England and Wales High Court (Queen's Bench Division) Decisions

IN THE HIGH COURT OF JUSTICE
QUEEN'S BENCH DIVISION

		Royal Courts of Justice The Strand London WC2A 2LL
		Friday, 11th October 2002

Friday, 11th October 2002

J U D G M E N T

THE DEPUTY JUDGE:

1. The claimant, Pauline Elizabeth Hutchinson, is the widow of Gerald Hutchinson who died on 19th December 1998 aged 51. This claim is brought by her under the Fatal Accidents At 1976 and also as executrix of the deceased's estate, under the Law Reform (Miscellaneous Provisions) Act 1934.
2. It is alleged that his death resulted from the negligent failure by the defendants to provide him with adequate treatment resulting from his admission to Epson Hospital on 27th September 1997.

Background

3. The reason for his admission was that he was suffering from a painful, swollen left leg, headache and fever. He was admitted under the care of Dr Rom. He was seen by a house physician, it was noted that he had vomited that afternoon. A note was taken of his social circumstances. It is evident that he was asked how much used to drink. Three-quarters of a bottle of wine a day is noted. It was also noted that he was obese. He was about 6'2" and weighed 20 stone. Cellulitis was diagnosed and he was treated with antibiotics and inpatient rest. He was discharged home on 8th October.
4. Blood tests had been ordered on his admission; the results are of importance. They reveal that there was (1) a mean corpuscular volume (MCV) figure of 107.5. This was very high. The upper limit would not normally exceed 99 or 100. (2) A platelet count of 63,000 cubic millimetres. This was very low, the normal range being between 150,000 and 400,000. The discharge plan is at bundle 3 page 94. It simply stated:

"No anticipated problems on discharge."

The discharge note, bundle 2 page 10, simply refers to:

"Treated with eight days intravenous antibiotics and two days oral. Discharge home with five day course of oral antibiotics."

Significantly, however, (1) the deceased's general practitioner was not informed of the highly abnormal blood test results, and (2) no follow up tests were recommended.

5. Paragraph 6 of the defence admits:

"(1) that liver function tests should have been carried out in the light of the abnormal blood test results; (2) that liver function tests would probably have shown that the deceased was suffering from liver disease; (3) that as a result the deceased would have been advised to stop drinking and lose weight in or around October 1997."

The deceased returned to his work as an estate agent. He was unaware of the condition of his liver. According to Mrs Hutchinson he had been told in general terms at the hospital that he ate and drank too much and should cut down.

6. Over the course of the next year or so he was not well from time to time and saw various doctors, particularly in October and November 1998. Suffice it to say that he was readmitted to Epson on 3rd December of that year. He was noted to have a recent history of jaundice. According to Dr Lim, on 9th December 1998 she suspected he was suffering from "decompensated alcoholic liver disease". He died on 18th December. Dr Tina Matthews carried out the post mortem and gave the cause of death as "alcoholic liver disease".
7. It is not in dispute that the failures admitted in paragraph 6 of the defence amounted to negligence. The dispute in this case is one of causation. In a nutshell the defendants maintain firstly his cirrhosis of the liver was caused by his obesity, not alcohol, and secondly if his death was alcohol related, he would probably not have stopped drinking even had he been told.

The issues

8. (1) What was the cause of the deceased's cirrhosis of the liver and consequential death? Was it (a) alcohol or (b) obesity or (c) a combination of the two. (2) If it was a combination of the two, was the alcohol a material contributory cause, i.e., was it more than de minimus? (3) If it is proved that the alcohol was at least a contributory cause, would the deceased have given up drinking had he been appropriately warned in 1997? These matters have to be proved on the balance of probabilities; the burden is on the claimant.
9. The first issue It is first necessary to determine this question: how much alcohol on average had the deceased been consuming? There are two sources of evidence: (a) the family.
10. Mrs Hutchinson. Her evidence was that Mr Hutchinson, the deceased, originally drank sherry but moved on principally to wine. At one stage she appeared to agree with the proposition that he drank about three-quarters of a bottle a day, but her evidence went rather further. She gave evidence that he would open a bottle and offer her a glass. Most evenings he had the better part of a bottle during the week and more at weekends. He would occasionally have a day off. He would also binge drink. After he was told to eat and drink less in September 1997, he appeared to drink less but was still drinking about a bottle a night. In 1998 he was not really well enough to go out and binge drink.
11. At paragraphs 29 to 31 in her supplemental statement, she describes his drinking history. The picture painted is of a heavy drinker, becoming drunk on occasions to such extent as to be something of an embarrassment to the family, even to the extent of not going to a family wedding in Australia for fear that he would drink so much and embarrass them. She refers to certain male friends he enjoyed a drink with, and to two occasions when he was so drunk he did not return home until the following day. Paragraph 31 (page 30) of her statement, she set the matter out in this way:

"He would always have excuses for a drink; a good week at work, the end of a long day, something to help me unwind, needs drinking up, a special offer, makes the food taste better, feel more confident, it's Sunday tomorrow, children's good news, feeling sorry for myself, a reward for mowing, and so on. Holidays were difficult for me because there were endless opportunities for his over-drinking."

12. Sophie Hutchinson. She describes how he would have a beer before a meal before moving on to wine. He would open the bottle, mother would have one glass and the bottle would be finished by bedtime. She describes (page 81) him drinking mostly beers and wine. She said that on occasions when they had been on at him about his drinking, he would give up for an evening or longer, just to prove that he could. She also makes reference to his binge drinking.
13. (b) The documentation. (1) The 1997 admission notes, 27-9-97: "ex smoker, gave up two years ago, ten a day, three-quarter of a bottle of wine a day". 1998 admission notes, 3-12-98: "Alcohol 40 units wine a week. Stopped past 2½ months." A further entry on the same day, 3rd December, "Alcohol for more than 30 years up to 6 a night (42 units a week) stopped three months ago." Thirdly, four days later on 7th December, "Alcohol approximately 70 units a week for years. The entries are contradictory. Three-quarters of a bottle of wine would amount, on the basis of eight glasses to the bottle, to six glasses which, on a daily basis, would produce 42 units. Of course, wine can vary in its strength. The higher figure of 70 units would obviously indicate substantially more.
14. Is there any reason to conclude the reporting by the deceased of only 42 units per week is a substantial under-estimate?
15. Professor Summerfield His evidence was that it was well known that patients, asked about their level of alcohol consumption often under-reported it. He went on to point out that that included under-reporting even by doctors. Professor Summerfield on this issue was dealing with a point in relation to a paper by Becker and others on the prediction of risk of liver disease by intake, sex and age at page 262 in bundle 2, and in particular at the bottom of page 265 where there is a specific reference to the feature of under-reporting:

"Under reporting of alcohol may have occurred in the current study resulting in an over-estimation of relative risks for given levels of alcohol consumption."

16. The phenomenon is also referred to in Clinical Features and Natural History of Non-alcoholic Stiotosis Syndromes by Falkiter and others, page 313 of bundle 2 at page 314:

"Many patients who consume alcohol deny or under-estimate their degree of alcohol ingestion."

The entry for the 7th December 1998 "approximately 70 units weeks for years". Nowhere is there any suggestion that patients have a tendency to over-report their alcohol consumption. It is noteworthy that the history on this occasion was taken by Dr Lim, a consultant physician and gastroenterologist. There is no reason to suppose that she was careless in her history taking, or took it down incorrectly. Indeed, Mr Whitting realistically does not so suggest. He seeks to deal with this by saying it is a "rogue entry". He clarified that by saying it is not consistent with the earlier entries. Nor is it. Mr Hutchinson would, in truth, have known better than anyone what his real consumption was. He told Dr Lim this at a time when the stage of embarrassment or reluctance to be frank had passed. His condition was deteriorating. That embarrassment or reluctance may well have been there on the day of his admission on 3rd December in the same way as it may have been a factor at the time of his admission the previous year.

