearer to 0.2 kPa. In those patients, he explained that the metabolic rate would be reduced and the difference would thus be less than in conscious patients.

As to the second issue, it is common ground (see paragraph 248-249 above) that a normal PaCO₂ for a 14-year old girl is in the range of 4.61-5.92 kPa (although Dr Ross Russell said there were other ranges). Anything below that range has to be characterised as abnormal though, of course, relatively temporary periods of abnormality may not be potentially damaging.

Dr Ross Russell’s response to (and disagreement with) Dr Pappachan’s approach and calculations as at the time of their meeting was set out in the Joint Statement in the following terms:

1.

At presentation Morwenna was fully alert with a documented GCS of 15. There is therefore no reason to believe that her control of breathing was abnormal. Breathing control in the brainstem is determined by arterial CO₂ levels, which diffuse across the blood brain barrier to alter the pH of the cerebral spinal fluid. A low CO₂ level (as postulated by Dr Pappachan at admission) would cause a much reduced drive to breathing from the brain, and would have caused an increase (towards normal) in her CO₂. A sustained and significant hypocapnia is not physiologically tenable in an alert patient (as Morwenna was at admission).

2.

Dr Pappachan’s calculations of Morwenna’s arterial CO₂ levels are erroneously based on her respiratory rate without consideration of the tidal volume. Alveolar ventilation (as agreed above) is only related to minute ventilation if the tidal volume remains constant (as stated in … Wexler et al …). If Morwenna reduced her tidal volume then alveolar ventilation would reduce and CO₂ would remain in the normal range. For example, normal tidal volumes for Morwenna would be around 450m1. Of this dead space would be around 150ml leaving alveolar ventilation of -300 ml/breath. A doubling of her respiratory rate with a halving of her alveolar ventilation (per breath) would yield the same CO₂ levels. So a tidal volume reduction to 300 ml from 450 ml (down by a third) would compensate exactly for a doubling of respiratory rate and give an identical CO₂. Without knowing Morwenna’s tidal volume we cannot postulate what her CO₂ would have been.

3.

Dr Pappachan has not taken any account of her pneumonia in his calculations. Abnormalities of ventilation and perfusion matching would have caused venous blood to ‘bypass’ the lung, causing the mild drop in oxygen saturation seen. Whilst this would not have been a large effect, it would have further served to increase arterial CO₂, and reduce AV differences.

4.

Dr Pappachan has quoted normal AV difference in CO₂ levels to be --1 kPa. Reviewing the papers Dr Pappachan has quoted (Rang et al and d’Hollander et al) with which he was recently … provided, he notes that the actual AV difference reported in the papers was 5-7 mm Hg in the first (-0.8 kPa), and 0.2 kPa (for peripheral venous blood) and 0.65 kPa (for superior vena caval blood - from the brain) in the second. The blood sample in Morwenna’s case was almost certainly peripheral blood and so the figure of 0.2 kPa may be more relevant. If (to illustrate) a figure of 0.5 kPa were used, then a 20% increase in metabolic rate would only increase this to 0.6 kPa. We are agreed that increased cardiac output will serve to reduce this difference further and so Dr Ross Russell cannot accept that there could ever have been an AV difference of greater than 1 kPa in Morwenna’s case.

5.

Lastly, and practically, he notes that children are seen every day with a fever and tachypnoea. If these children suffered hypocapnia of the degree suggested by Dr Pappachan, and this caused cerebral injury, he believes that this would be seen as a regular problem. He does not recall ever having seen brain injury as a result of such a combination.”

Dr Pappachan’s answer to these points as raised at their meeting was in the following terms:

1.

Dr Ross Russell eloquently describes the negative feed back mechanism that controls breathing in health and thus maintains CO₂ levels in the normal range …. I therefore agree with everything but the last sentence. During illness, other stimuli (hypoxia, pyrexia, metabolic acidosis, neurological disease, fear anxiety and pain) can influence breathing control and thus override the normal influence of arterial CO₂. During illness therefore Dr Pappachan argues that acute and sustained hypocapnia is not only possible but very common in an alert patient.

2.

Both experts would seem to agree on the relationship between minute ventilation and arterial CO₂ if tidal volume is constant. Dr Pappachan argues that his calculations conservatively assumed that [Morwenna’s] tidal volume remained normal. As increased respiratory drive tends to increase both rate and tidal volume (and following Dr Ross Russell’s logic a proportionately greater increase in alveolar ventilation) the decrease in [Morwenna’s] arterial CO₂ might well have been greater than predicted by Dr Pappachan.

3.

Dr Ross Russell has correctly pointed out that V/Q abnormalities are an almost universal finding in respiratory disease including pneumonia. Dr Pappachan argues that this is very unlikely to have caused an increase in CO₂ levels especially as artificial ventilation with modest minute ventilation allowed the arterial CO₂ to fall to 2.94 kPa. This would have been very unlikely if there was a significant V/Q abnormality.

4.

Dr Pappachan included the d’Hollander paper to add a historical perspective but in the population studied the metabolic rate and AV difference was reduced by anaesthesia and muscle relaxation. The mean AV difference of most relevance is that quoted in the Rang paper which studied the mean peripheral AV difference in unwell patients who, like [Morwenna], were admitted through the emergency department. This value was 6 mmHg or 0.8 kPa. A 20% increase in metabolic rate would increase this to 1 kPa. We are agreed that a reduced cardiac output would serve to increase this difference and so Dr Pappachan cannot accept that there could ever have been an AV difference of less than 1 kPa in [Morwenna’s] case.

5.

Dr Pappachan agrees that this combination of fever and tachypnoea associated with a low arterial CO₂ is a common presentation in both unwell and critically ill children. However he goes on to state that the combination of these findings with a history of previous encephalopathic episodes, abnormal peripheral (weakness and hypo-reflexia) and central (double vision) neurology and a rapidly falling GCS is extremely rare. Dr Pappachan would therefore disagree with Dr Ross Russell’s conclusion that, if his causation argument were correct, brain damage in children with fever and hypocapnia would be seen as a regular problem.

Dr Pappachan’s reference to a V/Q abnormality in numbered paragraph 3 above relates, I think, to what is known as the V/Q ratio, or the ventilation/perfusion ratio, which is a measure of the efficiency and adequacy of ventilation (namely, the air that gets to the lungs) and perfusion (namely, the blood which reaches the lungs).

I will isolate and deal with the various challenges made to Dr Pappachan’s approach. I will start with the challenge (not previously identified by Dr Ross Russell) to the initial calculation (referred to in paragraph 252 above) relied upon by Dr Pappachan which appears to be based on an assumed respiratory rate of 38 breaths per minute throughout the whole period. Mr Browne suggested to him that any calculation failed to take account of the fact that at 12.30 the respiratory rate had declined to 28 breaths per minute (which is, of course, still above the normal, but less than 38 breaths per minute) and by 13.07 had further declined to 20 breaths per minute (the high end of normal) would be misleading. (At a later stage, at about 14.15, it had apparently dropped further to approximately 14 breaths per minute.)

