FAMILY DIVISION
33 Bull Street, Birmingham B4 6DS. |
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B e f o r e :
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DERBYSHIRE COUNTY COUNCIL |
Applicant |
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A MOTHER And A FATHER |
1st Respondent 2ndRespondent |
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1st Floor, Quality House, Quality Court, Chancery Lane, London WC2A 1HP.
Telephone No: 020 7067 2900. Fax No: 020 7831 6864
MISS KNOWLES, Q.C. and MISS HEALING, of counsel, appeared for the First Respondent
MISS CHEETHAM, of counsel, appeared for the Second Respondent
MISS ROGERS, of counsel, appeared for the younger children
MISS BUDDEN, of counsel, appeared for the older children
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Crown Copyright ©
MRS. JUSTICE KING DBE:
Events leading up to the Proceedings
"A disorder comprising a history of many physical complaints, beginning before the age of thirty-years, occurring over several years, resulting in treatment seeking or significant impairment in function."
The Law
i) The burden of proof lies on the local authority.
ii) The standard of proof is a simple balance of probabilities, neither more nor less. Re B UKHL 35 [2008] FLR 1413.
iii) The inherent probability or improbabilities are simply something to be taken into account, where relevant, when deciding where the truth lies.
iv) Medical evidence needs to be considered in the context of all the evidence and against the backdrop of all circumstances, often called the broad canvas.
"In a child case involving complex and serious injuries the expert evidence has to be carefully analysed, fitted into a factual matrix and measured against assessments of the witness's credibility. To achieve justice for parents and for children medical evidence given in court is tested fully by the advocates, the family judges and subjected to rigorous analysis."
'The court invariably needs and invariably depends on the help it receives from experts in this field … The experts advise but the judge decides. The judge decides upon the evidence. If there is nothing before the court, mere facts or no circumstances shown to the court which throw doubt on the expert evidence, then that is all with which the court is left, the court must accept it.'"
Events Leading up to the Care Proceedings.
"A was brought to PEB at the hospital by his mother on 8th of June with concerns about pain in his left thigh. Mother stated that he had been referred to the orthopaedic team by the orthopaedic team at another hospital. This was not the case. A had attended that hospital where the orthopaedic team had suggested some investigations and management and mother had discharged A against medical advice. A was found to have tender swelling of his left thigh but was otherwise well. This was felt to be a localised infection and he was commenced on antibiotics. On the evening of 9th of June he became unwell and had an episode of apnoea. He was transferred to the paediatric intensive care unit for further management in the early hours of 10th of June. He was intubated and ventilated and required medication to help his profusion and blood pressure. It was felt that this was compatible with serious infection at the septic shock. He went to theatre for further exploration of his left thigh, but no pus was found. His condition improved and he was extubated on the morning of 13th of June and went back to the ward."
"On the morning of 6th of July his heart rate was about 60 ml and the PICU Team reviewed this. He was otherwise well and this was monitored at about 18.00 hours, it was returned to 90 to 100 beats per minute and has been normal ever since. He has since had a twenty-four hour ECG, which was normal. Due to bradycardia he had blood tests done on 6th of July. These showed an unacceptably high sodium level, NA 176, this had been normal the previous day."
"On 1st of July, when in ICU, A was kept nil-by-mouth as he was due to go to theatre for a procedure. He had a plasma sodium of 155, which is high. The medical records also suggest he was vomiting around this time. Therefore, one would assume that he could have been dehydrated. However, there were no increases in his urea or creatinine, which would be expected when someone is dehydrated. He was not weighed and no urine electrolytes were measured and, therefore, it is not possible for me comment on why he developed hypernatraemia."
