Coakley v Rosie

In January 2008, at the age of 42 years, the Claimant suffered bacterial meningitis. As a result of that infection she suffered total loss of her sight and substantial loss of hearing, with other significant but less serious neurological damage. She claims damages for these devastating injuries and consequential losses. She alleges that but for the negligence of the Defendant, then a general medical practitioner, in failing to recognise or suspect, and consequently failing to treat, the infection, when she attended the Defendant’s surgery on Monday 7th January 2008, she would not have suffered the injurious sequelae. Further or alternatively, she alleges that the Defendant’s negligence materially contributed to the injury she sustained as a result of the bacterial infection. The Defendant denies that she was negligent or that the injury sustained by the Claimant was caused thereby. It is her case that anything which it is proved she negligently did or failed to do, did not affect the course and consequences of the bacterial infection from which the Claimant was then suffering. The parties have reached agreement as to the damages recoverable by the Claimant in the event that she succeeds on the issues of breach of duty by the Defendant and causation of injury and loss; consequently, this judgment is limited to determining those issues.

In the course of the trial I heard evidence from the Claimant, her husband, the Defendant and eleven expert witnesses representing six medical disciplines. There were substantial disputes of fact, as well as differences of medical opinion, which I have had to resolve. Notwithstanding her blindness and substantial impairment of hearing, the Claimant was able to give oral evidence clearly. In particular, she was able to deal with questions which arose from her witness statement (standing as evidence-in-chief and which had been taken at her dictation and then read back to her before she signed a statement of truth) as well as other documentary material, although relevant passages to be read to her before questions were put, particularly during cross-examination. The fact that the Claimant is an obviously intelligent and determined woman, facilitated what might otherwise have been a very difficult process in adducing her evidence. Throughout the trial, counsel adapted their presentation of written material so as to allow the Claimant to follow the evidence as it progressed.

Because some of the expert evidence, particularly that which related to the duty and standard of care of general medical practitioners, was dependent upon findings of fact, this judgment will be divided into four distinct sections, each with subsections identified by capitalised headings. In the first, I will deal with evidence of fact; in the second section I will deal with expert evidence; in the third section I will determine the issue of the Defendant’s alleged breach of duty; in the fourth section I will determine issues of causation. However, as a preface to those sections of this judgment, I will provide an overview of bacterial meningitis. Without an understanding of the basic medical matrix it is difficult to appreciate the significance of much of the factual evidence and the opinions which have been expressed by the expert witnesses about it.

In what is an agreed Glossary of Medical Terms attached as an Appendix to this judgment, meningitis is defined as an inflammation of the meninges and especially of the pia mater and arachnoid mater. The meninges are the membranes that envelope the brain and spinal cord. The cranial meninges comprise of three membranes lying between the skull bone and the cerebrum. Immediately below the skull is the first of these membranes, namely the dura mater. Immediately below that is the arachnoid mater. Between the arachnoid mater and the pia mater (the third membrane) is the subarachnoid space containing blood vessels and cerebrospinal fluid (CSF). When, as some bacteria are capable of doing, they breach what is known as the ‘Blood-Brain Barrier’ (Footnote: ²), and enter the CSF, the endotoxins (Footnote: ³) released by the bacteria attack the membranes bordering the subarachnoid space and surrounding the brain, but not the brain itself, causing irritation and inflammatory swelling. This is known as meningitis. If there is irritation, inflammation, and swelling of the brain matter, this is known as encephalitis. Where meningitis and encephalitis co-exist, this is known as meningo-encephalitis.

The bacterial aetiology of meningitis in 305 patients was the subject of a Special Report by the Research Committee of the British Society for the Study of Infection ('the BSSI') (Footnote: ⁴). A total of 177 (58%) of those patients suffered meningitis caused by meningococci (bacteria of the genus Neisseria meningitidis). In the second largest group of 61 patients (20% of the total), the pathogen was Haemophilus influenzae. In 39 cases (12% of the total) the pathogen was Streptococcus pneumoniae. In the remaining 22 cases where bacteria were identified, there were no fewer than eight different pathogens, six of them in only one or two of the 177 cases and thus rarely implicated in meningitis.

Despite the fact that Professor Shaunak, the expert witness in infectious diseases called on behalf of the Defendant, had concluded in his report that the infecting bacterium was probably Streptococcus pneumoniae, in his closing submissions Mr. Balcombe QC conceded that "on the totality of the evidence a finding that the Claimant had a meningococcal disease would not be inappropriate." This was not surprising, given that all other relevant expert witnesses had agreed that the infection was probably meningococcal, and that Professor Shaunak, when giving evidence-in-chief, had said that he did not dissent from that opinion (Footnote: ⁵), notwithstanding some misgivings. Nonetheless, Mr. Balcombe QC expressed concern that classification of the Claimant's condition as 'meningococcal meningitis' would be an oversimplification. That reservation sought to highlight the fact that the evidence suggested a concurrent, rather than an alternative, condition of meningo-encephalitis. Whether, if that reservation is justified, it is material to the issues I have to determine, will be considered later.

In the context of meningococcal disease, at least four conditions have to be met before invasive disease can occur in an individual person (referred to as ‘the host’ in bacteriology). Firstly, there has to be exposure to the pathogen, in this case Neisseria meningitidis (Footnote: ⁶); secondly, there has to be colonisation of the naso-oropharyngeal mucosa; thirdly there has to be passage through that mucosa, and finally there has to be survival of the meningococcus in the bloodstream (Footnote: ⁷).

When bacteria enter the bloodstream they can survive and proliferate by virtue of particular bacterial virulence factors or incompleteness of the host defence. Importantly, the proliferation of bacteria is exponential with a doubling of numbers, and thus bacterial ‘load’ or ‘biomass’, about every 45 minutes. This exponential growth is illustrated in Exhibits C2 and C3, both of which relate to the time period which is relevant on the particular facts of this case, and is of particular importance to the issue of causation viz. whether earlier antibiotic treatment would have prevented or materially reduced injury. Once viable meningococci have reached the bloodstream, known as bacteraemia, different disease manifestations can develop. Where there are low degrees of bacteraemia, meningococci are cleared spontaneously by the individual’s immune system (the ‘host immune response’), leaving behind a so-called transient meningococcaemia, characterised by a short febrile flu-like episode. Where the bacteraemia is not cleared, clinically overt disease develops; one such is meningococcal septic shock, another is meningitis:

“In nearly all patients who develop shock and in most patients with meningitis, the beginning of the bacteraemic phase is marked by the onset of chills, acute fever, low back pain, thigh pain or generalised muscle aches. Within a few hours ‘fulminant meningococcal sepsis’ (FMS) may develop without signs of meningitis. This condition is characterised by high concentrations of endotoxin and cytokines (Footnote: ⁸) in plasma. Because one of the striking features of meningococci is their propensity to invade the meninges, patients with less marked bacterial proliferation in the bloodstream and less cytokinaemia, present after 18 to 36 hours with meningitis. In these patients (of whom, as I will find, the Claimant was one), blood cultures are often negative at the time of hospitalisation. Due to the limited growth of bacteria in the bloodstream and the seeding of meningococci in the subarachnoid space, patients with meningitis have compartmentalised high concentrations of endotoxin and cytokines in the CSF.” (Footnote: ⁹)

Once meningococci cross the Blood-Brain Barrier and enter the CSF, then, without antibiotics, they are initially able to proliferate uncontrolled, because the host defence mechanisms, principally immunoglobulin and complement (Footnote: ¹⁰), are absent in the CSF. Consequently:

The diagnostic signs and symptoms of meningococcal meningitis include fever, headache, meningeal irritation (neck stiffness and / or photophobia) and non-blanching petechial or purpuric rashes, although in some patients rashes may be non-specific. Because it is the Claimant's case that she presented to the Defendant with rashes which are characteristic of meningococcal meningitis, the presentation and identification of rashes has been considered in detail in the context of the expert evidence adduced at trial. In one paper relied upon in the course of that evidence (see paragraph 5 above), indicating a very high proportion (58% of the total) of purpuric and petechial rashes in meningococcal disease presentations (Footnote: ¹⁴):

“Of the 177 patients with meningococcal infection (six of whom were diagnosed on clinical grounds alone), 70 (40%) had a purpuric rash on presentation, 32 (18%) a petechial rash and 10 (6%) erythematous or maculo-papular rashes.....”; 65 (36%) patients were without a rash,

and in another, relied upon by Dr. Cranfield, the expert in general medical practice called on behalf of the Defendant:

“Majority of bacteriologically proven cases of meningococcal disease develop a rash during some stage of the illness

•

the rash can be extremely diverse (with different presentations in different skin types) and the rate of progression may vary rapidly as well

•

a non-blanching haemorrhagic rash is a characteristic feature of meningococcal disease

•

the rash may be absent, scanty or it may be blanching in the early stages

•

a blanching maculopapular rash at early stages of the disease may develop into a non blanching rash as the disease progress” (Footnote: ¹⁵)

The types and characteristics of rash which will be referred to throughout this judgment are as follows:

So far as treatment is concerned, in a paper to which repeated reference was made during the course of oral expert evidence, and which will be considered again later in this judgment - not least because it is particularly relied upon by the Claimant's expert witnesses in formulating their opinions on causation - it is stated:

For the purposes of this overview, there is no clear, accepted wisdom in the medical literature as to the rate of progression of meningococcal disease process, although there is literature as to the consequences of the disease process if treated at particular stages of that progression. It is these issues, which lie at the heart of the issue of causation, which I have to determine with the benefit of the expert witnesses called by the parties. In general terms, even with antibiotics, bacterial meningitis remains a life-threatening condition (see the BSSI paper, footnote 14) with a significant morbidity rate. However, such a generality involves recognition of the fact that patients, as individuals, will have presented at different stages in the progress of the disease, with different immune responses and differences in the virulence of the pathogen.

Much of the factual history is not in dispute. At the time of the events with which this judgment is concerned the Claimant lived with her husband in the village of South Wonston near Winchester. They had two sons then aged 17 and 18 years, and a family retail business based in Guildford. In addition, the Claimant was a talented artist undertaking a degree in 3 Dimensional Design at the University of Creative Arts; she was in the final year of her course and was due to finish a dissertation at the end of the week in which she became seriously ill. Despite her disability she achieved a First Class degree.

On Saturday 29^th December 2007, whilst on a short visit with her husband to France to stay with their eldest son Patrick, who was working in a ski resort, the Claimant began to feel unwell with what, to her, felt like the first signs of flu. In her witness statement she describes feeling ‘so awful’ and wanting to get home as quickly as possible. They were due to fly home that day in any event. She went to bed as soon as she and her husband arrived home on the evening of 29^th December and on each succeeding day she felt worse than the day before. Her symptoms included headache, nasal congestion, lethargy, loss of appetite, “enormous pressure in my head” and difficulty in focusing and concentrating, particularly on the work she was required to do to complete her dissertation. She stayed at home during the whole of the following week feeling “generally grotty”, self-medicating with Lemsip Max and Anadin Extra, only leaving the house to accompany her youngest son, Christopher, to his driving test on Friday 5^th January 2008.

In the first account she gave of what occurred on Monday 7^th January 2008, namely that contained in Draft Particulars of Claim attached to a Letter of Claim dated 21^st December 2010, it was stated:

“4.

