QUEEN'S BENCH DIVISION
Royal Courts of Justice
Strand, London, WC2A 2LL
B e f o r e :
|KING'S COLLEGE HOSPITAL NHS FOUNDATION TRUST
Mr Michael de Navarro QC and Ms Nina Unthank (instructed by Kennedys Law LLP) for the Defendant
Hearing dates: 19, 20, 21, 22 & 26 March 2018
Crown Copyright ©
Mrs Justice Yip:
"2. The said brain damage was caused by seizures which started after 19.15 hours on 17 November 2008 and continued thereafter into 18 November 2008. The cause of the said seizures was sepsis which provoked seizures in a child who was susceptible and vulnerable thereto as a result of pre-existing Tuberous Sclerosis ("TS") and recent surgery.
3. In breach of duty, the Defendant failed to treat the Claimant's infection with antibiotics in a timely fashion and failed to intubate, sedate and ventilate the Claimant: which would have been neuroprotective, and would have avoided any brain damage until the antibiotics could take effect and treat the sepsis. But for the said breaches of duty, the brain damage would not have occurred and the claimant's neuro-development would have returned to its prior state."
"I am extremely unhappy and distressed about the terrible events which occurred on the 17th of November. This patient developed a serious, life threatening problem which was inadequately managed by doctors of insufficient expertise and seniority.
A paediatric neurosurgical patient has been left with severe permanent damage due to an inadequate response by paediatric/PICU medical staff and I believe this Trust will be found entirely liable if this comes to litigation (and I believe this will come to litigation and strongly recommend the Trust Medico-Legal Team are involved now). It highlights significant issues about the expertise of certain members of the PICU and paediatricians. There was a lamentable primary failure of a paediatric junior doctor to inform the neurosurgical team looking after this patient at an early stage which allowed a catastrophic chain of events to develop. I remain deeply concerned that the serious issues surrounding the events of 17/11/2008 concerning the paediatric staff have still not been addressed within Kings."
"I emphasise that in my view it will seldom be right for a judge to reach the conclusion that views genuinely held by a competent medical expert are unreasonable.
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 benchmark by reference to which the defendant's conduct falls to be assessed."
"(1) In certain circumstances a court may be entitled to draw adverse inferences from the absence or silence of a witness who might be expected to have material evidence to give on an issue in an action.
(2) If a court is willing to draw such inferences they may go to strengthen the evidence adduced on that issue by the other party or to weaken the evidence, if any, adduced by the party who might reasonably have been expected to call the witness.
(3) There must, however, have been some evidence, however weak, adduced by the former on the matter in question before the court is entitled to draw the desired inference: in other words, there must be a case to answer on that issue.
(4) If the reason for the witness's absence or silence satisfies the court then no such adverse inference may be drawn. If, on the other hand, there is some credible explanation given, even if it is not wholly satisfactory, the potential detrimental effect of his/her absence may be reduced or nullified."
Factually, this case is rather different from Wisniewski. In that case, there was an issue as to whether a doctor should have been called and what he would have done had he attended. The defendants did not call the duty doctor. The judge found (and the Court of Appeal agreed) that a weak prima facie case was strengthened if for no good reason the doctor was unwilling to submit him/herself to questioning about was he/she would probably have done.
"The factual evidence from both C's family and the medical witnesses requires to be evaluated against [the medical records], but bearing in mind that D has not chosen to call key witnesses."
It seems to me that this is a sensible approach, and the correct one in this case. When considering the evidence, if there are gaps that could have been plugged by the defendants, I will bear that in mind in evaluating the evidence overall. I am inclined to give the benefit of any doubt to the claimant. I bear in mind the principles set out in Wisniewski, while taking care to analyse the whole evidential picture.
"In the evening became febrile and shivering ++
Subsequently around 7.30 pm 17.11.08 began to seizure. Multiple seizures but Mum very clear that whilst motor component improved she was continuing to seize (eyes) until phenytoin given at 10.45 pm. Subsequently further breakthrough seizures additional phenytoin & midazolam infusion. (Also had initially rectal diazepam, then lorazepam iv without Mum noting complete seizure control). Subsequently brief seizures when midazolam reduced but otherwise nil and EEG does not show any subclinical seizures."
