Royal Courts of Justice
Strand, London, WC2A 2LL
Before:
MR JUSTICE FOSKETT
Between:
XYZ (A Child by his Mother and Litigation Friend MYZ) | Claimant |
- and – | |
MAIDSTONE AND TUNBRIDGE WELLS NHS TRUST | Defendant |
Christopher Gibson QC (instructed by Leigh Day) for the Claimant
Alexander Antelme QC (instructed by Weightmans LLP) for the Defendant
Hearing dates: 4-7, 10, 12 and 14 October 2016
Judgment
MR JUSTICE FOSKETT:
Introduction
This case concerns the quality of the treatment and attention that the Claimant received at what was then the Pembury Hospital in Tunbridge Wells in May 2001 when he was 23½ months old. The hospital as it was then has since ceased to exist.
The Claimant was referred to throughout the trial by his first name (as were his mother and maternal grandparents), but because this judgment is to be anonymised I will for convenience refer to him in the somewhat impersonal way as “the Claimant” and to his mother and grandparents in similar fashion.
The primary issue is whether his presentation when he was taken to the hospital and during the hours thereafter was such that steps should have been taken that would have halted his developing pneumococcal meningitis.
As a result of the development of pneumococcal meningitis he now suffers from epilepsy, a residual left hemi-syndrome, a substantial loss of vision and severe cognitive impairment leading to significant learning and behavioural difficulties.
Master Cook directed a trial of the issues of liability and causation and it was with those issues that the hearing before me was concerned.
The focus of the trial has been on the events of 22 and 23 May 2001, but there is a relevant history prior thereto to which it is necessary to refer briefly. That history, and indeed the events of 22/23 May 2001, will be informed by an appreciation of what is known as a “febrile fit” (or a “febrile convulsion” or “febrile seizure”).
A “febrile fit”
A “febrile fit” is a fit, convulsion or seizure experienced by a child with a fever. More often than not the underlying fever is caused by a benign viral illness and is self-limiting – in other words, it resolves itself without any long term effects.
It is broadly accepted by the paediatric experts in this case that many or most children who have suffered a febrile fit caused by a benign viral illness will be more or less back to normal (albeit with a continuing fever) within 60 – 90 minutes of the fit, although in some cases the recovery may be slower or less complete.
The underlying illness giving rise to a febrile fit may, of course, be caused by a bacterial infection rather than a viral illness. Such an infection will usually require antibiotic treatment, treatment that is ordinarily ineffective in relation to a viral illness.
Whatever the underlying cause of the fever, a febrile fit is a highly alarming event for any parent to witness, many parents thinking that their child is dying. Nonetheless, as already indicated, in the vast majority of cases, the fit is a harmless event and the child makes a good and rapid recovery from it.
Before turning to the issues, factual and otherwise, I should record the identities of the experts on each side who have contributed to the debate in the case. There has been a substantial measure of agreement about many of the issues. This judgment will primarily focus on the differences where those differences are relevant to any conclusion that needs to be reached by the court.
The expert witnesses called were as follows:
Paediatrics
Dr Ben Lloyd (for the Claimant)
Dr Adrian Hughes (for the Defendant)
Infectious diseases
Dr Gareth Tudor-Williams, a paediatrician with particular expertise in paediatric infectious diseases (for the Claimant)
Professor Nigel Klein, a paediatrician with a special expertise in Paediatric Infectious Diseases and Immunology (for the Defendant)
Microbiology
Professor Keith Cartwright (for the Claimant)
Professor Robert Masterton (for the Defendant)
Paediatric Neurology
Dr Martin Smith (for the Claimant)
Professor Rajat Gupta (for the Defendant)
Each expert was eminently qualified to offer opinions within his area of expertise. I need not set out anything further about their individual backgrounds.
Events prior to 22/23 May 2001
The Claimant was born in June 1999. His mother was aged 17½ at the time of his birth. Leaving aside one hospital admission of no relevance to the present case, he was admitted to hospital following a febrile fit at home on 21 November 2000 (when he was aged 17 months). The fit lasted about 10 minutes.
He was taken to the A & E Department at the Kent and Sussex Hospital in Tunbridge Wells where his temperature was recorded as 39.2º C. He was given paracetamol and intravenous antibiotics more or less immediately. He was then transferred to Jacoby Ward at Pembury Hospital which contained the Paediatric Unit. He was seen by Dr Martin Robards, then the Consultant Paediatrician at the Unit and head of the paediatric team. The Claimant was kept in the hospital overnight but discharged home the following day, advice being given to his mother on febrile convulsions.
Essentially, he made a full recovery. It was recorded that organisms resembling pneumococci were seen in the blood cultures.
He suffered another febrile convulsion at home on 29 March 2001 (when he was 21 months old). It lasted about 5-6 minutes. He was taken by ambulance direct to the Jacoby Ward at Pembury Hospital where he was seen initially by Dr Rebecca Fisher, then a paediatric SHO. His temperature on admission was 38.1º C. Dr Fisher’s assessment was that he was “still fitting”. She discussed the situation with the Registrar, Dr Olga Slater, and a decision on whether to perform a lumbar puncture was delayed until the results of a full blood count (‘FBC’) and a CRP test (see paragraphs 26 and 56-60 below) were available. If those tests had revealed evidence of bacterial infection intravenous antibiotics would have been introduced before the carrying out of any lumbar puncture.
The results were not indicative of infection, but the Claimant was kept in hospital overnight because of his continued raised temperature and the previous history. He was allowed home the following day.
