Commentary
Having written in Hospital Update, 48 years ago, about routine parenteral thiamine alongside prophylaxis or treatment of alcohol withdrawal symptoms, I read this with great interest. It should be of interest to physicians and psychiatrists but what is striking are the lessons for all experts. There is a long section in which the judge is critical of some of the experts and their evidence.
Learning points
An expert's credibility is less dependent on preparing a flawless report than demonstrating the qualities expected of an expert witness, including:
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meticulous preparation,
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careful review of all relevant evidence,
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logical and transparent reasoning,
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familiarity with authoritative guidance,
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prompt correction of errors,
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willingness to make fair concessions,
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avoiding speculation,
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respecting contemporaneous evidence, and
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maintaining independence and humility.
The judge in this case observed that errors and omissions are understandable in a complex case. However, what most influenced the court's assessment was the experts' response when those errors were exposed.
Lessons for experts
The case offers several important lessons for experts, particularly experts who provide evidence in areas where the scientific literature is limited or evolving.
The key lesson is that expert evidence must be case-specific, evidence-based and proportionate to the strength of the available science. Rather than simply demonstrating that a mechanism is possible, an expert must explain how the evidence supports or undermines that mechanism in the particular circumstances of the case. Where an opinion depends on rare events, limited literature or personal experience, the expert should be especially careful to disclose limitations and avoid overstating certainty.
Case
The Claimant in this clinical negligence claim is now a 47 year old man who has developed functional neurological disorder ("FND") and functional cognitive disorder ("FCD") and a depressive disorder. There was no dispute that these give rise to profound physical disability and also functional cognitive and memory disorder. With minor differences, the consensus was that the prognosis was bleak for any meaningful improvement.
The issue in this case was how the Claimant came to have those conditions and whether they are related to the Defendant's admitted breach of duty. It was accepted by the Defendant that when the Claimant was admitted to its Freeman Hospital for treatment of a facial lesion, in August 2016, the Defendant failed to administer a course of prophylactic thiamine (vitamin B1) in the form of Pabrinex, given he was a known alcoholic being treated with chlordiazepoxide for symptoms of withdrawal from alcohol.
The Claimant's case was that the Defendant's breach caused him to develop thiamine deficiency which caused a Wernicke's encephalopathy ("WE"), and then a disabling functional disorder affecting him physically and cognitively, and giving rise to major reactive depression.
The Defendant did not materially dispute the Claimant's current condition but denied causation. Its case was that the symptoms arose coincidentally or more likely were pre-existing, but worsened markedly, albeit unrelated to the failure to administer thiamine. As part of that denial, the Defendant also disputed the notion that the Claimant ever developed WE.
Medical records
Prior to the events in question, the claimant’s medical history was characterised by long-standing poor mental health, chronic alcoholism, spinal surgery in 2006, surgery to the right knee in 2011 and some left leg symptoms, the aetiology of which was not definitively established at the time.
The first pertinent entry is the Claimant's attendance at his GP surgery on 1 June 2016, with his then partner and now wife, Mrs Dickinson. The main focus was the Claimant's ongoing substantial alcohol consumption: 10-20 cans [of lager, at c.2 units per can, so 20-30 units] at the time.
There was some difference between the parties about the level of consumption at the relevant time:
1 June 2016 (as summarised in the preceding para.): GP: 10-20 cans per day.
17 June 2016: alcohol key worker: 8-20 cans daily; shakes and sweats; been drinking like this "for the past year".
18 August 2016: alcohol support worker: had drunk for many years; from 7 cans to 20 cans daily; reduced to 7 "shandys" and 3 cans a day after assessment (presumably after 17 June 2016); but since 18 July (when as will be seen, the Claimant's wife's evidence was that she left home for regular periods to care for her father who passed away a few weeks previously) "increased back to 20 cans daily". This would seem to be the last contemporaneous record of his drinking prior to the day of his admission to hospital on 26 August.
26 August 2016:
i. GP: 9-10 cans per day and awaiting help gradually to reduce
ii. Hospital: 10 cans per day.
30 August 2016: alcohol liaison nurse: 10-year history of daily alcohol consumption at heaviest 20 cans lager daily (40 units), but with work over previous 3-4 months, reduction to 10 cans (20 units).