Dr Pappachan accepted that had he, for example, repeated the calculation utilising a respiratory rate of 20 beats per minute, the PaCO2 would have been higher and, as I understood the matter, higher than any part of the range of figures he mentioned in sub-paragraph (h) referred to in paragraph 252 above. He said that it would still not have been normal, but that it would have been higher than within that range. He also accepted that he could have repeated the physiological construct for each of the respiratory rates. However, his answer to the criticism made is that, whilst he could have performed that exercise, there was no need to do so because objective data (particularly in the form of the venous blood sample taken at 13.44) was available that demonstrated that Morwenna was indeed hypocapnic at that point. In other words, the conclusion he reached in sub-paragraph (e) referred to at paragraph 258 above confirmed the general message conveyed by the calculations to which I referred in paragraph 252 above.

Stopping at this point in my analysis of what Dr Pappachan has said, and reviewing his report, I can see that what he said in the witness box does indeed reflect the way he thought about the issues in the case. He may, however, perhaps take away from this case the thought that the written presentation of his thinking needs to be tightened up because, as will have emerged during the case, very close attention is paid to the precise wording of what is said. As will be apparent from observations I have made elsewhere (see, e.g., paragraph 214), I do not think he was the sole culprit in this regard in this case. However, since I am quite satisfied that his report was not intended to be deliberately misleading (and probably the addition of a few words of explanation, linking the first part of his analysis with the second, would have put paid to any such suggestion), I think that the essential issue is whether his analysis bears logical scrutiny and withstands the other criticisms levelled at it. It follows, therefore, that the point that Dr Ross Russell might have raised with Dr Pappachan at the joint meeting concerning the respiratory rate of 38 breaths per minute, but which he did not raise in the terms that founded the cross-examination by Mr Browne, was not truly a significant point at all from Dr Pappachan’s perspective. That having been said, however, it is clear to me that the confident assertion to which I referred in paragraph 241 above cannot really be accepted in the terms in which it was expressed as reflecting the reality of what occurred. It is based on a calculation that, whilst not wrong in itself as a calculation (subject to the other matters to which I will refer below), it is too absolute in terms of the figures it generated. That may not, subject to the other matters to which I will turn, undermine the broad proposition that Morwenna was hypocapnic during this period, merely that working to precise figures derived from this calculation would connote an accuracy that cannot be achieved. It is, of course, to be observed and repeated that had a further blood gas been taken during the morning as it should have been (see paragraph 130-131), no-one would be struggling with the effect of calculations such as these.

I will turn now to the specific criticisms made of Dr Pappachan’s approach as articulated by Dr Ross Russell in the joint statement to which I have referred. The first is that set out as numbered paragraph 1 set out in paragraph 262 above.

It is not in issue that there is within the brain stem a central respiratory control mechanism that receives information from various sensors and, in consequence, sends messages out which regulate “the respiratory muscles in a fashion coordinating both breath frequency and tidal volume”. That quotation is from a passage in one of a series of lectures on respiration given by Dr Michael J Mason, who I believe is or was associated with the Department of Physiology in Cambridge. It was one of a number of pieces of literature produced on behalf of the Third Defendant at a very late stage in these proceedings. The lecture describes the circulatory route that various messages to and from the brain follow in order to maintain breathing frequency and tidal volume. It describes the sensors that feed back to the central controller and the information that is conveyed as a result. It says that “it is generally accepted that the variable under closest control in the respiratory control system is arterial PCO2 … [and] as such input from sensors sensitive to this parameter, or chemically interrelated … are overwhelming modulators of respiration”. It goes on to describe other matters and concludes by saying “the output from the controller, in response to the input from the sensors, modulates both the frequency and tidal volume to obtain optimum alveolar ventilation”.

As I have indicated, this essential position is unchallenged. Mr Browne questioned why Dr Pappachan had not mentioned it in his report, or factored it directly into his calculations, but his response to Mr Browne’s question was that there was no need to make any adjustments because the central control system is overridden when the patient is in what he described in his evidence as a “diseased state” – in other words, when affected by the kind of stimuli identified in answer numbered 1 under paragraph 263 above. As I understood Dr Ross Russell’s evidence, he accepted that other factors (e.g. temperature) could affect the mechanism, but the issue between him and Dr Pappachan was “how much?” He also accepted, in principle, that the control mechanism may be overridden where the brain has been damaged. However, he said that he could see no reason why the central control mechanism should have been overridden during a period when there had previously been episodes of neurological disturbance (namely, double vision, weakness and reduced reflexes) and a period during which there was a deterioration in conscious level. Dr Pappachan asserted to the contrary and said that respiratory alkalosis with reduced CO₂ is a common finding in critical illness.

I have not found this issue an easy one to resolve. One feels that there ought to be agreement on what, according to Dr Ross Russell, are fundamental and well-established physiological principles. The substance of his argument means that Dr Pappachan has either deliberately ignored a major problem from the point of view of his belief about what occurred or that he is ignorant of basic respiratory physiology. I am not prepared to accept either proposition. In one sense the conclusion will be answered if the evidence derived from the blood gas analyses to which I will refer shortly do demonstrate that Morwenna was hypocapnic at any material point. If that is so, it means that the central control mechanism has not operated to ensure the usual equilibrium. If, however, I was convinced at this stage that hypocapnia was simply not possible because of the operation of this mechanism, it would render futile an analysis of the effect of the blood gas readings. It is the Third Defendant’s case that the blood gas figures at 13:44 (which adjusted to reflect a PaCO2 result that, whilst low, was not unacceptable) demonstrate that the central control mechanism was working, even after the Morwenna’s GCS had fallen to 7 or less and it is argued that for Dr. Pappachan’s “physiological construct” to work, it has to be assumed that it was not working even when her GCS was normal. It is also contended that the 2.94 kPa PaCO2 result following the 14.29 sample was simply the result of the hand-bagging carried out by Dr Evans.

I will defer my final conclusion about this issue until I have examined the basis upon which Dr Pappachan contends (by a route other than through his “physiological construct”) that the blood gas results demonstrate the existence of hypocapnia. However, my tentative view at this stage of the analysis is that Dr Pappachan is probably right in what he says. He says (and I have no basis upon which to doubt it) that he has seen the mechanism overridden in what he termed “diseased” states, a reflection of what he said in the joint statement at paragraph 1 as referred to in paragraph 263 above. Dr Ross Russell had to accept that he had not mentioned in his report this fundamental objection to the case being advanced on Morwenna’s behalf (which he did correctly understand at the time the report was prepared) and equally he had to accept (as Professor Kirkham also suggested) that there is no research literature that confirms the position that he is taking. Although Dr Thomas lent his support to the proposition in his oral evidence, by describing the hypocapnia as “biologically” or “physiologically” implausible, he did not specify it in that way in his report. In his report he rejected as implausible hypocapnia for what appeared to me to have been other reasons. He, of course, would have been approaching this issue from his vantage point as a paediatric neurologist, not as a respiratory or anaesthetic specialist.