His mother took him back to the hospital the following day because she could not get the temperature to settle, but a diagnosis of tonsillitis was made and he was discharged home again.
There was, therefore, a history of two occasions of febrile fits prior to the events with which this case is concerned. It is plain that the Claimant’s mother (and her parents also with whom she and the Claimant were living at the time) had a good appreciation of what a febrile fit involved and what to do in the event of one occurring.
Before turning specifically to the events of 22/23 May 2001, it would be helpful to highlight features of pneumococcal meningitis which, as indicated above (see paragraph 3), is the condition that led to the Claimant’s permanent disabilities. It was also the pneumococcal bloodstream infection that he developed that was the probable cause of the Claimant’s 3-minute self-resolving febrile fit that occurred on the evening of 22 May (see paragraphs 27-32 below) according to the infectious disease and microbiology experts.
Pneumococcal meningitis
Pneumococcal meningitis is a form of bacterial meningitis. When a lumbar puncture was carried out on the Claimant in order to obtain a sample of his cerebrospinal fluid (‘CSF’) no bacterial organism was in fact detected when the CSF was cultured. However, all the relevant experts in the case are agreed that Streptococcus pneumoniae was the most likely cause of his bacterial meningitis.
The pneumococcal bacteria are usually carried in the throat of a young child. The bacteria colonise the throat in a symptomless fashion before, at some stage, entering the blood stream. Once the bacteria enter the blood stream bacteraemia is said to be in place.
For a time, the bacteria simply remain in the blood stream and (unless checked by the administration of antibiotics) continue to multiply, but do not invade the central nervous system. At this stage the symptoms displayed by the child are usually very non-specific, but can include fever and poor feeding. Professor Keith Cartwright, the Consultant Microbiologist called on behalf of the Claimant, said that it is widely believed that there is a threshold level of bacteria in the blood stream that must be exceeded before the meningeal membranes, which exist to protect the brain, can no longer withstand the penetration of the bacteria into the CSF. Once that occurs it is said that the blood/brain barrier has been broken or crossed.
It is generally thought that it can take 12 – 24 hours of bacteraemia (possibly a little longer, according to Professor Cartwright) before the blood/brain barrier is crossed. When this barrier has been crossed, the bacteria will continue to multiply, both in the blood and the CSF, if unchecked by antibiotics. For some period (in the region of 8 – 12 hours) the replication of the bacteria will continue without any additional clinical symptoms being exhibited other than the non-specific symptoms associated with the bacteraemia. It is generally accepted that clinical examination alone will not distinguish between the effects of the bacteraemia and the effects of that subsequent period when penetration of the bacteria into the CSF has occurred, sometimes called a period when “asymptomatic meningitis” is occurring. Professor Cartwright described it as a “silent period”. (If the infection in the bloodstream progressed to the stage of septicaemia, then the serious symptoms associated with that condition would be manifested. However, that did not occur in this case and is thus irrelevant to the present analysis.) After this asymptomatic period, symptomatic meningitis can occur with, typically, symptoms such as headache, fever, photophobia and neck stiffness. Once this stage has been reached, unless the progress of the illness is halted, the consequences may include seizures, coma and even death. The onset of symptoms in this period generally occur or start to develop at the time when what is termed the “host inflammatory response occurs”, namely, when the tissues of the brain start to mount an immune response to the bacterial invasion.
The inflammatory response is usually accompanied by a rise in the white cell blood count (‘WBC’) in the CSF, a rise in the CSF protein level and a fall in the CSF sugar level. The CSF protein level is a reference to the level of C-reactive protein (‘CRP’). An elevated CRP level in the blood may be indicative of an inflammatory or an infectious process (see paragraphs 56-60 below).
The febrile fit on 22 May 2001
For a day or so prior to 22 May the Claimant had, according to his mother and her parents, been slightly unwell with a slight cold, but on that day he appeared a little better and was able to go to his nursery school. When his mother and grandmother collected him at about 15.30 they were told that he had slept for an uninterrupted period of 3 hours at some stage during the day. His mother says that he did not appear particularly well and seemed to have a temperature and, whilst not particularly unhappy, was not his normal, chirpy self.
When they got home she gave him some ibuprofen and paracetamol (Calpol) to reduce his temperature. This had some effect, she recalled, but did not cure things completely. He was behaving reasonably normally but appeared to be tired and out of sorts.
At about 18.00 she gave him his evening bath and put him to bed. He refused the milk he usually had. She was unable to get him to settle and his temperature began to rise again. She feared that he might to be heading for another febrile fit. She brought him downstairs to somewhere cooler than his bedroom, but that did not improve things. Just before 19.45 she telephoned the out of hours GP service and was advised to bathe him in tepid water to reduce the fever. The GP also suggested further ibuprofen to reduce the fever. Because they were running low on ibuprofen she and her mother, at her father’s suggestion, went to buy some more.
He, the Claimant’s grandfather, felt that his wife and daughter were being over anxious about the situation and he wanted to try his own method of calming the Claimant which involved some active play and distraction. He managed to get him to eat some chocolate and drink some Ribena. It seems that the Claimant did indeed laugh at some stage during the time he and his grandfather spent together.
However, when his mother and grandmother returned, they described him as irritable and tired and attempts were made to get him to sleep in his cot. The Claimant’s mother stayed with him and whilst she was with him he had the fit foreshadowed in paragraph 21 above.
She called for her parents to summon an ambulance, which they did. The story can be taken up by reference to what occurred once he was at Pembury Hospital. Where there are conflicts of fact about what occurred and when, I will indicate my findings. I will deal with the allegations of negligence later.