Other potential indications around the relevant time of the effects of excess alcohol consumption include:
2 August 2016: GP: vomited blood last week; referred for gastroscopy.
30 August 2016: endoscopy: gastric ulcer/erosions at the gastric antrum; generalised gastritis. Oesophagitis was diagnosed and advice given to start proton pump inhibitors (PPI).
5 September 2016: histopathology: report on gastric ulcer biopsy showed appearances in keeping with reactive gastritis.
There was a GP attendance with a left sided facial infection on 23 August 2016 and an attendance at the Emergency Department ("ED") without being seen that day. There was a further GP attendance on 26 August [1367], when a diagnosis of cellulitis of the face was made. On the same day, the Claimant was admitted to the Defendant's Freeman Hospital.
Following that admission, it was appropriately noted that the Claimant was alcohol dependent, would need CIWA scoring (to assess alcohol withdrawal) and chlordiazepoxide. A cannula was inserted but apparently fell out. The Claimant was correctly prescribed Pabrinex, which was mandated under NICE Guidelines to mitigate the risk of thiamine deficiency and WE. But the consensus between the experts, based on the records, is that even the first dose was not properly administered: Neurologists' joint statement "a complete vial of Pabrinex was not given".
In any event, the Defendant agreed no further doses of Pabrinex were administered during the admission and had admitted that this was a breach of duty.
There was nothing of particular significance to note in the first part of the Claimant's time as an inpatient. There was discussion about the Claimant being unable to "vape" on the ward or to consume alcohol. He was documented to be awake and orientated. There was no suggestion in the records of unsteadiness or confusion at this point. He was mobile and off the ward at times. He discussed HIV testing on 27 August.
At 1700 on 28 August, a facial abscess was identified by ultrasound and the plan was for the Claimant to go to theatre. He underwent drainage of the left facial collection that evening. The next day, he continued with antibiotics and a drain was in situ.
On 29 August, the records document the Claimant expressing some concern about how he would cope after discharge without chlordiazepoxide and there was a plan to contact the alcohol liaison nurse.
On the ward round of 30 August, the Claimant felt groggy with pain around the wound. On examination there was no sign of facial weakness, and he was noted to be alert, orientated and eating breakfast. The plan was for a discussion with microbiology regarding antibiotics and with the alcohol liaison nurse, with discharge home "later if no issues".
The alcohol liaison nurse made a detailed record of her discussion with the Claimant at 1000 on 30 August 2016. She noted his history of alcohol consumption (already summarised above). The specialist nurse recorded "no evidence of acute alcohol withdrawal symptoms - some anxiety which he agrees is a chronic condition he manages by "walking his dog" and leaving ward for "fresh air" for an hour or so at a time." The specialist nurse was of the view that his detoxification was nearing completion, and it was not appropriate to discharge on chlordiazepoxide for anxiety. She encouraged engagement with his key worker to sustain his abstinence on discharge. The plan was for discharge when medically fit and CIWA score of less than 8 for 24 hours. In this regard, she advised, "please take into consideration chronic anxiety and agitation associated with his anxiety".
It was noted by nursing staff that the facial drain was removed around 1100 on 30 August, who also recorded in relation to CIWA that "Liam gets agitated which he is scoring on but that is his personality & not his withdrawal". There was a plan for follow up in 3 or 4 weeks after discharge.
On 31 August, it was noted that the Claimant had been for a wander in the hospital grounds. He was seen on the ward round at 0810. No cellulitis or new collection was found. There were complaints of constipation, but no abdominal pain, nausea or vomiting. The gastroscopy results were explained and the plan was for follow up in 3 to 4 weeks. There is no reference to confusion or unsteadiness in this entry. At 0910, the negative HIV result was communicated to him.
At 1240, the following nursing entry was made:
"R/v on ward round. Patient fit for discharge...patient went off ward for 2 [hours?] this morning & on return c/o felt drunk when outside & had to sit down. D/w alcohol liaison nurse who stated that this should not hinder d/c plans. Pt & his partner aware to contact support worker to arrange community follow up. Discharged from ward."
The Claimant was discharged on 31 August at approximately lunchtime and this generated various discharge documents summarising his inpatient stay and advice.
The Claimant's wife described the Claimant's confusion on returning home, becoming upset before going to bed. She described researching the Claimant's symptoms, sitting up all night (of 31 August to 1 September 2016). She says she tried to call the "alcohol liaison officer" but they were not available. She came across a reference to thiamine deficiency, and the condition Wernicke's encephalopathy. There is an account of an untimed telephone call to the ward in which she discovered that the Claimant had not been given his thiamine medication. There is also an untimed call to the GP.