As I have said, I will defer a final decision on this issue until I have considered the evidence relating to the blood gases.

Before I deal with that aspect directly I should deal briefly with the second of Dr Ross Russell’s criticisms of Dr Pappachan’s use of the Wexler paper, namely, not having allowed in the calculations for changes in the tidal volume in Morwenna’s breathing. (For the meaning of ‘tidal volume’, see sub-paragraph (a) in paragraph 252 above). Dr Pappachan’s answer to that is short: he recognises that the formula provided for in the Wexler paper is invalidated if the tidal volume changes significantly, but he asserts that there is no evidence that this occurred at any stage during the period with which his calculations were concerned. He said that there was nothing in the records to indicate respiratory failure or other inadequacies of breathing. Accordingly, it was right, he says, for him to have assumed for the purposes of his calculations that the tidal volume remained constant and normal, albeit maintained at a respiratory rate of 38 beats per minute. He agreed that to maintain the tidal volume at 38 breaths per minute would require considerable physical effort and that it would have been necessary to reduce the tidal volume by approximately one third to stabilise the PaCO2. That would, he said, have been clinically obvious. Dr Ross Russell had not himself advanced any suggested reduced tidal volume as being likely and, whilst there was debate about whether a reduction of one-third in Morwenna’s tidal volume would have been apparent clinically, this does not seem to have advanced the debate much beyond the issue of whether it was right to assume a consistent respiratory rate of 38 beats per minute throughout the whole of the period under consideration. I have already dealt with that issue in paragraphs 265-267 above.

Turning to the two blood gas measurements at 13.44 and 14.29, it needs to be recalled that the first was obtained from a venous sample and the second from an arterial sample. Although Dr Ross Russell in his report had simply asserted that the 13.44 result was “normal”, he accepted that it was appropriate to apply a conversion factor to that result to obtain the equivalent arterial result in order to determine whether it was “normal”. Having done that, on his (Dr Ross Russell’s) approach, the equivalent arterial result would be about 4.31 kPa which was below the normal range, but not to such an extent as to be concerning. He suggested that it was an acceptable level “clinically and physiologically”. That level was arrived at by deducting 0.8 kPa from the venous result which, Dr Ross Russell had said, was the maximum that should be deducted, but in cross-examination he said that 0.8 kPa represented an acceptable reduction based upon a reasonable interpretation of the two papers to which I referred in paragraph 260 above. Dr Pappachan says that the adjusted result would yield an arterial PaCO2 of “less than 4 kPa”. Given his view that the deduction should be 1.2 kPa, his position is that, in absolute terms, the adjusted figure should be 3.91 kPa.

It follows, therefore, that despite the debate and the length of time it took to arrive at this point, the adjusted figures should be in the range of, say, 3.9 to 4.3 kPa. I do not propose at this stage to try to be more precise for present purposes. The net effect of this analysis is that the arterial PaCO2 at this time (which was before intubation and ventilation), and which was below what had been agreed as an acceptable normal range (see paragraphs 248-249 above), was at a level that was hypocapnic. I will return to the implications, if any, of this in due course.

I will turn now to the vexed issue of the blood gas taken at 14.29. I have already analysed the evidence concerning the circumstances in which it was taken (see paragraphs 152-160 above) and I will not repeat it. The reading is acknowledged on all sides to be low and, as a result of my finding (based upon what Dr Evans said), the reading must inevitably reflect the effects both of the hand-bagging by Dr Evans and a period (albeit relatively short) of mechanical ventilation on a ventilator with a setting designed to produce normal respiration in a 14-year old. Dr Ross Russell was cross-examined on the basis of the blood gas being taken at a time when Morwenna was “stable” (whatever that may mean precisely in this context, but it appears to have been assumed to represent a period of between 10 and 30 minutes on a mechanical ventilator) and he accepted that, if that was so and the result of 2.94 kPa was yielded, it would be an indication that she was hypocapnic before the blood gas was taken. Whilst he was not asked to address the issue on the basis of my finding, I suspect he would say had he done so that the result was still largely driven by the effects of the hand-bagging and that the mechanical ventilation would have made some, but not much, difference. The only matter that might militate against that answer is the opinion he expressed in his report, when dealing specifically with the 14.29 blood gas result, namely, that “[it] is not uncommon to have a low CO₂ immediately after intubation, especially if the patient requires bagging, and this is usually corrected over the next minutes when the ventilator is set up.” (My emphasis.) Dr Pappachan, as I have said, seems to have appreciated that what now is my finding was indeed essentially what Dr Evans said finally in the witness box. He appeared comfortable with maintaining his previously stated position in the light of that and was clearly of the view that, whatever the impact of hand-bagging, it could not have brought the PaCO2 down as low as 2.94 kPa if it had started at or about normal.

I do not think it is possible on the evidence to reach a firm conclusion about the precise level of PaCO2 at any one moment – or indeed over any precise period save as I shall indicate in paragraph 280 below. However, what the two blood gas results reveal, set in the context that by 15.19 Morwenna’s PaCO2 was clearly and incontestably back in the normal range, is that on the balance of probabilities she was hypocapnic at 13.44 and that the PaCO2 level at that time was probably nearer to Dr Pappachan’s estimate (of in the region of 3.9 kPa) than the estimate of Dr Ross Russell. I say that because I accept as a matter of inference and, I trust, commonsense that the effects of the “nervous” hand-bagging would not have driven the PaCO2 down to 2.94 kPa from something like 4.3 kPa in the relatively short time that it took place. The bagging might have been “nervous”, but Dr Evans did have time, as Dr Pappachan correctly observed, to arrange for Morwenna’s transfer to the resuscitation unit and to speak to her Consultant about the technique to be adopted. It follows that this was not handled in the manner of a “crash” call and, of course, Dr Driver had been administering high-flow oxygen for a while before Dr Evans arrived.

That conclusion of fact does lend support to Dr Pappachan’s view that the central control mechanism had, at least to some extent, been overridden in Morwenna’s case. The essential question, for present purposes, is whether that conclusion evidences or indicates a pre-existing period of hypocapnia.