The history of the Claimant’s admission to Pembury Hospital on 22 May 2001
The records show that the ambulance was called at 21.36 and the Claimant arrived at the hospital at 22.02.
The ambulance records show the following “observations”:
“23-month old child has experienced a febrile convulsion which lasted approximately 3 minutes. [XYZ] on our arrival is still very irritable. 3rd episode of f/con. Mum has given calpol – tepid sponge - to no avail. [XYZ] was in a very ‘hot’ room.”
His pulse was noted to be 130 and he was recorded as being “alert” and that his “breathing” and “circulation” were normal.
It is not quite clear precisely who saw the Claimant immediately on his arrival. There is a note composed and signed by the Paediatric Registrar in retrospect the following day (after the fitting to which reference is made in paragraph 54 below) in the following terms:
“Happened about 2200, 22.5.01
When [XYZ] came to ward by ambulance he was not fitting.
When he looked at us (myself and nursing staff) he cried. Then I went to SCBU.”
It would seem that the Registrar saw him at the same time as the nursing staff. I have not heard from the Registrar. On any view, the note reveals that this was the briefest of encounters, an occasion of “eye-balling” as it was described by Dr Hughes. The paediatric experts said of that occasion that it was “a rapid ‘once-over’ type examination” that led to the conclusion that the Claimant could be left to Dr Fisher to carry out the full assessment. In other words, the Registrar did not consider that the Claimant was critically ill.
At all events, the Claimant was seen initially by Nurse Ronald Carrido who was a staff nurse at the hospital. He completed the Ward Assessment Form at about 22.15 and the relevant contents were as follows:
Reason for admission
Febrile convulsion lasting three minutes = 3rd episode
Respiration & Circulation
…
On admission
Not in distress
Diet and fluid intake
Prior to admission
No problem
Elimination
Prior to admission
No problem
Play, development and communication
Prior to admission
No problem.
Comfort, rest and sleep
On admission
sleepy, slightly floppy
Comments
was well throughout the day highly febrile at night – fit happened at 2135 – 3rd episode.
Whilst the precise sequence is not wholly clear, it appears that Nurse Carrido conducted an examination and recorded some observations at about this time although they were not transposed into the Clinical History until after 23.00. This is to be deduced from the reference in the note to an event of vomiting at that time. The record is timed at 22.00 but, as I have said, was not recorded in the history until after 23.00:
“Admitted a 1 11/12 boy with mum via 999 with febrile convulsion lasting 3 mins at home. Highly febrile. Mum bath him but still febrile since episode had happened around 2135.
Condition: sleepy, looks tired, quite miserable but awake, able to take medicine well.
OBS: Fever 39.4ºC, warm to touch, tachycardic other obs stable.
Drugs: given Calpol and junifen (Footnote: 1) when he came in.
Fluids/diet. Given Ribenna (sic) – not interested – eating and drinking well before he had a fit. Vomited at 2300.
Social: mother is with him all the time.”
He was next seen by Dr Fisher who had, of course, seen him a few weeks previously. Given the criticisms sought to be made of Dr Fisher’s examination and record, I should set it out in full. It is in the form of a 4-page document headed “Paediatric Admission” with various sub-headings, the material headings being those underlined below:
“History from mother and grandmother
Presenting complaint
? fit/fever
History of Presenting Complaint
2 previous fits, 2nd 3 months ago – tonic afterwards given Diazepam. 1st - 6 months before that treated for meningitis IV abs as prolonged recovery.
Temp yesterday about 100-101, woke up well bounding around this am. E+D (Footnote: 2). Went to nursery – on return felt hot mother gave antipyretics immediately.
Temp up later – contacted GP who advised doses – due next at 10pm
Tepid sponging/shivering ++
About 9.40pm – eyes up; slight drooling; jerking of limbs; stiff; lasted 3 minutes. Sleepy afterwards but not stiff.
This episode not as severe as quicker recovery.
Called ambulance.
Has had slightly runny nose but often has one. Has temp every 2-3 weeks. Children in nursery today had feverish illnesses.
Current medication
Calpol/ibuprofen.
Immunisations
Fully immunised.
Past Medical History
2 previous feb fits. No known medical problems.
Birth/Neonatal history
36 weeks. No problems. NVD (Footnote: 3). No SCBU.
Development
Normal, although speech slow but good comprehension.
Family history
nil known. Mother had UTIs as a child. Living with parents at present.
Physical Examination:
14.7kg, 39.4ºC; Pulse 174; oxygen 96%.
General appearance and skin
asleep on arrival, woke up for exam, alert then slept again. CRT (Footnote: 4) <2 secs. No rash. No neck stiffness.
Cardiovascular System
Resp. RR36. Clear chest. No distress. Nil added.
Abdomen
soft, no masses, non tender.
ENT
ears - mild hue waxy; Throat mild erythema, but not exudal. Nose - yellow/green nasal discharge in nose.
CNS
PERL (Footnote: 5) Normal tone. CNS NAD. PNS – using all four limbs. N[ormal]. No asym.
Diagnosis of problem list
Fit + fever. Likely febrile convulsion – previous episodes - quicker recovery this time – probable viral illness – signs of discharge in nose.
Initial investigations and results
Urine MICS. Throat swab. If temp not settles needs RV (Footnote: 6) + bloods. Informed N staff to call if any concern or temp not ↓.
Initial management plan
Observations
close obs.
Food/fluids
oral as tolerates.
Drugs – calpol ibuprofen.
Information given to parents
discussion with mother re above.”