On 7 January 2008 the Claimant woke up late feeling much worse. She noticed she had a rash on the palm of her left hand, across both her lower arms and across her midriff. Her right arm was spotty and dark pink. The rash was spidering and the spidery parts were purple with gaps between the dots. However, the rash was not raised or itchy. The rash did not hurt save for a spot on her arm that felt sore when she pressed it.

5.

The Claimant telephoned the surgery arranged an appointment to see the Defendant at 5.20 pm.”

In the Particulars of Claim dated 11^th April 2012, which were served, it is pleaded that:

“4.

On 7January 2008 the Claimant woke up late feeling much worse. She

noticed she had a rash on the palm of her left hand, across both her lower arms and, later in the day, across her midriff. The Claimant telephoned the Surgery and arranged an appointment to see the Defendant at 5.20 pm.

5.

The Claimant remained unwell during the day and slept for the most part. By the time she was driving to the surgery for her appointment she noted that her right arm was spotty and dark pink. The rash was spidering and the spidery parts were purple with gaps between the dots. However, the rash was not raised or itchy. The rash did not hurt save for a spot on her arm that felt sore when she pressed it.” (emphasis added)

In her witness statement, dated 24^th June 2013, she described events as follows:

“25.

On 7 January I woke up late. I was feeling really horrible. I had woken up at about 10.30 and saw that I had a rash on the palm of my left hand, both of my lower arms and across my midriff."

She then described, in detail, how, on getting out of bed, she had first been alerted to the rash on her midriff, of what was then her unclothed body, by the reflection in a large mirror in her bedroom, and how she had had used the mirror to check other parts of her body as best she could. She then referred to a telephone call to her husband preceding her call to the Surgery, and to telling him that she “felt really unwell and .... had a strange rash.” It was her husband she said, as he confirmed, who suggested she should telephone for an appointment at her GP Surgery.

In paragraphs 27, 28, 29 and 30 of her witness statement the Claimant gave extremely detailed descriptions of the rashes as they had been on waking, including the fact that “on touching the rash with my fingertips the surrounding capillaries did not change colour” - for the context of which, see below. She affirmed the account given in her witness statement when she came to give oral evidence, particularly the descriptions of the areas of rash, adding only that, on waking, as well as the rash, she had a headache and a sore throat, congestion, lethargy and a tickly cough. She said that the description of the rash “comes from my memory ; it was the last thing I saw and is a vivid memory”.

The description of the rashes given by the Claimant in her witness statement and confirmed in her oral evidence is one of the central features of her case in respect of breach of duty by the Defendant, and thus needs to be included within this judgment in full. It is the Claimant’s case that the rashes were typical and characteristic of the rash where there is a meningococcal infection and that this was not recognised by the Defendant. I take the descriptions from her witness statement (Footnote: ²³):

“27.

In the morning on my left lower arm the rash extended from the inside crook of my elbow approximately 5-7 inches down my arm. The rash did not extend as far as my wrist. The rash was only on the inside of my arm and not on the outside of my arm. I had a number of pinky small dots on that arm. I did not count them but would estimate there were around 30 or more. The size of the dots were about the same size as if you made a mark with the tip of a felt pen or the same size as the head on a flat headed dressmaker pin. The dots were not joined together, they were several millimetres apart. I would describe them as evenly distributed; they were not clustered. The spots were not as dark as a port wine stain but they were darker than a pink Angel Delight whip.

28.

On my lower right arm I had a couple of large spots. These spots were on the inside of my lower right arm not on the outside of my lower right arm. The largest spot was approximately 4 inches down from the crook of my elbow with the second spot approximately a further 3 quarters of an inch along the inside of my lower right arm. One of the spots was slightly larger than the other and was about the same size as the end of a cigarette. Both of these spots had spidery like tentacles radiating from them like a starburst. At this stage, meningitis had not occurred to me, however, on touching the rash with my fingertips the surrounding capillaries did not change colour. It was tender to the touch and looked more like a very fresh and livid bruise. I can recall that in the morning both spots on my lower right arm were a few shades darker than the spots on my lower left arm.

29.

On the palm of my left hand I had 4 small reddish spots. These four spots were smaller than the spots on my lower right arm. They were about the same size as a compass prick. They were more of a reddish colour than the spots on my lower right arm and were more spaced apart. They had about 1.5 cm between them and were like the four corners of an offset square.

30.

The spots on my midriff appeared to look slightly larger than the ones on my lower left arm but were the same colour. I would estimate that there were at least double the amount of spots on my midriff than my lower left arm. The spots covered a good roll of fat around my middle. The spots were more congested towards the middle area of the rash and towards the outer edges they became more spread out and random.”

Mr. Balcombe QC, whilst making it clear that he was not suggesting dishonesty, did suggest to the Claimant that in the respects which I have identified by emphasis in paragraphs 4 and 5 of the Particulars of Claim, and, in addition and in particular, the very detailed descriptions of each area of rash, her factual account had ‘evolved’ over time. This she disputed; she said that her account had been "clarified", and that she was not responsible for what was or was not pleaded by her legal team. It was suggested to her that having got up and dressed she could only have discovered the rash on her midriff ‘later in the day’ (as pleaded, but abandoned in the witness statement and her oral evidence) because it was itchy. This she denied.

In his written and oral evidence, Mr. Coakley, not only confirmed the telephone call at about 10.30 am and that it was he who had suggested she should see the GP, but also that the Claimant had told him that she now had a rash, adding “she did not explain what the rash looked like and she did not say it was itchy.” At this point I should make it clear that apart from two other very short telephone calls from the Claimant, the first simply confirming that an appointment had been made with a GP and the second after she had returned home from the appointment “at about 5.45pm” (so Mr. Coakley thought), Mr. Coakley never spoke to the Claimant before she emerged from the coma in which she was admitted to hospital at 11.28 pm the same day. Furthermore, the only time he saw any rash was when an ambulance driver “pointed to the rash on my wife’s stomach and arm. I cannot recall which arm” –after he had found the Claimant, some time after about 9.15 pm, “lying on the wrong side of the bed with her eyes open and not responding and at the same time choking on vomit.” Neither in his witness statement nor in his oral evidence did Mr. Coakley give any description of the rash he had seen. At that time he could not have known that it would be significant, and undoubtedly had far more important matters on his mind, namely the dire condition in which he had found his wife and the need for her to be removed to hospital where she could be cared for.

Having made an appointment to see a GP, which she has always recalled as being at 5.20pm, the Claimant’s evidence was that she set an alarm for 5.00 pm and slept for the rest of the day until shortly before it was due to go off when she was half awake. The alarm did go off. She said:

“I can recall trying to wake myself up but did not feel like I could get up. The alarm went off and I just lay there until I suddenly realised that unless I moved quickly I was now going to be late for my appointment at the surgery...”

Before leaving her home and driving the short distance of 3.5 miles from her home to the Surgery at which the Defendant worked in Sutton Scotney (Footnote: ²⁴), the Claimant said that:

“I checked my midriff and lower arms to see if the rashes were still there and the rashes on both lower arms appeared to be slightly darker than when I inspected them in the morning.”

adding:

“...it was whilst driving to the appointment with my sleeves rolled up that I looked at the rash on my forearms and hand and I noticed that the spots were darker, in particular the ones on my lower right arm and the left palm of my hand.”

The Claimant was not the Defendant’s patient; Dr. Anna Wilson was her usual doctor, but she was absent with long-term illness. Having arrived at the Gratton Surgery, the Claimant was directed to an upstairs waiting room from which she was collected by the Defendant. Although there is no document identifying these times, it was the Defendant’s evidence that

“..... according to the practice records, she is registered as having arrived at reception at 17.07. According to the computer records, I commenced the consultation in my room with Mrs Coakley at 17.10 and she left my room at 17.22. The consultation therefore lasted 12 minutes.”

A photograph of the room used for the consultation is exhibited to the Defendant’s second witness statement (1/C77). The Defendant told me that her surgery that afternoon finished at 6.00 pm and that she had other patients not only before, but after the Claimant.

Although she could not recall whether she had made the record of the consultation immediately after the Claimant had left the consultation room or at the end of the surgery, the Defendant did make a computer record of the consultation [1/C78], reproduced below as it set out in the original record, and shown in Bold (with explanation of abbreviations in italic, as were provided by the Defendant during her oral evidence):

There are significant disputes of fact as to how the consultation proceeded both in terms of what was said and what was done. The Defendant’s witness statements dated 17^th March 2011 and 14^th October 2013 (responding to just two paragraphs of the Claimant’s witness statement, namely paragraphs 32 and 36), and particularly the former, contain significantly more information than the notes she made at the time, some 3 years earlier. The Defendant revealed that about one month after the consultation when, of course, she had become aware of what had become of the Claimant, she made some typed notes independently explaining:

“I realised the Claimant was very ill and her family were angry. I put down what I could remember - but not to defend myself - what I could recall of the consultation. Some of it is what is in the witness statement and not in the notes.”

Neither this additional record, nor what the Defendant thought had been a transmission of the substance of this record to the Medical Protection Society, was disclosed. I have already observed that the Claimant’s witness statement contains significantly greater detail than had been revealed prior to its disclosure.

The Claimant described walking from the upstairs waiting room, on the seat nearest the door, and walking from there, no more than 12 to 15 steps, to the consulting room. The Defendant said that the Claimant walked freely and easily, observing this when she went to collect the Claimant from the waiting room. The Claimant described, in her witness statement, entering the consulting room and sitting in a chair “almost on the corner of a very large desk” some distance away from the Defendant who was typing in front of a computer screen. The relative positions of the Claimant and Defendant is confirmed in a photograph of the consulting room at 1/77 if, as the Claimant said it was, her chair was further back than is seen in that photograph. However, the Defendant stated that the patient’s chair was always alongside the end of the desk and that “when I take a history, I move my chair slightly away from the desk, towards the patient.” The significance of this evidence relates to the ability of the Defendant to see, inspect and examine the rash which the Claimant said she had on her arms, left hand and midriff, but, in cross-examination the Claimant accepted that she was close enough for the Defendant to see the rash when she held her arms out.

The Claimant agreed that there were three phases to the consultation; a conversation about why she had attended, an examination and a discussion. The Claimant specifically recalled explaining that she

“felt really poorly and I had been suffering from ‘man flu’ for over one week that wasn’t getting better, that I had pressure in my head that made me feel as if my head was going to explode and now I had this awful rash on both my lower arms, midriff and strangely on the palm of my left hand. I specifically remember referring to the spots on the palm of my left hand as “weird” and pointing them out to her ... I described the pressure in my head as similar to the ‘man in the iron mask’ ”.

This latter reference was explained as being a reference to a television advertisement for Lemsip [ see screenshots: Exhibit C1] and, the Claimant said that this prompted the Defendant to ask about the medication which the Claimant had been taking and to consult a book, which the Defendant confirmed was the OTC Directory. This, in turn, led the Defendant, as she agreed, to conclude that because Lemsip Max contained phenylephrine, the rash was probably (“might well be”, was the Defendant’s evidence) an allergic reaction to this.

