Derbyshire County Council v A Mother and A Father [2013] EWHC 1864 (Fam)

Case No ER12C00080[2013] EWHC 1864 (Fam)
IN THE HIGH COURT OF JUSTICE
FAMILY DIVISION
Venue Birmingham Civil Justice Centre,, 33 Bull Street, Birmingham B4 6DS.Date 25/06/2013
Before
MRS JUSTICE KING DBE
Between
DERBYSHIRE COUNTY COUNCILApplicantA MOTHER1 st RespondentA FATHER2 nd Respondent
Tape Transcription by Marten Walsh Cherer Ltd.,1 st Floor, Quality House, Quality Court, Chancery Lane, London WC2A 1HP.Telephone No: 020 7067 2900. Fax No: 020 7831 6864
MR A HAYDEN, Q.C. and MR G SEMPLE, of counsel, appeared for ApplicantMISS KNOWLES, Q.C. and MISS HEALING, of counsel, appeared for First RespondentMISS CHEETHAM, of counsel, appeared for Second RespondentMISS ROGERS, of counsel, appeared for younger childrenMISS BUDDEN, of counsel, appeared for older children
JUDGMENT
[1]These are care proceedings concerning the children of the mother & the father.[2]This hearing centres around, but is not exclusively concerned with the children A & O. O has quadriplegia, secondary cerebral palsy and is visually impaired. A is in no way disabled, although he has been exposed to frequent invasive medical treatment, which has meant that he has been artificially fed throughout his life and has spent protracted periods of time in hospital.[3]During the course of children’s lives there has become increasing concern that the mother was misrepresenting the state of A’s health to medical professionals in order to gain greater treatment for him than was necessary or in order to obtain various resources. The mother now accepts that this was in fact the case and the concessions she has made are set out in the agreed threshold criteria.

Events leading up to the Proceedings

[4]A was admitted to hospital on 8th of June 2012 with a suspected infection of his right thigh. He remained an in-patient for a number of weeks. On 1st of July 2012, and again on 6th of July 2012, blood tests revealed an unexpectedly high level of sodium in A's blood. The usual cause of such high sodium levels is dehydration and on each occasion it was felt by the medical team that A was showing no clinical signs of dehydration. The consultant nephrologist was concerned, therefore, that the only alternative cause of the elevated sodium levels was that salt had been administered to A by a third party.[5]Against that backdrop care proceedings were issued by the local authority on 10th of July 2012. A decision was rapidly reached that a finding of fact hearing would be required in these proceedings to determine the cause of the hypernatremia. Pending such a hearing, the mother moved out of the family home, the children having remained at home in the care of the father, assisted by the grandmother.[6]As part of the preparation for the hearing, two reports have been prepared by Professor Anne Mortimer, consultant psychiatrist who, following inspection of the mother's medical records and clinical assessment, diagnosed her as having suffered from Somatization disorder, which is defined as:
"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."
[7]Dr. Mortimer also found that the mother's medical history was "incontrovertibly consistent" with a diagnosis of fictitious disorder. The medical records identified:
"An extensive history and presentation of foreign bodies, burns and somewhat mysterious wounds that heal with great difficulty."
[8]The mother accepts the conclusion of Professor Mortimer's report so far as the diagnosis, briefly set out above, is concerned.

The Law

[9]The relevant law is well established. In summary: 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.[10]In the present case the allegation in relation to salt poisoning depends largely upon expert medical testimony. I remind myself, therefore, that in W v. Oldham MBC [2006] 1 FLR 543 and Webster v. Norfolk County Council [2009 EWCA (Civ) 59. Lord Justice Rose stated that: "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.”[11]Ward LJ considered the balance as between the judge and expert in Re B (Care: Expert Witnesses) [1996] 1 FLR 667 at 670 and said: '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.[12]In the early months following his birth and discharge home A became seriously anaemic due to iron deficiency. This required blood transfusions and intravenous iron. He lived with a nasogastric tube in place, but the mother said that he frequently pulled it out and wished instead for there to be an insertion of a gastrostomy, which would allow him to be fed directly into the stomach. This was done on 7th of July 2009.[13]The excellent medical chronology prepared by Mr Semple (junior counsel on behalf of the local authority) shows A's constant referrals to doctors and hospitals. By 14th of April 2011, (by which time A was rising three), there were serious concerns being expressed by various health professionals about the constant referrals and about the mother's behaviour in relation to A's health.[14]A professional's meeting was convened at hospital which highlighted what were felt to be the mother's exaggerations in relation to A's medical needs and well-being and they questioned the continuing need for a gastrostomy.[15]On 8th of June 2012 A was again admitted to hospital. Dr S, the consultant paediatrician at the hospital prepared a report about this admission and described it as follows:
"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."
