Alder Hey Children's NHS Foundation Trust v (1) Mr Thomas Evans
| Jurisdiction | England & Wales |
| Judge | Mr Justice Hayden |
| Judgment Date | 20 February 2018 |
| Neutral Citation | [2018] EWHC 308 (Fam) |
| Docket Number | Case No: FD17P00694 |
| Court | Family Division |
| Date | 20 February 2018 |
[2018] EWHC 308 (Fam)
IN THE HIGH COURT OF JUSTICE
FAMILY DIVISION
Royal Courts of Justice
Strand, London, WC2A 2LL
Mr Justice Hayden
Case No: FD17P00694
Michael Mylonas QC (instructed by Hill Dickinson) for the Applicant
The First and Second Respondents representing themselves
The Third Respondent represented by Ms Melanie Carew of CAFCASS
Hearing dates: 1 st and 2 nd February 2018 & 5 th – 9 th February 2018
Judgment Approved
This judgment was delivered in public. The judge has given leave for this version of the judgment to be published.
I am concerned here with an application made on behalf of the Alder Hey Children's NHS Foundation Trust concerning Alfie Evans who was born on 9 May 2016. The Trust seek a declaration that continued ventilatory support is not in Alfie's best interests and in the circumstances it is not lawful that such treatment continue.
Alfie's parents, Tom Evans (F) and Kate James (M), both resist the application. In the hope of resolving the dispute and endeavouring to forge an agreed resolution, a mediation meeting took place on the 8 January this year. No agreement as to the way forward was forthcoming.
Background
Alfie was born at the Liverpool Women's Hospital. He was delivered at full term with a healthy weight and discharged home three days after the birth. Alfie's mother was then 18 years old and this was her first pregnancy. Alfie's father Tom was 19 years of age. Though self-evidently very young and though Alfie had not been planned his parents were delighted by him. They were both determined to be good parents and, from what I have seen and read, were instinctive and natural. The couple were well-supported by their respective extended families. Alfie was a happy smiling baby who seemed to be perfectly well.
The first indication that all might not be well occurred in July 2016 when Alfie was noted to have a ‘divergent squint’ for which a hospital referral was considered appropriate. He was seen again by his General Practitioner, at four months, for his first child development check. It is clear that M already had some concerns about her son's general development. Alfie's smile had become less frequent, he was sleeping to an extent that had begun to alarm her and quite commonly she had to wake him up. She was concerned too with Alfie's lack of general interaction and disinclination to reach out for or play with his toys. I sense also that M considered that the squint was something rather more serious. She queried Alfie's ability to see. It is apparent that concern was shared by others, the health visitor was troubled by Alfie's lack of age-appropriate head control.
By six months of age there was no doubt that Alfie was showing marked signs of significant developmental delay. He was reviewed in the general paediatric outpatient clinic in Alder Hey Hospital in November 2016. On examination he was there found to be functioning in a range appropriate to a six week – 2 month old infant. An MRI brain/spine scan was arranged for 30 November 2016. The report of Dr M, a Consultant Paediatrician, specialising in intensive care medicine, records the following:
“The MRI brain scan done on 30.11.2016 showed evidence of borderline delayed myelination for his chronological age and unexplained diffusion restriction along sensory motor cortex, the cortical-spinal tracts and fibres leading into the medial temporal lobes. The appearances were not typical for any specific disorder. Suggested possible diagnoses to be excluded included mitochondrial disorders and non—ketotic hyperglycinaemia.”
On 14 December 2016 Alfie was admitted to Alder Hey Accident and Emergency Department with a history of coughing, high temperature and a reported episode of rhythmic jerking of all four limbs and his jaw. His parents reported that this episode had lasted approximately 20 minutes, after which Alfie had a sleep. He was taken to Accident and Emergency about 20 minutes after the episode. The following is recorded in the paediatrician's report:
On review in the Accident and Emergency Department, Alfie was noted to have a temperature of 38.4°C (normal body temperature 37°C) and he was tachypnoeic (fast breathing rate) with a breathing rate of 60 breaths per minute. (The normal breathing rate for this age is 20 – 30 breaths per minute). He had moderate increased work of breathing with signs on auscultation (listening) to the chest of wheeze and scattered crepitations (crepitations are heard with secretions in the lungs). A microbiology test on a nasopharyngeal aspirate (NPA) showed rhinovirus/ enterovirus. (The test cannot differentiate these two organisms — infection could be with either or both pathogens). We commonly isolate these viruses in infants with acute viral lower respiratory tract infections. Alfie was diagnosed with acute viral bronchiolitis and a possible prolonged febrile convulsion.