I will return to the criticisms made of Dr Fisher in relation to this examination in due course (see paragraphs 62-74 below), but I will first complete the chronology of events by reference to the medical notes so far as it is possible to do so.
There is an unresolved issue about precisely what “close” observations meant (see paragraph 43 below). However, there is an untimed note written by Nurse Carrido which, under the heading “Care Required”, included the following:
“4 hourly TPR (Footnote: 7)
cooling measures remove clothing
fan, open window
encourage fluids
paracetamol/junifen as ordered or as needed
note for signs/symptoms of seizure
prevent injury when or while having seizure
O2 as needed”
Neither Dr Fisher nor Nurse Carrido could remember what Dr Fisher would have said, but it seems tolerably clear that this was Nurse Carrido’s understanding of what was required and it was presumably completed soon after Dr Fisher’s examination. Dr Fisher’s note indicates that she spoke to the nursing staff and the obvious inference is that this is what she conveyed to them. Nurse Carrido thought that he should make the relevant observations every 3-4 hours. Dr Hughes (who felt that the observations should have been every 2-3 hours) did say that in 2001 matters such as this were dealt with in a less prescriptive way than they would be now, but did concede that if neither Dr Fisher nor Nurse Carrido knew what was intended, that would not be acceptable. If this uncertainty led to a failure to make observations when they should have been made, then there would have been a “system failure” for which the Defendant would be responsible. The essential issue, however, is whether in fact the observations were carried out at intervals that were reasonable in the circumstances.
The drug administration chart shows that the Claimant was given paracetamol at 22.15 (thus shortly before Dr Fisher’s examination) and Ibuprofen at 22.50 (and thus shortly after Dr Fisher’s examination). He is recorded as having vomited at 23.00 (see paragraph 39 above) and his temperature and pulse rate were recorded at 23.30 as about 38ºC and 144 respectively.
The Claimant would have been awake to take the paracetamol, the Ibuprofen and when he vomited, but I understand that the temperature and pulse rate could have been taken whilst he was asleep. He may well, therefore, have been asleep at 23.30.
There is an issue about whether the Claimant vomited again at about midnight. There is a record which on one interpretation might indicate that that was so. However, it seems clear that Dr Fisher was told before her review at 02.40 the following morning that he had vomited only once (see paragraph 47 below) and I do not think the record relied upon on behalf of the Claimant to suggest another occasion of vomiting is indicative, even on the balance of probabilities, that that was so. It appears to have been completed by someone who was not on duty at the material time and may well have been an attempt to record the one instance of vomiting at 23.00. It is quite correct to observe that the Claimant’s mother must have told the staff at Guy’s Hospital (where the Claimant was taken later on 23 May) that he had vomited three times “overnight” and indeed she mentioned in her witness statement that there were two occasions of this in the early morning of 23 May. Had he vomited on at least three occasions before Dr Fisher saw him at 02.40 then it is accepted that this would have operated as a “red flag”. However, I do not consider that the evidence supports such a conclusion of fact and I consider it more likely than not that he vomited only once between Dr Fisher’s first examination at 22.20 and her review at 02.40.
There is no record of any further observation before Dr Fisher conducted her review at 02.40. It is not in issue that the Claimant was asleep when Dr Fisher arrived and that she did not wake him up. The note she completed was as follows:
“Reviewed
Temp 36.9, after antipyretics
Vomited x 1 → now back asleep.
O/e nasal obs audible.
CRT < 2 secs.
No rash. Well perfused.
Looks well. Asleep.
P – ct observations close.”
In short, his temperature was effectively normal, his CRT (see paragraph 40 above) was normal, there was no rash, he looked well and well perfused. The plan was to continue the close observations.
There is an issue about whether the Claimant’s mother was awake when this review took place. She has no recollection of it, but Dr Fisher’s witness statement suggests that she “did not raise anything with me to express concern … or to suggest there had been any significant deterioration.” This suggests a recollection that the Claimant’s mother was awake.
I do not really believe that anything turns on this, but I am more inclined to the view that the review took place without the Claimant’s mother being woken. I imagine that Dr Fisher might have woken her if she was concerned about the Claimant. That she made no note, for example, to the effect of “discussed with Mum” or “reassured Mum” suggests to me that she saw no reason to wake her and did not do so. Whilst Dr Hughes expressed the view that it would be highly unlikely that a young child would be reviewed at night without speaking to the mother (which he said would be “the norm for all junior doctors”), I think that this did occur on this occasion. The Claimant’s mother says that she recalls being woken when the nurses came to see the Claimant during the night, but does not remember seeing the doctor in the middle of the night. I think it unlikely that she would have forgotten this if it had occurred.
According to the records, the next event was the taking of the Claimant’s temperature and recording of his pulse rate by Nurse Carrido at 03.00. He was, it appears, unaware that Dr Fisher had recorded the temperature. Nonetheless, the temperature was recorded at 38.2ºC so that it had gone up again from what it was when Dr Fisher took it. (I should say that it is common ground that this kind of fluctuation can occur.) His pulse rate was 135. These observations would have been performed whilst the Claimant was asleep. He was then woken at 03.10 to be given some Calpol. Nurse Carrido recorded in the Clinical History at 03.00 or 03.10 “pyrexial – paracetamol given – temp settled afterwards.”
The next recorded observations were at 04.45. The temperature was as before and the pulse was 140. Nurse Carrido recorded the following in the Clinical History: “still pyrexial – junifen given. No seizure.”
