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Regina v. Shipman (Harold Frederick) (1999, unreported) Day 21:

Transcript for Trial Day 21
Wed 10 Nov 1999

 

The following cases were referred to on this day:
Kathleen Grundy, Muriel Grimshaw, Ivy Lomas, Jean Lilley, Winifred Mellor, Joan May Melia, Bianka Pomfret, Marie Quinn, Irene Turner.

[COMMENT1] No. T982105

THE HIGH COURT OF JUSTICE

Sessions House,
Preston Crown Court,
Lancaster Road,
Preston.

Wednesday, 10th November, 1999

BEFORE:

THE HONOURABLE MR. JUSTICE FORBES

R E G I N A

v.

HAROLD FREDERICK SHIPMAN

____________________

MR. R. HENRIQUES, Q.C., MR. P. WRIGHT, Q.C. and MISS K. BLACKWELL appeared on behalf of the prosecution.

MISS N. DAVIES, Q.C. and MR. I. WINTER appeared on behalf of the defendant.

____________________

Transcribed from the Stenotype notes of
Cater Walsh & Co.,
Official reporters to the Crown Court at Manchester.

___________________

P R O C E E D I N G S

I N D E X

JULIE EVANS, recalled

Cross-examined by MISS DAVIES .. .. .. .. .. 2
Re-examined by MR. WRIGHT .. .. .. .. .. 41

JOHN ASHLEY, recalled

Cross-examined by MR. WINTER .. .. .. .. .. 54
Re-examined by MR. WRIGHT .. .. .. .. .. 67

ROBIN ADRIAN BRAITHWAITE

Examined by MR. WRIGHT .. .. .. .. .. .. 70
Cross-examined by MISS DAVIES .. .. .. .. .. 79
Re-examined by MR. WRIGHT .. .. .. .. .. 83

STEVEN BERNARD KARCH

Examined by MR. WRIGHT .. .. .. .. .. .. 88

Wednesday, 10th November, 1999.

MR. JUSTICE FORBES: Yes, Mr. Wright.

MR. HENRIQUES: My Lord, once Mrs. Evans has been recalled I have discussed matters with my learned friends this morning and there are no other matters that I would seek to elicit in examination-in-chief at this stage. There may be matters in due course that may require her to be recalled but on a different point entirely.

MR. JUSTICE FORBES: Right. Are you content to start your cross-examination now?

MISS DAVIES: Yes, thank you my Lord.

MR. JUSTICE FORBES: Mrs. Evans, if you would come back into the witness box please.

MR. WRIGHT: Furthermore, there is the schedule now, there is a schedule now available and will be distributed.

MR. JUSTICE FORBES: Thank you.

MISS DAVIES: My Lord, overnight we have prepared a schedule which deals with, in respect of each of the 9 exhumations, the date of death, the date of exhumation, whether or not each body was embalmed, the postmortem interval both in weeks and days, and the finding so far as Mrs. Evans is concerned, be it thigh alone or liver and thigh. I have shown it to my learned friend. He agrees it as a document and perhaps I could then hand it in.

MR. JUSTICE FORBES: Thank you very much.

MISS DAVIES: Can I also say during the course of the questioning of Mrs. Evans I will want to refer to some of the liver weights, we have put those into a chart, and also an extract from a textbook relating to weights of livers and skeleton muscles. These documents I hope Mrs. Evans received yesterday. Therefore, to avoid any delays in cross-examination perhaps I could hand all those documents in now.

MR. JUSTICE FORBES: Yes. Very well.

MISS DAVIES: My Lord, perhaps as we have now produced them they can go into the defence bundle, probably the easiest position be at the end of the defence bundle.

MR. JUSTICE FORBES: Into the front of which bundle?

MISS DAVIES: I was going to suggest the end but I don’t feel strongly, the defence bundle my Lord.

MR. JUSTICE FORBES: Yes.

JULIE EVANS, recalled
Cross-examined by MISS DAVIES

Q. Mrs. Evans, the position in the Autumn of last year was this, that you were carrying out your analysis over a period of time as samples were being produced for analysis?
A. That’s correct, yes.