That account was given when events were fresh in KAX's mind. The outcome was not yet known, and hindsight is unlikely to have played a part. Further, I have no doubt KAX was being careful to give a full and accurate account to assist in her daughter's diagnosis and treatment. The account seems broadly consistent with the notes. As I read Dr Hughes' note, she did not doubt what KAX said and was recording it on the basis that it was likely to be accurate. Dr Parker, the expert neurologist called by the claimant (who has particular experience of HHE syndrome) told me that this account was very similar to accounts he had heard from parents in other HHE cases.
Breach of duty
"(1) Delay in Dr Raj's attendance after being called at the onset of fitting.
(2) Failing to take the following steps in the light of C's high and rising temperature (41.1°C at 19.35 and 41.7°C) and prolonged seizure: (i) treat with broad spectrum antibiotics; (ii) admit to the HDU for a CT scan; and (iii) intubate her.
(3) Planning to postpone active management, as identified under (i) to (iii), until 23.00 hours.
(4) By Dr Tait failing to contact Mr Chandler immediately, and delaying until after 22.00 hours
(5) Generally failing to suspect a serious problem unfolding, 4 days after major brain surgery, and in the face of very high temperatures, status epilepticus, and deteriorating condition.
(6) Wrongly assuming NAX was experiencing a simple episode of seizures."
i) Failure to arrange a CT scan;
ii) Delay in intubating and sedating for neurological protection.
These allegations overlap. It is accepted that a CT scan would not itself have shown anything that would have altered the course of treatment. However, it is the claimant's case that she would have had to have been intubated and sedated to undergo the scan and that the drugs used to sedate her would have stopped her fitting. It is also apparent from the expert evidence that a decision to perform a CT scan would call for consideration of the likelihood of intubation and sedation being required.
"everybody who saw her seemed to have one bit of information or have one particular interest in the case, but nobody actually put it altogether."
Even before he said this, the thought had occurred to me that there appeared to have been a lack of "joined up thinking".
"I don't think there was a breach of duty by not doing a CT scan. I would have done a CT scan and but I think Professor Hayward touched on this before: neurosurgeons despite their slightly confident appearance are slightly insecure and we do when we do when we have an intubated patient or we have something changed, we like to reassure ourselves. So we're partly treating ourselves, not the patient there necessarily."
He then went on to say:
"actually, I think it was reasonable for him not to perform a scan, particularly in the scenario with these really acute medical problems developing on days two and three."
"there was no indication for a CT scan either following the first seizure, or subsequently up until the time that the claimant was intubated at around 02.50 hours."
Dr Darowski therefore adds to the body of opinion that would regard it as proper not to perform a scan before the child had already been ventilated.
Protective intubation and sedation
i) In his report, Dr Darowski said that there were several cogent reasons for not intubating NAX during the evening of 17 November. His opinion was that the risk/benefit balance was in favour of not intubating her until she showed signs of respiratory failure. He modified his position in the joint statement, concluding that "intubation and ventilation were not required until 00.40 on 18th November when the claimant suffered a prolonged (20 minutes) predominantly right sided focal seizure."
"We are agreed that intubation should have occurred sooner to reduce the risk of neurological injury but disagree as to the required timing of intubation."
Dr Whiteley maintained intubation was mandatory at 22.00. Dr Darowski said it was not necessary until 00.40.
"from a neurosurgeon's perspective we have handed over that patient when they're intubated, we can't really assess them very well."
Dr Darowski explained that there is a reluctance to intubate "because you lose that window into the brain". He did not accept that a patient needed to be intubated just because she remained unconscious, saying:
"We are all used to looking after patients who have GCS's of 3, or slightly more, during recovery from anaesthesia. And protecting the airway doesn't necessarily mean intubating it. It means ensuring the patient is in a recovery position, that the airway is open, that they have adequate suction and that there is somebody who is looking after the patient."
"Yes, I have to modify that to a degree. It was pointed out that clinically NAX had a series of seizure events. When clinically assessed, she wasn't in a relentless period of hours of seizure activity and, for that reason, I went back to the literature and did some floating around Realising that we didn't have, in this case a history of relentless status epilepticus lasting several hours, I went back to my literature that I collected on this syndrome and was relieved to find, in terms of appropriate diagnosis in this case, that trivial seizures and minor seizures anteceding the full recognition of the HHE syndrome has been documented. "
Dr Nelson did not produce the literature to which he had referred.