[16]Dr S then went on to describe his progress and continued:
"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."
[17]Dr T, consultant paediatric nephrologist, was asked for his opinion, which opinion is set out in a letter dated 24th of July 2012. In the report he deals with A's presentation on 1st of July 2012 and on 6th of July 2012. He says:
"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."
[18]In relation to 6th of July he said:
"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."
[19]It is in relation to these two periods of hypernatraemia that the court is concerned. Parameters of Investigation[20]A, therefore, in July 2012 had had two episodes of acute hypernatraemia. That is to say, episodes where his plasma sodium reading (or salt level) was found to be abnormally high. On each occasion A was an in-patient at hospital. There are, undoubtedly, questions as to whether A's admission and continued stay in hospital at this time was in some way caused or contributed to by the actions of his mother. The court has heard no evidence about this and this judgment deals only with the single issue of whether A's hypernatraemia on those two occasions was caused by the mother poisoning A with salt. The mother has not been called to give evidence and I have been invited to decide the issue on the basis of the medical evidence alone.[21]Given the substantial concessions the mother has made in respect of her inappropriate behaviour in relation to the medical issues concerning A and O, and her acceptance of the entirety of the report of Dr. Mortimer, this is the approach that the parties invite me to take and I agree that it is indeed an appropriate way to proceed.[22]For the purposes of these proceedings Dr Malcolm Coulthard was asked to consider the issue of salt poisoning. Dr Coulthard is an Honorary Consultant Neuphrologist at the Royal Victoria Infirmary in Newcastle. Dr Coulthard has a special interest in the diagnosis of, hypernatrenia of and the safest treatment regimes for hypernatraemia in babies and children and, in particular, as to how to distinguish salt poisoning from other causes.[23]Together with Professor Haycock Dr. Coulthard was involved in 2009 in the production of evidence-based guidelines entitled The Differential Diagnosis of Hypernatraemia in Children with Particular Reference to Salt Poisoning. Those guidelines, co-written by Dr Coulthard, have been referred to by all the physicians considering A's case.[24]Dr Margaret Fitzpatrick, Consultant Paediatric Pathologist at the Paediatric Neuphrology Unit in Leeds, has also prepared a report and given expert evidence in this case. Dr Fitzpatrick’s, expertise, she told the court, is more clinically based than that of Dr Coulthard and she would not seek to suggest that she has a level of expertise of Dr Coulthard in relation to salt poisoning. She relies heavily on the guidelines devised by Dr Coulthard and regularly deferred to his enhanced expertise.[25]As the views of Dr Coulthard and Dr Fitzpatrick largely, but not entirely, coincide, it is not necessary for the court to analyse the entirety of the complex medical evidence in the case. In failing to do so it should not in any way be thought that the court is disregarding the immense amount of work carried out by Dr Coulthard and Dr Fitzpatrick and the court is especially grateful to Dr Coulthard for the lucid and accessible way in which he explained what is a very complex subject. His evidence was undoubtedly of benefit not only to the court but also to the parents as they struggle to understand what happened to A.[26]Dr Fitzpatrick and Dr Coulthard had an expert meeting, conducted by telephone. On 16 May 2013 following which their views were reduced to a schedule of agreement and disagreement. Put shortly, both experts are of the opinion that the second episode (6th of July) of hypernatraemia was caused as the result of salt poisoning. In relation to the first episode on 1st of July, Dr Coulthard is equally convinced. Dr Fitzpatrick, however, expresses reservations.[27]With respect to Dr Fitzpatrick, it was somewhat difficult to record with precision the cause of what she described as her "lack of certainty". By piecing together her report, comments in the expert's meeting and her oral evidence in relation to episode one, it would seem that she felt significantly handicapped by the absence of urine chemistry or weight calculations and that although she is able clinically to exclude severe dehydration, she feels there is insufficient clinical data to be confident about a diagnosis of salt poisoning.[28]The absence of this clinical data (required by the guidelines), together with the fact that A was on intensive care at that time and, therefore, by definition an unwell child, created for Dr. Fitzpatrick the degree of uncertainty, particularly where the sodium reading was 155 on 1 July and therefore elevated although not by the dangerous levels seen on 6th of July. Dr Fitzpatrick was unable to give the court an alternative unified diagnosis, but said she thought the elevated sodium level seen in A on 1 July was “multi-factorial.”