The Defendant said in her witness statement that she “observed the rash on her hands (note the incorrect use of the plural) and on her arms”. Her witness statement also refers to “the rash was also present on her back. There were discrete lesions about one or two centimetres in length in an oval shape, infrequent and coloured pink to red.” Apart from the computer note she made, which makes no reference at all to a ‘rash’, or to the location of any rash or other skin lesion, or to any suggested treatment of any skin lesion she was referring to (‘urticarial patches’), the Defendant’s evidence in respect of any skin signs was very limited. During her evidence-in-chief she said she had seen only one previous meningococcal purpuric rash when she was a junior doctor in Sheffield in the mid 1970s, although she said she had encountered purpuric rashes with other conditions, including cancer, and in a condition suffered by her son-in-law. She said that most surgeries would have a patient with “a rash of some sort”, the most common being eczema and allergic rashes. She agreed she had not touched the rash on the arms. The Defendant contended that the Claimant had told her that the rash was itchy, and that was why she recorded ‘itchy’ in her note. This was disputed by the Claimant who said she had only described the rashes as ‘awful’. The Claimant also, and materially, said that she had never been aware of there having been any rash on her back until she had seen the Defendant’s witness statement many years later. It was submitted on her behalf that had the rash been itchy it is likely that she would have been aware of this back rash (assuming it is correctly recalled by the Defendant as having been seen).

The Defendant also said that she checked the Claimant’s neck for stiffness, by holding the neck and asking the Claimant to lift her head up and down, and was “certain there was no neck stiffness present”. The Claimant disputes ever having been aware of such a physical check as part of the examination, although she accepted that her lymph glands and throat were examined. Neck stiffness is one of the signs that is looked for if meningitis is suspected, although it may not always be present. The Claimant’s evidence was that the Defendant had “asked if I had a stiff neck. I said that I had a stiff neck but I also said that I quite often had a slightly stiff neck and back so it was difficult to tell”. Crucially, the Claimant, having, she said, been alarmed by the reference to neck stiffness, asked the Defendant “whether she was checking for meningitis and she said that the rash was definitely not a meningitis rash.” The Claimant was able to make this enquiry because one of her sons had suffered viral meningitis some three years previously. The Defendant agreed that there was a reference to meningitis but that this occurred whilst she was actually testing for neck stiffness.

In her oral evidence the Claimant said:

“I did mention cough and headache. I don’t recall being asked if I had a bad cough. I didn’t convey the impression that the cough was the worst symptom. I believe I used the expression ‘I think my head is going to explode’ and conveyed ‘pressure’ in my head [the Claimant then demonstrated this by drawing her hands down across both cheeks from the area between her eyes]. I did use the expression ‘the man in the iron mask, like the Lemsip advert’. I was trying to convey that I had a very severe headache. She said nothing specifically in response.”

It was common ground that the Defendant did not take the Claimant’s temperature or blood pressure, that she had not required the Claimant to undress to examine any parts of her body that were not visible or shown, that she had not examined the Claimant on a couch and that she had not checked her skin for signs of blanching. In the course of her cross-examination she said that she regretted not examining the rash closely, and regretted not examining the extent of the rash or doing a blanching test. She also agreed in cross examination that : “ I was checking for meningitis as part of my examination” - something she resiled from in re-examination when she said “Meningitis was not in my mind at the time!”, and notwithstanding that she had agreed that meningitis had been specifically referred to by the Claimant.

The consultation concluded with the issuing of a medical certificate, but without any medication or advice beyond to go home to bed to rest.

Whether, in the conduct of this consultation and in the conclusion she reached, the Defendant was negligent, will be considered discretely when I analyse the evidence and make findings on the issue of breach of duty. Because this issue is informed by expert evidence, it is inappropriate to deal with it now.

At the conclusion of the consultation the Claimant left the surgery (she said in her witness statement that this was at 5.35 pm) and drove home. She described having had “an incredible thirst” half way through the short journey and thinking she would stop at the village store to obtain a can of Coca-Cola. However, “when I arrived at the shop I started to feel really awful and I could not face going into the shop so I drove home”. When she reached her home she used her mobile telephone to call her husband whilst sitting in the car on the drive where there was a good signal. As I was informed, the use of the phone involved manually entering several sequences of numbers. Mr. Coakley told me that he had received a telephone call from his wife at about 5.45 pm. It was short. The Claimant told him that the Defendant had told her that her condition might be a respiratory infection, that she was to have lots of bed rest and that she had been given a medical note. She recalled her husband reminding her that he had a committee meeting that evening, and telling him that she would go straight to bed. Mr. Coakley confirmed the telephone call but also recalled the Claimant telling him that she was very thirsty and asking him to get her a can of Coca-Cola (which he said he did). The Claimant then went straight to bed where she was seen, asleep and shivering, by her husband when he returned home from work at about 6.15 pm. He did not disturb her. Having made himself something to eat, Mr. Coaklely left the house for the meeting in the village which was due to start at 7.00 pm. He returned home at about 9.15 pm where, having “heard noises coming from upstairs which sounded like my wife vomiting”, he found his wife “lying on the wrong side of the bed with her eyes open and not responding and at the same time choking on vomit.” Having turned his wife on her side he called the ambulance service.

The first ambulance to arrive was one that had, coincidentally, been passing near to the Claimant's home at the time of Mr. Coakley's call and was consequently diverted. There is no separate record of this ambulance or what was observed and done by the female paramedic driver, who was alone. It is not clear at what time that first ambulance arrived; Mr. Coakley called for it at some time after his arrival home which was at “about 9.15 pm”, after he had begun to prepare a hot drink, and after he had found his wife in the state which prompted the call. He thought it took approximately 12 minutes to arrive. If Mr. Coakley did indeed arrive home at 9.15 pm, it is likely that the first ambulance arrived between about 9.40 pm and 9.45 pm. However, given that a second ambulance was summoned to support the solitary driver of the first, with a recorded 'Call Time' of 10.23 pm, the timing of the arrival of the first ambulance would mean that there is an unexplained period of almost 40 minutes before the second ambulance was summoned. Mr. Coakley’s evidence was that having taken the first ambulance paramedic to the bedroom, where they found his wife had “fallen on the floor with her head wedged between the bed and the bedside table, her body on the floor”, she “made an assessment that she needed help and radioed for another ambulance.” In my judgment this is unlikely to have taken 40 minutes! It is more likely, as I find, that Mr. Coakley is mistaken about the time he arrived home and that it was somewhat later than he recalled.

As I have already observed (paragraph 22 supra), it was when the first ambulance paramedic was assessing the situation that she “pointed to the rash on (the Claimant’s)stomach and arm”, the Claimant’s shirt top having ridden up in her fall from the bed. Mr. Coakley was unable to recall the nature or characteristics of the rash.

The Ambulance Service's 'Patient Clinical Record' [3B/643] was prepared by one Carol M Cole, presumably one of the second ambulance crew paramedics. It shows the arrival at the Claimant's home of the second ambulance at 10.30 pm (although this is at odds with 'primary' observations recorded as having been undertaken at 10.20 pm). It did not leave the Claimant's home until 11.18 pm, arriving at the Royal Hampshire County Hospital at 11.28 pm where the Claimant was admitted to the Accident and Emergency Department [3A/289 and 3B/643] and came under the care of the hospital's medical staff. During the time the second ambulance's crew were at the Claimant's home, the following is recorded as having occurred:

It is clear from the documentary evidence of the involvement of the ambulance service, that there was significant delay in the administration of the first dose of antibiotics, even after the arrival of the second ambulance. It is also clear that there is no evidence to support a conclusion that any delays by the ambulance service were causative of injury which, but for that delay, the Claimant would not have suffered in any event. As will be seen, the Claimant's case, as advanced by expert witnesses called on her behalf, is that the 'window of opportunity' for administering antibiotics which would have prevented or significantly reduced lasting damage, was closed before the arrival of the first ambulance, but open at the time the Claimant was seen by the Defendant.

The first record following the Claimant's admission to hospital is a nursing record at 11.30 pm (Footnote: ²⁵) recording a Glasgow Coma Scale assessment score of ‘3’, the lowest possible score and indicating deep unconsciousness. Shortly after arrival, at 11.35 pm, a Neurological Assessment Form was completed showing a GCS of ‘6’ (Footnote: ²⁶), subsequently falling to ‘3’ again at midnight and, apart from an assessed score of ‘6’ at 12.30 am (by Dr. Ritchie – see below) remaining at that level until admission to the hospital’s Intensive Care Unit at 01.45 hours on 8^th January. 'On arrival' at hospital a 2g dose of Ceftriaxone (Footnote: ²⁷) was administered again intravenously.

An Observation Chart (Footnote: ²⁸) was commenced at 11.44 pm. This recorded:

The Claimant was reviewed at 12.30 am on 8^th January 2008 by Dr. J Ritchie, a Specialist Registrar in the Emergency Medical Assessment Unit. He identified the ‘Problems’ as being ‘1. ? Bacterial meningitis 2. ? Intracerebral event’ and, having discussed the situation with a member of the microbiology department, antibiotic prophylaxis was given to the Claimant’s husband and ‘staff’ (Footnote: ³⁰). In the course of his attendance upon the Claimant, and in an extensive four pages of notes, Dr. Ritchie made the following relevant records:

The Claimant was admitted to the hospital's Intensive Care Unit some time after 1.50 am (when it was noted by a nurse that she was to be admitted to ITU, also referred to in hospital records as the Critical Care Unit). In what appears to have been the first record (Footnote: ³²) made in the intensive/critical care unit a provisional diagnosis of 'meningitis / encephalitis' is noted by one R.Vandabone (a doctor whose precise status is unclear). This was before any tests results had been received (see under 'Investigations' at 3A/307). The first series of detailed blood gas records in the Critical Care Unit, began at 2.08 am on 8th January.

At 8.30 am there was a ward round by Dr. Thomas, an ICU Consultant, noted (Footnote: ³³) by Dr. Giles (a Senior House Officer). In addition to previous findings he noted 'Grand mal seizure in A&E', although there is no confirmatory note of this in the nursing record. He also noted an elevated white blood cell count and an elevated CRP (C-reactive protein) suggesting inflammation. In particular he noted:

At 9.00 am, a ward round by Dr. Shire, a Consultant Physician, noted (Footnote: ³⁴) by Dr. Ritchie, reviewed earlier history but notes, in contradiction of the note half an hour earlier:

At 11.00 am a ward round by Dr. Dryden, a Consultant Microbiologist, was noted (Footnote: ³⁶) by a junior doctor as follows:

The next notes are untimed, (Footnote: ³⁸) but made by Dr. Thomas. Because Dr. Dryden was anticipating Lumbar puncture at 11.00 am, it is likely that Dr. Thomas's notes are after that time. They are reproduced in full:

In another untimed note (Footnote: ³⁹) made by Dr. Thomas on 8th January, the following is recorded:

On Dr. Shire’s ward round at 10.00 am on 9th January it is recorded (Footnote: ⁴⁰):

On 10th January Dr. Thomas noted another discussion with Mr. Coakley at the Claimant's bedside. He recorded (Footnote: ⁴¹) that there was

On 11th January, bilateral eyelid swelling was noted (Footnote: ⁴²) by Dr. Goldsmith (another ICU Consultant), and Dr. Dryden noted negative PCR results. On 12th January, an 'essentially normal' CT scan with no evidence of raised intracranial pressure was noted. Also on 12th January, Dr. Goldsmith made a very long summary note (Footnote: ⁴³), including a note of a further discussion with Mr. Coakley. Among the comments he recorded, was the following:

On 14th January the Claimant's case was discussed with, and referred to, a Dr. Kipps, a Consultant Neurologist. (Footnote: ⁴⁵) He noted a history of headaches, rash and seizure and agreed with treatment for meningo-encephalitis even though the diagnosis was still unclear; he also raised the possibility of post infectious demyelination. However, following an MRI scan, Dr. Kipps recorded (Footnote: ⁴⁶):

On 16th January there was the first specific ophthalmic investigations. On examination (Footnote: ⁴⁷) both pupils had poor reaction to light and bilateral papilloedma was noted and thought to be 'probably part of cerebral oedema/infarction'.