"I think you are saying with two hours ten minutes less of the deleterious process, on the assumption that it was finished with strong sedative drugs with strong anti-epileptic effect. I think she that would have reduced the extent of her subsequent long-term disability."
He said that he was unable to quantify that further.
"although the exact causes of the pathogenesis of HHE syndrome, and their interactions are not clear, we do know that the factors outlined by RG below contribute.* In terms of duration of epileptic activity, some children with exceptionally long periods do not develop HHE and other children with shorter periods of seizure activity do. However, it is clear that in the population of children who develop HHE, the hyperthermia / seizure activity is much more prolonged, and similar to that described in this case. AP is of the opinion that if HHE does not occur with short periods of seizure activity, if the seizure activity in this case had been dramatically shortened, it would have been unlikely to have occurred."
(*The "factors outlined by RG" included prolonged seizure activity, hyperthermia, inflammation and blood brain barrier damage.)
"In most other cases I have seen with HHE, we have debated whether earlier intervention could have occurred and if so whether it would have altered the outcome. In most of those cases, the reduction in the length of the injurious process would have been minor, and hence any possible improvement in outcome less certain."
When giving evidence, he told me that when he has seen HHE, junior doctors have asked whether they should have intervened earlier and have felt very bad about the outcome. He tells them that it is likely the child had been in status epilepticus for a long period but HHE is a very rare sequela of status epilepticus (so rare it does not feature in the training of a SHO). Dr Nelson's evidence also pointed to the difficulty in predicting when HHE will occur. It seems to me, ultimately, that it is more likely that this was another unfortunate case of HHE which cannot be directly linked to fault on the doctors' part.
i) Is it correct (as the Claimant understands) that the finding that there were no further seizure[s] after 01.30 includes a finding that after that time there was (a) no subtle fitting activity that was unrecorded; (b) no further subclinical (i.e. clinically undetectable, but still part of a damaging process) seizures; (c) resolution at that point of status epilepticus that has been found; and (d) accordingly, that the 'deleterious process' identified by Dr Parker stopped at that point?
ii) If so, what is the reasoning and evidential basis for that finding?
iii) Does the Court find that there [was] any clinical recovery after 01.30 before intubation at about 02.50? If so, what was the extent of this, and the evidential basis of such a finding?
iv) What was [the] clinical cause of the deterioration that led to the concern about respiratory status (and hence intubation at about 02.50), and the evidential basis for that cause?
i) There was no evidential basis for a finding that there was further seizure activity after 01.30. The evidence I heard, taken as a whole, did not establish that a "damaging process" continued after 01.30. The claimant may have been considered to be in status epilepticus beyond 01.30 because she had not recovered. However, Dr Parker's evidence suggests that the term "status epilepticus" does not have a universal definition. Further, the evidence before me did not persuade me that being in status epilepticus (in the sense of not recovering rather than having ongoing ictal activity) meant that the process causing the damage was continuing. On a balance of probabilities, the deleterious process had ceased by 01.30.
ii) I consider that this question risks reversing the burden of proof. The claimant did not establish on the basis of all the evidence before me that the deleterious process continued after 01.30. There was no direct evidence that it was continuing. Dr Parker's evidence in the end was that it continued "a little bit longer" than the last witnessed convulsion. That evidence was vague. Having regard to all the evidence, including the literature and the other expert opinions, I was unable to infer that a damaging process was continuing beyond 01.30.
iii) I did not make a finding that there was any clinical recovery between 01.30 and 02.50. My only finding about this period was that there were no further seizures.
iv) This issue was not one addressed at trial and I consider it inappropriate to make a finding now. The claimant was septic, pyrexic (her temperature was recorded as 40 C at 9am on 18 November) and she was systematically very unwell. If the implication is that I should have found that ongoing seizure activity led to reduced respiratory effort and the need for intubation, I reject this as being unsupported by the evidence. No evidence was presented that continuing seizure activity caused NAX to deteriorate after 01.30.