[29]At the conclusion of her evidence Dr Fitzpatrick said that salt poisoning was a possible diagnosis. The data did not, she conceded, point to a significant dehydration and, really, she said, the difference between herself and Dr Coulthard came down to "shades of uncertainty". She remained troubled by the absence of some clinical data. Hypernatraemia: a Starting Point[30]The normal plasma sodium concentration in a child of A's age is 135 to 145. On 1st of July 2012 his plasma sodium level was found to be 155 and on 6th of July 167, the latter being very dangerous level which could undoubtedly have been fatal.[31]There are three possible causes for hypernatraemia: i) Malfunctioning kidneys. ii) Too much salt. (salt overload). iii) Not enough water. (dehydration).[32]A's blood and urine samples confirmed that he has normal kidneys.[33]In order to decide which of the two remaining causes - salt overload or dehydration is the cause of the elevated plasma sodium - the doctors have to consider the following matters: 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.[34]Before looking at the two Episodes against each of the four matters it is helpful to understand in simple terms the biochemistry and recovery process as they are seen respectively in dehydration and salt overload.[35]A number of biochemical measurements are of assistance to doctors and neuphrologists in deciding whether a child is dehydrated or overloaded with salt:(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.[36]The period of recovery marks the most dangerous phase for a child who has been poisoned with salt. A child who is dehydrated responds in an entirely different way from a child who has salt overload. A dehydrated child will desperately hang on to what salt he or she has in their body. As a consequence, there will be little or no urine voided by a dehydrated child and the normal treatment would be to catheterise the child in order to measure the urine accurately by weight and a clinician “would hope” (as Dr Coulthard put it), for a few mls to be voided.[37]The opposite happens with a child who is salt overload. Such a child will void copious amounts of urine as their body struggles to get rid of the salt. In Episode One timed volumes of urine were recorded and can, (give or take a10% allowance for error), give a value of mls per kilogram per day of urine.[38]No urine was collected after Episode Two, but Dr Coulthard was nevertheless able to calculate A's fractional excretion rate (FEs); this is a measure used to understand how kidneys are responding to a clinical situation by calculating whether they are actively conserving or excreting large amounts of either water or sodium.[39]Having calculated fractional excretion values for both water and sodium, Dr Coulthard was able to extrapolate from the results the quantity of urine A was voiding in the hours following the discovery of his elevated plasma sodium on 6th of July 2012.[40]The Two Episodes of Elevated Plasma Sodium: Episode One.[41]In episode one the plasma sodium concentrate was 155, the equivalent, if it was salt overload, of 2.5 teaspoons of salt. History.[42]At this time A was on the PICU awaiting further surgery to put a PICC line in place. He was seen at 22.40 hours by Dr U at the nurse's request and in the presence of the mother. His well documented examination did not reveal any signs of dehydration and his observations were normal. Dr U considered that he had a flow murmur of his heart, which he took to be secondary to his anaemia. An intravenous line was erected and he was prescribed a bolus of 0.9 saline of 20 mls a kilo. That is to say, 320 mls, which was administered over twenty minutes. A blood sample, which was taken at 23.30 showed the elevated plasma sodium already referred to.[43]The examination also disclosed that at 16.20 A had vomited a large amount of undigested food and fluids and that he'd had three large, loose bloodstained stools from 21.30 and was continuing to vomit.[44]Dr Coulthard having considered this history concluded: 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.[45]A’s weight was not recorded before or after the discovery of his hyperactivity.[46]A's EGFR and plasma bicarbonate concentration were normal throughout Episode One and his plasma chloride was elevated. All of which tests militate against dehydration being the cause of the increased plasma sodium.[47]No urine chemistry was carried out or rates taken, both of which form part of the guidelines for identifying salt poisoning. Recovery from Episode One.[48]The timed urine loss was 175 mls per kilogram per day, compared to a normal rate of 60 mls per kilogram per day. Dr Coulthard called this:
"An enormous amount, two or three times the amount you would expect in a boy of this age."