It is not possible to determine the precise timing and sequence of the early clinical contacts on 1 September 2016. Subject to that caveat, there were the following:
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A timed record was made in the Progress Notes, by the alcohol key worker at 1133, who had spoken to Mrs Dickinson and noted matters including:
i. Mrs Dickinson had been "by his side since discharge" and confirmed that he had remained abstinent, with there being no alcohol in the house.
ii. She reported "increasing concern" about the Claimant and "sounded very distressed and concerned on the phone".
iii. She described the Claimant's condition as "like he is 'brain damaged'".
iv. The details she provided were that he could not walk in a straight line, kept falling over and was impulsive.
v. The record confirms that by this point she had informed the GP and spoken to the ward, who apparently advised her to speak to the key worker. The key worker felt this matter was not for them as they were not medically qualified, so recommended telephoning the GP or taking the Claimant to hospital.
vi. There is no reference to WE, thiamine or to Pabrinex, although this differed from Mrs Dickinson's recollection in her witness statement.
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The Claimant was taken for wound care following surgery, but the appointment is not timed, although it would seem to come before the GP's assessment.
i. The nurse also confirmed that the Claimant had not had any alcohol for 6 days. She described him as "very unsteady shaking etc.". Mrs Dickinson had apparently left a message for the key worker. The nurse spoke to the GP.
ii. The GP, the first clinician to see the Claimant after his discharge from hospital, also recorded that the Claimant had had no alcohol. The note of the presentation includes "Hasn't been himself today - confused this morning, dizzy, 'not himself'. Sleepy."
iii. The examination seems to have been normal save for a "mildly ataxic gait". No tremor or ophthalmoplegia was noted.
iv. In terms of diagnosis, the GP wondered "about Wernicke's encephalopathy".
v. There is no documented awareness about the failure to administer Pabrinex during the hospital inpatient stay, at this stage.
vi. It appears that the GP initially prescribed oral thiamine, but later reconsidered and felt that parenteral (not oral) thiamine may be required so telephoned and spoke to Mrs Dickinson. She was then to take him to A&E.
So it was that the Claimant arrived in the Emergency Department ("ED") of The Defendant's Cramlington Hospital at 1920 on 1 September 2016. The ED Assessment Documentation included the following summary at 1950 and a recognition at that point that the Claimant had not been taking thiamine:
"Recent detox while in hospital having an abcess removed. C/o acute confusion and feeling generally unwell. Has not been taking thiamine. Seen by GP today who advised A+E. Acute confusion ?Wernicke"
Medical clerking was documented between 2245 and by 2340 that day. The matters noted included the following:
a. The doctor was told that no Pabrinex had been given during his recent admission to hospital, although chlordiazepoxide had been.
b. The doctor recorded two presenting complaints:
i. Confusion; and,
ii. Balance problem.
c. In the presenting history, a two-day history of "problems with memory/confusion". A rudimentary bedside test of cognition (the six-item screener or "SIS") was undertaken and the Claimant scored 5/6, having wrongly answered as to the day of the week).
d. It was noted that the Claimant felt drunk without drinking.
e. The Claimant complained of his left eye flickering and of paraesthesia (abnormal sensation) in his hands and legs. He had suffered a single episode of faecal incontinence that night.
f. The note relating to the examination of eye movements is not entirely legible, but suggests some blurred vision was reported.
g. The doctor made a note of "cerebellar signs" using the DANISH mnemonic (a test designed to identify signs of cerebellar dysfunction). All appeared to be negative/normal save for a specific note of "Ataxic [with] no heel toe walk". [3]
h. The conclusion of this medical clerking, like the GP, was of "- Possible Wernicke's - Vit B1 deficiency". The plan was to admit the Claimant and amongst other things start intravenous Pabrinex, which appears to have commenced at 0020 on 2 September.
A further medical review was performed by CT1 Shevlin at 0120 on 2 September 2016, so about an hour after IV Pabrinex had started. The presenting complaints were recorded as "confusion, ataxia and paraesthesia in glove & stocking distribution". The Claimant was noted to be feeling a little better. He was described as alert and orientated, scoring 9/10 on another rudimentary test of cognition (forgetting his [sic] address, apparently). The doctor noted that the Claimant's fingertips and toes "still feel tingly". It was recorded that the Claimant was "still ataxic on walking". The working diagnosis was still "? Wernicke's".
