Bailey v The Ministry of Defence & Anor

On 26 January 2001, when an inpatient on the renal ward at St Mary’s Hospital, Portsmouth, the Claimant suffered a cardiac arrest that caused her to suffer hypoxic brain damage.

For the previous twelve days she had been an inpatient in the Intensive Therapy Unit (ITU) at the Queen Alexandra Hospital, Portsmouth, to which hospital she had been transferred following treatment at the Royal Hospital Haslar in Gosport.

The Claimant is now seriously disabled and, if it is established that the brain damage she suffered arose from negligence, she will recover substantial damages. The trial before me has been confined to the issues of breach of duty and causation.

Until shortly before the trial the claim advanced on her behalf embraced allegations against those responsible for her treatment at the Royal Hospital Haslar (at the material time it being managed by the First Defendant, the Ministry of Defence) and against those responsible for her care at the Queen Alexandra and St Mary’s Hospitals (for which the Second Defendants, the Portsmouth Hospitals NHS Trust, are and were responsible).

The essence of the case against the Second Defendants was that Claimant should not have been transferred from the ITU to the renal ward when she was and that once there she should have been more closely monitored than she was. Mr Christopher Gibson QC, representing the Claimant, explained to me at the outset of the trial that following (i) the eventual disclosure of the large ITU charts that the Second Defendants had been unable to find initially and (ii) the meeting of the experts in intensive medicine, he and the team advising the Claimant’s family took the view that there was no realistic prospect of establishing the case against the Second Defendants. Against that background, and subject to the Court’s approval, it was agreed that the claim against the Second Defendants should be dismissed with no order as to costs. After the background was explained to me, I approved that course.

The Claimant’s case against the First Defendant was maintained. I will say more about it in detail shortly, but in essence it is that the alleged negligent treatment whilst at the Royal Haslar Hospital left her so significantly weakened that it caused or materially contributed to the cardiac arrest.

The First Defendant has accepted certain criticisms of the care and treatment at the Royal Haslar Hospital, though not all levelled against it, but has argued that the Claimant cannot establish a sufficient causal link between any negligence that may have been admitted or established and the eventual cardiac arrest some two weeks later.

The Claimant was aged 35 at the time of the material events and was engaged to be married to Mr Shawn East. She and Mr East went to Kenya on holiday between 24 September and 9 October 2000. Although otherwise healthy she had been experiencing some stomach upsets during the earlier part of the year. Following her return from Kenya, where she had had some gastric problems, she appeared jaundiced and continued to experience further gastric difficulties. The overall working diagnosis during November and December of those who saw her at the Royal Hospital Haslar where she had been referred was of infective hepatitis. This working diagnosis was not substantially criticised during the trial and the clinicians may have been thrown off the scent by the holiday in Kenya. However, by early January 2001, with things getting progressively worse, attention was being focused on the possibility of gallstones having been the cause of the problem.

Bile, which is made in the liver, is stored in the gall bladder awaiting the ingestion of food. When food is ingested bile is exuded from the gall bladder into the main bile duct and passes along that duct into the duodenum. Gallstones occur when stones are formed in and from bile. Often they are entirely benign, remain within the gall bladder and cause no symptoms. However, they can be dislodged and if a gallstone becomes lodged in the bile duct such that bile cannot pass into the gut it passes into the blood stream leading to jaundice. The yellow staining of the tissues that is the hallmark of jaundice is caused by an increase in the serum bilirubin level. When the Claimant’s gall bladder had been made the subject of an ultrasound scan on 13 November 2000 gallstones were found, but there was no evidence of bile duct dilatation. A repeat ultrasound scan on 5 January 2001 showed a markedly dilated common bile duct at the head of the pancreas where it was thought that there was probably a gallstone.

Against that background the opinion of Wing Commander (now Group Captain) Mark Watkins was sought. He was (and remains) a Consultant Surgeon at the Royal Hospital Haslar with a particular interest in endoscopic retrograde cholangio-pancreatography (ERCP). The question was raised as to whether the Claimant required an urgent ERCP given the suggestion of an obstructive jaundice, that perception being evidenced by the most recent ultrasound scan.

ERCP is a procedure used to diagnose and treat conditions of the bile ducts, liver, gall bladder and pancreas. The patient is sedated and asked to swallow the first section of the endoscope (a thin flexible fibre-optic telescope). The operator then guides the endoscope to the desired destination by watching its path through the eyepiece or on an associated television monitor. The endoscope also has a side channel down which other tubes or instruments can be passed. A contrast dye can be introduced into the bile or pancreatic ducts and X-rays used to show the details of the ducts. This can show the presence of gallstones lodged in the bile duct. If that is demonstrated the operator can create a small cut (a sphincterotomy) which may allow removal of the stone with a balloon or basket or simply allow the stone to fall out into the intestine thus relieving the blockage. If a narrowing or blockage of the bile duct is discovered, the operator can insert a stent (a small plastic tube like a straw) into the bile duct thus allowing the bile to drain into the duodenum in the usual way.