On 17th January the Claimant was finally extubated. Large dilated pupils were noted to be 'poorly reactive to light' and the Claimant complained (obviously, for the first time) that she could not see (Footnote: ⁴⁸). Later on 17th January there was a note (Footnote: ⁴⁹) : 'pupils : non reactivity'

The PCR results are found at Trial Bundle 3B/678 et seq. A specimen of the Claimant’s blood was collected 8^th January, received on 10^th January and reported upon on 11^th January by the HPA Southampton Laboratory at Southampton University Hospitals NHS Trust; this tested negative for meningococcal PCR (Footnote: ⁵⁰). A sample of the Claimant’s CSF was taken on 12^th January, received by the Southampton Laboratory on 16^th January and tested positive for meningococcal PCR (Footnote: ⁵¹). This was reported by telephone on 17^th January. Another sample of the Claimant’s CSF was also sent to the Manchester Medical Microbiology Partnership on 21^st January. The meningococcal screening PCR test was negative as was a pneumoccocal PCR test. It was made clear in the report that a negative PCR test does not exclude either meningococcal disease of pneumococcal infection. Although some questions were raised by the Defendant’s experts as to the status of the Southampton Laboratory, it was established that this laboratory had been duly accredited by Clinical Pathology Accreditation (UK) Ltd in April 2007 for a period of four years. (Footnote: ⁵²)

In the ICU Discharge Summary (Footnote: ⁵³) dated 18th January, when the Claimant was moved to the hospital's Victoria Ward, it was clearly stated that:

No suggestion has been made that the Claimant’s subsequent medical history and rehabilitation has features which are relevant to the issues I have to determine. Nor, apart from the clinical records to which I have referred, has any reference been made to anything in the nursing or other medical records prior to discharge from the ICU, which might assist in the resolution of the issues in this case.

Dr. Ineson and Dr. Cranfield, expert witnesses in general medical practice, instructed by the Claimant and Defendant respectively, considered the alleged negligent failure of the Defendant to suspect or diagnose meningitis and, consequently, the failure to treat the same. There was no dispute that the Defendant owed a duty of care to the Claimant to exercise reasonable skill and care in her treatment of the Claimant, and that the standard of care she was required to exercise was the ordinary skill of an ordinary competent general medical practitioner being one which accorded with a practice accepted at the time as proper by a responsible body of medical opinion. Despite the variety of formulations which have been offered by appellate courts, probably the best known and most often quoted definition of the standard of care required of medical practitioners is McNair J’s direction to the jury in Bolam v Friern Hospital Management Committee [1957] 1 WLR 582:

“But where you get a situation which involves the use of some special skill or competence, then the test as to whether there has been negligence or not is not the test of the man on top of a Clapham omnibus, because he has not got this special skill. The test is the standard of the ordinary skilled man exercising and professing to have that special skill. A man need not possess the highest expert skill; it is well established law that it is sufficient if he exercises the ordinary skill of an ordinary competent man exercising that particular art ... he is not guilty of negligence if he has acted in accordance with practice accepted as proper by a responsible body of medical men skilled in that particular art ... Putting it another way round, a man is not negligent if he is acting in accordance with such a practice merely because there is a body of opinion who would take a contrary view.”

In Sidaway v Governors of Bethlem Royal Hospital [1985] A.C. 871 at 881F Lord Scarman reformulated it thus:

“ a doctor is not negligent if he acts in accordance with a practice accepted at the time as proper by a responsible body of medical opinion even though other doctors adopt a different practice.”

In Maynard v West Midlands Regional Health Authority [1984] 1 WLR 634 the House of Lords held that the ‘Bolam test’ was applicable to diagnosis.

Because six out of a total of nine pleaded ‘particulars of negligence’ (Footnote: ⁵⁴) were concerned with the Claimant’s ‘rash’ viz. alleged failures to inspect it properly, check if it was non-blanching, appreciate its nature and significance and wrongly diagnosing it as being probably an allergic reaction, there was an understandable emphasis on this issue when the experts, having submitted their reports, met to discuss their conclusions. Both of them agreed that “the appearance of the rash is a matter of dispute which must be for the Court to resolve”. (Footnote: ⁵⁵) In his report, Dr. Ineson had concluded that “...the appearance of the rash will determine whether Dr. Rosie’s actions were acceptable or not.” (Footnote: ⁵⁶) In her oral evidence-in-chief Dr. Cranfield stated that “In this case all depends on the nature of the presentation.”

The only area of disagreement in the joint statement related to whether the Claimant’s description of her rash was consistent with meningococcal disease. Dr. Ineson considered that the description given was consistent and could not be described as ‘urticarial’, whereas Dr. Cranfield “does not consider it entirely consistent with the rash of meningococcal disease – Julie Coakley describes the rash as spidering and the spidery part was purple with gaps between the dots”. Dr. Cranfield did accept, however, that a rash where the surrounding capillaries do not change colour on pressure, is consistent with a non-blanching rash. (Footnote: ⁶²)

In his oral evidence Dr. Ineson made it clear that a general medical practitioner “is expected to suspect the diagnosis, not to diagnose” and that if meningococcal disease is suspected a standard bolus dose of penicillin must be given preparatory to admission to hospital. He added that “if meningitis comes into your thinking, which it always does if there is a temperature, headache and rash, you must exclude it.” Dr. Cranfield agreed with this. Exclusion involves the blanching test, that is, the application of pressure to the area of rash to seen whether or not the rash will blanch. It was Dr. Ineson’s opinion that when suspicion of meningitis is missed, this is usually because there is no rash or because the rash is misinterpreted. He was critical of the Defendant’s notes; an adequate note would, critically, comment on where the rash is, he said, adding “where it is, is relevant to whether it was actually seen!” and that “a doctor must see all areas of rash a patient is concerned about.” It was his opinion that “If you cannot exclude meningococcal disease, manage it as if it is.”

When giving her evidence-in-chief, Dr. Cranfield said that, when reporting on the case, she had understood that the rash with which the Claimant had presented was (as a matter of fact) non-blanching: “I had not appreciated that an attempt had not been made to test non-blanching.” However, it was her opinion that there was little to be gained by touching a rash and “most of the diagnosis is visual .... If you think it’s purpuric, you know what to do. If it’s purpuric there is little it can be confused with.” She thought that an urticarial rash could not be confused with a purpuric rash. It was her opinion that because meningitis was actually raised during the consultation “there was a need to confidently dismiss this as a differential diagnosis.”

It is noteworthy that in answering the question in the agenda for the joint meeting - “...what history, assessment and examination should a reasonably competent practitioner have taken and performed in order to reach a diagnosis or a differential diagnosis” - both expert witnesses only referred to the appearance of the rash (“The key would be the appearance of the rash”). There was no mention of checking for neck stiffness being a necessary assessment, particularly bearing in mind that the Defendant’s note contained no reference to a neck examination. This was referred to by Dr. Ineson in his main report, albeit in the context of suggesting the absence of neck stiffness would not exclude a diagnosis of meningococcal disease. It was not a point relied upon by Dr. Cranfield in her report, other than pointing to the existence of a factual dispute about whether or not there was an examination. She agreed with Dr. Ineson that a neck examination was a ‘screening’ assessment and would not be diagnostic, adding that early meningococcal disease might not be picked up by a neck examination. Nor were either of these experts critical of the fact that the Defendant did not take the Claimant’s temperature or blood pressure.

It was suggested to Dr. Cranfield that there were many examples within both her main report and the joint report where she demonstrated a lack of objectivity in her assessment of the materials with which she had been provided, and was acting as an ‘advocate’ for the Defendant, looking for reasons to disbelieve the Claimant and reasons to believe the Defendant. Particular examples were identified in her responses to Questions 5 and 7 in the joint statement, and in paragraphs 7.25, 7.30 and 7.31 of her report. An entire Appendix of the Claimant’s closing written submissions was devoted to a critique of Dr. Cranfield. Dr. Cranfield robustly defended her contention that she had been objective, pointing out that her conclusion, in paragraph 7.41 of her report was that if the Claimant’s account of her rash and neck stiffness was accepted “then failure to administer penicillin and arrange immediate admission to hospital would not be supported by a responsible body of competent general practitioners” (Footnote: ⁶³) .

My findings of fact relevant to the issue of breach of duty will follow my summary of the remainder of the expert evidence because that evidence informs those findings.

By the end of the evidence, and notwithstanding many excursions, during the course of it, into medical backwaters, it was clear that the issue upon which these experts could assist the court was whether, on the balance of probabilities, any finding of a negligent failure by the Defendant to administer antibiotics, caused or materially contributed to the damage caused to the Claimant by the meningococcal infection and its sequelae. Putting this issue another way, and bearing in mind that the Claimant was treated with intravenous penicillin at 11.00 pm, on the balance of probabilities, would the damage suffered by the Claimant have been prevented, or the outcome have been materially better, had penicillin be administered, and followed by admission to hospital, earlier than was actually the case? In the context of this case, it is clear that ‘earlier than was actually the case’ means (a) the administration of penicillin by the Defendant and (b) arrangement of admission to hospital as a matter of urgency immediately thereafter, there being no other opportunity for either of these events to have occurred prior to the arrival of the first ambulance, and it being common ground that it was probably too late by then for there to have been any difference in the outcome.

Despite their different fields of expertise, each of the experts in the fields of infectious disease, microbiology and neurology were able to express opinions on the issue as defined in the preceding paragraph, and it is sensible for their evidence to be dealt with together. The evidence of the experts in the fields of ophthalmology and the sole expert (Dr. West) in the field of audivestibular medicine, whilst also very relevant to the issue of causation, are dealt with separately.

The fact that it was considered necessary for the six experts with whose evidence this subsection is concerned, to meet together to produce a joint statement, reinforces my decision to consider their evidence together, even though that exercise was not entirely successful. Due to lack of time, and a misunderstanding as to what would happen subsequent to initial discussions, the six experts only managed to consider the first eight of a number of questions posed by what is described as ‘the defendant’s agenda’.