A nursing note at 0130 confirmed the Claimant "remains confused".
At 0650, the Claimant "appears less confused this AM..." according to nursing notes [1477]. CIWA scoring started at around 0800.
Dr Bennett, the Consultant, conducted the Post-Take Ward Round at 0935 on 2 September. The presenting complaint was documented to be "confusion & ataxic". The Claimant was noted to feel sore and tired and frustrated by being in hospital. A history recorded "unsteadiness, forgetful and confused, came on over the last few days". He "seemed drunk" and had difficulty walking. An abnormal neurological sign was found on examination; namely left side "past pointing", a clinical sign of cerebellar dysfunction. The Claimant was noted to be "unsteady on standing" and "pins & needles" in both fingertips and toes were highlighted. The Consultant's provisional differential diagnosis was "Vitamin B1 deficiency ? Wernicke's". Of note is that this was the third doctor in hospital consecutively to make this diagnosis, a point discussed further below.
At 1100 on 2 September, ASN Laura Brown had an apparently detailed discussion with the Claimant which she wrote up as follows:
"...Liam settled at present no signs of alcohol withdrawal at present. States abstinence for 8 days, as recently detoxed in hospital. Liam stats a long history of heavy alcohol use 20 cans daily for approx 10 years. Denies any withdrawal symptoms. Is aware of medical condition, long discussion re thiamine + nutrition highlighting the importance to health. Liam is aware of the danger of sudden cessation + implications to health of continuing drinking. He plans to abstain on discharge and engage with key worker Amy at NTRP. Message left with Amy to inform her of admission. Liam lives at home with partner + her two kids aged 13 + 14. Discussed concerns re alcohol dependency and duty of care to social services. Will discuss with Amy when returns call..."
At some point on 2 September a CT head scan was performed which was reported to show normal intracranial appearances [1508].
The next ward round documented was on 5 September 2016, in which Dr Warren noted "Confusion improving" and in a discussion with Mrs Dickinson "explained [the] probable diagnosis of Wernicke's encephalopathy", which was a "clinical diagnosis based on kind of ataxia, ophthalmoplegia, confusion". By this point, Mrs Dickinson was documented as expressing concerns about "memory impairment and neuropathy, which is new". Dr Warren explained that Pabrinex had been started [to be administered] and symptoms might improve but it was likely to take weeks or months rather than days. Mrs Dickinson said she had written a letter of complaint.
A series of physiotherapy appointments between 5 September and 13 September revealed significant ongoing problems with mobility.
On 6 September, the Claimant told the assessing clinician that he was "struggling with physio as cannot remember the commands & steps" required and was concerned Pabrinex had been stopped the previous night. He expressed concern about his memory to nurses at 1110 on the same day. In the same entry there is an update about the referral to children's services "no further action".
On 7 September, physiotherapy could not be undertaken "...In bed, [patient] asked if we could leave it today asked p[atien]t why, p[atien]t pulled sheets over his head and started to cry." The Claimant seemed unable to answer questions other than wanting the physiotherapist to leave. On the same day, the doctors noted that he felt upset about everything that was going on; felt confused, but able to remember the name of a doctor who reviewed him on the preceding day. A discussion was had about WE and his condition.
At the ward round on 8 September, it was noted that the Claimant had been upset on the previous day, was of low mood and wanted "to die". His mobility was limited by burning pins and needles in his legs, like a dead weight. The doctor recorded the following impression: "No clinical evidence of Wernickes, ?cause of [illegible]...if not improvement... MRI spine, May be behavioural [therefore] hold."
On 9 September, the note of the ward round indicates that the Claimant was mobilising to the toilet with a Zimmer and felt very unsteady on his legs. There is reference to a normal neurological examination. The Claimant's frustration about poor mobility was noted.
On 12 September, an elevated ALT was noted and the cause queried, including, "??alcohol over weekend/end of last week as was off ward for period of time...". However, this was later confirmed to be likely secondary to antibiotics (see discharge letter of 14 September.
On 13 September, the Claimant was encouraged to use crutches around the ward rather than a wheelchair.