The Claimant was seen by Group Captain Watkins on the morning of 9 January. His note made following the examination was as follows:

“I note the history. It now looks likely that she has a stone at the lower end of the [common bile duct]. Her coagulation is currently too abnormal to allow a sphincterotomy safely and whilst I could do an urgent ERCP and place a small stent safely and return for a definitive ERCP later I think she is well enough to wait till a planned list [on] Thursday when I hope her INR will have returned to normal. On the other hand if she deteriorates in any way I will review and perform urgent ERCP.”

‘INR’ is the abbreviation for International Normalised Ratio which is a measure of the time it takes the blood to clot compared with an average. If an INR is too high then there is a risk of uncontrolled bleeding. Group Captain Watkins obviously wanted that to be better controlled if possible before performing the ERCP. Vitamin K was prescribed to assist in restoring her coagulation.

The ERCP was carried out on 11 January, starting at 16.00. There is no doubt that this particular ERCP proved to be a difficult one. It lasted approximately 90 minutes before it was abandoned. The Claimant had been given the sedative Hypnovel, 7.5 milligrams at 16.00 and 2.5 milligrams at 16.20. Whilst nothing in fact turns on it, it was, I think, common ground between the relevant experts that even this amount of Hypnovel was at the top end of what was acceptable at the time. However, according to the operation note, a further 6 mg of Hypnovel was administered at 17.28. Although, of course, some of the Hypnovel initially administered would have been metabolised by that time, there is no doubt that a further 6 mg did contribute to a very large overall administration of sedation. The very nature of the procedure, particularly if prolonged, can give rise to distress and discomfort on the part of the patient. Group Captain Watkins confirmed in cross-examination that the reason for administering this additional quantity of sedative was because he would have preferred to continue for a little while longer despite having already taken a long time with the ERCP procedure. I will say more about the significance of this shortly, but it represented an important insight into Group Captain Watkins’ perception of the outcome of the ERCP at the time.

During the course of the ERCP, the conduct of which as such is not criticised, the Claimant sustained very considerable bleeding. Group Captain Watkins estimated that the total blood loss was 1-1½ units. Whilst it is acknowledged that bleeding is a well-recognised complication of ERCP, Dr Dickinson, a Consultant Physician based at Hinchingbrooke Hospital, who has always had a particular interest in ERCP procedures and who gave evidence for the Claimant, said that he had never seen bleeding of this magnitude in over 5,000 ERCPs of which he had experience. Dr Goodman, a Consultant Gastroenterologist and General Physician based in Manchester, who gave evidence for the Defendant, seemed less willing at the joint meeting of the experts to accept that the blood loss was unusually considerable, but he too said that he had not seen blood loss in this quantity in an ERCP. I do not think there can be any doubt that it was indeed very considerable. It was sufficient for Group Captain Watkins to note in handwritten form immediately after the procedure finished that the Claimant would ‘need close observation and possibly transfusion.’ Again I will return to this in due course.

As I have indicated, that bleeding (even significant bleeding) can occur as a result of the procedures involved in an ERCP, particularly a sphincterotomy, is a well-recognised complication and not necessarily indicative of negligent performance of the procedure. When it occurs, particularly when it is significant, it can obscure the view of the endoscopist. That is what occurred here. Group Captain Watkins noted, both in his handwritten note and the typed note the following day, that his view was obscured and consequently he could not be sure that the stone had been removed (because he never saw it), but he thought that it probably had been removed.

The net result of the ERCP was that there could be no certainty that the blockage had been cleared, no stent had been inserted, the Claimant had been heavily sedated and she had lost considerable blood. The immediate post-ERCP note also recorded ‘continued bleeding with clots’. As thus noted, this is ambiguous as to whether the bleeding had in fact ceased. Group Captain Watkins’ note the following morning was that ‘probably active bleeding ceased by end of procedure’. He did accept in cross-examination that he could not be sure that the bleeding had stopped and that he had some anxiety in that regard. He said that he thought that if there was continued bleeding, it was no longer dangerous, though he remained concerned.

As I have indicated, Group Captain Watkins emphasized that he wanted to continue with the procedure if possible and that is why he administered more sedation. He said he was uncertain as to where he stood and was hoping to get a bit more time to settle the Claimant and assess what else was required. He said he felt he could have put a stent in had she become sufficiently settled and he either wanted to do that or insert another balloon to see if the bile duct had cleared. In the event he did not proceed further because the Claimant could not be settled sufficiently. Although Dr Dickinson felt that Group Captain Watkins should have taken the opportunity to insert a stent that evening, it was recognised that this was a matter of clinical judgment and it was not unreasonable to abandon the procedure that evening. However, this would have to have been on the basis that there was, in effect, ‘unfinished business’ to attend to and, very significantly, that she was properly monitored and resuscitated overnight.