The next observation recorded by Nurse Carrido looks from the Observation Chart to be at 06.00 when the temperature was 37.2ºC and the pulse rate 129. It is difficult to read the timing, but he thought it was about 06.50 which would be consistent with the note he made in the Clinical History at 06.45 that the Claimant was “offered milk, refused, apyrexial.” Nothing of significance turns on the precise timing of these observations and I need not resolve the difference.
In due course, at about 10.00 the Claimant’s mother and a nurse observed what they considered to be some twitching. This was confirmed at 10.39 and thenceforth his condition was treated as an emergency. There are aspects of what occurred during that day before the Claimant was transferred to Guy’s that, in other circumstances, might have called for an explanation, but they are not material to the case advanced on the Claimant’s behalf and I propose not to refer to them.
The issues and the criticisms
It is common ground that by the time that the Claimant’s twitching was finally identified at about 10.00 or shortly thereafter on 23 May (see paragraph 54 above), he was suffering from established pneumococcal meningitis. Piecing together from the various strands of evidence the way this condition evolved has not been an easy exercise for the experts. However, there is a tolerably clear agreement about that to which I should refer briefly.
They have had to try to recreate the evolution of the meningitis from various pieces of evidence, some more reliable than others. There is no doubt that the Claimant’s CRP level in the blood was raised to 207 mg/L by the morning of 23 May. The normal level would have been in the region of 6-8. It had increased to 352 the following day. There was evidence of fitting by about 10.00 on 23 May and the febrile convulsion occurred at 21.30 on the previous evening. Putting all these factors together against the background of the general understanding of the medical profession about the evolution of bacterial meningitis, the consensus amongst the experts was that, whilst the blood/brain barrier had probably been breached by the time of the Claimant’s admission to hospital on 22 May, the immune response did not commence until about 04.00 the following morning and that no symptoms attributable to meningitis as such would have been apparent until then. What would have been apparent were the effects of the continuing bacteraemia (see also at paragraph 25 above and paragraphs 66 and 81 below). As will be apparent in due course, it is agreed that if a CRP test had been carried out at any time following the Claimant’s admission to hospital, it is likely that his CRP level would have been found to have been raised. However, this would not have been associated with the manifestation of overt to clinical symptoms until after 04.00 on 23 May.
There is an issue between the Consultant Paediatric Neurologists for each of the parties as to the effect of the administration of intravenous antibiotics at various times. They were asked to say what the outcome would have been, on the balance of probabilities, if intravenous antibiotics had been administered by (i) 01.30 on 23 May or (ii) 04.00 on 23 May. They have differing views about the answers to this question which it will be necessary to resolve if it can be established that the Defendant was in breach of duty in not securing the administration of such antibiotics by either of these times. I propose, therefore, to address that question at this stage since it is the logical place to start.
There is one background feature that I should mention before undertaking this analysis. I referred above (see paragraph 56) to the relevance of a CRP test. A raised CRP level in the blood is, it is common ground, a typical response to, and thus an indicator of, an inflammatory or infectious process. Although there appears to have been an increased interest in this phenomenon as a test in the published literature since 2001, the utility of the CRP test was certainly recognised at the time. It was, of course, one of the tests required by Dr Fisher to be carried out when the Claimant presented on 29 March 2001 (see paragraph 17 above).
The potential importance of the test is reflected in the agreement of the infectious diseases experts and the microbiologists in this case that they would have expected a hospital in 2001 that admitted potentially seriously sick children at night to have overnight testing facilities for CRP levels. The paediatricians agreed that when a blood test is decided upon in relation to investigating a febrile child in 2001 it should have included a CRP test. Dr Lloyd said that the CRP test was more reliable (with less false positives or negatives) than the white cell count. I did not understand Dr Hughes to disagree with that proposition and it is consistent with the literature.
It has emerged during the process of preparing for this case that all the staff at Pembury Hospital, from Dr Robards downwards, believed that CRP testing was not available overnight. That (it seems through no fault of theirs) was their belief. However, it has also emerged that such testing was available out of hours. It was agreed on behalf of the Defendant that the case should proceed on the basis that such testing, had it been thought necessary or appropriate, could have been carried out.
On any view, it is highly unsatisfactory that the system in place at the hospital should have been such that the paediatric team were unaware of the facility. Had the evidence been that, for example, Dr Fisher would have ordered a CRP test at any time after the Claimant’s admission, but felt that she could not pursue it because it was not available, whilst she would have personally been blameless, the hospital would have been held responsible for any consequent failure to carry out the test. I will come to deal with this feature below (see paragraph 74 below), but it is important to appreciate the position in relation to CRP testing at night at Pembury Hospital at the time.
The first allegation made against Dr Fisher is that she failed to carry out an adequate assessment of the Claimant during her examination that started at 22.20 on 22 May. It is alleged that she should not have made the presumptive diagnosis of a febrile convulsion that was viral in origin. Given what is said to have been his condition on admission and his history, she should either have sought a review at a more senior level or ordered blood tests which would have included FBC, CRP and blood cultures. The nature of the case is that had she ordered such tests, the tests would have been available in time to begin intravenous antibiotics by 01.30 on 23 May. That is the way the case was pleaded against her in relation to this assessment.
The position became a little more refined following the discussion between Dr Lloyd and Dr Hughes. They agreed that if the Claimant’s condition were to be found by the court to have been as described by his mother in all respects (other than neck stiffness: see paragraph 64 below), he should have undergone blood tests and had been referred for senior review. As Mr Christopher Gibson QC, for the Claimant, rightly observed in his closing submissions, the precise extent of what was meant by “as described by his mother in all respects” was not defined in their joint statement. They were presumably referring to her witness statement where she said that, even after the fit had concluded, the Claimant at no stage “[seemed] better or like himself” and that to her “he was clearly very unwell”. Although not in her witness statement, it was pleaded in the original Particulars of Claim that the Claimant was unable to sit up and “remained slumped”. She described this in her evidence by saying that he largely sat leaning to one side against her.