The Claimant was discharged on 14 September 2016, with the following summary in the discharge letter:
"Presenting Complaints and Clinical Summary
This 37 year old was admitted with confusion, unsteadyness, forgetful. He has a history of alcohol excess. He was very recently discharged by the Freeman ENT team for abcesses (?parotiditis). He was treated with possible Wernickes with a long course of Pabrinex. He was also seen by the alcohol nurse whilst an Inpatient. He improved clinically and was discharged. He was seen by the physio and on discharge could mobilise with crutches and was safe on the stairs. He had some equipment put into his house including rails. His abcesses were still an issue so will be seen by the ENT team on 14/9/16. We noted an ALT of 288 but this is likely secondary to antibiotics. We would be grateful if the GP could check this in 1 week to ensure it is settling. Liam will have an outpatient gastro appointment - date and time TBC.
Diagnosis
Possible Wernickes - high dose pabrinex given
Discharge medication included Thiamine tablets; 100mg x 2 per day orally."
Factual evidence
The Claimant's wife gave oral evidence. There was a witness statement from Ms Valerie Dickinson, the Claimant's mother, but the Defendant did not require her to be tendered for cross-examination. This evidence concerned the claimant’s alcohol consumption and dietary habits prior to the hospital admission and their observations of his physical and mental state over the course of the admission and following discharge.
Expert evidence
The court heard oral testimony from neurologists and neuropsychiatrists.
The claimant’s case, supported by expert evidence was that he had developed WE and subsequently a FND. The defendant’s case was that the claimant had not developed WE and his FND was pre-existing.
A number of unsatisfactory aspects of some of the expert evidence were recognised by the judge.
One expert’s report had no page numbering. He could not explain why he had not discussed the endoscopy report in his report, which was a minor part albeit important. He did not know why he had not included it. He accepted that he had not asked to examine the Claimant and commented "[The Claimant] had never volunteered to do it." This meant he had not been able to ask about his bowel transit and there was no evidence about whether it was increased.
He was taken to the NICE guidelines and it was put to him that a dependent drinker should receive prophylactic oral thiamine irrespective of their nutritional status. He interrupted to say that Counsel was looking at the wrong section. But he then accepted that section 1.2.1.2, indicating the need for oral Thiamine, irrespective of nutritional status if undergoing a medically assisted withdrawal, there being no requirement in that part of the guidance to need harmful drinking or malnourishment (or the risk thereof).
In discussing the diagnoses of ataxia, the expert was sceptical about whether it was actually present and in a form relevant to WE. The Claimant had not been under the care of neurology but under acute physicians. The standard of assessment would not have been to the standard of a neurologist or might not be. He worked a lot with acute physicians and their clinical acumen had deteriorated, with clinicians over relying on tests. Most acute physicians were pretty bad at neurology, although he had no knowledge of the consultant physician in this case. He had no basis to think these doctors do not do things properly.
He was challenged about the brevity of his review of the ward round through to his discharge on 14 September, being dealt with in a few short phrases. He accepted that he may have had some loss of focus there. It was said in his report he had moved very quickly from the conclusion about normal nutrition to concluding that the Claimant did not have WE. He accepted that he was not forensic enough in his analysis at the beginning. But he since had had a lot of information and his opinion remained the same.
Another expert was taken to his report and accepted that saying "at the time of the accident" was an error as this case was not about an accident. At the time the Claimant was 37 not 32 years as stated. It was not intended to be a verbatim note. When challenged on the basis that it was not the Claimant who was studying but his wife, his response was "that is what she told me". Asked to explain what the phrase "foredge waste" meant, his response was "I have no idea what that is." It was put to him that Mrs Dickinson denied using the phrase "very muscled" about the Claimant or that he ate normally and had a good diet. He denied picking those points up from another expert’s report. He did not accept that his report was so riddled with mistakes that one needed to be careful about relying on it. His response was that there would be no reason for him to make those words up and he cannot speak to their accuracy.
He was challenged on the lack of evidence, such as anyone suggesting he smelt of alcohol, in records in relation to his theory about the covert consumption of alcohol after the detoxification. He did not abandon the theory, but said he did not want to overemphasise the point. He did not know whether it had happened.
The judge went on to refer to how it was a complex case with extensive records, so it was not that surprising that all of the experts had made one or two errors. They had also overlooked or failed to mention entries which the other party thought significant. What was instructive for the judge was the contrast between how they dealt with those matters.