Q. Because as a matter of fact bodies were exhumed over a period of time between August and the latter part of last year and as bodies were exhumed samples were taken and were sent or brought to you and you began and indeed continued your process of analysis?
A. Yes, that’s correct.

Q. And is it right to say that as you gave your evidence to the Court yesterday, beginning with the case of Mrs. Grundy and ending with the case of Mrs. Grimshaw, that represented your chronological process of analysis, save where you might go back to a case for further investigation?
A. Approximately, yes.

Q. When you began with the very first case, which was Mrs. Grundy, that was an analysis done on its own, it was the first exhumation and it was one exhumation and one exhumation alone?
A. That’s correct.

Q. In respect of that very first sampling you attempted to analyse 3 types of samples, one was blood, one was liver and the other was thigh muscle?
A. Yes.

Q. And was that in accordance with what would be perceived as good practice, namely to obtain a number of samples so that you can use them for comparative purposes?
A. Yes.

Q. Insofar as the blood was concerned you told the Court yesterday that there you encountered difficulties because the blood was solid clotted material which in your opinion had been caused by the embalming process?
A. I think that was the most likely explanation, yes.

Q. And therefore of the 3 samples that you received only one you could actually test and the testing was so limited that in fact you could take it no further at all?

A. That’s correct, yes.

Q. And is it fair to say this, that following your attempt to sample the blood on Mrs. Grundy there was no further blood sampled on any of the other bodies?
A. That’s correct yes.

Q. Then moving on to the first 4 cases, do you have a copy of this chart Mrs. Evans?
A. No I don’t.

Q. Let me give you one. It would be easier for you. I will hand you two documents to save time. It is the top document. Members of the jury, I am working off that long schedule. Mrs. Evans, what you can see there simply in chart form are the names of the various women whose bodies were exhumed, the date of birth, the date of exhumation, whether or not each body was embalmed, the postmortem interval in weeks and days and the total morphine findings both in thigh and liver, yes?
A. Yes.

Q. And I will say at once that the total morphine findings are from your reports and your evidence?
A. Yes.

Q. We can thus see that in the first 4 bodies, Mrs. Grundy, Mrs. Pomfret, Mrs. Mellor and Mr. Melia, there you did sampling of both thigh muscle and liver?
A. I did, yes.

Q. And in the remaining 5, Lomas, Quinn, Turner, Lilley and Grimshaw, you sampled only thigh?
A. Yes.

Q. Is my understanding of your evidence yesterday thus, that although you were able to analyse the liver in the first 4 cases, in the remaining 5 the state of the liver was such that you could not analyse it?
A. I could have attempted analysis but any interpretation would have been very much flawed, the decomposition was so far.

Q. So that by the time you get to the last 5 cases you have had to abandon two means or bases of analysis, namely blood and liver, and you have to rely on thigh muscle alone?
A. Yes. There were other tissues which we could have sampled but again because interpretation would have been difficult that was not attempted.

Q. When yesterday you were speaking of your decision not to sample liver in certainly Mrs. Lomas and Mrs. Quinn, in respect of Mrs. Lomas you said of the liver the extensive decay would not give a reliable result and in respect of Mrs. Quinn you said the decomposition would make meaningful interpretation extremely difficult?
A. Yes.

Q. Could you help please, why would extensive decay produce an unreliable result?
A. Just in that we could not be sure of which areas of the lobes we were sampling. You do get variations across livers anyway. There was a lack of tissues, tissue areas that were amass, there were holes evident within that liver tissue.

Q. And in respect of decomposition, for example in Mrs. Quinn, where you said it would make meaningful interpretation extremely difficult, how does a certain degree of decomposition make meaningful interpretation extremely difficult?
A. Meaningful interpretation of any liver, even a relatively fresh liver, is difficult because the differing lobes of the liver can have differing levels of a drug in them. The liver can act as a storage site. This isn’t going to apply to especially exhumed bodies, it could apply even to fresh bodies. So, given that we have these problems to deal with anyway it was felt that it was better to rely on the thigh muscle.