By 13.44 Morwenna had been in a coma for a while, but nonetheless her respiratory rate had diminished and her temperature had also reduced, both factors that would militate in favour of her PaCO2 being normal, or at least returning to normality. When she was admitted to hospital her respiratory rate was 38 breaths per minute and had been elevated (at 25-30 breaths per minute) when Dr Hurton saw her earlier. Mrs Ganz told Dr Lloyd during the early hours of the morning that she had been breathing “a little bit more than usual”. All this suggests that prior to admission there had been a number of hours of hyper-ventilation, the intensity of that hyper-ventilation increasing with the passage of time. Since it is, at least in principle, not disputed that the central control mechanism can be compromised to some extent by, for example, fever and fear and there is evidence of both these elements in Morwenna’s case, I do not see what is wrong with drawing the inference that she was hypocapnic to a degree when she was admitted to hospital and had probably been so for a period prior to that. The evidence of the fever, of course, is clear. She may well have been anxious during the night as well, but more particularly her father spoke of her worries about being taken to hospital in an ambulance and about whether she was going to die. All those factors provide justification for the inference I have drawn. Some further justification is afforded because of the Third Defendant’s failure, through Dr Kapse, to take specimens for blood gas analysis during the morning that would have revealed the true position. Such a failure seems to me to justify drawing a reasonably robust inference provided, of course, it sits reasonably comfortably with all the other evidence. At all events, the evidence justifies drawing the inference that there had been a lengthy period of a degree of hypocapnia at least since admission, and probably before, that had not been corrected. As I have indicated previously (paragraph 278), it is difficult to be precise and I am not able to conclude that the hypocapnia was as profound as Dr Pappachan confidently asserted in his report (see paragraph 241 above), but I do not think it unreasonable to infer that, given the conclusion I reached in paragraph 276 above, the general level of Morwenna’s PaCO2 was in the region of 4 kPa throughout the time she was at Kingston before ventilation took place and probably a little longer than that.

That inference is, as will be apparent, drawn principally from the evidence derived from the two blood gas readings at 13.44 and 14.29 in the context of a normal reading at 15.19. This, to my mind, is more convincing than Dr Pappachan’s physiological construct given some weaknesses in the analysis that led to it, although the construct itself does help to support the legitimacy of the inference. The period in question coincided with a time when, although apparently reducing, Morwenna’s respiratory rate was still elevated: it was certainly still elevated at 12.30 and at 13.07 if 14 breaths per minute (as it was at 14.15 and later at Guy’s) was normal for her. It also coincided with a period, at least until shortly after 13.07, when she was receiving no supportive measures to stabilise her position.

I do not think that I need to take the analysis of the evidence on this issue further. I am alive to the fact that the advice given to Kingston Hospital from the Guy’s Paediatric Intensive Care Unit (‘PICU’) was for the CO2 level to be maintained at between 4.0 and 4.5 kPa so the mechanical ventilator would have been set to maintain that level. That could be taken to suggest that maintaining a level of 4 kPa was perfectly acceptable. However, that is a different matter from determining whether, as a matter of fact, Morwenna’s PaCO2 level was less than normal and would be likely to result in cerebral vasoconstriction. I will deal with the latter point later (see paragraph 285 et seq).

The two remaining criticisms of Dr Pappachan’s approach made by Dr Ross Russell were reflected in numbered items 3 and 5 referred to in paragraph 262 above. As to the first, Dr Ross Russell confirmed in his evidence-in-chief that the effects of this on CO2 levels would be minor and the issue did not figure materially in the argument. Again the issue raised in numbered item 5 did not assume great significance during the trial. Dr Pappachan’s answer to it appears in paragraph 263 above and, when asked about it by Mr Browne, he said that he agreed that children who are unwell can have a high respiratory rate and low CO₂ and in general they do not succumb to significant brain injury. He recognised that spontaneous hyperventilation can cause hypocapnia which itself can lead to (usually) reversible neurological deficit in normal healthy individuals. There are two examples where hypocapnia is, he said, probably more important in the generation of neurological deficit leading to hypoxia: one is acute mountain sickness the other is a child with Leigh’s syndrome (a form of mitochondrial disorder). I do not think that either of these issues truly affects the central issue of whether the existence of hypocapnia is established in this case. Neither issue rules it out.

Having established the existence of the hypocapnia on the basis I have described, it is necessary now to consider its effect.

It was agreed that hypocapnia causes cerebral vasoconstriction. One issue is the extent by which cerebral blood flow (‘CBF’) is reduced. Dr Pappachan drew attention to a paper by Ito and others entitled ‘Changes in human cerebral blood flow and cerebral blood volume during hypocapnia and hypocapnia measured by positron emission tomography’, published in 2003, in support of the contention that where the PaCO2 level falls from normal to about 4 kPa, there is an approximately 37% reduction in CBF. Although challenged about this by Mr Browne, Dr Pappachan maintained his position and there was no evidence that really controverted his evidence. He distinguished a paper to which Professor Kirkham had contributed (apparently suggesting a much lower percentage reduction) as arising in the context of cardiopulmonary bypass.

Dr Pappachan said that a fall to 4 kPa in a normal brain in the absence of other factors is unlikely to cause a sustained neurological effect, but in different circumstances, different degrees of hypocapnia are better tolerated than others.

Whilst absolute figures are not material, it is clear from the evidence of Dr Pappachan (supported by the Ito paper), to which no meaningful challenge has been mounted, that a significant degree of vasoconstriction will arise from the kind of reduced PaCO2 level that I have found occurred in Morwenna’s case. I have to say also that Professor Kirkham’s analysis of the Curless paper (see paragraphs 236 and 237 above) and the effects which the hypocapnia in those few patients was thought to have given rise to the basal ganglia damage seemed measured, logical and persuasive. I accept her opinion that, in a broad sense, it supports hypocapnia as a possible cause of basal ganglia damage. That helps me towards thinking that Dr Pappachan’s general analysis is correct.

What this means, therefore, is that at least for the period when Morwenna was in Kingston Hospital until intubation and ventilation she had been subject to a significant degree of vasoconstriction. As a result less blood was perfusing the brain cells than would otherwise have been the case. I am unable on the evidence to say that this, of itself, would have caused brain damage. The question, it seems to me, is whether, taken with any other factors that might affect the well-being of the brain cells, it contributed to the brain damage.

I must turn to another factor that has been said (by Professor Kirkham) probably to have been in play, namely, hypoxia.

I have referred to Professor Kirkham’s view about this in paragraph 227 above. Should I conclude, on the balance of probabilities that Morwenna was hypoxic to any material degree during the period after her admission to Kingston Hospital and before oxygen was administered to her, starting with the high-flow oxygen soon after 13.07?

That there are no imaging changes that are specific for hypoxia or hypoxic ischaemic damage is not conclusive that there was no hypoxia: see paragraphs 183 and 184. Indeed the preponderance of the neuroradiological opinion is that the neuro-imaging changes could be attributable to hypoxic ischaemia, but there could be other causes (see paragraph 184). As I have indicated (paragraph 215), Dr Thomas conceded one possible cause of the cerebral atrophy seen on the neuro-imaging was hypoperfusion and hypoxia. However, his view was that there was no evidence of significant hypoxia from the blood gas measurements. It is, of course, the case that a further blood gas should have been taken some time after about 11.30 (see paragraph 130 and 131). In the light of my finding at paragraph 137, Morwenna was not given any oxygen until Dr Driver arrived although, as Dr Markovitch said, she should have been given oxygen when it was realised that her GCS was falling.