Deficiencies in the post-ERCP monitoring and resuscitation of the Claimant have been acknowledged on behalf of the First Defendant for some time. Group Captain Watkins has accepted responsibility for not giving adequate instructions to the nursing and junior hospital staff. Whether the responsibility was his or that of the nursing and other medical staff does not matter for present purposes: what matters is to determine the extent to which the failure to deal with her immediate post-ERCP condition and its development thereafter fell below reasonable standards of care and then to see what direct or indirect effect, if any, that had upon the Claimant’s condition in due course. That having been said, Group Captain Watkins did go so far as to acknowledge that what had happened overnight following the ERCP on 11 January was ‘probably a serious deviation from what is acceptable.’ It will be necessary to spell out what this involved before investigating whether there were any further deficiencies in the treatment afforded thereafter and the overall effect on the Claimant’s condition.

It is not in dispute that there was negligently inadequate resuscitation/fluid replacement in the 24-hour period following the ERCP. So much was agreed by Dr Dickinson and Dr Goodman when they (together with a Dr Anderson who had reported for the Second Defendant) discussed the case. Bearing in mind that the ERCP took place between 16.00 and 17.30 on 11 January, this covers the period until about the same time following day.

It is important to note that it is the view of Dr Dickinson, supported by Mr Scurr to whom I will refer in due course, that, given the uncertainties over what had actually been achieved during the ERCP on the evening of 11 January, it was necessary for further intervention the following morning. I use the word ‘intervention’ to encompass a number of options to which I will refer below. Group Captain Watkins admitted that had the Claimant been treated as she should have been overnight, she would have been significantly better off the following morning such that she would have been in a better condition and fitter for a further procedure.

She had lost 1-1½ units of blood with no certainty that the internal bleeding had stopped, yet no intravenous fluid replacement therapy had been instituted. Dr Goodman, who was generally more supportive of aspects of the treatment given than the other experts, said that the Claimant was ‘on the cusp of requiring a blood transfusion’ after the ERCP and said that she should have been given intravenous fluids before leaving the endoscopy room. He suggested 1 litre of normal saline immediately and further tests (including a full blood count) within a few hours to reassess the position. He would, I think, share the view of Dr Ryan (a Consultant Anaesthetist and Clinical Physiologist with specialist experience in intensive care) and Dr Dickinson, both of whom said that she should have been given 1-1½ litres of fluid initially and maintenance volumes thereafter. They all thought that her urine output should have been monitored by the insertion of a catheter. As it was, the Fluid Balance Chart shows that from 01.00 on 12 January she received only small amounts of oral fluid intake with a fair amount being vomited back. It demonstrates that intravenous fluid replacement (with an associated catheter to monitor urine output) was not commenced until about 16.00. It is clear from this chart why the experts reached the agreement to which I referred in paragraph 19 above. There were other criticisms made of what was (or, more accurately, what was not) done overnight, but the substantive criticism is the lack of fluid replacement therapy.

I will deal with the effect of this failure on the Claimant’s overall condition below, but there was, I think, no real dispute that, had she been properly resuscitated by an acceptable level of fluid replacement therapy, she would have been materially better than she was in fact on the morning of 12 January. She would, I find on the balance of probabilities, have been fit for a further procedure had such a procedure been deemed necessary. As it was, she was not sufficiently fit for a further procedure and that option was not available to the treating clinicians. From then on, or at least from later that day when proper resuscitation was eventually undertaken, the process became one of clinical catch-up.

I recorded the net effect of the ERCP in paragraph 16 above. Leaving aside other matters for the present purposes, there was no guarantee that the biliary blockage had been cleared, though Group Captain Watkins thought that the stone had ‘probably’ been removed. In fact it had not. It is not clear precisely when Group Captain Watkins saw her on the morning of 12 January, but she was seen by the Surgical Registrar at 08.00 that morning when she was noted, inter alia, to be jaundiced with a pulse rate of 120 bpm. There was uncertainty about her urinary output and when blood tests were done later her bilirubin level was still significantly raised suggesting that the biliary blockage had not been cleared.

At that stage, albeit undiagnosed, the Claimant was developing another well-recognised complication of ERCP, namely, pancreatitis. This is inflammation of the pancreas. It will be necessary to consider the impact of this condition on the Claimant’s general well-being, but the fact that it was undiagnosed at this stage is not criticised.

However, the balance of the expert evidence is, in my view clear: that had she been properly resuscitated overnight she would have been fit for and, if correctly cared for, would have been subjected to a further intervention on 12 January to resolve the two areas of uncertainty left over from the previous evening – whether the biliary blockage had indeed been removed and whether the internal bleeding had been stopped. Whilst Mr Scurr, looking at things from the perspective of a surgeon, would have favoured an immediate surgical approach by way of laparotomy, I think that the most favoured approach in the circumstances would have been a further endoscopy under general anaesthetic. This would have enabled an investigation into whether the stone had been removed and it would have presented an opportunity to insert a stent if it was clear that it had not. The placing of a stent was, it is to be recalled, what Group Captain Watkins would have done had he felt the conditions towards the end of the ERCP on 11 January had enabled it. If it was apparent that there was continued bleeding at this second endoscopy, or the endoscopic procedure had disturbed a clot that had previously formed, then it would have been possible to proceed to laparotomy there and then. Group Captain Watkins was himself a surgeon and this approach would have been perfectly feasible. In other hospital settings it might have been necessary to have an endoscopist attended by a surgeon who could take over and move to laparotomy if necessary, but that situation would not have presented itself here.