The modest amount of fluids A had had administered via the bolus could not possibly account for it and, said Dr Coulthard, is inconsistent with the same bolus being desperately needed in the body if he had in fact been dehydrated.[49]When giving her evidence Dr Fitzpatrick said that she felt uncertain of the relevance of the heart murmur and was concerned by the absence of urine chemistry and the evidence of weight. A, she said, was unwell and in intensive care and had been given fluid so fluid management could have affected the plasma sodium level.[50]Dr Fitzpatrick accepted Dr. Coulthard's biochemical calculations and the relevance of the data. She also agreed there was no kidney abnormality. She would not, however, agree that in a sick child choleric loss (in the form of diarrhoea) would be necessary in order for there to be plasma sodium of 155.[51]Dr Fitzpatrick agreed that Dr U's description points away from dehydration and the fact that he passed a great deal of urine also points away from dehydration, even with the bolus.[52]In conclusion, Dr. Fitzpatrick said, that she was not saying the elevated reading was caused by dehydration, but that it could be multi-factorial with a degree of water loss. Salt poisoning, she said, “is a possible diagnosis, but before you make it you need the information.”[53]Whilst Dr Coulthard has a greater understanding of the physiology of salt poisoning, she said, there was no urine chemistry and no weights, both of which are required by the guidelines and, as a clinician, she would not make the diagnosis on the basis of the information available. Episode Two.[54]The second episode, the plasma sodium was 167, the equivalent of four teaspoonfuls of salt. History/Clinical[55]On 5th of July the medical notes record A as having been moved out of his cubicle to the high observation area of the open ward with the arrangement that he would remain, with his curtains open, to allow the nurses to see him. This was done in the light of the safeguarding concerns which were held about the mother's actions and behaviour in regard to A. The notes record the mother being “stressed” and of drawing the curtains around A, despite being asked not to do so. The records further show her threatening to take A home, against medical advice, and of her actually taking him out of the ward.[56]A pragmatic decision was made by the medical team that in order to ensure that A stayed on the ward that A should be, would be moved back into the cubicle once again with the mother. The following morning A was examined by cardiology and ward doctors. He was well and stable with only a mild sinus bradycardia. In the morning and early afternoon he had seven small diarrhoeal stools, amounting to only 300 mls and a single vomit. His pulse slowed and so a blood test was taken and that revealed his plasma sodium at 167. Clinically, therefore, A had been well and the diarrhoea and vomiting in the morning, too little and too late to have caused even mild hypernatraemia due to dehydration.[57]Once again, there was no evidence of weight change available. Biochemistry.[58]Once again, A's EGFR is normal and had not fallen, as it would have done had he been dehydrated. His plasma bicarbonate was also normal and plasma chloride was elevated, again consistent with salt overload rather than dehydration. On this occasion a urine sample was taken and a fraction excretion of sodium calculated from the urine sample and the blood sample, as opposed to a blood sample alone, as in episode one) and was approximately 2%. This, it was agreed by both Dr Coulthard and Dr Fitzpatrick, is not in keeping with severe dehydration when the FE would be generally less than 1% and is consistent with the kidneys actively trying to excrete salt rather than conserve it.[59]The plasma sodium level returned to the normal range within twelve hours after commencing administration normal and of thereafter half normal saline and both experts agree that it would not usually occur so quickly in a child with significant hypernatraemia dehydration. Recovery.[60]Although A's urine was not measured after the second episode, Dr Coulthard was able to estimate the volume by reference to the fractional excretion values and, once again, they showed a very high volume of urine voided, 175 mls per kilogram per day as against the norm of about 60. Those computations are supported by the medical notes, which record "PU +++" indicating that A was passing large volumes of urine which would be inconsistent with dehydration. The Mother’s case.