I will return to these matters shortly after a brief explanation of the reference to neck stiffness and why it should have been excluded from the consideration given by the experts to the Claimant’s presentation. The case for the Claimant was originally pleaded on the basis that he was suffering from meningitic symptoms on admission to hospital and that his mother’s alleged reference to neck stiffness was something that should have been acted upon and confirmed on examination. However, after the experts had considered the position, it became their view that he would not have been showing signs of meningitis at that time (see paragraph 66 below) and, accordingly, the suggestion that he was showing relevant signs of neck stiffness at the time was withdrawn. That is the explanation for the exclusion of the mother’s complaint concerning neck stiffness. (She has not withdrawn her evidence that she mentioned that, from her perspective, the Claimant had manifested difficulties with his neck, but the suggestion that this was something associated with meningitis was withdrawn.)
Returning to the way in which the case was advanced at trial, it was to the effect that the Claimant was sufficiently unwell for Dr Fisher to have been negligent in not noting it and taking the initial steps of ordering a blood test and then seeking a more senior review. Reliance was placed on other contemporaneous evidence that he was unwell: for example, the ambulance record that he was, on the arrival of the ambulance, “still very irritable” (see paragraph 34 above), that he was “sleepy and slightly floppy” when seen by Nurse Carrido (see paragraph 38 above), that he cried when the Registrar looked at him (see paragraph 36 above) and that he had gone to sleep prior to the examination by Dr Fisher (see paragraph 40 above).
Before recording my conclusions concerning Dr Fisher’s assessment, it should be noted that, as indicated above, the infectious diseases and microbiological experts are now agreed that, whilst the Claimant’s blood/brain barrier had probably been breached by the pneumococcal bacteria by the time of his admission to hospital, he would not have been demonstrating any overt signs of meningitis at that time. His symptoms at that time would have been those derived from his continuing bacteraemia.
A number of matters seem to be absolutely clear from Dr Fisher’s note: first, she plainly had in mind the possibility of meningitis because she recorded that there was no neck stiffness. She would not have recorded that if she had not tested for it and I accept that she did. That would have involved examining and manipulating the Claimant’s neck whilst he was sitting on his mother’s lap. She also examined for the characteristic rash that could appear if meningitis has become established. That involved checking the whole body. It cannot, therefore, be said that she overlooked the possibility of there being established meningitis. It is equally clear from her plan (namely, of keeping the Claimant in hospital overnight for close observations) that she realised that there was a possibility, notwithstanding her provisional diagnosis of a viral illness, that something more sinister or serious underlay the fit that the Claimant had suffered and the fever that he was demonstrating.
The essential first issue is whether other features of his presentation should have led to a request for blood tests. Dr Lloyd, who gave evidence to support the criticisms of Dr Fisher, said that it was not possible to say from her note how alert and responsive the Claimant was and how he was sitting. He said that if he was sitting up well, was alert, responsive and interacting, immediate blood tests were not called and Dr Fisher’s management plan was reasonable.
Whilst views might reasonably differ about the quality of Dr Fisher’s note, Dr Lloyd himself was advocating a standard that that even he recognised was not achieved by all doctors in Dr Fisher’s position and the criticism he made was, in my view, incapable of being sustained by the usual approach to deciding whether an action fell below reasonable standards. The more important question is whether the examination itself was inadequate.
Taken as it stands without any oral elaboration, the note is suggestive of a thorough review and examination. Having looked at the note, Dr Fisher, who was a very undemonstrative witness, thought that it signified a review lasting between 10 and 20 minutes. Mr Gibson indicated that he had assumed it was about 15 minutes and I would myself have thought that it was certainly not less than 15 minutes when all aspects, including the note-taking, were taken into account. She described the CRT test which involves pressing on the sternum for five seconds and then counting how long it takes for the blanching of the skin to disappear and the skin reassume its normal colour. Whilst that test would not take long, it would have involved some obvious physical contact between the doctor and the Claimant. The examination of the cardiovascular system would have involved the use of a stethoscope at various places on the chest and in the groin area (the removal of a nappy being required for this purpose) and then the examination of the respiratory rate would require the listening through a stethoscope both on the front and the back of the chest. Examination of the abdomen would require the palpation of that area of the body. The examination of the ears, nose and throat would have required the use of an otoscope to look in the ear and the tongue would require to have been pressed down to looked at the back of the throat. The examination of the eyes would have required the shining of a torch into the Claimant’s eyes.
Those matters will have formed the basis of the physical examination. Plainly, some of the period of time that Dr Fisher was with the Claimant would have been spent speaking to his mother and grandmother. However, the inter-reaction between Dr Fisher and the Claimant would certainly have been sufficient to enable her to decide whether he was “alert” and, notwithstanding that he may not have walked, sufficient for her to conclude that he was using all four limbs and that there was no asymmetry. I do not believe that she would have recorded this if it were not the case. It would also have been obvious to her that the Claimant was “slumped” on his mother’s lap if that was the case. He would undoubtedly have been tired after the events of the previous few hours, but it seems to me to be clear that if he was, to borrow an expression used by Dr Lloyd, disported like “a sack of potatoes” that would have been obvious to Dr Fisher. She did not record that: indeed her record is to the contrary.