The evidence of these experts is found in their individual reports in Trial Bundle 4 and the following joint statements:

By way of general comment I would observe that whereas, in some cases, agreed agendas may help experts to focus upon issues, the fact that there are separate agendas in this case has, in my judgment, caused unnecessary duplication, confusion and lack of proper focus. Also by way of a general comment, I am quite satisfied that the fact that all experts relied upon a substantial body of literature, enables me to rely upon it in formulating my judgment, if and to the extent that it is demonstrated to provide reliable support for opinions expressed by those expert witnesses. As was made clear by Stuart-Smith J in Loveday v Renton [1990] 1 Med LR 182:

“The works of learned and qualified authors forms part of the general corpus of medical and scientific learning on the subject and can be relied upon and adopted by suitably qualified experts. These experts may have their opinions tested in the light of the literature”

Putting on one side the fact that it is now agreed that the Claimant in fact suffered meningococcal disease (as opposed to the other possible conditions / pathogens raised by the Defendant’s experts, discussion of which can now be dispensed with) the following particular areas of agreement emerge from the joint reports which are relevant to the issue of causation.

The main area of disagreement was thus whether or not the earlier administration of penicillin and hospital treatment (with intravenous antibiotics) would have made any difference to the outcome in the particular case of the Claimant. The evidence on this discrete, but crucial, issue is now summarised below.

Dr. Lynn’s evidence was that antibiotics given at the time of the consultation with the Defendant would have rapidly started killing bacteria and because she was neurologically intact at this time, this would, more likely than not, have prevented the visual loss. He concluded that it would have been too late to prevent visual loss if antibiotics were administered after 8.00pm on 7^th January, although this timing was, he opined, conservative given that she was functioning sufficiently well to drive home from the Defendant’s surgery. In maintaining his opinion in the course of his oral evidence he relied particularly upon the paper produced by Aronin et al. The Aronin paper was agreed to be reputable by all of the expert witnesses, and had led to the strengthening of guidelines for the antibiotic treatment of suspected meningitis because it demonstrated a difference in morbidity, not just mortality, by reason of the earlier administration of antibiotics. Three stages of the progress of bacterial meningitis were identified by reference to factors which were demonstrated statistically to affect clinical outcome namely, hypotension, altered mental state and seizures. In Stage I there were none of the adverse features. It was agreed that the Claimant was in this Stage at the time she saw the Defendant and remained in that Stage until she lost consciousness at some time before she was found by her husband ‘at about 9.15’ (although note the finding I have already made about this). In Stage I there was one adverse feature and in Stage III two or more adverse features. The Claimant reached Stage III when she suffered the seizure in the ambulance at 11.15 pm. Patients in the Aronin cohort who remained in Stage 1 before receiving antibiotic treatment did not necessarily suffer a poorer outcome notwithstanding a delay in treatment. However, those who were allowed to progress, particularly those who progressed untreated from Stage I to Stage III, suffered significantly worse outcomes, their chance of an adverse outcome increasing from 9% to 75% viz. a patient who was treated with antibiotics whilst in Stage I had a 91% chance of a good outcome, whereas that patient only had a 1 in 4 chance of avoiding a poor clinical outcome once they had progressed to Stage III. (Footnote: ⁶⁵)

Professor Wilson’s evidence

The effect of timing of antibiotic therapy on clinical outcome is considered in detail under this specific subheading at page 5/1012 of the Trial bundle:

“The effect of antibiotic timing on clinical outcome was analysed in two ways. For patients who remained in the same prognostic stage from arrival in the emergency department until their first dose of antibiotics, the time of delay in initiation of therapy was compared for those with and those without adverse clinical outcomes (viz. death or serious neurological damage) – (Table 5). As shown for the total cohort of 227 patients who remained in a given prognostic stage, the median delay in initiation of antibiotic therapy was 4.0 hours and did not significantly differ between patients with and those without an adverse outcome. ..... The results for patients whose prognostic stage advanced from arrival in the emergency department until the initiation of antibiotic therapy are shown in Table 6. Of the 45 patients who were in Stage I at the time of their arrival in the emergency department, 35 were in Stage I at the time of initial antibiotic therapy; however, 6 advanced to Stage II and 4 advanced to stage III. (As referred to above at paragraph 73) As noted, patients who advanced from Stage I to stage III before initiation of antibiotic therapy had a greater proprtion of adverse outcomes (3 of 4 [75%]) than those who remained in Stage I at the initiation of antibiotic therapy (3 of 35 [9%]) (P=0.008) (Footnote: ⁶⁸) Similarly, of the 191 patients who were at Stage III at the time of arrival in the emergency department, 159 were in Stage II at the time of initial antibiotic therapy but 32 advanced to Stage III. Patients who advanced from Stage II to Stage III before initiation of antibiotic therapy had a significantly greater proportion of adverse outcomes (20 of 32 [63%]) than those who remained in Stage II at the initiation of antibiotic therapy (56 of 163 [34%]) (P=0.003).

In the case of the Claimant one, of course, substitutes ‘leaving the Defendant’s surgery’ for ‘arrival in the emergency department’.

Finally, Professor Wilson was referred to the Proulx paper op.cit., and the passage cited at paragraph 12 above. He relied upon the fact that the Claimant had made “a remarkable recovery” notwithstanding the recorded Glasgow Coma Scale, suggesting that her immune response was good and was aided by antibiotics when given. Although the Proulx paper was dealing with mortality rather than morbidity, Professor Wilson confirmed that its findings accorded with his clinical experience.

Professor Schapira’s evidence, as provided in the joint statement following his meeting with Dr. Lecky, provided, of all the experts’ opinions in this case, what in my judgment was the clearest exposition of what would have been the probable outcome for the Claimant if intramuscular penicillin had been administered “at or about 17.20 and she had been immediately transferred to hospital”. He stated that:

“... timely administration of an appropriate dose of penicillin at 17.20 would, as opposed to its later administration at 23:00, have had a significant impact on outcome and ... on the balance of probabilities, Mrs. Coakley would have had a much better outcome. Importantly, this was an important “window of opportunity” to significantly affect outcome. The earlier treatment would, on the balance of probabilities, have prevented visual loss, deafness and also her facial weakness. (He) cannot exclude the possibility that she may have had some deafness or optic nerve injury, even with this earlier treatment but this would not have been as severe as currently and would not have been so severe as to cause actual functional impairment. This view is based upon the agreement that earlier effective treatment of meningitis leads to better outcome, particularly if treatment is given prior to the onset of neurological deficit including altered consciousness.” (Footnote: ⁶⁹)

As will be seen, it is noteworthy that Dr. Lecky did not totally disagree with Professor Schapira’s opinion, but expressed ‘better outcome’ as a possibility, rather than a probability, having regard to what he thought was “the rapidity of onset of neurological deficits”, agreeing that, in general, “the earlier the treatment the better the outcome and (the) later (the) treatment the worse the outcome”.

In his report on causation, Professor Schapira identified that:

“There were probably two processes that combined to cause her loss of vision. The first comprised the meningitic inflammatory process affecting the optic nerves, and the second involves the elevated intracranial pressure as documented at lumbar puncture and as seen on the CT scans. ...

There is unanimity amongst the experts that earlier treatment offers the best prognosis and particularly in the case of meningitis, the earlier administration even by an hour or so can have a dramatic beneficial effect on outcome... At the time Mrs Coakley presented to her general practitioner on 7 January 2008, she had no neurological deficits and had a normal Glasgow Coma Scale. There were no features of vascular collapse. She was therefore in a good prognostic group (no hypotension, no altered mental status, no seizures) in contrast to her condition when she was admitted to hospital”.

He went on to express the opinion as to the probable avoidance of serious neurological damage which he repeated in the joint report. In his evidence-in-chief he expanded on the mechanisms of neurological damage and particularly the relationship between the bacterial ‘load’ or ‘biomass’ and the triggering of inflammatory responses which are capable of causing progressive damage to blood vessels (including infarction) or the structure of nerves (including demyelination) whether alone or in combination, as well as raising intracranial pressure. He stated that the inflammatory response was proportionate to bacterial load, and hence to the amplifying cascade process, and that the greater the inflammatory response, the greater was the potential for neurological damage. Consequently, as he said, “killing bacteria is a good thing!” because it limits the potential for damage. He made it clear that if the Claimant had not had antibiotics at 11.00pm on 7^th January it is likely she would have died, but that there was nothing in her case that was unusual in terms of disease progression rate. Although he agreed that the outcome of blindness (without brain damage or death) was unusual he could see nothing in the unusualness of the case to justify departure from the general principle that earlier treatment is good. He emphasised the fact that the Claimant was neurologically intact when she saw the Defendant and that the much later seizure was a consequence of cerebral irritation caused by the presence (at that time) of bacterial toxins in the CSF. He too relied upon the Aronin paper to support his evidence, describing it as “a valuable guide as to what happens to a patient who remains in the same group as opposed to one who progresses from group to group”. Nor did he consider that the evidence as to total loss of sight having probably occurred as late as 11^th January presented any difficulty, this being simply a consequence of progressive accrual of damage to the optic nerve as a result of the inflammatory cascade. However, as he made clear, the cytokine response at 5.30pm on 7^th January would not have been the same as the response at and after 11.00 pm on that day because at the earlier time there would have been a much lower bacterial biomass and therefore a lower number of ‘triggers’ for the inflammatory response.

Cross-examination of Professor Schapira merely strengthened, by further elucidation, Professor Schapira’s explanations of the relationship between the bacterial load and the inflammatory response, including reference to, and reliance upon, the van Deuren paper (Footnote: ⁷⁰). Notwithstanding the fact that the inflammatory process was responsible for the damage to the optic nerve (and, as Professor Schapira accepted) possibly for the papilloedema discovered later, the Claimant’s immune response was effective and did not cause any damage beyond the optic nerve (for example to the brain itself or death). He made it clear that timely antibiotic treatment when there was a small pathogen biomass could abort the inflammatory process, thereby limiting the inflammatory response.

Professor Shaunak’s opinions on causation had begun from a mistaken base of opinion that the Claimant had “probably suffered from pneumococcal pneumonia with the infecting organism being streptococcus pneumonia and meningitis” (despite not having seen the Claimant’s chest xrays and the absence of any respiratory signs and symptoms), a position from which he was effectively removed during his oral evidence when he conceded that he “did not dissent” from the majority view as to the effective pathogen. In part, his stance had been affected by the fact that he was unwilling to accept the Southampton Laboratory’s positive PCR finding of meningococcal disease, mistakenly believing that the laboratory was not accredited, and because “we only ever use Manchester!” In paragraph 80 of his report he had identified the factors associated with “a bad outcome” (albeit at time of admission to hospital), but it was clear that these related to streptococcus. He also raised suggestions of stress related diabetes, a (totally unsupported) ‘history of alcohol excess’, and penicillin encephalopathy, none of which remained as either accurate or relevant matters by the end of his evidence. He had also emphasised, at the time of his joint meeting with Dr. Lynn, that in his opinion the Claimant “did not have a clinical indication to be treated with antibiotics at 17.20 hours” having formed that opinion solely on the basis of his conclusion that “Mrs Coakley’s rash was never purpuric in nature” despite this being one of the main issues of fact in the case. He also mistakenly believed that “the crucial damage to the optic nerve, auditory nerve and facial nerve” had occurred “within the brain” and “early on in the course of her bacterial meningitis” (this was the witnesses emphasis) concluding:

“it is in the context of cytokine mediated tissue injury within the brain itself that I have concluded that giving the antibiotics at 5.30 pm would not have changed the long term clinical outcome for her.” (Footnote: ⁷¹)

When it was pointed out to him (during examination-in-chief) that Dr. Hodgkins and Mr. Elston, the ophthalmic experts had, in fact, agreed – by way of a change in their opinions - that the loss of vision had occurred on 11^th January and not 7^th January as originally thought, Professor Shaunak stated that this did not affect his opinion!