The essential issue is what significance should be attached to the one oxygen saturation result that is available, namely, 93% saturation at about 10.30. After Morwenna had been properly oxygenated her saturation increased to 99-100% after about 14.30. 93% was, therefore, low and, as Professor Kirkham said, it was at the lowest end of the range for a child (see paragraph 230). Dr Markovitch concurred that it was “borderline” but that oxygen “should be given to an unwell child with that measurement”. There is really no evidential basis for saying that it would have improved over the next couple of hours or so and the inference seems to me to be irresistible that she was, putting it colloquially, “short of oxygen” during that period. It may well be, as the evidence demonstrated, that an oxygen saturation of ≤92% is one indicator provided for in the British Thoracic Society guidelines for admission to hospital in an older child suspected of having community acquired pneumonia (the corollary being that an oxygen saturation of ≥92% does not of itself justify admission), but that does not mean that a level of 93% is not evidence of a very low oxygen saturation which is the relevant factor for present purposes. It follows that if not corrected, it could lead to hypoxia in an individual child, particularly, as Professor Kirkham said, if the child is also hyperventilating which Morwenna plainly was doing for much of this period.

Professor Kirkham said that, in her opinion, on the balance of probabilities Morwenna did become hypoxic during the period between the taking of that initial blood gas and Dr Driver’s intervention. She attached some significance to the fact that Morwenna’s GCS fell during this period also. Dr Thomas did not, as I understood him, disagree that this consequence could follow from an effective starting point of a 93% saturation in the circumstances, but rejects hypoxia because of the lack of neuro-imaging changes and because there is no other evidence (in the form of acidosis) that would ordinarily confirm it. The former is not conclusive for the reasons already given. As to the latter, it seems to me that Professor Kirkham’s answer was convincing, namely, that where there are in place two processes, one leading to hypoxia and one leading to hypocapnia, the first making blood acidotic and the second making it alkalytic, there is in place an effective balancing mechanism. Her response to the normal pH seen in the blood gas taken at 13.44 was that that was how it came about, though she had some reservations about the validity of a venous sample for this purpose in any event.

Professor Kirkham’s analysis has a logic about it which convinces me that I should accept her opinion that Morwenna did become hypoxic at some stage in the period until oxygen was administered. If the presence of imaging changes or evidence of acidosis was crucial, then, of course, my decision would have been different – and indeed I am sure Professor Kirkham’s view would also have been different.

It is impossible to say precisely the extent to which she became hypoxic save to say that, given the starting point of 93% saturation at about 10.30, a falling GCS over the next couple of hours and no oxygen administration in the meantime, it is clear that it cannot be regarded as minimal.

It is equally not possible to say with real precision when she became hypoxic to a degree that, combined with the hypocapnia, cell damage was likely. However, I will indicate below (see paragraph 312) my conclusion of when, on the balance of probabilities, this occurred.

I have, therefore, found that both hypoxia and hypocapnia were present during the period between Morwenna’s admission to Kingston Hospital and when she was ventilated and also that it is likely that there was some degree of hypocapnia present before her admission. I have been unable to conclude on the evidence whether the hypocapnia in itself would have been sufficient to cause brain damage and the question, as I see it, is whether it was likely to have operated together with any other factor to cause or contribute to a brain damaging process. I have found that there was a more than minimal level of hypoxia at some stage during the period from about 10.30 onwards. Cumulatively each will have contributed to a lack of oxygen perfusing Morwenna’s brain cells during this period. There can be no doubt that Morwenna was running a very high temperature on arrival at Kingston. It is impossible to know to what extent and for how long it remained at that level because no further reading was taken until 12.30. It was still elevated at 12.30, albeit less than when she was admitted. The extent to which the temperature of her brain had reduced, if it did, is, of course, unknown. It is against that background that there seems to me to be a compelling logic in the view expressed by Professor Kirkham in her report (which she developed in her oral evidence) that Morwenna’s “basal ganglia, in the context of her underlying condition, would have been vulnerable to the combination of a very high temperature and a low PCO2”. The hypocapnia would result in less blood getting to the brain when it was most needed (because of the high temperature) and, if the blood itself contained less than a full oxygen saturation, the probability of cell damage following this combined process seems clear. The more difficult issue, to which I will turn later (see paragraph 300 et seq), is whether this combined process led to irreversible brain damage which follows cell death. As Dr Pappachan said, cell dysfunction does not imply cell death and it can, therefore, be reversible. He described the damaging process as a “graded process that can be recoverable”.

The conclusion to which I have referred is a conclusion that I can (and should) reach on the evidence I have heard and accepted. If it was possible to conclude that Morwenna had a mitochondrial disorder, then it could make it easier to explain why what was not necessarily, and in the overall scale of things, serious hypocapnia and serious hypoxia may have had the very serious effect that they did in this case. However, I do not think I can conclude, on the balance of probabilities, that Morwenna suffered from such a disorder. There is a broad consensus between, for example, Professor Kirkham and Dr Thomas, that Morwenna probably does suffer from some underlying metabolic or genetic condition that makes her more vulnerable than others to intercurrent infections (the previous episodes of encephalopathy suggest this), but the condition remains undiagnosed. Professor Kirkham thinks that mitochondrial disorder is a possibility, but has not really felt able to go further than to say that it is merely a possibility. She did indicate that she had recently found some literature that suggested that, contrary to the position taken at the joint experts meeting, there could be a mitochondrial disorder without imaging changes, but I do not think that I could possibly conclude on the evidence as it is that, on the balance of probabilities, such a disorder existed. One day it may be proved by clinical means to have existed: on the evidence before me I am unable so to conclude.

Where does that leave the combined hypocapnia and hypoxia as a cause of Morwenna’s brain damage? It seems to me that it must be treated as at least a contributory cause of cell damage or dysfunction. If no other cause can be identified, then it has to be regarded as the sole cause of such damage or dysfunction. If I am wrong about my conclusion on MPE (see paragraphs 202-220 above) and that MPE did indeed contribute to the damage in its own right, that would be a non-negligently caused contributory factor, but it would not prevent the combined effect of the hypocapnia and hypoxia also being a contributory cause such that a full award of damages could be made if the damage occasioned was irreversible brain damage: see Bailey v Ministry of Defence [2009] 1 WLR 1052. Indeed even if there was some other unidentified contributory cause, the same conclusion would be reached.