None of her findings is inconsistent with the chronology of the evolution of the bacterial processes continuing within the Claimant’s bloodstream or CSF at the time of the examination. It needs also to be emphasised that by the start of Dr Fisher’s examination, the Claimant had ceased fitting some 45 minutes or so previously. When seen by the ambulance crew (who arrived commendably quickly), the fit had only just subsided. Equally, Nurse Carrido’s note that the Claimant was given Calpol and Junifen on arrival at the hospital is consistent with him being alert.
Although he sought to do so under cross-examination, I do not think that Dr Lloyd was truly able to maintain his criticisms of this examination or the management plan and, of course, Dr Hughes considered that both were acceptable and met reasonable standards. As it happens, Dr Tudor-Williams ventured the view during his cross-examination that what Dr Fisher had recorded was “thoughtful and appropriate”, that she concluded that the Claimant was not well enough to be sent home and that he should be admitted for close observation. That, he said, was reasonable from his perspective. He was not, of course, one of the breach of duty experts and this might have been an unexpected forensic bonus from the point of view of Mr Alex Antelme QC, for the Defendant. He placed reliance upon it in support of the Defendant’s case. Not unnaturally, I do not ignore it, but my conclusion in relation to Dr Fisher’s assessment at this stage is based upon the appraisal set out above, namely, that the evidence demonstrates the assessment to have been thorough and the management plan reasonable by reference to what, as it seems to me, was in truth and on proper analysis the combined view of Drs Lloyd and Hughes. If there was any residual difference between them, I thought Dr Hughes’ evidence represented the more mainstream view on this particular issue.
It follows that I do not consider that Dr Fisher’s examination and management plan having seen the Claimant soon after admission to the hospital can legitimately be criticised. The examination was thorough and the management plan, involving close observations by the nursing staff and a subsequent review by her, was entirely acceptable. It also means that her misconception about the availability out of hours of CRP testing (which, as I have said, was not her fault) makes no difference to the position: no blood tests of any kind were called for at that time. It is right to observe that the paediatric infectious disease experts and the microbiologists agreed that a CRP test carried out shortly after admission would probably have been moderately raised (to between 50-70 mg/L) and Dr Fisher herself acknowledged that this would have led her to order antibiotic intervention had she been aware of it. However, since the clinical picture did not demand a blood test (and hence a CRP test), this information did not enter the picture.
That is not, however, the end of the story because criticisms are made of Dr Fisher’s review at 02.40. In essence, what is said is that it was negligent not to have woken the Claimant at that stage and, by failing to do so, she deprived herself of the opportunity to observe what would, it is said, have been clear signs of a deterioration in his condition, or at least no clear, positive signs of well-being, which would have led to antibiotic administration.
I will address shortly the issue of whether the Claimant should have been woken (see paragraphs 77-85), but if the failure to wake him were to be characterised as a breach of duty, I would need to be satisfied, on the balance of probabilities, that what would have been revealed would have been such as to demand the commencement of intravenous antibiotic treatment. That in itself raises the question of what observation would have driven the taking of that step.
Dr Lloyd advocated the need to wake the Claimant in order to look for positive signs of well-being. What that constituted was examined when he gave his evidence. It is a fair point that, as Mr Antelme suggested in cross-examination, Dr Lloyd’s position in relation to the 02.40 examination was predicated on the premise that the examination the previous evening had been insufficiently reassuring. However, I will address the 02.40 examination as a matter separate from that consideration.
There can be no doubt that the Claimant’s temperature had (albeit temporarily and after antipyretics) returned to normal when Dr Fisher saw him and his pulse rate had reduced. There was no evidence of any rash, his CRT was normal, he looked well and was “well perfused” (see paragraphs 47-48). Without more, overall these observations represented an improvement in his condition compared with what it was at the time of Dr Fisher’s first examination, or at the very least indicated no worsening in his condition. The perfectly legitimate question is what else would have been discovered if he had been woken which ought to have led to the administration of antibiotics?
In the joint statement with Dr Hughes, Dr Lloyd had identified “sitting up and drinking - or better still standing up and drinking” as “positively reassuring behaviour” that needed to be looked for at 02.40. He also said that evidence of “responsiveness/interaction with mother or nurses” would be a positive sign. The absence of these signs ought, he said, to have led to antibiotic intervention.
He varied that position when giving his evidence. It was suggested to him that the Claimant was woken to take his medicine and that that constituted appropriate interaction. Dr Lloyd denied that it constituted proper interaction and said that “some words, some positive thing” was required.
I regret to say that I felt that the target was moving during this part of Dr Lloyd’s evidence and the target itself was, in any event, somewhat elusive. However, perhaps more importantly, I consider that the requirement to look for something positive in the way of improvement was inconsistent with the accepted position of the infectious disease experts in particular. It was common ground that a viral illness may take 3-4 days to settle so that clear evidence of some improvement only a day or so into such an illness (which, for this purpose, would be what should be assumed in the Claimant’s case) would be unlikely. But additionally, what is now known is that there was in the Claimant’s case an emerging bacterial meningitis which at 02.40 was asymptomatic. What was causing any symptoms at that time was the bacteraemia. There is no consensus amongst the experts that there would, in the period from, say, 22.40 on 22 May to 02.40 on 23 May have been any significant deterioration in the Claimant’s presentation because of the evolving bacteraemia. The symptoms would remain non-specific and would, classically, be of fever and poor feeding. Professor Cartwright said that a young child might be “grizzly, clingy, not making good eye to eye contact, really lethargic and maybe even a little bit drowsy”.