17. In my judgment, on the basis of the totality of the evidence, what he told Dr Lim is likely to have been closer to the reality. I do not make a finding of an exact weekly consumption figure. That would not be possible in these circumstances, nor is it necessary. However, for reasons which will become apparent, I am satisfied on the balance or probabilities that his weekly consumption exceeded 56 units.
18. The medical evidence I have heard evidence from two distinguished experts, firstly Dr Murray Lyon. He is a consultant physician and gastroenterologist at Charing Cross Hospital. He has just retired from the NHS and is still in practice in Harley Street. He has had a particular specialist interest in the liver for over 30 years. Secondly, Professor Summerfield, he is also a consultant physician and gastroenterologist based at St Mary's Hospital in Paddington. He was made a Professor in 1993. He also has a specialist interest in the liver and has published about 140 articles on liver disease.
19. They are both of the view that morbid obesity such as existed here can cause cirrhosis of the liver. So far as alcohol intake is concerned, Dr Murray Lyon says a weekly consumption about 42 units is sufficient to cause it; Professor Summerfield says it is not. Professor Summerfield maintains the probable cause of the cirrhosis is non-alcoholic stiato hepatitis ("NASH"). He says he would have to have a weekly intake of at least 56 units of alcohol for it to be hazardous. In view of my finding as to the probable level of intake, it is not necessary to journey in detail through the gripping statistics set out in the 141 pages of articles, extracts and reviews to which reference has been made in this case.
20. I consider, however, the relevant aspects of Professor Summerfield's evidence in the light of my earlier conclusions: (1) the thrust of his evidence was that it was common ground that Mr Hutchinson was morbidly obese. Morbid obesity is a known cause of NASH. Levels of alcohol intake at 42 units a week are highly unlikely to cause cirrhosis of the liver, and therefore the probable diagnosis is one of NASH rather than alcohol related cirrhosis. He pointed to various references in the literature. Amongst these were (a) the paper from Andrea Reed, "Non Alcoholic Stiato Hepatitis", bundle 2, page 183 at page 184:

"Obesity is the condition most often reported in association with NASH. The earliest report of 'fatty liver hepatitis' an early name for what was later called NASH, was in a cohort of obese patients."

(b) The book by Sherlock & Dooley, "Diseases of the liver Bilary System", 11th Edition, bundle 2 page 248, which he said indicated that the chance of alcohol related cirrhosis at a level of 42 units per week was remote. (c) The paper by Ballantoni & Others, known as the Italian Paper, entitled "Prevalence of and Risk Factors for Hepatic Stiatosis in Northern Italy", bundle 2, page 318:

"Compared with controls, the risk for stiatosis was higher by 2.8 for heavy drinkers and 4.6 fold in obese persons."

He drew my attention to the difference set out in that paper in support of the proposition that liver disease was more likely to occur in obese persons, rather than those who were heavy drinkers. He said that he had come across hundreds of patients with alcohol related cirrhosis and about twelve with cirrhosis caused by obesity. He would expect there to be more with the alcohol caused condition than the condition caused by obesity, because there were many more heavy drinkers than those with morbid obesity.