[61]Miss Knowles, Queen's Counsel (on behalf of the mother) properly tested the evidence of Dr Coulthard, although given the significant degree of consensus between Dr Coulthard and Dr Fitzpatrick she was, necessarily, somewhat limited in how much challenge she could mount.[62]In particular, Miss Knowles drew the court's attention to what were, clearly, a number of inconsistencies in the record keeping within the medical notes and, in seeking to undermine the powerful evidence in relation to A's urine output on both occasions, emphasised the fact that urine output had not been measured on the second occasion.[63]Dr Coulthard's evidence was that there was roughly the same margin of error (10%) regardless of whether you measure the urine output or carry out the calculations by reference to FE values. Dr. Fitzpatrick took no issue with any of Dr Coulthard's calculations. Conclusions.[64]I bear in mind how serious the allegations are in this case. In considering the medical evidence I take into account that in neither episode was all the data available which would, ideally have been available under the guidelines and that the absence of that data (and particularly the urine chemistry and lack of weights) has left Dr. Fitzpatrick with a sense of unease in relation to the first episode.[65]I also bear in mind that in an e-mail dated 17th of January 2013 when Dr Coulthard had skim-read the medical records but had not carried out a detailed analysis, he said:
"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."
[66]When asked about his change of view, Dr Coulthard explained that she initially could not see how A could possibly have been given salt in circumstances where she was on each occasion under observation in hospital. She said that salt tastes “horrible” and A, would have kicked, struggled and resisted very vocally to being given it to drink. He would, in all likelihood Dr. Coultard said, also have vomited.[67]Whilst Dr. Coulthard had seen in the notes that A had had a gastrostomy as a very young child, not unreasonably, it had not occurred to Dr Coulthard that he still had one in place by July 2012. Dr. Coulthard told the court, that once he appreciates that A still had a gastronomy in place and so salt could have been dissolved in a small amount of water at room temperature and thereafter simply put into the gastrostomy tube, he was certain that that was the explanation.[68]I accept Dr Coulthard's explanation for his seeming change of view and note that he at no time expressed any doubt about the cause of the readings being salt overload rather than dehydration.[69]In my judgment both episodes of hypernatraemia were caused by the mother putting salt into A's gastrostomy tube. I am satisfied in relation to the first episode, notwithstanding Dr Fitzpatick's anxiety about it, which I judge to be based largely upon her reluctance to rely on the undoubted and unequivocal clinical and recovery picture in the absence of all the chemical data advocated by the guidelines. I bear in mind that they are guidelines and not mandatory and that whilst I look at each episode separately, I also look at it in the context of the bigger picture, namely the mother's overall behaviour as conceded by her, and by the fact that she, undoubtedly, poisoned A five days later by the same means.[70]I bear in mind also that Dr Fitzpatrick is, as she made clear to the court, primarily a clinician and appropriately cautious thereby in making such a serious diagnosis where all the data the guidelines recommend are not available.[71]Dr Coulthard, however, has the specific expertise and depth of understanding of the physiology of elevated plasma sodium levels which allow him to diagnose salt poisoning (taking into account all the elements considered above, and by the use of alternative calculations) in order to ascertain the necessary biochemical data and make a diagnosis to the appropriate standard of proof notwithstanding the absence of a complete urine profile and weights.[72]I am satisfied, therefore, that Dr Coulthard is able to diagnose salt poisoning, notwithstanding the absence of all the guideline data.[73]I am, satisfied, on the balance of probabilities, that the mother administered salt to A on both occasions.