It is, of course, the case that Dr Fisher, not having woken the Claimant, was unable to see for herself whether he was responsive towards his mother or indeed to her. However, he was woken within less than 30 minutes of her examination in order for him to take his medicine. I have no doubt that Nurse Carrido would have woken his mother before attempting to give him the medicine – indeed she confirmed in her witness statement that she recalled being awake two or three times during the night when the nurse came in. There was a clear opportunity, therefore, to see whether he was capable of interacting at that stage. No adverse comment was recorded and nothing that his mother said suggested any particular concerns on her part at the time.
One obvious problem, which has a bearing on the decision whether to have woken the Claimant at 02.40, is that almost inevitably he would have been sleepy and not very alert simply because of the time of the night and bearing in mind that he had had a disturbed evening from about 18.00 until 23.00 the day before after a day when he had been generally “off colour”. It is not difficult to see how a doctor might be criticised for starting intravenous antibiotic treatment simply because a child was sleepy and not very alert at this time. In the Claimant’s case there were reassuring signs at the time of the previous examination, he had interacted with Nurse Carrido and/or his mother at 23.00 or thereabouts and the objective signs at 02.40 were such as to suggest continued improvement or, at the very least, no sign of deterioration. Since Dr Lloyd himself agreed that it was not necessary to wake every sleeping child in the middle of the night and that the issue is largely one of judgment on the part of the clinician, it is impossible to characterise Dr Fisher’s decision as negligent. At all events, as I have said, even had she woken him (as the nurse did shortly afterwards) it is more probable than not that no adverse signs would have been noted and no concerns raised.
It is, of course, known now that the Claimant was in a state of asymptomatic meningitis (see paragraph 26 above), but that very fact means that the kind of symptoms that would have led inevitably to the immediate intravenous antibiotic treatment were simply not present.
Mr Antelme has reminded me that the allegation that it was negligent not to have woken the Claimant only emerged when the pleadings were amended in March 2016 and had not been made previously despite the Claimant’s case being examined closely by various experts and his legal team over the years. I agree with him that this is a secondary point and is by no means conclusive, but it does highlight the need for caution in holding that Dr Fisher’s decision was one which no reasonably competent clinician could have taken in the circumstances. I do not consider that such a proposition has been demonstrated.
Conclusion
The foregoing analysis results in the conclusion that Dr Fisher was not guilty of any negligence in either of her examinations and that the steps she took were entirely appropriate in the circumstances and in accordance with the practice of a reasonable body of clinicians in 2001. The mere fact that events turned out unexpectedly in a tragically different fashion is not, of course, a reason for being critical of her conduct. There is evidence that she was very upset when she learned the true position later in the morning of 23 May. That is an entirely understandable human reaction and demonstrates a caring disposition that one would expect of all medical practitioners, certainly one at the stage that she had reached in her career. I am sure she has looked back on what she did and thought at the time on many occasions subsequently and has asked herself whether she should have acted differently. She said, when giving evidence, that she regretted what had happened, but felt that what she did was correct in the circumstances. In my view, she was right to express herself in this way. There is evidence in her CV that she had impressed her examiners some two years previously that she was a highly competent and conscientious student. Whilst that does not mean that she might not have fallen below reasonable standards on this particular occasion, it strengthens support for the conclusion that she would have approached her tasks concerning the Claimant competently and conscientiously. I am sure that she did.
This conclusion will, of course, come as a disappointment to the Claimant’s mother. Leaving aside the principal allegations made in these proceedings, she will know that there was one particular aspect of the regime at the Pembury Hospital that might have been relevant (namely, the availability of CRP testing out of hours) that was lacking (see paragraphs 56-61 above). That may have encouraged her to believe in the strength of the case. However, it has in the event proved not to be an important consideration. Nonetheless, she has fought tenaciously but with dignity for her son and will, I am sure, have examined her own conduct and asked herself whether she could have done anything more. The short answer to that question is “no”. As soon as she observed his fit she got him to hospital quickly. Earlier in the evening she had taken medical advice. She did everything that a caring and devoted mother, which plainly she is, could have done. The same applies to her mother (and indeed her father). Her mother was at one stage a little tearful in the witness box, feeling that she should have said or done something more. These are all understandable human reactions from decent people. They should take some comfort (if ‘comfort’ is the right word) from the fact that the experts did find piecing together the evolution of the Claimant’s pneumococcal meningitis difficult. Professor Cartwright ventured the view that its development was at the rapid end of the spectrum which, if he is right, means that it may well have developed too quickly for the observations that were reasonably required to have been carried out to have provided evidence of the underlying condition such that it could have been arrested by antibiotic treatment.
I should, perhaps, say that, had I been satisfied that antibiotic treatment should have been started after the review at 02.40 I would have been inclined to accept Dr Smith’s approach to the issue of the effect of that treatment rather than the approach of Professor Gupta. On this occasion I felt the Dr Smith’s approach was better thought out and was supported by the literature to which he referred. However, that situation has not arisen. I am satisfied that Dr Fisher’s conduct has not been shown to have been negligent and, accordingly, the issue does not arise.
It follows that this claim must be dismissed.
Expression of thanks
I am grateful to Mr Gibson and Mr Antelme for their extremely helpful submissions and to both firms of solicitors for agreeing to commission a daily transcript. In a case where there is a good degree of conflicting evidence, particularly expert evidence that falls to be tested, it is often very helpful to the trial judge to be able to focus on the evidence without having to take his or her own note. It also operates to save time. I am grateful to the transcribers for producing the daily transcript so efficiently.