"On 6th July morning there were no concerns regarding A's low heart rate. The nurse looking after him has documented that A had two loose stools that morning. Although he had a heart rate of 55 beats per minute, he was looking well and eating and drinking. A junior doctor reviewed him at 12.45 hours and noted that A appeared well; had a BP of 120 over 80, which is slightly elevated, and was warm and well profused. All this suggests that he had no clinical signs of moderate or severe dehydration. He was commenced on 0.9% saline and 5% Dextrose, sixty-eight ml per hour, which is more than his calculated for maintenance. Blood tests were performed because of the low heart rate at 14.00 hours and this showed severe hypernatraemia in a one sixth second. His urea and creatinine were low normal. Although he had further episodes of loose stools, his fluid balance charge showed input at 608 mls and output of 526 mls of urine. Following the blood results showing severe hypernatraemia he was reviewed by the same junior doctor who, once again, noted that A appeared very well and did not have any signs of dehydration. The blood test was repeated. His plasma sodium had improved. His urine sodium this time was 312 mls. The fractional excretion of sodium was 1.8 which suggests he was actively trying to excrete salt and not conserve salt as avidly as a child with severe dehydration would be expected to do. The plasma sodium came back to normal within ten hours of commencing intravenous normal saline and 0.45 saline, a little more than full expected maintenance, which would be unusual for a child with severe hypernatraesion dehydration."
Parameters of Investigation
Hypernatraemia: a Starting Point
i) Malfunctioning kidneys.
ii) Too much salt. (salt overload).
iii) Not enough water. (dehydration).
i) The history and clinical examination of the patient at the time.
ii) Weight loss.
iii) Biochemistry.
iv) How the patient recovers from the high salt levels.
(a) Plasma creatinine is used to measure an aspect of kidney function. A's highest reading at the estimated normal glomerular filtration rate, (eGFR) (which measures plasma creatinine), would be 80. It is common ground that the eGFR consistently falls during dehydration in children.
(b) Plasma sodium. As already noted, the normal range is 137 to 145. A's was 155 and 167.
(c) Plasma bicarbonate concentration is reduced in cases of dehydration and remains normal with salt overload.
(d) Plasma chloride: Increased levels indicate that increased sodium levels are due to an increase in sodium chloride or common salt.
(e) The urinary chemistry results disclose the level of salt. In A's case they were not taken in respect of Episode One, 1 July 2012 but were for Episode Two 6 July 2012.
Episode One.
History.
i) that the diarrhoea was not anything like as profuse as it would need to be for dehydration. In evidence Dr Coulthard talked about the dramatic and catastrophic levels of diarrhoea which would have been necessary in order for A to have had the degree of dehydration necessary to result in the elevated salt level seen. He equated the level of diahorrea with that seen with cholera, "floods of diarrhoea filling the bed" continuing over several days. He would expect diahorrea of a type not seen in the UK where children have ready access to medical care and are, therefore, treated before they get into that state. The episode of vomiting and diarrhoea, he said, was too brief and too late in time for the hypernatraemia to have been developed.
ii) Dr Coulthard regarded the murmur, heard by Dr U, as being indicative that he was not dehydrated, as it showed full circulation and volume of blood, whereas, inevitably, dehydration necessarily results in a significant reduction in blood volume and, therefore, it would be unlikely that a full circulation would have been heard.
iii) Dr Coulthard did not think that the 20 mls per kilogram bolus of normal saline would increase his plasma sodium above normal as it was a small volume relative to the body weight and the sodium concentrate in normal saline is 154. That is to say, below the value of 155 in his blood.
iv) A's haemoglobin was low at 8.8 and if a child is dehydrated the haemoglobin goes up as the blood becomes more concentrated
v) Dr U (it was agreed between both Dr Coulthard and Dr Fitzpatrick) had carried out an unusually careful and thorough examination for such a junior doctor and Dr U saw no clinical signs of dehydration, such as sunken eyes, grey skin, dry skin and mouth and cold hands and feet.
Recovery from Episode One.
Episode Two.
History/Clinical
Biochemistry.
Recovery.
The Mother's case.
Conclusions.
"What is absolutely clear is that A's episodes of hypernatraemia … were due to him developing a salt overload without dehydration, but I am about 90% certain that this was due to his acute illness at a time combined with his medical fluid management and not due to the deliberate administration of salt."