This approach was supported explicitly by Dr Dickinson. Mr Derek Sweeting QC, who represents the First Defendant, has reminded me that Dr Dickinson did not mention a further ERCP on 12 January in his report and that this only emerged at the experts’ meeting. That is true, but it is clear that his essential position was that a stent should have been inserted during the ERCP on 11 January. If, as has to be accepted in the light of the evidence, Group Captain Watkins cannot really be criticised for not doing that in the particular circumstances, the question arises of what should happen if there is uncertainty about whether the blockage had indeed been relieved. If it had not or there was uncertainty about it, it is difficult to see how logically one could simply do nothing thereafter, particularly if there is evidence (as there was here when the bilirubin results were obtained) that there had been no material improvement. The logical progression of Dr Dickinson’s view must be that, provided the patient is fit enough to undergo another procedure, then such procedure should be carried out as soon as possible. I do not think that Dr Dickinson, or indeed Dr Goodman for that matter, had actually focused on what ought to have been done on 12 January if proper resuscitation had been implemented. That may simply have been a function of the way in which the issues in this litigation had developed. But I consider that Dr Dickinson’s view has the force of logic behind it and, coming from someone whom I regarded as an impressive witness with considerable knowledge of the kind of issues involved, it is a view I accept. Dr Goodman, who had produced a very lengthy report with a considerable amount of extremely helpful material attached to it, was no less experienced, but I felt that occasionally the wood was concealed by the trees and that there were areas where his evidence did not stand up to close scrutiny. Certainly on this issue, I prefer and accept Dr Dickinson’s view. In fairness to Dr Goodman, however, I should record that when asked about the possibility of further intervention he did accept in his evidence that by the afternoon of 12 January “the evidence [gave] enough room to hesitate” by which I understood him to mean that it ought to have been seriously considered then. He said that by 13 January it was a “no-brainer” that there should have been further intervention. As I have said, though, the more compelling and logical view is that this should have been carried out earlier on 12 January.

It follows, therefore, that had the Claimant been properly resuscitated following the inconclusive ERCP on 11 January, and had she been followed up properly the following day, she would have had her continued biliary blockage attended to and any continued, or recommenced, bleeding stopped. It also follows that if this had occurred, as in my judgment it should have done, on 12 January the percutaneos transhepatic cholangiogram (PTC) carried out on 15 January would not have been necessary. (A PTC is a procedure by which the hepatic and common bile ducts can be x-rayed to see if they are wholly or partially blocked. If a blockage is detected, a catheter may be inserted to effect biliary drainage.) Dr Dickinson had (together with Dr Anderson) said that had biliary drainage been achieved, as it should have been, on 12 January the PTC would have been avoided and indeed that must be so as a matter of fact.

This additional procedure on 12 January would not have prevented the continued development of the pancreatitis and the complications to which it gave rise to the significance of which I will return below. However, it would have avoided the PTC which, as a matter of fact, resulted in a tear to the liver with consequent further extensive bleeding. The Claimant was taken back to theatre in the early hours of 16 January and underwent an emergency laparotomy at which the sphincterotomy was over-sown, the gall bladder was removed (cholecystectomy) and the liver was packed because of bleeding from the gall bladder bed. A T-tube was inserted. As I have indicated, the gall bladder was removed and four stones were also removed in the process.

It hardly needs stating that this was a very major operation (incidentally by now the Claimant had been transferred to Queen Alexandra Hospital, Cosham) the outcome of which, in common parlance, was ‘touch and go’. She did, of course, survive, but her family had been prepared for the worse. The operation took place at a time when the full impact of her acute pancreatitis (see paragraph 32 et seq below) was also being felt.

Because of the need to pack the liver on 16 January it was necessary for a further laparotomy to remove the packing to be performed on 19 January. It does follow from my previous conclusions that if, as I have found, the need for the 15 January PTC should have been avoided, then all that followed (including this further laparotomy on 19 January) should also have been avoided.

I will have to address in due course my conclusions as to what impact, if any, those events and the build up to them had upon the Claimant’s overall condition some 7-10 days later when she suffered her cardiac arrest. However, there can be no doubting the seriousness of the overall condition she was in by the time of the operation on 16 January, an operation that would have been avoided had she received proper treatment overnight on 11 January and then during 12 January.