21. In cross-examination he was asked about various aspects of the literature. Firstly, at page 205 the letter from Bode, in the New England Journal of Medicine, indicating that daily indicate of 30 grams in males could be sufficient to cause alcohol-induced liver disease. He disagreed. Secondly, at page 206, the paper by Dixon & others, entitled "Non Alcoholic Fatty Liver Disease, Predicators of Non-alcoholic Stiato Hepatitis and Liver Fibrosis in the Severely Obese", bundle 2, page 206, and in particular at page 208 table 2. He was asked about the 105 patients in the study where it was indicated that only one had cirrhosis amongst the severely obese, a percentage figure of .95 per cent.
22. He was asked to compare that with the paper by Becker (already referred to) at page 262 and in particular at page 263 table 1, showing that with an alcohol intake of between 42 and 69 units per week, 25 of the sample, equivalent to 6.5% had alcohol-induced cirrhosis. (It was here that he pointed out at page 265 the fact that Becker and others recognised under reporting of alcohol intake may have occurred). The essence of what he was saying in relation to the comparison that he was asked to make by Mr Pershad was that in reality it was not comparing like with like. He was asked whether an intake of 42 units per week was significant alcohol abuse; he agreed it was. He was then taken to page 245 of bundle 2, chapter 72 of "Non Alcoholic Fatty Liver Disease" by Deale and Pordett, which at page 246 sets out the diagnostic approach to determination of non alcoholic fatty liver disease. NASH in the paper is considered to be part of the spectrum of non-alcoholic fatty liver disease.
23. Step 2 in the diagnostic approach to NAFLD is "exclude significant alcohol use and other forms of liver disease based on history". Professor Summerfield then said that for the purpose of this diagnostic tool, 42 units was not significant, because it was not sufficiently hazardous at that level. His evidence in this context was to the effect that a weekly intake of 56 units would be significant, and therefore 56 was accepted as the lower limit of hazardous drinking. It follows that on the basis of my earlier finding, if the level was in excess of 56 units, Professor Summerfield would accept that he could not conclude that NASH was a proper diagnosis in this case.
24. Dr Murray Lyon gave evidence, as I have indicated, to the effect that the deceased suffered probably from alcohol caused cirrhosis. He accepted that obesity played its part. He considered alcohol probably was the major causative factor. In support of this conclusion he replied on parts of the literature to which I have already made selective reference. He also relied on a paper by Navaho at page 270 of the bundle to which I need not specifically refer.
25. In addition he said: (1) the MCV here was very high, and that was much more typical of alcohol related cirrhosis than that caused by obesity. He pointed out that it is used as a surrogate marker for alcohol consumption. (2) He pointed to the speed of deterioration of the deceased's condition, more common, he said, with alcohol driven liver disease than that caused by obesity. (3) He pointed out that there had been found in 1998 multiple spidaniva which, he said, were more commonly found in cases of alcohol induced liver disease. These, he said, pointed to alcohol rather than obesity. Suffice it to say, Professor Summerfield did not agree with the proposition set out in page 3, aspects relied upon by Dr Murray Lyon.
26. It can be seen from the medical evidence that whilst there is substantial dispute as to the level at which alcohol related cirrhosis of the liver can be caused, in broad terms, Professor Summerfield and Dr Murray Lyons' evidence appears to be in agreement, at least in this respect, that if there is alcohol consumption above the level of 56 units per week, it is not possible for a diagnosis of NASH to be made.
27. I have come to the clear conclusion that: (1) the level of intake in excess of 56 units was such as to exclude by definition and on the evidence of both Dr Murray Lyon and Professor Summerfield the diagnosis of NASH; (2) the strong probability is that both obesity and alcohol were causative factors in this case.
28. Would the deceased have given up drink had he been properly warned? This is not an easy question to decide. It is clear on the evidence, as I have found, that he was a considerable drinker. He was very fond of his wine in particular, he needed it for a host of reasons. Clearly, the family had nagged him to control his drinking in the past. What would he have been told? The evidence is that he would have been told, "If you don't stop drinking you will be dead in 12 months or perhaps two years". That is a stark warning. Mrs Hutchinson gave evidence on this issue. She said, "I believe he would have given up had he been told this." She pointed to the fact, first of all, that he had given up smoking in 1995. He had been smoking since the age of 14 and they got him to give up eventually because of the health risks. Secondly, she pointed to the fact that they have a very difficult son. She said Ricky was very, very supportive. He would not have wanted me to have had to look after him alone. Thirdly, she pointed to the fact that "we had many good things in our lives. He adored and cherished the children and there is no way that he would have jeopardised that". Lastly, she pointed out, "He had me, and I would have killed him if he hadn't have done it".
29. Having listened to Mrs Hutchinson in the witness box and seen her during this trial, it is clear to me that there is considerable force in what she says. Undoubtedly he would have had the motivation. In my judgment, she is probably right. Had he been given that stark warning when he should have been, he would, on the balance of probabilities, have stopped drinking.
30. The Law

I have been referred to three authorities, Bonnington Castings Ltd v. Wardlow [1956] AC 613, secondly Wiltshire v. Essex Area Health Authority [1988] AC 1074, and thirdly Tahir v. Haringey Health Authority [1998] Ll LR 104. The principles to be distilled from these authorities are straightforward and uncontroversial: (1) the burden of proving causation is on the claimant; (2) causation is a question of past fact to be decided on the balance of probabilities; (3) if it is proved that negligence was the sole cause or substantial cause or that it materially contributed to damage, the claim succeeds in full. Material contribution means a contribution which is more than de minimus.

31. For the reasons set out earlier in this judgment, it follows that the claimant has proved that negligence in this case was at least a material contribution to the damage that was suffered, that damage was the cause of the deceased's death, and in consequence this claim must succeed in full. Damages have helpfully been agreed in the sum of £175,000. It follows that there must be judgment for the claimant for that sum.