The essential question, however, having reached those conclusions, is whether earlier intervention to reduce the effects of the hypocapnia and hypoxia would have arrested the damaging process sufficiently and quickly enough to avoid the permanent damage that ensued. Put another way, in order for the conclusion to be reached that some antecedent breach of duty caused or materially contributed to the irreversible brain damage, it is necessary to determine when the condition of irreversibility was reached. It does not necessarily have to be a moment in time or indeed a few moments in time; it could be a prolonged period or it could be a shorter period when a “cascade” into material cell death occurred. But it is necessary to say with some degree of precision, albeit on the balance of probabilities, when it was.

The experts who addressed this question did so by reference to times associated with the fall in the GCS score. The following answers by Dr Pappachan and Dr Ross Russell indicate the position they each took before the case started:

Q. If the court accepts C’s case that basal ganglia damage without radiological correlate was caused by hypocapnia-induced cerebral vasoconstriction, what in your opinion is the latest time by which ventilation would have had to be achieved to avoid lasting brain damage?

A.

Dr Ross Russell believes that ventilation would have to have been commenced by 11:00 or 11:30 at the latest. Dr Pappachan believes that the reduction in C’s GCS from 15 at 1022 to a GCS of 12 recorded at 1130 should have lead to a sequence of events that would have lead to the initiation of ventilation at 1200 at the latest.

Professor Kirkham and Dr Thomas, addressing the question of when, if the court accepted that brain injury was caused by a prolonged period of hypocapnia causing cerebral vasoconstriction, ventilation would have had to be achieved to avoid lasting brain damage, each replied as follows:

Dr Thomas: should the court accept that brain injury was caused by a prolonged period of hypocapnia causing cerebral vasoconstriction, to prevent brain damage, the Claimant would need to have been intubated an hour before her coma score deteriorated i.e. by 1130 a.m. ….

Professor Kirkham: should the court accept that brain injury was caused by a prolonged period of hypocapnia causing cerebral vasoconstriction, which she thinks is the most likely explanation, to prevent all of the brain damage, she thinks that the Claimant should have been intubated before her coma score deteriorated from 12 (intubation not mandatory but close watch for deterioration essential) to 7 (intubation mandatory), i.e. between 1130 and 1230. However, she thinks that the insult to the brain would have been cumulative so that any reduction in the duration of exposure to hypocapnia would have resulted in less severe dystonia ….

Notwithstanding the way these views were expressed, it was accepted on all sides during the trial that whilst a fall in the GCS score represents an important indicator of conscious state, it does not of itself indicate that brain damage is occurring or has occurred. Professor Kirkham spoke of children under her care whose GCS had fallen to 3 and yet had “survived intact”. It was common ground between Dr Pappachan and Dr Ross Russell that the fall in GCS represented a progressive deterioration in Morwenna’s cerebral function, but that such a deterioration would not of itself indicate irreversible cerebral damage. Dr Thomas said that loss of consciousness is to do with impairment of the systems that enables consciousness to be maintained (he cited the reticular activating system in the brain stem and the cerebral cortex) and, consistent with what the others said, asserted that loss of consciousness does not necessarily mean that cells are dying. He also said that whilst hypoxia becomes more likely as the GCS falls, in the majority of situations patients maintain their oxygen saturations (and presumably do not therefore become hypoxic with the risk of hypoxic brain damage) until deeply unconscious. It does seem to follow from all this that, whilst a fall in GCS may be a strong indicator for clinical intervention, it does not necessarily indicate that lasting neurological damage has been or is being caused.

When cross-examined by Mr Browne about the way she had expressed herself in the joint statement, Professor Kirkham clarified what she had meant. She said that the position in this case was different from the birth asphyxia cases so frequently considered in the courts where, certainly in that particular medico-legal context, a relatively clearly defined period when the asphyxial or hypoxic episode occurred is identified as the period when the relevant damage was caused. Here, she said, there was a continuum starting on Morwenna’s admission to Kingston Hospital. She said that somewhere between that time and when Morwenna awoke at Guy’s she had suffered “irreversible neurological damage”. She said, however, that it was “impossible to say when the brain damaging process became irreversible” and that it is “very difficult to say” with any precision “how irreversible the damage [was] at any specific time”. She said that the risk of getting brain damage “is accruing all the time” and, in response to a repeated challenge from Mr Browne about the meaning of her contribution to the joint statement, she said that she was “definitely not” saying that everything was irreversible after 12.30. Her view was that “the process” (by which I understood her to mean that the process during which cell damage, though not necessarily cell death, occurred) began between 11.30 and 12.30, when matters became “critical”, but that it was a continuous process from admission through to intubation. Describing the effect of the combined hypoxia and hypocapnia, she said that Morwenna, who had an underlying condition, had pneumonia, had low oxygen saturation, a low oxygen content and a low CO2 level, would gradually have been taken below what she described as “the ischaemic threshold” with the result that damage was caused.

Not surprisingly, Professor Kirkham’s view was that, particularly in the case of children, the better the clinical management, the better the outcome. However, she said that, unlike the birth asphyxia cases, this particular scenario did not reflect a “time-locked situation” and emphasised that she saw it as a continuous process.

Because I have broadly accepted that Morwenna was subjected to the combined effects of a degree of hypoxia and hypocapnia during a period from some time after 10.30 onwards on 19 December, and because that is what Professor Kirkham has advanced as her perception of what occurred, I have attached particular significance to her views on the mechanism in play in causing the irreversible brain damage. I have not ignored the views of Dr Thomas, but he found it difficult to subscribe to this scenario as a likely explanation for Morwenna’s damage. His view, on the assumption of a scenario such as that contended for by Professor Kirkham, was that Morwenna would need to have been intubated before 11.30 for brain damage to be avoided. His reasoning was not fully investigated, but I imagine he would say that intubation (and presumably ventilation) was required before her decline in conscious state took place.

The real difficulty I face is the way in which both Professor Kirkham and Dr Thomas (and indeed Dr Pappachan and Dr Ross Russell) seem to tie their opinion to the fall in GCS. Since that, by common consent, does not connote cell death (which is what must occur for permanent brain damage to be caused), I have difficulty in seeing how it helps me to conclude when or even during which period, on the balance of probabilities, cell death occurred. Given Professor Kirkham’s view (which, in my judgment, is the most authoritative view in this context), I do not see how I can find that cell death occurred at any particular time or during any particular period in the overall period from when Morwenna was admitted to Kingston Hospital and when she awoke from her coma at Guy’s save to say that it plainly occurred during that overall period. I can accept, as Professor Kirkham says, that the risk of brain damage was accruing all the time, but a mere increase in risk does not permit a conclusion that the risk has eventuated and does not help identify when it eventuated (as, of course, it did) given the kind of mechanism involved here. Furthermore, if the logic of the situation is that if there had been a period of combined hypoxia and hypocapnia prior to 11.30 (which is the starting time for what Professor Kirkham has called a “critical period”), how could it necessarily be said that material cell death did not occur during that earlier period? Since conscious state and cell death are not necessarily related, it would, as it seems to me, be impossible to exclude the possibility that material cell death occurred during that period. If it did occur during that period, how could the possibility be excluded that the cell death that had occurred during that period was not itself sufficient to lead to the brain damage without the contribution of any other subsequently caused cell death?