I have already alluded to the emergence of this condition following the ERCP. It was an unfortunate, but non-negligently caused, complication of that procedure. According to Dr Dickinson, it usually takes about 6-8 hours to develop. By 15.00 on 12 January Group Captain Watkins thought the Claimant may have ‘post-ERCP pancreatitis’. By then she was displaying many of the accepted diagnostic features – raised white blood cell count, raised amylase, abdominal pain, raised C-Reaction Protein (CRP) and raised urea. It is not in dispute that she was developing then and continued to develop thereafter acute pancreatitis the management of which as such is not criticised. When she was operated on in the early hours of 16 January (see paragraphs 28 and 29 above) the surgeon noted ‘severe pancreatitis’.

As already noted (paragraph 24), pancreatitis is inflammation of the pancreas. As I understand it, the pathophysiological process involved is that the digestive enzymes that normally do not become active in digesting food until they reach the small intestine begin acting upon the walls of the pancreas itself. If this becomes severe, as it did in this case, the process can lead to reduced or impaired kidney function – normally called renal ‘impairment’ or ‘insufficiency’ – or to kidney (or renal) ‘failure’ which requires dialysis.

Professor John Williams, a Consultant Physician in the Institute of Nephrology at the University of Wales College of Medicine, who was in fact the only nephrologist to give evidence, assessed the Claimant’s renal function as having become ‘significantly abnormal’ by the time the provisional diagnosis of pancreatitis was made in the afternoon of 12 January and said that by 19.00 that evening she could be described ‘as being in acute renal failure.’

By that time she had been put on intravenous fluids, albeit belatedly, which itself is an important element in the clinical response to acute pancreatitis. Later in the evening of 12 January she was transferred to High Dependency Unit at the Royal Haslar Hospital where she stayed until she was transferred to the ITU at Queen Alexandra’s on 14 January.

I have referred to the impact on renal function that pancreatitis can have. It is common ground in this case that the severity of the Claimant’s pancreatitis was such that she would inevitably have had to go to the ITU and would have required a period of dialysis irrespective of any component of her impaired kidney function that may have been attributable to the failure to treat her appropriately on 11 and 12 January. I will return later to the issue of the extent to which there was remaining by 26 January (the day of the cardiac arrest) a relevant component of her overall condition that was attributable to that failure. It is not disputed that the failure to resuscitate properly would have made the Claimant potentially more likely to sustain renal impairment than otherwise would have been the case. Before returning to that issue I should say a little more about pancreatitis in general and the Claimant’s history of it in particular.

Dr Goodman helpfully produced the UK ‘Guidelines for the Management of Acute Pancreatitis’ that were extant at the time of material events, together with updated guidelines. It is plain that acute pancreatitis in its severe form can be life-threatening. The guidelines say that ‘all patients with severe acute pancreatitis should be managed in a High Dependency Unit or Intensive Therapy Unit with full monitoring and systems support…’

Dr Ryan said in his report, and Mr Sweeting has emphasized it, that ‘pancreatitis is a very difficult condition to manage – often with a remitting and relapsing course – [and that] it is quite unpredictable…’ I think it is right to bear that in mind, though, that his comments appeared to have been directed to management outside an ICU or ITU environment. Nonetheless, his evidence was that the course of pancreatitis is unpredictable.

As I understand the evidence, the essential non-surgical treatment for acute pancreatitis is effectively to allow the pancreas to rest by not permitting the patient to eat whilst the inflammation settles naturally. This means feeding the patient by tube and, of course, monitoring closely all other functions. The Claimant was indeed being fed by Total Parenteral Nutrition (TPN) and by Percutaneous Endoscopic Jejunostomy (PEJ).

I have already referred to the stormy passage between leaving the Royal Haslar Hospital and the removal of the packing of the liver following the second laparotomy on 19 January. That also had involved a blood transfusion of 3 units on 13 January and a gastroscopy on 14 January to investigate upper gastro-intestinal tract bleeding. She was mechanically ventilated from 14 January onwards. She was being dealt with in this way in that period whilst at the same time active efforts were being made to bring her pancreatitis under control. She was commenced on dialysis on 17 January.

Following the removal of the packing on 19 January, the Claimant remained on mechanical ventilation, tube feeding and dialysis until 24 January. She was taken off the ventilator that day and the Consultant Nephrologist who saw her noted that she remained a ‘very sick patient with pancreatitis’, though he anticipated a transfer to the Renal Unit in due course. She was restarted on dialysis on 25 January and by the following day she was still being tube fed.

The foregoing is merely a summary of the position at that time. As I indicated at the outset of this judgment, it had originally been the Claimant’s case that she should not have been transferred from the ITU to the Renal Ward on the morning of 26 January. It was apparent that Dr Ryan was still of the view that she should not have been discharged from the ITU when she was, but he acknowledged, having seen the detailed ITU records, that there was evidence that she could maintain her own airway and had some control over swallowing by then. Given those factors, he acknowledged that the discharge from the ITU to the Renal Ward was within the applicable guidelines and that it could not be characterised as negligent to have done so.

