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England and Wales Court of Appeal (Civil Division) Decisions |
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You are here: BAILII >> Databases >> England and Wales Court of Appeal (Civil Division) Decisions >> Bailey v The Ministry of Defence & Anor [2008] EWCA Civ 883 (29 July 2008) URL: http://www.bailii.org/ew/cases/EWCA/Civ/2008/883.html Cite as: [2008] EWCA Civ 883, (2008) 103 BMLR 134, 2008] LS Law Medical 481, 103 BMLR 134, [2009] 1 WLR 1052 |
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COURT OF APPEAL (CIVIL DIVISION)
ON APPEAL FROM THE HIGH COURT OF JUSTICE
QUEEN'S BENCH DIVISION
Mr Justice Foskett
Strand, London, WC2A 2LL |
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B e f o r e :
Vice-President of the Court of Appeal, Civil Division
LORD JUSTICE SEDLEY
and
LADY JUSTICE SMITH
____________________
Grannia Geraldine Bailey (by her Father and Litigation Friend, Maurice Bailey) |
Respondent |
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- and - |
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The Ministry of Defence and Anr |
Appellants |
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Derek Sweeting QC (instructed by Treasury Solicitors) for the Appellant
Hearing dates : 1st, 2nd July 2008
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Crown Copyright ©
Lord Justice Waller :
Introduction
The Facts
". . .
3. The record of the ERCP by Mr Watkins indicates there was at least one stone in the dilated duct system, but the view was obscured by considerable bleeding, estimated at 101.5 units of blood, and that it had 'probably' stopped by the end of the procedure.
4. There is no recovery chart available. The patient was sent to the ward with a pulse around 115 beats per minute.
5. There are no nursing records of her condition on return to the ward after the ERCP or subsequent ward care.
6. There is no medical [record] of the patient being seen by any clinical staff until 0800 on the 12./01/2001 when she was clearly unwell.
7. She was reviewed again at 15.00 hours, 12/01/2001 when she remained unwell and diagnosed as possibly developing "? Post-ERCP pancreatitis." She continued to deteriorate and was moved to a High Dependency Unit [HDU] that evening for further management of her fluid balance with a central line and bladder catheter. She started to vomit 'coffee grounds' – a term used to signify altered blood from her stomach, a sign of serious illness.
8. She deteriorated over the next 24 hours despite strenuous efforts to reverse the situation. She was given a blood transfusion of 3 units on the 13/01/2001. A transfer to intensive care [ICU] was requested early on 14.01/2001. At this stage she had started to bleed from the gut, had developed renal failure, had developed acute pancreatitis, and was requiring circulatory support and was developing respiratory failure. She was clearly going to die unless the situation was reversed.
9. She was taken later that day safely to ICU at Queen Alexander Hospital, Portsmouth, 14/01/2001
10. At Queen Alexander Hospital ICU she underwent gastroscopy that night. This was to further investigate her upper gastrointestinal tract bleeding. There was found to be fresh blood in the stomach, but no obvious source was found. The most likely site was the ampulla, at the entrance to the pancreatic duct. She was at this stage aggressively supported by a variety of appropriate drugs including a local injection of adrenaline down the gastroscope, different clotting factors and an anti-ulcer agent to try and curtail the bleeding.
11. On the 15/01/2001 she received blood and clotting factors and then the patient underwent a percutaneous transhepatic cholangiogram [PCT] and biliary drainage which showed the ampulla to be distorted and full of blood clot. That evening she underwent surgery for massive bleeding to the liver caused by the PCT procedure, as well as oversewing of the sphincterotomy, a cholecystectomy, and packing of the liver for bleeding.
12. She could have died at this point. She was aggressively supported with a lot of blood products and intropes. She was stabilised after much effort. She survived and subsequently had her surgical packs removed on the 19/01/2001.