Although Professor Shaunak maintained during cross-examination that if antibiotics had been given at 5.30 pm “in my opinion there would have been no difference”, he did not, in my judgment, provide a reasoned basis for this opinion. He was asked why, if there is no difference in outcome, antibiotics should be given at all, to which he responded “because GPs have it and it may save life!” - adding that “I agree this is counterintuitive” - ‘this’ being the opinion he had expressed as to no difference in outcome. He was also asked why, bearing in mind his opinion, he had referred to the Aronin paper in his report, to which he responded “I don’t know. I agree its a good paper ... I’ve spent many hours going through Aronin!” It was quite clear that this witness appreciated that his opinion was not supported by the Aronin paper.

Professor French also began from a base in which he suggested that the Claimant had suffered from a condition “closely resembling fulminant meningococcal meningo-encephalitis .... (which) usually comes on very suddenly and progresses very rapidly” from which he later resiled. In his report, he too had relied upon the original conclusion of Mr. Elston that the damage to the optic nerves was “very early in the course of the illness” (Footnote: ⁷²) as supporting his view on causation. When, by the time he came to his meeting with Professor Wilson, he had been made aware that the ophthalmology experts “agree that the vision loss occurred as a result of inflammatory infarction of the optic nerves on the 11^th January, that is after 3-4 days intravenous antibiotics”, he observed “this confirms (my) view that antibiotics do not immediately stop continuing inflammation”. He then added that “giving an additional single dose of penicillin on the 7^th January would not have altered the outcome for vision.” Leaving aside, for the moment, the fact that any penicillin administered by the Defendant would have been followed by immediate referral to hospital and intravenous antibiotics (rather than the ‘single dose’ to which he refers), Professor French also gave no reasoning for the opinion he expressed, even though he did agree (Footnote: ⁷³) that “the earlier treatment was given the better the result.”

In the course of his oral evidence he suggested that because blindness was not prevented by the giving of antibiotics at 11.00pm on 7^th January and at the hospital thereafter, it was his opinion that “she wouldn’t have responded (to antibiotics) earlier”, because “if we don’t know why blindness was caused, we can’t say it would probably have been cured.” When cross-examined he agreed that bacterial load was related to outcome, that treatment timing was important because “the earlier you kill, the earlier you stop the replication (of bacteria)”, and that it was widely accepted that the greater the delay, the worse the prognosis. He also agreed that prevention of the exponential multiplication of bacteria reduces the inflammatory response which would otherwise have occurred. He also agreed that the rate at which the Claimant’s condition had deteriorated without treatment was within the normal spectrum. He also acknowledged that the Aronin paper accorded with clinical experience and its message was intuitive. Notwithstanding these concessions he maintained his opinion that earlier antibiotic treatment would not have affected the outcome, but without clearly explaining why.

Dr. Lecky had never expressed a firm opinion on the issue of causation. In the joint report he had said:

“ treatment at this time (5.20 pm) may possibly have led to a better outcome but ... even with the administration of intramuscular penicillin at 17.20, Mrs. Coakley would still have had the possibility of major neurological deficit.”

When giving his evidence-in-chief, and mindful of the fact that the ophthalmic evidence had changed, Dr. Lecky offered a new opinion. His new opinion was that the outcome would not have been altered by the delay in the administration of antibiotics: “a delay of a few hours would not alter an event (the blindness) which was so remote in time”. He was unable to offer any reason for this opinion. In cross-examination he accepted that meningococcal disease was progressive and that the exponential increase in the bacterial load meant that the inflammatory response was also exponential, and that “killing the bugs stops the multiplication which will reduce the response, but won’t switch it off.” He also agreed that the neurological outcome was affected by effective treatment and the stage at which it was given as well as the virulence of the strain and the individual host immune response. He agreed that it was likely that there was demyelination of the optic nerves with progressive loss of axons by this cause or, indeed, any other mechanism caused by the inflammatory response. Finally he agreed that, in terms of considering outcome, there was “no better paper” than the Aronin paper and that it was “a reliable guide”. During very extensive cross-examination by Mr. Latimer-Sayer, Dr. Lecky frankly struggled to provide answers to the questions put to him, it being quite apparent that he had not thought about the case sufficiently when preparing his report viz. “when I prepared my report Aronin was not on the horizon” – “it was not clear to me what questions I would be asked in court” – “there is no mention of literature in my report”. At the end of his cross-examination he said:

“I do not have a reason to explain why severe optic nerve damage occurred on 11^th January other than it was related to the infarction.”

The ophthalmic experts, Mr. Hodgkins for the Claimant and Mr. Elston for the Defendant, did not address the issue of whether earlier administration of antibiotics would have affected the damage to the optic nerve, and deferred to the other experts on that issue. Notwithstanding that they were to some extent misled by proceeding from a baseline in which they assumed that the Claimant had suffered ‘fulminant bacterial meningoencephalitis’ (even though Mr. Elston said that he understood the word ‘fulminant’ to be purely descriptive), they did agree that the damage to the optic nerves was a consequence of vasculitis which was progressive, leading to infarction: “the pathological process causing permanent visual damage was initiated in the acute (fulminant) phase of the infection but continued over the next few days” (Footnote: ⁷⁴) (my emphasis added). They also agreed that damage had not been caused by raised intracranial pressure or by optic neuritis. Little reliance was, or in my judgment, could be, placed on the original reports prepared by either of these experts given the later change in opinion as to when the damage to the optic nerve was complete and the fact that both of them resiled from much of what they had said, because it was based upon an incorrect view of the nature of the disease. Nor did the oral evidence of either expert add to the store of knowledge that bears on the issues I have to determine, save that Mr. Elston did explain that for reasonable visual function to exist it is only necessary to have 10% of the axons of the optic nerves; in other words, the gradual destruction of axons over a period of time will not result in blindness until 90% of them have been destroyed.

Dr. West, a Consultant Audivestibular Consultant, was the only expert to be instructed (by the Claimant’s solicitor, and not on a joint basis) in respect of the Claimant’s hearing loss. Much of his report was concerned with the Claimant’s condition and prognosis, but he did deal with how the damage had been caused. He stated that the hearing loss clearly resulted from the bacterial meningitis and that this was due to “direct spread of the infective organisms into the inner ear either via the internal auditory meatus or via the cochlear aqueduct.” He continued:

“Damage occurs as a direct result of inflammation and the release of bacterial toxin. There is good evidence that vestibulo-cochlear damage occurs as a relatively early complication of bacterial meningitis and therefore early intervention with antimicrobial treatment is of particularly crucial importance in the avoidance of deafness. Delayed diagnosis and treatment in this case is likely to have contributed materially to the development of deafness.” (Footnote: ⁷⁵)

Dr. West gave oral evidence. When asked specifically about the likely outcome if the Claimant had been given antibiotics when seen by the Defendant, he said that it was very likely, to a high level of probability, that the outcome would have been much better than it was and that it was likely that it would have been prevented. The reason for this was that because there was a direct invasion of bacteria up the cochlear aqueduct, the exponential growth of the bacteria, and hence the direct damage caused, would have been prevented by antibiotics. During the course of his cross-examination Dr. West made an important point upon which more general reliance is placed by the Claimant. He stated that because the ear is so exquisitely sensitive and a “very energy requiring organ”, if there were very small numbers of bacteria in the CSF it is likely that they would be in the fluid of the inner ear and the patient would be aware of something and complaining with an expression such as ‘my ear feels funny’. Consequently, Dr. West continued, if there were no symptoms associated with hearing, then there would be very small numbers of bacteria in the CSF and it would be very early in the disease process.

As is made clear in the opening paragraphs of Mr. Balcombe QC’s written closing submissions, where a patient presents to a general medical practitioner with signs and symptoms which either warrant a diagnosis of meningitis or where meningitis should be strongly suspected, and, I would add, cannot reasonably be excluded, that medical practitioner would be negligent (by the standards already identified) if penicillin was not administered and the patient was not referred to hospital. This was agreed by the expert witnesses in general medical practice.

Thus the question of fact is whether the Claimant did present with those signs and symptoms. It is agreed that relevant signs and symptoms of meningococcal meningitis (the disease from which it is now clear the Claimant was in fact suffering when she presented at the Defendant’s surgery – and as I find as a fact if it is necessary to do so) include a history of being unwell, petechial and / or purpuric rash, fever, headache, neck stiffness. It is agreed that the question of whether the Claimant was indeed suffering from meningitis was actually raised during the course of the consultation. Whilst this does not, per se, give rise to a suspicion, let alone a strong suspicion, that it was present, it is clearly relevant to the question of whether there was a reasonable basis for excluding it.

Given the apparent significant differences in the accounts of the Claimant’s presentation I have had to determine whose evidence, on material disputes of fact, I accept. Fortunately, this is not a case in which there is any evidence of dishonesty or deliberate exaggeration. Also, fortunately, determination of disputed facts is not something that is dependent solely upon my assessment of the accuracy and reliability of Claimant and the Defendant as witnesses. I have been assisted by facts which are not disputed including that:

Despite careful and lengthy cross-examination the Claimant maintained her description of the signs and symptoms with which she presented. She did not concede any doubt about the accuracy of her witness statement notwithstanding that it was suggested to her that this account was one that had changed from earlier accounts. Her response to that suggestion was that any changes in account were the consequence of her desire to clarify rather than introduce facts which were inaccurate. It is noteworthy that the original draft Particulars of Claim, accompanying the Letter of Claim in December 2010, whilst considerably less descriptive than the witness statement, nonetheless referred to rashes on four separate areas of the Claimant’s body which were neither raised nor itchy. The witness statement is not inconsistent with the original draft pleading. The only alleged inconsistency is between the original draft pleading and the served pleading, the latter including reference to the rash across her midriff having been noticed ‘later in the day’ than the rashes on her arms and left hand. I am quite satisfied that if this is indeed an inconsistency, it is neither material, nor such as to undermine the reliability of the Claimant’s witness statement and oral evidence. In my judgment, the reference to ‘later in the day’ is likely to have been a consequence of the fact that the Claimant did in fact check her rashes before leaving for the Defendant’s surgery, and not a contradiction of the fact that she said that she had in fact seen that rash when rising from bed, naked, at 10.30 in the morning.

I reject the submission that the Claimant’s account of her signs and symptoms has ‘evolved’. I accept her evidence that when it came to her providing the content of her witness statement for the purposes of trial she clarified earlier descriptions. It is likely that she was aware that she needed to give the best, and fullest, description that she could. The suggestion of an ‘evolution’ of her account was never particularised (other than by references to alleged differences), as it should have been were it intended to caste any serious doubt on the accuracy and reliability of the witness statement. Although there were passing references, or veiled suggestions, that the account might have been the product of the Claimant’s discussions with expert witnesses, or even her legal team, or researches undertaken by the Claimant (notwithstanding her disabilities), these were never the subject of direct accusation.