Dr Ryan did, however, draw attention to the fact that the Claimant was extremely weak. For example, she needed a hoist to get her in and out of bed. He said that she ‘had only just achieved a degree of safety’, meaning that there had been some improvement in her overall condition, but that she remained very weak and continued to need a lot of nursing care. That was his view as an intensivist, but I do not think that there was any disagreement about it as a conclusion. I accept it as a matter of fact.

It would be the natural reaction of anyone to the brief history of the Claimant’s condition that I have given that she had been through an extremely tempestuous period of about 14 – 15 days from the time of the initial ERCP to the time of her transfer out of the ITU to the Renal Ward. Anyone would say that it is not surprising, bearing in mind that she could easily have died some ten days before 26 January, that she was still very weak by then.

That layman’s reaction is supported by the evidence given by Dr Ryan. In his report he had said this:

“[The Claimant] had had two life-threatening incidents. Her body would have responded by a process of catabolism which…means she breaks down muscles to provide energy. This leads to profound weakness and tiredness during recovery. She was unable to sleep. She had swollen tissues. She had until two days before discharge a tube in her airway that could cause local trauma and discomfort with swallowing. She was unable to metabolise drugs and excrete in the normal way because of her liver and renal failure. The [scan] shows the bowel to be swollen and free fluid in the abdomen. She had ongoing pancreatitis.

All of these factors could contribute firstly to the inability to swallow safely and thus protect the airway, and secondly to the delay of the bowel to recover its normal function and motility. ”

He expanded on the process of catabolism in a supplementary report. He described it by saying that the body goes into a hyperdynamic state and breaks down muscle mass as a fuel for itself. He said that the more severe the injury and the longer it is sustained, or repeated, the greater the effect and the longer it takes for recovery to occur. He said that severe weight loss and muscle fatigue can occur for months. He said that the severity of the Claimant’s illness initiated a process of severe catabolism which he believed would have been reduced markedly if she had been dealt with promptly and appropriately on 11 and 12 January with the avoidance of the debilitating treatment she received over the next few days as a result.

I will return to this evidence shortly, but I must deal with a controversial part of the evidence given by Professor Williams which has a bearing on how the Claimant’s physical well being was affected by the negligent treatment on 11 and 12 January and its relationship to the effect which the pancreatitis was having, and did have, upon her well being and strength over that period.

Professor Williams had said in his initial report that proper resuscitation after the ERCP would, on the balance of probabilities, have prevented the need for dialysis. When he discussed the position with his colleague who had provided a report for the Second Defendant (Professor Sacks), he modified his view to accept that she would have gone on to suffer renal failure and would have required dialysis in any event (presumably on the basis of the pancreatitis), though he maintained the position that she would have been less ill and would have sustained a lesser degree of renal impairment if she had been properly resuscitated. He clarified that in a supplemental report provided shortly before the trial when he said that had she been resuscitated properly over the first twelve hours or so then, although she would have probably gone into renal failure, the periods of dialysis would have been shortened significantly and may have lasted for 3 – 4 days only. He concluded that the failure to resuscitate properly overnight on 11/12 January, combined with the failure to deal definitively with the problem on the morning of 12 January, led to a significant worsening of her overall illness and meant that her recovery was unnecessarily prolonged.

Professor Williams had not specifically addressed the scenario that involves concluding that the PTC and then the subsequent emergency laperotomy could have been avoided if there had been proper resuscitation and treatment over 11 and 12 January. When he gave his evidence he said that he thought that if those procedures had been avoided then the need for dialysis would also have been avoided.

With some justification, Mr Sweeting protested that this was a new proposition that had not found its way into any of the written material provided by Professor Williams and ought, accordingly, to be approached with considerable caution. Mr Gibson did not dissent from the proposition that it was an unsatisfactory way for the evidence to emerge, but asserted that this was the evidence of Professor Williams and he was the unchallenged expert in nephrology. It is a fair point that the First Defendant had not chosen, it seems, to instruct a nephrologist and, to that extent, disabled itself from being able to challenge evidence of this nature.

Professor Williams is plainly a very distinguished expert with considerable experience in this field. It is, I think, unfortunate that matters emerged in the way that they did, but it has to be said that neither Dr Dickinson nor Dr Goodman had addressed this specific scenario in any detailed degree in their reports, although there was an indication from Dr Dickinson at the joint meeting of his views as I have already recorded. Whilst I do not doubt that what Professor Williams said represented his genuine view, I am troubled about accepting it as it is formulated because of the manner in which it has emerged. However, for reasons which I will give shortly, I do not think that whether dialysis was or was not required represents the full answer to the causation issue that lies at the heart of this particular piece of the dispute between the parties. To the extent, however, that dialysis forms part of the picture, I do accept the view that Professor Williams put forward in his supplementary report to which I referred above.

I must now turn to what happened at the time of the cardiac arrest and endeavour to draw together my conclusions as to what caused or contributed to it.