One expert made a date error in the JER when he recorded the date of discharge as 30 August, rather than 31 August 2016. He accepted that he did not routinely provide letters of clarification after the JER, but he did in this case and it was dated 23 January 2026. By the time of trial, the parties had agreed it should go into evidence. He said he wanted to correct the error in the date of discharge. He said in the letter that the Counter Schedule "appears to misrepresent my views" about when the Claimant started to suffer FNSD. The judge said that this was probably a poor choice of words which implied blame. When pressed in cross-examination he said that it was a misunderstanding of his view and he wanted to clarify what he had said in the JER to help the Court to understand the progression of this complex condition and explain his view on when it started. That was a sensible concession, properly made, recognising that these were complex matters, but that it appeared his views had been misunderstood and needed clarification. It would have been better if he had recognised this from the outset, but that he did ultimately do so in his oral evidence was to his credit.
By contrast, whilst recognising their eminence and experience as clinicians and expert witnesses, in this particular case the court found the way that two of the defendant’s experts dealt with errors and omissions in their reports and evidence less satisfactory.
The judge felt that one expert had been uncharacteristically less careful than his previous experience of him, in the preparation and presentation of his evidence in this case. There were the odd references to "at the time of the accident", which a proof read would have identified as an error. At one point he tried to refer back to an accidental fall in the medical history, when the reference was clearly to the index admissions in August and September 2016, which had nothing to do with an accident. Rather than accepting that he had probably misunderstood who was studying and that it was the Claimant's wife, not the Claimant, his response was "that is what she told me". Asked to explain what the phrase "foredge waste" meant, his response was "I have no idea what that is." The court found it curious that his response was not to apologise for the error or recognise it as such, but to express his lack of understanding of it. Almost as if it was something in a document which he had not created, let alone put before the Court.
Another expert accepted some sequencing errors and a lack of detail on important parts of the chronology in his report. The expert got the entry about the Claimant being given IV Pabrinex out of chronological sequence, after the 2 September ward round, whereas it was started at 0020. He was challenged about the brevity of his review of the period from the ward round through to his discharge on 14 September, this being dealt with in a few short phrases. He accepted that he may have had some loss of focus there. The judge agreed with the Claimant's observation, put to him, that in his report he had moved very quickly from the conclusion about normal nutrition to concluding that the Claimant did not have WE. He accepted that he was not forensic enough in his analysis at the beginning. His response was that he since had had a lot of information and his opinion remained the same. The judge felt that this lack of rigour in his analysis of the key parts of the chronology was a lacuna in his evidence which deserved greater explanation, rather than a readiness simply to stand behind the confident assertion that nothing he had since seen changed his view. This glossing over of detail and high degree of confidence in his conclusions, notwithstanding a lack of attention to detail, did not sit well with his readiness to undermine the skills and conclusions of the treating clinicians, especially those who were more junior in their careers.
What was surprising was less the making of errors and omissions themselves, as we all can and do make errors and omissions, but the reaction to them being pointed out. This gave an impression of loftiness on the part of the Defendant's experts which gave the judge pause for thought about the cogency of their overall opinions.
Two other aspects of one expert’s evidence which did not impressive the court were, (a) the way he introduced for the first time in his oral evidence-in-chief the audit he said he had carried out in his hospital of WE cases; and (b) the calculation of how long the Claimant's reserves of Thiamine would have lasted, which he introduced for the first time in re-examination. Unlike the claimant’s expert, he did not seek to deal with points of clarification, correction or supplemental opinion by a follow-up letter prior to trial, he left it to his oral evidence. However, he knew about the audit prior to finalising his report and dealing with the JER, but he did not mention it. The judge found his explanation that he did not think the case would go to trial, so had not mentioned the point sooner, difficult to understand and an insufficient explanation. As he recently observed, albeit in different and much more troubling circumstances than apply here, in Mew v The General Dental Council [2026] EWHC 1116 (Admin), it is not open to an expert consciously to hold back matters relevant to their opinion until they give oral evidence. Such a matter should be set out in their report or, if it arises later, included in a promptly prepared and disclosed supplemental report or letter.
The introduction in re-examination, of his calculation of how long the Claimant's stores of thiamine would have lasted, had the air of an after-thought about it. The judge said that one might be tempted to say colloquially, that this had a whiff of a 'back of a fag packet calculation' about it. The way it was introduced, at that stage and without being put to the claimant’s expert struck the judge as giving rise to likely unfairness to the Claimant. He felt that if important and helpful, it could and should have been introduced sooner in the case or at the least earlier in the trial. Similar concerns arose from mention of the audit for the first time in his evidence-in-chief. The judge did not put any weight on either the audit or the calculation for those reasons.