13. Miss Bailey then made steady progress in the ICU, although she continued to show signs of sepsis. A computerised tomography [CT] scan on the 21/01/2001 confirmed what had been seen at the time of previous emergency surgical intervention on the 15/01/2001. This was pancreatitis, swelling of the surrounding tissues and bowel, the presence of fluid in the abdomen (ascites), and some liver defect after surgery. The bases of the lungs are collapsed with some fluid around them. She was receiving antibiotics but there were no positive bacterial cultures. She was being fed by a combination of intravenous [TPN] and direct feeding into the gut (PEJ).
14. Antibiotics were stopped 24/01/2001. She was removed from mechanical ventilation and it was noted she needed a Bird Ventilator to help expand the lung bases. She continued to have a high temperature. She was receiving intermittent haemofiltration (renal support). There were problems in establishing enteral feeding. The volume used was small (30ml) and was being varied daily; she was relying principally on the TPN. She was not sleeping.
15. She was visited (24/01/2001) by the Consultant Nephrologist, Dr Hedger, who noted her to be "very sick patient with pancreatitis, GI (gastrointestinal) bleed sepsis". He anticipated a transfer to the renal unit "probably w/e (weekend), early next week?" He did not revisit this patient or see the patient in the renal ward subsequently.
16. On the 25/01/2001 there was another CT scan because of concerns about an infective focus. This was basically unchanged from the report of the 21/01/2001 (described in section 12 above). She was also restarted on haemodialysis because of her abnormal electrolytes and she was still very oedematous (swollen with fluid) due to water retention.
17. On the 26/01/2001 she appeared well, but was still very jaundiced. She was being fed by a combination of TPN and a nasogastric feed. The written clinical comments include "reculture today" "Central line out later? Needs new line? ?re-filter today". There is a typed note of the decision by Dr Taylor to discharge to the renal unit. [Dr Ryan accepted once records had been produced that the claimant was properly assessed as able to cope in a ward.]
. . .
18. Miss Bailey arrived safely at the renal ward at about 6pm. Her condition was safe. She was initially seen by Dr Blakeley, an experienced Registrar. She noted that Miss Bailey was to receive 1L via her PEJ and 500mls free oral fluids over 24 hours. She comments the patient 'now – hyperdynamic (likely ongoing sepsis)'.
19. Miss Bailey became nauseated and vomited at about 20.15 hours after drinking about 100ml of lemonade. She became rapidly unwell. Her oxygen saturation which had been 98% on room air fell to 82%; her pulse previously at 70 went up to 120, her blood pressure was OK, but her temperature had risen from 37.5C to 38.5C.
She was seen by Dr Patel (who had been an SHO on the Unit for 6 weeks) at 20.35 who examined her and elicited all the signs of aspiration but did not record a diagnosis. He contacted Dr Blakeley and they gave her oxygen, but it was low flow oxygen. She had a chest X-Ray, she was given antibiotics and an H2 blocker. Her condition improved. No other member of the medical staff was contacted at this stage. No anti-emetic was given.
20. Nurse Hanson was the nurse initially responsible for Miss Bailey's care – in her witness statement she recorded that the patient was to be given 500mls free fluids a day. She recorded the 100mls of lemonade.
21. Nurse Drum took over the care for the night shift and was responsible for 3 patients – the other two were 'lighter' in regard to their nursing needs. There were two other nurses on duty that night, one had 4 patients and one had 3 respectively.
Miss Bailey was sat up, encouraged to cough which was unproductive. Her PEJ feed was recommenced at 22.30. She had no further oral intake.
22. At around 23.30 while Dr Patel was reviewing her chest X-ray on the ward, Miss Bailey vomited about 100ml of 'coffee grounds' (altered blood).
23. Miss Bailey suffered a cardiac arrest at around 24.00. The doctor and nurse were not at her bedside when this happened. The patient was unconscious when the alarms sounded and the nurse returned to the bedside. She was resuscitated and returned to the ICU."