Raising these questions without being able to answer them demonstrates the impossibility of determining when, in what Professor Kirkham described as an “acute” situation (see paragraph 230 above), irreversible brain damage occurred once a combination of sufficient hypoxia and hypocapnia as may lead to damage was in place. It might have been early in the process: it might have been late in the process. But unless the steps necessary to arrest the effect of the process before irreversible damage was caused can be said to have been negligently omitted, the causal link between that negligent omission and the damage cannot be established.

Establishing when a sufficient degree of hypoxia was present to add to the effect of the hypocapnia (see paragraph 312 below) is not itself easy. That it is not easy does not absolve me from the responsibility of endeavouring to reach a sustainable conclusion on the basis of the evidence.

Professor Kirkham felt that it would have been some time after the time when the first blood gas was taken between 10:22-10.36, but was not specific as to when. Until Morwenna did become hypoxic, the damaging mechanism that I have found occurred would not have been in place. As is already plain from a number of comments I have made (see paragraphs 130-131), one significant omission in the period after about 10.30 was any further measurement of oxygen saturation. There is a temptation in such a situation to draw a robust inference adverse to the Third Defendant (the party responsible for this omission). That would involve reaching a conclusion that Morwenna did not become sufficiently hypoxic such that the hypoxia, in combination with the hypocapnia, was at a level to cause cell death until after a relevant breach of duty on the part of the Third Defendant occurred. However, I do not consider that to be a permissible approach and I do not think that the evidence justifies such a robust inference.

The oxygen saturation at around 10.30 did not represent a “standing start” on the downward slope of the physiological process by which the oxygenation of the blood diminished. At some stage prior to that time, Morwenna’s oxygen saturation must have been 99-100% and it will have diminished over a period of time until the sample for analysis was taken at around 10.30. Morwenna was undoubtedly ill at that time with a high temperature and high respiratory rate. In those circumstances, I think it would be unrealistic to suppose that the development of hypoxia would have been much delayed beyond that time. The evidence suggests that within, at most, an hour of that level of oxygen saturation, her GCS had dropped from normal to 12. It is not suggested that hypoxia could not exist until such a diminished GCS was evident – indeed it seems logical to suppose that diminished cerebral function, as evidenced by a fall in GCS (see paragraph 302), would follow rather than precede the development of hypoxia.

At all events, whether that be correct or not, it is necessary to advance some realistic working assumption upon which to base the rest of the analysis in this case even though it is impossible to place a precise time upon the moment when the combined effect of the hypoxia and hypocapnia became damaging. On that basis and with that kind of approach in mind, I have to say that I do not regard it as unreasonable to conclude that the hypoxia had developed to an extent that, in combination with the hypocapnia, it was capable of causing cell damage from about 11.00. If I am right that the evidence means that from that time onwards it is impossible to say when material cell death was caused by that damaging process, the consequence is that any breach of duty that failed to arrest that process would have to have occurred before 11.00 to have causal effect from the legal point of view.

Given Morwenna’s general condition at that time, such a step would probably have involved intubation and ventilation. Professor Kirkham, Dr Thomas, Dr Pappachan and Dr Ross Russell all spoke of this as the step that would have to have been instituted for an effective arresting and reversal of the damaging process (on the assumption from the point of view of Dr Thomas and Dr Ross Russell that it was in place). They differed as to when it was necessary, but that issue is concluded, it seems to me, by the finding I have made in the preceding paragraph. Even if that finding is too generous to the Third Defendant (which I do not think that it is), then given that the earliest time at which a breach of duty on the part of the Third Defendant could potentially be identified is about 11.45 (see paragraphs 314 and 315 below), I am quite satisfied that the combined damaging process was well in place by then. I do not reject the possibility that, as Professor Kirkham has said, the damage was even by then still reversible, but equally I cannot discount the possibility that it was not: no-one knows and there is little that truly assists in yielding the probable answer. Whilst the longer the damaging process goes on the greater the risk of damage, the effect that Morwenna’s predisposition to damage arising from her unidentified condition is a factor that might swing the pendulum the other way and result in earlier damage. Sadly, the truth (even on the basis of a probability) simply cannot be determined.

I have alluded to the earliest point at which it could be said that there was negligence on the part of the Third Defendant (see paragraph 313 above). I consider it to have been about 11.45. I reach that time by concluding, not on the basis of absolutely precise times (which seems to me to be unrealistic), but by taking 10.50 as the time by which, given the orange category into which Morwenna was put following the triage, Dr Kapse should have commenced her examination of her subject to one matter to which I will return below. (I have taken 10 minutes from completion of the triage as a “target” for commencing the examination, not an absolute requirement, as Dr Marcovitch accepted.) An examination taking 30 minutes is not criticised, but I think it is right to say that Dr Kapse should have realised that Morwenna’s GCS was less than normal and should have called Dr Driver as soon as she realised that this was so. Dr Marcovitch did accept that it could have been not until near the end of the examination that it was incumbent on her to make that decision. For this purpose I will take it to have been about 10 minutes before the end of the examination. The situation would not have been critical at that point, but urgent. On that basis Dr Driver should have been summoned at about 11.10 and should have been present within 5 or 10 minutes, say, by 11.20. On that basis he would have been presented with Morwenna whose GCS was 12 and who presented in the way previously described. She was not then in the acute state she was in when Dr Driver in fact arrived at 13.07 (see paragraph 138 et seq). As Dr Marcovitch accepted (see paragraph 173), he would have had “time on his side” to some extent then. I have already indicated that a period of 15 minutes for the arrival of the anaesthetic team could not be criticised in those circumstances. In those circumstances I do not think a delay until 11.35 of a readiness for intubation could be criticised legitimately in the circumstances of Morwenna’s presentation at the time.

To that can, in my judgment, be added a period of about 10 minutes or so when Dr Kapse dealt with the other child before examining Morwenna (see paragraph 118 above). It is quite right to say, as Mr Maskrey has emphasised, that no disclosure has been given about that patient in order to determine how urgent it was for the child to have been dealt with before Morwenna. It is equally right to say that matters of confidentiality could have been dealt with by anonymising the records of that child. However, there are two observations to be made: first, it is not disputed that there was indeed another child perceived to have required more urgent attention. Mr and Mrs Ganz confirmed that. Second, these choices do have to be made from time to time. It is a matter of judgment and I do not think a court should readily entertain criticisms of this nature. The judgment was effectively made by Nurse Theobald-Smith, who appears to have generally made proper judgments in this case and, accordingly, I do not think there is any fair basis for making the criticism advance. It follows that another 10 minutes or so to the timescale I have mentioned.