One expert raised in his report his theory that there might have been covert consumption of alcohol. That seemed to be based more on his general experience of the regularity of relapse than any sound evidential foundation in the case, beyond a question being asked in a single entry in the records, much later in the chronology on 12 September and which was never corroborated. There was no suggestion that this could explain earlier symptoms, such as anyone smelling alcohol on the Claimant's breath upon examination, whereas there was plenty of evidence of abstinence being maintained from the August admission onwards through the relevant events. Whilst he did recognise the limitations of the theory, given the lack of evidence, one might have expected him to concede in oral evidence that the Court could not realistically conclude on the balance of probabilities that this was the explanation for what was wrong during the admission on 1 September. He did not do so.
The court also found the defendant’s experts’ attitude to the contemporaneous notes and conclusions of the treating clinicians unconvincing. There was a sense that their eminence led them to two unconvincing positions. First, they had what came across as an excess of confidence in their ability retrospectively to second-guess the contemporaneous notes, when they did not fit with their theory on diagnosis and causation. During his evidence asked one of them why if the treating clinicians were "so bad at [identifying ataxia]" they were all getting it wrong in the same direction and why some were not saying it was functional, on re-admission and in the early days of September. He clarified that he was not seeking to say they were so bad at it (which see had been the view of the other defence expert) but that it was a difficult skill to work it out. If they were thinking this might be WE, they started to see things through that lens.
Second, at times they also displayed an unfortunate and undue scepticism about the competence of the treating clinicians at all levels of seniority, none of whom were in Court to comment. Even the treating Consultant, Dr Bennett who conducted the post-take ward round on 2 September, did not escape this approach. One expert sweepingly observed that "most acute physicians are pretty bad at neurology", although he had "no knowledge of Dr Bennett".
For one expert, this attitude apparently extended to the authors of one of the academic papers cited. The way he dealt with the status of that paper, published in the Lancet Neurology, had more than a hint of academic de haut en bas about it which, coming from him, was as uncharacteristic as it was unfortunate.
There was also another relevant theme in some of the Defendant's expert evidence of undercutting the admission of breach of duty. Entirely properly in the court’s view, there was no attempt made prior to or at trial to withdraw that concession. But there was a sense at times that the Defendant's experts were not entirely comfortable with or accepting of it and/or that the Defendant itself perhaps regretted it. The judge referred to the expert’s observation that he did not know who made the decision to give the Claimant Pabrinex and there were no witness statements from any clinicians, but he doubted that an ENT doctor was best placed to make those judgments. The implication was that if he had been the treating clinician, he would not have prescribed it. Whilst he was driven to accept that it was in accordance with the NICE Guidelines to do so, this was general guidance in his view and he gave the impression of thinking that it was defensive medicine and/or not really necessary in this case.
The audit he belatedly referred to appeared to be grounded in his belief that Pabrinex was overprescribed. He mentioned that as Pabrinex was becoming more difficult to obtain from the manufacturer, this seemed a reason to take stock and get resident doctors to be a bit more alert to the symptoms and signs of WE, by looking at those who had Pabrinex and did not go on to develop WE.
One expert's firm view was that the Claimant had had FND since long before the index events, dating its onset to 2012. Whilst not exclusively on this basis, it was largely predicated upon (a) the diagnosis of CRPS in 2012 and references to that condition and related symptoms since then in the medical records; and (b) his view that the treating clinicians in 2016 had not known about the pre-existing functional condition so had mistaken a functional presentation for WE. The difficulty the judge had accepting those opinions arises from the records which call into question those conclusions. The expert was taken through the history in cross-examination. The diagnosis of CRPS was initially made, via its precursor condition Reflex Sympathetic Dystrophy ("RSD"), in November 2011, in the Orthopaedic clinic. But when seen by a Consultant in Pain Medicine on 10 September 2012, who would be better placed to make the diagnosis, the conclusion was "I do not think he has CRPS..." Whilst there was further mention of it in the GP records, perhaps also overlooking the Pain Consultant's view, the 10 September 2012 opinion that this was not CRPS appeared to be the most recent authoritative view. Whilst the expert had included that pain medicine reference in his records review in his report, the judge was not convinced that he had taken it into account. The judge did not find his explanation for why, notwithstanding that, and despite not having seen the Claimant prior to the index events, he was able to second guess the Consultant in Pain Medicine.