It follows that I am satisfied, and find as a fact, that the Claimant’s account of her signs and symptoms in her witness statement is reliable and accurate, not only in terms of the various rashes, but also in terms of her complaint of neck stiffness. She had every reason to recall those signs. She presented as a witness who did in fact have recall of the signs and symptoms about which she was speaking. Overall, even on matters which were not significant to my findings, I found the Claimant to be an entirely reliable and careful witness. This being so, it follows that the Defendant failed to identify and record what were, as all experts have agreed, rashes typical and characteristic of bacterial meningitis. It is significant that the Defendant had never seen a menigococcal purpuric rash in general practice, and referred to having seen only one case of a meningitic purpuric rash in a hospital in Sheffield in her early years as a doctor. I am not satisfied that she was able to distinguish between different types of rash, and formed a fixed view early on in the consultation that what she was shown was an allergic reaction to medication and therefore likely to be itchy. I am satisfied, and find as a fact, that she was never told that any of the rashes were in fact itchy, because, as is common ground, the meningococcal rashes from which the Claimant was undoubtedly suffering, are not in fact itchy.

My finding that the Defendant negligently failed to identify rashes which would have led her to a very high suspicion of meningitis, is reinforced by the evidence of the Defendant herself. She said the following in the course of cross-examination:

“I agree that the Claimant could have been suffering from meningitis which I did not identify.

I presume she had a meningococcal rash on the basis of what the experts say.

I agree she could not have been suffering from an urticarial rash at the time she consulted me.

Therefore I was wrong!”

In my judgment, this concession was not the product of hindsight. The Defendant was accepting that, given the agreement of the expert witnesses that the Claimant was indeed suffering meningitis at the time of the consultation, she did not have the type of rash (an urticarial rash) which she had in fact identified. It was in this respect that she acknowledged that she had made a mistake. That being so, it follows that the Defendant’s evidence is unreliable on a crucial (probably ‘the’ crucial) matter of fact.

In the event, I find that the Defendant’s error was not confined to mistakenly describing the rash as ‘urticarial patches’, as opposed to a purpuric and / or petechial rash, as I find as a fact it was, but that she also failed to examine the Claimant’s neck for stiffness, which she would probably have elicited had she done so. There is nothing in the Defendant’s record of the consultation to suggest that she did examine for neck stiffness notwithstanding the fact that it is agreed the Claimant referred to meningitis. The Claimant’s evidence, which I accept, is that the Defendant merely enquired about neck stiffness. The Claimant told her that she did have a stiff neck but that she had this quite often. In my judgment, this response distracted the Defendant from performing an actual examination, and because, as I have found, she was unable to correctly identify a meningitic rash, responded that the rash was ‘not a meningitis rash’ in answer to the Claimant’s direct question. I am also satisfied that the Defendant was not sufficiently aware of the symptoms of meningitis to make any proper enquiry about the Claimant’s complaints of headache. The Claimant has always described the headache as being a ‘pressure’ headache, not sinus pain. The fact that she may have put her hands to her face and drawn them across it was not sufficient to allow the Defendant to dismiss the reported headache, particularly in the context of a lengthy prodromal illness.

If further support was needed for my rejection of the Defendant’s evidence, it is found in the wholly unsatisfactory evidence as to the record she made. Whilst I can accept that the Claimant’s case is memorable because of its tragic outcome, I cannot accept that the Defendant had any reliable memory of the consultation for very long after it had occurred, particularly bearing in mind her actual diagnosis was not a memorable one (respiratory infection), and the fact that she saw many patients that afternoon both before and after the Claimant. She was unable to say when she had made the note of the consultation with the Claimant, but given the time allocated for each patient it is likely, as she accepted, that the notes were not made until after the surgery had finished at 6.00 pm, as I find. The most significant omissions from the note she actually made was the finding of lesions on the Claimant’s back and the recording of rashes which I am satisfied she had been shown by the Claimant on her arms, left hand and midriff. The mere noting of ‘urticarial patches’ has led me to conclude that she paid no particular attention to the rashes she was shown, because she did not believe they were relevant to the conclusion she had already reached. She did not carefully examine the rashes or conduct an examination to discover the location of other rashes. She did not even mention to the Claimant the rash she did find of the Claimant’s back. She did not test for blanching and I am not satisfied that she understood that she should have done, even though, in her oral evidence she conceded regret in not having done so. She prescribed no medication for the rash or relief of any itch she thought was present. She made no note of thinking the rash was an allergic reaction. The Defendant told me that the expanded account of the consultation (including reference, for the first time, to a rash on the Claimant’s back) was based on other notes she had made after she had become aware of the Claimant’s injuries. Those notes, or evidence of those notes, were never produced and I am not satisfied that they ever existed in any formal context. If the Defendant had considered that it was necessary to clarify or expand her note of the consultation she could, and would, have supplemented the computer record with clear notation that it was being amended retrospectively. All in all, the Defendant’s note was, in my judgment, such as leads to a conclusion that she never began to consider meningitis seriously even when it was mentioned. Had she done so, she would undoubtedly have made a note to this effect. The actual content of the note, coupled with conceded omissions from the note is, in my judgment, supportive evidence of the lack of care which I have found there was. In addition, and giving due allowance for the position in which she found herself, it was clear that the Defendant was less than confident in the evidence she gave.

In seeking to persuade me that I should reject the Claimant’s evidence as to the rashes with which said she presented to the Defendant, great reliance was placed on the records made much later in the history by others, not least because it was agreed that the rashes which the Claimant described would not disappear within the time frame of those records. The Defendant relied upon those records which were not consistent with the Claimant’s description. In fact, in my judgment, there is only one record that appears to be inconsistent, and that is the one made by a junior doctor called Giles following a ward round by Mr. Thomas. The other records including the ambulance record are either not inconsistent with the Claimant’s evidence or supportive of the existence of a characteristic purpuric rash. Amongst the records which are not inconsistent, I include the short note made (again by a junior doctor) following Mr. Dryden’s ward round on 8^th January; that note reads “no pupura (mis-spelt!), but non blanching” which is suggestive of either an error in the note or some other kind of non-blanching rash. Given the agreed condition, this could only be a petechial rash. Both the first and second hospital records refer to purpuric rashes. So far as the record of Mr. Thomas’s ward round is concerned viz. “No obvious purpuric rash, occasional erythematous papules ? itchy” there is no evidence as to who it was that formulated this note or whether Mr. Thomas ever approved it. Clearly he relied upon it to note the opinion “skin lesions not characteristic of meningococcus” [3A/309] but that does not mean that the note was itself, reliable. In respect of the one discrete note made by Dr. Ritchie, that refers to ‘History from Husband’, and includes a reference to ‘blotchy rash’, I find that this does not assist me one way or the other. There is no doubt that at one point Mr. Coakley had been shown a rash by one of the paramedics, but whether the expression ‘blotchy’ came directly from him (which he disputed) or from elsewhere, does not in my judgment undermine my conclusions in respect of the Claimant’s evidence. In my judgment, given that none of those responsible for the Claimant’s care in hospital were required to make witness statements or called to be examined about their notes, the weight I am able to give to anything which is arguably inconsistent with the Claimant’s evidence, and the agreed factual matrix surrounding it (including, particularly, the working diagnosis of meningitis adopted by those in charge of the Claimant’s hospital care pending test results), is very slight compared to the weight I give to the Claimant’s evidence. Whilst I have been made aware of a volume of correspondence between solicitors as to the status of the medical records and the need to call hospital staff as witnesses, the parties always had the right as well as the opportunity to adduce any additional evidence beyond the physical medical records, if they really thought it necessary to do so. The fact that I have only the records themselves, whilst undoubtedly forming part of the evidence I have had to consider, means that the weight I can give to their contents is limited.

I am mindful of the fact that I received a total of 64 pages of typed submissions on behalf of the Defendant and 80 pages of typed submissions on behalf of the Claimant, dealing with every detail of the 14 days of evidence. In dealing with the issue of breach of duty, and reaching the conclusion that breach of duty has been established for the reasons I have given, I have not sought to answer each and every point made on behalf of the Defendant or to rely on each and every point made on behalf of the Claimant in the many pages devoted exclusively to that issue. That is not to say I have not carefully considered each of them. In my judgment there are none which undermine my conclusion that the Claimant’s evidence is reliable on those facts which she gave in evidence as to the nature of her illness, and the signs and symptoms which she had at and before the time she saw the Defendant. To the extent that there is a conflict as to fact between the evidence of the Claimant and that of the Defendant or those responsible for the Claimant’s care in hospital, I prefer the evidence of the Claimant for the reasons set out in the preceding paragraphs. There are no aspects of the Claimant’s evidence as to fact which I have found to be unreliable.

Thus, on the issue of breach of duty, in addition to those matters which I have identified upon which there is no dispute, I make the following findings of fact:

I agree with Mr. Balcombe QC’s submission that, in respect of the issue of causation, “the question that should be asked is whether the Claimant has established, on the balance of probabilities, that ‘but for’ the lack of penicillin at 17.30 and hospital admission immediately thereafter, she would not have suffered blindness and other injury”.

I also agree with Miss Rodway QC’s exposition, at page 35 of her closing written submissions, of the law relating to unexpected damage and remoteness, which I incorporate by reference. In particular, the fact that everyone agreed that the Claimant’s blindness was unusual, if not unique, cannot mean that she is unable to establish causation. The Defendant did not seek to argue this.

Although the Claimant’s primary case on causation is that ‘but for’ the failure to treat the Claimant with penicillin and by immediate referral to hospital (where she would undoubtedly have received intravenous antibiotics), she would, on the balance of probabilities have made a full recovery, avoiding blindness and the other injuries she sustained, Miss Rodway QC argued, relying upon Bailey v Ministry of Defence [2008] EWCA Civ 882 that:

“In the event that the court does not accept the Claimant’s primary case, in particular because it considers that the current state of medical knowledge does not allow such a finding to be made, the Claimant further argues that the principles in Bailey apply and she succeeds on causation if she can show that the Defendant’s breach of duty materially contributed to her injuries, in other words, that but for the negligence she would have had a materially better outcome.”

In Bailey at paragraph 46 Waller LJ stated:

“In my view one cannot draw a distinction between medical negligence cases and others. I would summarise the position in relation to cumulative cause cases as follows. If the evidence demonstrates on a balance of probabilities that the injury would have occurred as a result of the non-tortious cause or causes in any event, the claimant will have failed to establish that the tortious cause contributed. Hotson exemplifies such a situation. If the evidence demonstrates that ‘but for’ the contribution of the tortious cause the injury would probably not have occurred, the claimant will (obviously) have discharged the burden. In a case where medical science cannot establish the probability that ‘but for’ an act of negligence the injury would not have happened but can establish that the contribution of the negligent cause was more than negligible, the ‘but for’ test is modified, and the claimant will succeed”.

Miss Rodway QC argued that in the instant case the cumulative causes are the meningococcal meningitis and the delay in treating it. She referred me to the recent case of Pringle v Nestor Prime [2014] EWHC 1308 (QB) in which Michael Harvey QC, sitting as a Judge of the High Court, held that had he not found for the Claimant on the ‘but for’ test that he would have accepted her alternative argument based upon Bailey. This case involved very similar facts to the instant case. The Claimant suffered surgical amputations of her feet due to gangrene consequent upon meningococcal septicaemia. The judge found that there was a delay in providing adequate treatment (namely intravenous fluids), and that a delay of three hours would have materially contributed to the injuries because the progression of the disease was necessarily gradual and the delay made a non-negligible contribution. At paragraph 129 of his judgment he said:

“I do not consider that medical science can determine whether there was a critical time before which treatment would have been effective, and after which treatment would have been ineffective. The progression of the disease is necessarily gradual, and will vary between patients. What I think can be said is that the delay between 04.00 and 07.00 in the commencement of treatment would have made a material contribution, more than negligible, to the development of (the Claimant’s) gangrene and the amputation of her feet.”