On that basis the anaesthetic team should have been in place to decide whether to intubate at that time. It would not have been a rushed intubation because, even with a diminishing GCS, the position would not have been as acute as it subsequently became. Ventilation, if it was dictated, would probably not have been in place until about midday or thereabouts.

Whilst there could be minor variations in this timetable, the fact of the matter is that the combined effect of the hypoxia and hypocapnia would, on Professor Kirkham’s analysis, have been well and truly in place by the time effective ventilation was achieved and, for the reasons I have already given, I do not think it is possible to exclude the possibility that the irreversible damage had already occurred by then or that ventilation at that point was early enough to reverse the damaging mechanism.

In those circumstances, although it is not a conclusion I find particularly palatable given the failure to act with appropriate expedition on the part of Kingston Hospital, I do not think that it can fairly be concluded that the delays in the treatment that Morwenna undoubtedly experienced when she was there can be proved to the appropriate standard to have caused or materially contributed to her irreversible brain damage. That being so, the claim against the Third Defendant must be dismissed.

The question, therefore, reverts to what would have happened had Morwenna been admitted to hospital during the Saturday or earlier on the Sunday morning. The assumption for this purpose, of course, is that she would have been dealt with, once in hospital, in accordance with reasonable standards of care. If those reasonable standards of care would, more probably than not, have prevented the onset of a period of combined sufficient hypoxia and hypocapnia that, on the basis of my findings, at the very least contributed materially to her irreversible brain damage, then the failure to ensure that Morwenna was in hospital to receive that attention would result in the causal link between the negligence and the damage being established.

I have dealt with what would have been required by way of reasonable care had Morwenna been admitted the day before at paragraphs 161 et seq. It is necessary to assume for present purposes that the general deterioration in her condition that is described by her parents (and as articulated in Mrs Ganz’s telephone conversation with Dr Lloyd) would have been observed and that, by the evening of the Saturday, a chest x-ray would have revealed the presence of pneumonia. An inability to walk more than a few steps would have been noted, as would a raised respiratory rate. Her temperature would have been noted as being very high.

As a general proposition, and without particular recourse to the expert evidence at this stage, it would hardly be a testament to good standards of hospital medical practice for Morwenna to be allowed to progress to the serious condition she was in when she was seen, first, by Dr Hurton between about 8.30 and 9.30 on the Sunday morning – or when seen by Nurse Theobald-Smith at about 10.30 – if she had been admitted to hospital with a request by her GP to “exclude pneumonia” the previous day unless, of course, the outcome was effectively pre-determined by her illness. Whether the frequency of the monitoring was hourly or four-hourly (see paragraph 164), it seems to me clear that there would have been a time well before 11.00 on the Sunday morning when her diminishing oxygen saturation, her raised respiratory rate and her high temperature would have been noted and acted upon in the sense that steps would be taken to reverse these matters. The administration of oxygen would have been the starting point (see paragraph 167) and, in the light of my findings about the mechanism in play during the Sunday morning after Morwenna arrived at Kingston Hospital, the inevitable inference is that this would have arrested and put the potential development of hypoxia into reverse and would have helped to diminish the rapid breathing which had led to the hypocapnia. This would, in my judgment, have prevented the mechanism that arose from arising, certainly to a level that would have caused irreversible brain damage, and, accordingly, the process that in fact led to the irreversible brain damage would have been arrested before the damage became irreversible.

In my view, had Morwenna been admitted to hospital on the Saturday by about midday or thereabouts, steps would have been taken which would have prevented the combined hypoxia and hypocapnia. She would, of course, still have had the pneumonia, but since she did not, in my judgment, develop MPE there is no reason to suppose that she could or would have suffered irreversible brain damage from any other cause.

On that basis the case against the First Defendant is made out, both in terms of liability and causation.

What is the position of the Second Defendant? It is accepted that had he acted as he should have acted the likelihood is that Morwenna would have been admitted to Kingston Hospital by about 05.00 or 06.00 on 19 December. I have already reflected on what would have happened in that situation, again on the basis that proper care was given. At that stage a 14-year old girl, who had been ill for several days with a high temperature, vomiting and significant lethargy would have been admitted as an emergency by ambulance. Her respiratory rate was likely to have been somewhat raised, the hospital would probably have known that her GP had said the previous day that a chest x-ray was needed on the Monday if there had been no improvement and the hospital would have learnt about Morwenna’s previous episodes of encephalopathy. This would be a situation where it is likely, in my view, that her condition on admission would have been regarded (by competent practitioners) as sufficiently serious to warrant hourly monitoring of, amongst other things, the oxygen saturation. That it was diminishing, as it must have been prior to 10.30, would have been recognised at least in the hour or so before then, if not earlier, and steps would have been taken to reverse that process.

For reasons already advanced, this would have arrested and put the potential development of hypoxia into reverse and would have operated to diminish the rapid breathing which had led to the hypocapnia. The damaging process would thus have been avoided.

In those circumstances, in my judgment, the causal link between the Second Defendant’s admitted negligence and the development of the irreversible brain damage is established.

It follows that the claim against the Third Defendant fails because, whilst breach of duty has been established, it has been impossible to prove when the irreversible brain damage occurred during the material period. I have, however, rejected the case advanced by the Third Defendant that the irreversible damage was inevitable because it was caused by MPE.

The case against the First and Second Defendants does succeed on the basis that had Morwenna been sent to hospital earlier and had she received competent care, the circumstances that led to her irreversible brain damage would have been avoided or at least reduced such that the damage would not have occurred. It is likely that Morwenna’s susceptibility to such damage was increased by an underlying, as yet unidentified, condition. However, the law holds that a tortfeasor takes the victim as found and thus such a condition does not operate to absolve a tortfeasor from responsibility for the damage caused. I think, however, it should be recorded, on the basis of my findings, that neither Dr Childs nor Dr Lloyd could have known of the existence of such a condition. Their failings were simply getting Morwenna to hospital earlier so that proper care should have stopped the damaging process occurring.

This will result in a judgment for damages to be assessed against the First and Second Defendants and judgment for the Third Defendant on the claim brought against it.

I have recorded previously (at paragraph 199) Professor Kirkham’s view that this is a difficult case. I have little doubt that all her medical colleagues, by whomsoever instructed, would share that view. I have, of course, had the ultimate responsibility of arriving at relevant conclusions within the framework of the legal process, but I will not disguise the fact that it has been a difficult task both factually and in relation to the complex medical issues raised.

Against that background I should like to express my appreciation to all Counsel, their Instructing Solicitors and all experts for their assistance in an unusually difficult case. I would add my thanks also to Ms Bernadette McGhie, of the Claimant’s solicitors, for providing me and all other parties in the case with her typed notes of the proceedings as they progressed. In a case where the expert evidence was complex, the notes afforded a helpful check on my own notes taken during the proceedings. I would merely confirm that ultimately it was my own note that I relied upon supplemented, where relevant, to listening again to parts of the evidence where I was unclear about precisely what was said.