One piece of evidence given by Professor Williams, which is accepted by the Defendant, is the mechanism for the cardiac arrest. Professor Williams had said in his initial report that the probable scenario was that the Claimant had fallen asleep, vomited and then aspirated causing the subsequent cardiac arrest. This seems to be the generally accepted mechanism amongst all the experts. It seems also to be accepted that she remained at risk of vomiting largely because of her continued pancreatitis.

The essential question arises, of course, as to why she should have aspirated the vomit and not reacted in the normal way and cleared her airway by coughing and discharging the vomit from it. Dr Ryan’s evidence was that it was her weakened condition caused by the catabolism that prevented her from responding in the normal way to vomiting and which caused her to aspirate the vomit. He had said in his initial report that her ability to ‘swallow safely and thus protect the airway’ would have been disabled, a theme he took up when explaining how the epiglottis or larynx could be weakened in this way. Again, this is something that he had not developed in any of the written material previously and, whilst he may be right about what he says, I am disinclined to accept the precise mechanism he mentioned without further material to support it. What I am prepared to accept, because it seems to me to be a common sense assumption, is that the Claimant’s generally weakened and debilitated condition on 26 January caused her not to be able to respond naturally and effectively to the emergence of vomit from her gut with the consequence that she inhaled it. The question then arises as to whether the Claimant can be said to have proved to the relevant standard that the negligence that occurred on 11 and 12 January caused or materially contributed to her inability to deal with the vomiting in this way. Is there a sufficient causal link between that overall weakness and the established negligence that occurred over 11 – 12 January?

Irrespective of any other conclusion that might be reached about the influence that that negligence might have had, it is clear that it cannot have been the sole reason for her weakness. She had suffered acute and severe pancreatitis throughout the same period and, on any view, the effect of that must have played a part in her continued weakness as at 26 January. The First Defendant’s case is that it could only have been that that had any bearing on her weakness at that time, the events of 11 and 12 January being too remote for it to have had any material influence. The Claimant submits that I do not have to be satisfied that the effects of the established negligence represent the sole cause of her weakness; it is submitted that if it can be shown that those effects made a ‘material contribution’ to her weakness that would be sufficient. It is argued that a material contribution was indeed made here.

The issue of causation in clinical negligence cases has received attention at the highest level on a number of occasions in recent years: Hotson v. East Berkshire Area Health Authority [1987] A.C. 750; Wilsher v. Essex Area Health Authority [1988] A.C. 1074; Fairchild v. Glenhaven Funeral Services Ltd. [2003] 1 A.C. 32 and Gregg v. Scott [2005] 2 A.C. 176. It can be a difficult issue in such cases: see per Lord Hoffman in Fairchild at para 69.

Can a negligent course of treatment the consequences of which materially contribute to a Claimant’s injury be said to have caused the injury for the purposes of the law? It was conceded to be so in Constable v. Salford and Trafford Health Authority, etc., [2005] EWHC 2967 and represented the approach taken by Burton J in Miles v. Redbridge and Waltham Forest Health Authority, unreported, 18 February 2000. Mr Gibson has drawn my attention to what was said by Lord Bridge in Hotson at page 783. It was in these terms:

“As I have said, there was in this case an inescapable issue of causation first to be resolved. But if the plaintiff had proved on a balance of probabilities that the authority's negligent failure to diagnose and treat his injury promptly had materially contributed to the development of avascular necrosis, I know of no principle of English law which would have entitled the authority to a discount from the full measure of damage to reflect the chance that, even given prompt treatment, avascular necrosis might well still have developed. The decisions of this House in  Bonnington Castings Ltd. v. Wardlaw  [1956] A.C. 613 and  McGhee v. National Coal Board  [1973] 1 W.L.R. 1 give no support to such a view.”

My attention has not been drawn to any subsequent authority that has cast doubt on the formulation of the burden on the Claimant as set out in that passage. If this approach to causation is permitted it does, of course, mean that the ‘but for’ test is not being applied: see Fairchild v. Glenhaven, etc, at paragraph 129 per Lord Rodger of Earlsferry.

Wilsher v. Essex Area Health Authority needs consideration in this context. If I was satisfied that there were two contributory causes to the Claimant’s weakness in this case, each of which was significant, but in respect of which it was impossible to say, on the balance of probabilities, that one was more dominant than the other, would that mean that causation was not established? In Wilsher the Claimant was negligently over-oxygenated when a premature baby. This was one possible cause of the retrolental fibroplasia (RLF) from which he suffered and which resulted in his blindness. As the following extract from the judgment of Sir Nicolas Browne-Wilkinson V-C in the Court of Appeal in Wilsher (which was expressly approved by the House of Lords) demonstrates, there were five possible causes of the RLF of which over-oxygenation was only one. The Claimant could not prove on the balance of probabilities that the over-oxygenation was more likely than any of the other four candidates. The extract from the judgment of Sir Nicolas Browne-Wilkinson V-C was quoted in the opinion of Lord Bridge at page 1090:

“In the Court of Appeal in the instant case Sir Nicolas Browne-Wilkinson V.-C., being in a minority, expressed his view on causation with understandable caution. But I am quite unable to find any fault with the following passage in his dissenting judgment [1987] Q.B. 730, 779:

"To apply the principle in  McGhee v. National Coal Board  [1973] 1 W.L.R. 1 to the present case would constitute an extension of that principle. In the  McGhee  case there was no doubt that the pursuer's dermatitis was physically caused by brick dust: the only question was whether the continued presence of such brick dust on the pursuer's skin after the time when he should have been provided with a shower caused or materially contributed to the dermatitis which he contracted. There was only one possible agent which could have caused the dermatitis, viz., brick dust, and there was no doubt that the dermatitis from which he suffered was caused by that brick dust.

"In the present case the question is different. There are a number of different agents which could have caused the RLF. Excess oxygen was one of them. The defendants failed to take reasonable precautions to prevent one of the possible causative agents (e.g. excess oxygen) from causing RLF. But no one can tell in this case whether excess oxygen did or did not cause or contribute to the RLF suffered by the plaintiff. The plaintiff's RLF may have been caused by some completely different agent or agents, e.g. hypercarbia, intraventricular haemorrhage, apnoea or patent ductus arteriosus. In addition to oxygen, each of those conditions has been implicated as a possible cause of RLF. This baby suffered from each of those conditions at various times in the first two months of his life. There is no satisfactory evidence that excess oxygen is more likely than any of those other four candidates to have caused RLF in this baby. To my mind, the occurrence of RLF following a failure to take a necessary precaution to prevent excess oxygen causing RLF provides no evidence and raises no presumption that it was excess oxygen rather than one or more of the four other possible agents which caused or contributed to RLF in this case.

"The position, to my mind, is wholly different from that in the McGhee  [1973] 1 W.L.R. 1, case where there was only one candidate (brick dust) which could have caused the dermatitis, and the failure to take a precaution against brick dust causing dermatitis was followed by dermatitis caused by brick dust. In such a case, I can see the common sense, if not the logic, of holding that, in the absence of any other evidence, the failure to take the precaution caused or contributed to the dermatitis. To the extent that certain members of the House of Lords decided the question on inferences from evidence or presumptions, I do not consider that the present case falls within their reasoning. A failure to take preventative measures against one out of five possible causes is no evidence as to which of those five caused the injury."

It seems to me that there is nothing in Wilsher that would prevent the Claimant in this case from establishing a sufficient causal link between the established negligence here and the ultimate weakness if I was able to conclude that it made a material contribution to it even if the other non-negligent source of the weakness also made a material contribution.

I do not think it can be doubted that there were two components to the weakness of the Claimant as at 26 January, both very closely interlinked and having their foundation in the ERCP carried out on 11 January. One component was the weakness engendered by the pancreatitis, the other was the weakness engendered by the consequences of the negligence on 11 – 12 January which led to a very stormy passage for the Claimant ending (purely from a surgical point of view) on 19 January when the packing of the liver was removed. Even leaving out of account the independent effect of the pancreatitis, it defies all common sense to say that she had recovered from the effects of all that by 26 January. I am satisfied, on the balance of probabilities, that she had not and that she was weakened as a result. I cannot say whether the contribution made by this component was more or less than that made by the pancreatitis and it follows that I cannot say whether the contribution made by the pancreatitis was greater or smaller than the contribution of the other component. All I can say is that the natural inference is that each contributed materially to the overall weakness and it was the overall weakness that caused the aspiration.

Mr Sweeting has placed particular emphasis on the apparent improvement in the Claimant’s condition early on 26 January and the variable course of pancreatitis as a condition, the implicit suggestion, as I understood him, being that the Claimant’s inability to cope with the vomiting later on 26 January reflected a sudden downturn in her apparently improved condition associated with the pancreatitis. As with so many scenarios, this is a possible construction of the events. However, it is no more probable than any other construction and the issue would still remain of the contribution made to her overall condition at the time the aspiration took place of the component attributable to the negligent treatment. Why should it be said that such a component was totally eclipsed by a component attributable to the pancreatitis? There is no evidence that enables me to draw such a conclusion. Equally, if in fact there had by then been some small improvement in her overall condition because the effects of the pancreatitis were subsiding, then the inference would have to be that the weakness attributable to the earlier negligence would have played a more dominant role.

As I have said, in my judgment the two components contributed materially to her overall weakness at the relevant time and, accordingly, that is sufficient to establish the causal link between the 11 – 12 January and the brain damage she suffered in consequence of the cardiac arrest on 26 January.

It follows that there must be judgment for the Claimant with damages to be assessed.

I should like to express my appreciation Mr Gibson QC and Mr Dean and Mr Sweeting QC and their respective teams for their considerable assistance in this difficult case.