"25. As a result of the failures listed in para 15 above:
a) C became very much more ill after the first procedure than she would otherwise have been;
b) C underwent additional procedures which should have been avoided. In all, following the original ERCP, she underwent: (i) a gastroscopy on 14.1.01, (ii) a PTC on 15.1.01, (iii) a laparotomy in the early hours of 16.1.01, and (iv) a further laparotomy on 19.1.01. It is accepted that one further procedure would probably been undertaken as set out above, but it would have been only one, and it should have been carried out on or around 12.1.01.
c) the laparotomy which was undertaken as an emergency in the early hours of 16.1.01 was a very much more serious operation than a planned laparotomy taking place immediately after the ERCP or on 12.1.01 or 13.1.01 would have been, undertaken when C was in a significantly more weakened condition than she would have been. C very nearly died then;
d) because of the massive bleeding caused at the PTC, and the packing of the liver that this necessitated, a second laparotomy [which] had to be undertaken on 19.1.01. This is an episode of major surgery which C would otherwise have avoided.
e) although C would probably have developed pancreatitis and renal failure in any event, they would have been less severe and C would have been in a much fitter state to combat them;
f) although C would probably have required to go into the ITU, she would not have required prolonged haemofiltration and would not have needed to be discharged to the Renal Ward.
g) C would have spent less time on the ITU and would thus have become less exhausted.
26. The Claimant suffered her injuries when she vomited at about midnight on 26.1.01 on the Renal Ward, and then aspirated the vomit. The reason why she aspirated was her extreme weakness as a result of her lengthy illness. Dr Ryan in his supplemental statement has set out his view of the mechanism of developing weakness as a result of the process of catabolism.
27. C's case is that if she had been properly treated for the removal of her biliary obstruction, and with proper post-operative management, the probability is that she would not have become as ill as she did, and would have recovered sooner, with the result that she would not have been so weak that she aspirated on 26.1.01 – leading to her cardiac arrest and the consequent hypoxic brain damage."
The law before the judge
"If it is an established fact that conduct of a particular kind creates a risk that injury will be caused to another or increases an existing risk that injury will ensue; and if the two parties stand in such a relationship that the one party owes a duty not to conduct himself in that way; and if the other party does suffer injury of the kind to which the risk related; then the first party is taken to have caused the injury by his breach of duty, even though the existence and extent of the contribution made by the breach cannot be ascertained."
"To apply the principle in McGhee v National Coal Board [1973] 1 WLR 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 plantiff. The plaintiffs RLF may have been caused by some completely different agent or agents, e.g. hypercarbia, intraventricular haemorrhage, apnoeas 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 WLR 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."
"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 Casting Ltd v Wardlaw [1956] AC 613 and McGhee v National Coal Board [1973] 1 WLR 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."
"The idea of liability based on wrongful conduct that had materially contributed to an injury was . . . well established long before Wardlaw. But Wardlaw became a convenient point of reference, especially in cases of industrial disease. In such cases this basis of liability is of considerable importance. Since it is enough that the defendant's wrongful act materially contributed to the claimant's injury, the law is not applying the causa sine qua non or 'but for' test of causation. In Wardlaw, for instance, the pursuer did not need to prove that, but for the dust from the swing hammers, he would not have developed pneumoconiosis All he needed to prove was that the dust from the swing hammers contributed materially to the dusty atmosphere which he breathed and which caused his illness. As will be seen below, in the Court of Session in McGhee the judges lost sight of this important point."
"The medical evidence was that pneumoconiosis is caused by a gradual accumulation in the lungs of minute particles of silica inhaled over a period of years. That means, I think, that the disease is caused by the whole of the noxious material inhaled and, if that material comes from two sources, it cannot be wholly attributed to material from one source or the other. I am in agreement with much of the Lord President's opinion in this case, but I cannot agree that the question is: which was the most probable source of the respondent's disease, the dust from the pneumatic hammers or the dust from the wing grinders? It appears to me that the source of his disease was the dust from both sources, and the real question is whether the dust from the swing grinders materially contributed to the disease. A contribution which comes within the exception de minimis non curat lex is not material, but I think that any contribution which does not fall within that exception must be material. I do not see how there can be something too large to come within the de minimis principle but yet too small to be material."