Later in the afternoon Alfie was observed to have episodes of jerking of his whole body and referred to the Neurology team. An EEG was requested and the plan was to commence anti-convulsant therapy if the seizures worsened. On 15 December 2016 the seizures continued to the degree that it was thought necessary to prescribe Midazolam which is a benzodiazepine which is, I am told, a first line drug. This was administered for Alfie via the buccal route (placed against the inside lining of the cheek) which enables rapid absorption for patients who do not have an intravenous cannula. The medical records reveal that the seizures stopped after two or three minutes and Alfie slept.
There were more problems overnight on the 16 December 2016 and after discussion Alfie was commenced on a different anti-convulsant, Vigabatrin. On the 19 December Alfie was reviewed by Dr R, a consultant in paediatric neurology and on examination was found to have a slow breathing rate, apnoeas (pauses in breathing) and his most significant identifiable neurological response was to pain. The plan was to transfer Alfie to the High Dependency Unit for non-invasive respiratory support. Whilst preparing for this Alfie's condition deteriorated significantly, his heart rate dropped and the periods of apnoea became more prolonged. A cardiac arrest call was made and bag-mask-valve ventilation was commenced to support his breathing.
When the cardiac team arrived, the anaesthetist took over management. Nasopharyngeal and Guedel airways (an oral airway adjunct to maintain or open a patient's airways) were inserted and Alfie was given oxygen via a mask. In addition the plan to admit Alfie to HDU was abandoned and he was transferred to the Paediatric Intensive Care Unit (PICU). Dr R has given a summary of this period in a statement filed in this Application. It requires to be stated in full:
“I saw Alfie with his parents on the 15 th December 2016. He showed sudden unprovoked movements compatible with infantile/epileptic spasms. An EEG performed on the 16 th December 2016 confirmed hypsarrhythmia (electrical correlate to clinical epileptic or infantile spasms, disorganised EEG). The EEG captured a number of electro-clinical epileptic spasms. I commenced Alfie on Vigabatrin (anti-epileptic medication, first line treatment for infantile/epileptic spasms) with an increasing dose regime as per standard practice. Alfie did not show any neurological recovery following the severe respiratory deterioration and critical life threatening illness on the intensive care unit. Alfie showed signs of a severe infantile progressive encephalopathy with drug and ketogenic diet resistant seizures. He remained profoundly encephalopathic/ comatose and remained unresponsive to central noxious stimuli (i.e. painful/ uncomfortable stimulation delivered via rubbing of cranial nerve exit points in the area of his eyebrows). Encephalopathy is a general term that refers to brain malfunction due to brain disease or brain injury. The major symptom of an encephalopathy is reduced responsiveness or an altered mental state. Epileptic seizures and a movement disorder can also be a symptom of an encephalopathy. There are numerous causes for an encephalopathy in childhood. They include infections, brain malfunction due to lack of oxygen or reduced blood flow, metabolic and biochemical conditions, toxins, drugs, trauma, and neurodegenerative diseases. At times Alfie showed withdrawal of his legs to peripheral noxious stimuli (ie applying pressure to his nailbeds) and presumed spinal reflexes. This means that information of painful stimuli travel up the nerve, enter the spinal cord in the back and stimulate a motor response, i.e. withdrawal, extension or flexion, via exiting immediately through the frontal nerve roots in the spinal cord without being modified from central “higher” nerve cells in the brain. Similar to our immediate withdrawal to for example, touching a hot cooker plate, when we withdraw our fingers long before we realise there is pain. The majority of responses to tactile stimuli or to eye opening/light exposure were and are seizures as confirmed on repeated EEG examinations.”
A further EEG was performed in January 2017. This, however, was markedly different, showing attenuation with little in the way of reactive response for protracted periods of time. Changes only really occurred when Alfie had an epileptic seizure. Though there was no period of collapse between December and January all are agreed that Alfie was very unwell with a severe bi-lateral pneumonia. It was at this time that the treating clinicians thought it both necessary and appropriate to broach with the parents the real possibility that Alfie might not recover. In fact Alfie did not...
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