On point (b), his view was that if the treating clinicians had known about the CRPS they would have weighed up what they found on testing differently. He was taken to the entry at 01.20 on 2 September that did document CRPS in the history, contrary to his assertion. His response was that this was not necessarily factored into the neurological examination, even though it was in the history. He accepted that the clinicians were not being called to give evidence to answer this. Again, the court felt this was part of the tendency to doubt the treating clinicians and second guess what they did and their conclusions. The judge considered that much more weight could and should have been placed on the consistent picture which emerges from those contemporaneous records.
Findings
a. What was the Claimant's likely alcohol consumption prior to the admission on 26 August 2016?
This had on balance gone back up to approximately 20 cans of lager per day or 40 units, consistent with the last contemporaneous entry in the records prior to that admission, on 18 August 2016. The expert consensus was that if individuals did not give an accurate account of their drinking, which was common, they understated the amount, not overstated it. So this can probably be seen as a likely minimum consumption at the time.
b. What was his likely nutritional status prior to that admission? There was disruption to his diet, given Mrs Dickinson's absences from the home in the 2 weeks before and 3 weeks after her father's death on 26 July. The contemporaneous record on 18 August, which was in no way a self-serving document given it preceded the index events, corroborated her account at trial that she was not there to help him during this period. This was coupled with the rise in his alcohol consumption to maximal levels again. I therefore find that his nutritional status was poor at the point of admission and in the preceding weeks. At the very least he was at risk of malnourishment, which eating well in hospital, likely reflecting a return in his appetite once not consuming a large volume of lager every day, could not reverse sufficiently quickly, in the absence of Pabrinex.
c. Were his thiamine stores at the point of admission (a) normal or (b) impaired and to what extent? They were significantly impaired for the above reasons, putting him at risk of WE if IV Pabrinex was not administered.
d. How much Pabrinex was likely administered on 26 August 2016? At most 1/30th of the 250mg vial.
e. Were the Claimant's thiamine stores depleted by the admitted failure to provide him with Pabrinex between 26 August and 31 August 2016 to the extent that he was at risk of developing WE? Yes.
f. Did the Claimant develop a WE and, if so, when did this occur? Yes, he did, likely starting on 31 August and developing into 1 September 2016.
g. When did the Claimant develop the functional disorder (later diagnosed variously as FNSD, FND and/or FCD)? By 1 or 2 September 2016, the Claimant was subject to a significant psychological stressor, one of the DSM-V diagnostic criteria for FNSD. He became aware that he was facing a significant neurological condition, likely flowing from the negligent failure to administer appropriate Pabrinex. This stressor laid the groundwork for the development of overt symptoms of FNSD over the following days. These symptoms were probably present by the latest on 5 September and certainly by 7 and 8 September 2016, with a gradual worsening thereafter. This was not a pre-existing condition, whether dating to 2012 or otherwise.
h. What caused the development of the functional disorder and would it have been avoided with the proper administration of Pabrinex? It was caused by the significant stressor outlined in the preceding sub-paragraph and it would have been avoided by the proper administration of Pabrinex. The timing was not merely a coincidence or a milestone on an inexorable process of an allostatic load. The episode of WE and effect on the Claimant was the cause of his FNSD on a balance of probabilities.
Outcome
In the court’s judgment, but for the admitted breach of duty, the Claimant would not have developed the functional disorder and liability is established.
References
Cooke et al, 1988 Absorption of Thiamine is reduced by both alcohol and malnutrition acting separately or together – Unable to find.
G. B. Phillips, M. Victor, R. D. Adams, and C. S. Davidson (1952) A study of the nutritional defect in Wernicke's syndrome’ Journal of Clinical Investigation.
Sechi, Gianpietro & Serra, Alessandro. (2007). Wernickes encephalopathy: New clinical settings and recent advances in diagnosis and management. Lancet neurology. 6. 442-55. 10.1016/S1474-4422(07)70104-7.
Thomson AD, Marshall EJ, Bell D. Time to act on the inadequate management of Wernicke's encephalopathy in the UK. Alcohol Alcohol. 2013 Jan-Feb;48(1):4-8. doi: 10.1093/alcalc/ags111. Epub 2012 Oct 11. PMID: 23065147.