Grounds of Appeal
Ground 1
"24. 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.
25. 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.
26. 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."
"In relation to why I did not attempt to drain the biliary tree the day following the ERCP, I did not perform repeat ERCP for stent placement the following day because my assessment was that the cause of the patient's deterioration was the evolving acute pancreatitis and renal failure. Her pyrexia and raised white cell count I attributed to the pancreatitis. Between 10.00 hrs and 20.00 hrs on the 12th Jan her bilirubin fell from 456 to 398 and her alk phos from 464 to 410 further supporting my view that the obstruction had indeed been relieved. I also felt that further intervention represented further risk to an already unwell patient without any clear cut benefit."
Ground 2
"55. The essential question arises, of course, as to why she should have aspirated the vomit and not reacted in a 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?"
"The text continues P2 and I quote 'The commonest physical problem reported by intensive care patients is severe weakness and fatigue. Patients in intensive care can lose about 2% of muscle mass a day during their illness owing to a contribution of catabolism and atrophy secondary to neuropathic degeneration. They may lose half their muscle mass resulting in severe physical disability. Rebuilding such muscle losses may take a year. Initially such patients may be so weak that they struggle to feed themselves, their cough power is greatly reduced, and they may not have control of their swallowing and upper airways with a risk of aspiration. The nursing burden can be large."
"61. 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 pancreatititis 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."
Ground 3
"In the present case the evidence does not show – perhaps no one knows – just how dermatitis of this type begins. It suggests to me that there are two possible ways. It may be that an accumulation of minor abrasions of the horny layer of the skin is a necessary precondition for the onset of the disease. Or it may be that the disease starts at one particular abrasion and then spreads, so that multiplication of abrasions merely increases the number of places where the disease can start and in that way increases the risk of its occurrence.
I am inclined to think that the evidence points to the former view. But in a field where so little appears to be known with certainty I could not say that that is proved. If it were, then this case would be indistinguishable from Wardlaw's case. But I think that in cases like this we must take a broader view of causation. The medical evidence is to the effect that the fact that the man had to cycle home caked with grime and sweat added materially to the risk that this disease might develop. It does not and could not explain just why that is so. But experience shows that it is so. Plainly that must be because what happens while the man remains unwashed can have a causative effect, though just how the cause operates is uncertain. I cannot accept the view expressed in the Inner House that once the man left the brick kiln he left behind the causes which made him liable to develop dermatitis. That seems to me quite inconsistent with a proper interpretation of the medical evidence. Nor can I accept the distinction drawn by the Lord Ordinary between materially increasing the risk that the diseases will occur and making a material contribution to its occurrence.
There may be some logical ground for such a distinction where our knowledge of all the material factors is complete. But it has often been said that the legal concept of causation is not based on logic or philosophy. It is based on the practical way in which the ordinary man's mind works in the everyday affairs of life. From a broad and practical viewpoint I can see no substantial difference between saying that what the defender did materially increased the risk of injury to the pursuer and saying that what the defender did made a material contribution to his injury.
I would therefore allow this appeal."
"Small though the contribution of pollution may be for which the defenders are to blame, it was continuous over a long period. In cumulo it must have been substantial, though it might remain small in proportion. It was the atmosphere inhaled by the pursuer that caused his illness and it is impossible, in my opinion, to resolve the components of that atmosphere into particles caused by the fault of the defenders and particles not caused by the fault of the defenders, as if they were separate and independent factors in his illness. Prima facie the particles inhaled are acting cumulatively, and I think the natural inference is that had it not been for the cumulative effect the pursuer would not have developed pneumoconiosis when he did and might not have developed it at all."
Conclusion
Lord Justice Sedley :
Lady Justice Smith :