Miss Rodway QC went on to submit that if I were to conclude that the current state of medical knowledge precluded a finding that the Claimant’s blindness would have been averted had she been treated at about 5.15pm, the Claimant still succeeds if she can show that earlier treatment would have made a material difference to the outcome i.e. to her blindness. Subject to the caveat within this submission, I agree with it.

Miss Rodway QC referred to Mr Elston’s evidence that blindness was a progressive condition and that the extent of vision depended upon the number of remaining axons, arguing that:

“the natural corollary is that the timing of treatment has a direct and proportionate impact on outcome such that delay in treatment causes greater loss of optic nerve axons, resulting in a progressive worsening of vision. Any such worsening or deterioration in vision would amount to a material contribution to the claimant’s injuries. Bearing in mind Mr Elston confirmed that only 10% of optical nerve axons were necessary in order for the Claimant to retain functional vision, it would mean that the optical nerve axons would have had to have been already more than 90% obliterated (or an irreversible process already set in train for the optic nerve axons to become more than 90% obliterated) for the delay not to have made a material contribution to the outcome.”

Before considering further whether, on the facts of this case Bailey applies, it is necessary to consider the evidence which I accept bearing on the issue of causation.

There is no doubt in this case, and I so find, that but for the fact that the Claimant suffered bacterial meningitis she would not have suffered blindness, deafness and other neurological damage. There is no suggestion of any coincidental medical cause of any of these injuries. There is also no doubt that meningococcal meningitis is a treatable disease and that provided treatment is commenced early enough antimicrobial therapy is, in the case of an individual patient, more likely than not to be effective treatment whereby significant injury is avoided. None of the expert witnesses called in this case disagreed with this proposition. There will, of course, always be exceptional cases, where, because of an individual’s particular susceptibilities or vulnerabilities, treatment may not prevent injury or even death, however, there is nothing in the instant case to suggest that the Claimant falls into this category of patient. The mere fact that blindness is an unusual consequence does not mean that the Claimant had particular susceptibility or vulnerability to the type of injury she suffered, but even if she did, this would not mean that he claim would fail, given that a tortfeasor has to take their victim as they find them.

As is clear from my summary of the expert evidence in this case, the main difference between the expert witnesses was that some of them relied upon the intuitive, logical proposition that early treatment of meningococcal meningitis viz. at the time of the consultation with the Defendant, in its early stages would probably have avoided injury, supported by their own clinical experience and the literature, and the others simply pointed to the unusual outcome for this Claimant and, without advancing any sound reasoning for their opinion, simply refused to accept that blindness and other damage would have been avoided had treatment been given by the Defendant.

In my judgment there is powerful evidence which leads me to find as a fact that, when the Claimant presented to the Defendant she was indeed in the early stage of meningococcal disease, and that consequently the bacterial load and any consequent cytokine response present or inevitable at that time, was likely to be destroyed not only by the antibiotic which the Defendant ought to have administered, but also the antibiotic treatment which would have been provided when the Claimant reached hospital very much earlier than she actually did. As to this latter point, given the relative proximity of the Royal Hampshire Hospital to the Defendant’s surgery, and the fact that it would have been the Defendant who made the urgent referral of a case of suspected meningitis, it is reasonable to conclude that the Claimant would have been in hospital and being treated by no later than 6.30 pm, and possibly even sooner, that is some 5 hours earlier than was in fact the case.

Those expert witnesses who expressed an unreserved opinion that treatment at or about 5.30pm would have prevented injury (namely, Dr. Lynn, Professor Wilson and Professor Schapira) relied upon the fact, not disputed by any witness, that the Claimant was neurologically intact when she was seen by the Defendant, as well as the literature which supported a conclusion that the earlier the treatment, the better the outcome, particularly where there was no neurological damage. Beyond headache, she had no signs or symptoms of any neurological damage. In particular she had no problems with either her sight or her hearing, and nor did she have any symptoms of altered consciousness, let alone of seizures. Whilst it was agreed that it is likely that the meningococcal bacteria had crossed the blood-brain barrier by the time the Claimant saw the Defendant, the compelling evidence of Dr. West, which was unchallenged (indeed the evidence was illicited during cross-examination), was that the bacterial load was likely to have been very small at this time because of the particular sensitivity of the cochlea to bacterial attack and the absence of any complaint of hearing being adversely affected.

In addition to providing no cogent, reasoned argument for their opinion that injury would not have been avoided if treatment had been provided by the Defendant, I reject the evidence of Professors Shaunak and French and Dr. Lecky (to the extent that it conflicts with that of Professors Wilson and Schapira and Dr. Lynn) for the following reasons:

Although there are qualifications in respect of the conclusions reached in the Aronin paper, identified within the body of the paper itself, I am satisfied, and so find, that those witnesses (notably Dr. Lynn, Professor Wilson and Professor Schapira) who relied upon it in support of their opinion that the Claimant would have avoided injury had she been treated by the Defendant, were not only entitled to place reliance upon it but were justified in so doing. I was told that the paper was widely acknowledged to be authoritative and statistically valid. It had been relied upon in the United States of America to institute changes in clinical practice. Above all, it was the evidence of those who relied upon it, that it accorded with their experience of clinical practice. No-one has advanced any reason for excluding the Claimant from the Aronin prognostic model. There is no doubt that at the time of the consultation with the Defendant, the Claimant was on Aronin Stage I and that by reason of the failure to treat was allowed to progress to Stage III. In Stage I and if, as would probably have been the case had she been treated, she had remained in Stage I, then the prospects of a clinically adverse outcome were very small indeed, so small that it can confidently be concluded, as I do, that she would probably not have suffered any neurological damage at all. In my judgment, the failure to treat the Claimant, allowed her to move from Aronin Stage I to Stage II and then to Stage III as a consequence of the exponential growth of the bacterial biomass and the associated and proportionate cytokine inflammatory response. It was, in my judgment, as a result of these movements that progressive damage was caused to the optic nerve. In my judgment it matters not whether the process was purely meningococcal meningitis or meningo-encephalitis; both have meningococcal aetiology and both cause progressive damage.

It follows that I reject the criticisms made by Mr. Balcombe QC of the evidence given by Dr. Lynn, Professor Wilson and Professor Schapira. In particular, and to the extent that Dr. Lynn was criticised for asserting that early antibiotic treatment would have prevented the injury to sight ‘irrespective of the mechanism of damage’ (he having considered the mechanism to have been raised intracranial pressure), I reject that criticism. There were indeed a number of possible mechanisms for the neurological damage, ranging from direct bacterial damage, through raised intracranial pressure, cerebral oedema, nerve demyelination, vascular damage or even cortical damage. Whatever the ‘mechanism’ the underlying cause was the bacterial disease and the inflammatory responses to it. The probable mechansims were identified by Dr. West and Mr. Elston, and I accept their essentially unchallenged evidence in this respect. Both were indisputably the consequence of untreated meningococcal disease. For the reasons advanced by Mr. Balcombe QC at paragraph 4.9 of his written submissions, I was not assisted by the ophthalmic expert evidence of Mr. Hodgkins, although his explanation of how pus would form as a consequence of bacterial infection and collect at the base of the skull in an area where the optic nerves are situated, provided yet another credible mechanism for damage.

In reaching my conclusions I carefully considered whether the Defendant’s case, as summarised by Mr. Balcombe QC in section 12 of his written submissions, was actually supported by more than mere assertions (however dressed up) that treatment by the Defendant would not have avoided the damage suffered. In my judgment it was not. I reject the contention that the Claimant’s case was atypical in terms of its onset and progress; there was considerable evidence, as highlighted above and which I accept, was that it was not. Bacterial meningitis always presents as an emergency because of its rapid progression. Consequently, the submission (Footnote: ⁷⁷) that:

“Logically, the only plausible explanation for loss of consciousness so soon after the Claimant was seen by the Defendant is that by 17.30 the inflammatory process in the CSF that ultimately was to lead to optic nerve damage was already at an advanced stage, even though there were no overt neurological signs”

is not sustainable. Not only was the loss of consciousness not “so soon after”, as submitted, but rather, as I find, within the normal spectrum of progressive, exponential, advancement of the disease process, but it is illogical that if an inflammatory process in the CSF was “at an advanced stage” there would be no signs or symptoms of it at all.

Whilst it is true that the damage was very unusual it was within a spectrum of neurological damage that unfortunately still culminates in a significant proportion of cases where death is the outcome. For obvious reasons it is impossible to determine how many of those who die will have suffered damage to the optic nerves before death. However, in a chapter in Walsh and Hoyt’s textbook ‘Clinical Neuro-Ophthalmology’ (6^th Edition, 2005) produced and relied upon by Professor Schapira (Footnote: ⁷⁸), three such cases are reported. The fact that both Dr. Lynn and Professor Wilson identified a ‘window of opportunity’ of no more than about 2½ hours after the consultation with the Defendant for treatment leading to the avoidance of loss of sight does not, when loss of sight was not a final outcome until 11^th January, undermine their opinions. Mr. Elston made it clear that damage was gradual and progressive and therefore likely to have been caused by the cytokine response to the bacterial damage persisting beyond the time that all bacteria were killed. There was no suggestion that the Claimant’s sight was perfect until some sudden event occurred on 11^th January.

It follows from the conclusion I have reached that it is unnecessary for me to deal with the alternative case in detail. However, had I been unable to conclude, as I have, that the damage suffered by the claimed would probably have been avoided had she been given penicillin by the Defendant and referred to hospital, then, because this would necessarily have involved a finding that the medical evidence could not establish when it was that neurological injury would have been avoidable (given that there was no such injury at 5.30 pm), I would have concluded that this was a case where Bailey would have allowed the Claimant to have succeeded on the basis that the delay in treatment made a material contribution to that damage.

Whilst there can be no doubt that this was a case of meningitis with unusual consequences, in my judgment the final definition of the cases advanced on behalf of each of the parties, and consequently the resolution of the medical issues, was not assisted by the way in which expert evidence was prepared, particularly when it came to the preparation of joint statements. The fact that much of the evidence was only available shortly before trial and the lack of agreement about agendas for the meetings of experts (let alone the instigation of a meeting of six experts with a failure to complete it) led to unnecessary prolongation of the trial during the course of which much ‘dead wood’ had to be identified and then disposed of. If agendas for expert meetings are necessary (which, in my experience, is rarely the case), and cannot be agreed, then the court should determine them rather than separate agendas being placed before experts with the obvious potential for confusion and inconsistency. However, having made those criticisms I must pay tribute to the enormous assistance I have been given by all counsel, leading and junior, not only in terms of written opening and closing submissions but in the adducing of evidence particularly, as I have already remarked, having regard to the Claimant’s disabilities.

Thus the Claimant succeeds on the issues of liability in respect of both breach of duty and causation. The parties having reached agreement on damages, I hope that they can agree a form of order reflecting the consequences of this judgment.