Q. Can I then please just for the moment and deal with the first 4 cases and your readings in respect of the liver?
A. Yes.

Q. What we have done, and it is the second document that I have handed to you Mrs. Evans, it is the shorter of the two documents, is extrapolate from the reports of Dr. Rutherford, the Crown’s pathologist, the liver weights in the cases of Mrs. Grundy, Mrs. Pomfret, Mrs. Mellor and Mrs. Melia. You see there the liver weights for the 4 cases?
A. Yes.

Q. I very much hope that you have the third document that I have handed in this morning. It is a publication the back sheet of which says that it is Current Methods for Toxic Practice. It is published in 1979 and of particular note for this part of the questioning, Mrs. Evans, is that part on the very first page, page 677, where we have percentiles of weights of normal liver. Do you have that?
A. I am afraid I don’t have it to hand.

Q. But you have seen it?
A. I have seen that one, yes. Sorry, I have not seen this one, this isn’t the document.

Q. My apologies?
A. Yes I have. It is just that it is stapled. Thank you.

Q. And it is the very first page I wanted to look at, page 677, percentiles of weights of normal liver, yes?
A. Yes.

Q. And if we look at that it is the second part of the page where we see there various columns where we can see the age of persons and the observed maximum and minimum weight, yes?
A. Yes.

Q. And if we look at the very final entry in that column in terms of age we see there age 70 to 79?
A. Yes.

Q. And we see there a maximum weight of 1,595 grams and a minimum weight of 1,100 grams, yes? Just going to the far right hand column, Mrs. Evans?
A. Right, yes.

Q. Those are the observed maximum and minimum weights and obviously there is a range between the two?
A. Yes.

Q. If we then look at the liver weights in the cases of the first 4 women, we can see that the livers of Mrs. Pomfret and Mrs. Mellor, Mrs. Pomfret let me say at once is 49 and therefore her liver weight would in fact be in the range 2,130 to 1,250,, she is in any event within the range, but one can see both in respect of Mrs. Grundy and Mrs. Melia that both those weights are lower than the normal liver weights?
A. Yes.

Q. Does that surprise you?
A. Not tremendously. I didn’t do any dehydration measurements on the livers of Mrs. Grundy and Mrs. Melia. It is possible that there could have been some dehydration of those tissues, some degradation. That is one of the reasons why we abandoned the liver testing.

Q. When you say some degradation what do you mean by that?
A. Any changes, breakdown in cells, loss of water putrefaction.

Q. You have spoken of loss of water, you have spoken of breakdown of cells. You have used the phrase putrefaction. That is rotting really, isn’t it?
A. Yes.

Q. So what you have in, let’s take the liver, there can certainly be loss of water can’t there?
A. There could be, yes.

Q. But there is also another process going on, namely the rotting process?
A. Yes.

Q. And one result of that rotting process is not simply loss of water, it is a reduction in mass?
A. Yes.

Q. And as a proposition would you accept that it is likely that certainly the reduced liver weights in Mrs. Grundy and Mrs. Melia reflect precisely that degradation, rotting process, and resulting loss of mass?
A. That is a possibility.

Q. If we then look at the correlation between the morphine finding in the thigh and the liver, while there appears to be a reasonable correlation between Mrs. Pomfret and Mrs. Mellor, 0.6 to 1 and indeed 0.7 or .9 sampling the thigh and the morphine being in the middle between the two, there is in fact as between Mrs. Grundy and Mrs. Melia in the order of a four-fold variation in the morphine reading as the between thigh and liver?
A. Yes.

Q. And those are precisely the two livers that are under weight and where you accept the possibility of degradation and rotting?
A. Yes.

Q. Just take Mrs. Melia and what again we have done is to go to the reports of Dr. Rutherford, the Crown’s pathologist, as to his findings as to the state of decomposition. As you would no doubt expect, Dr. Rutherford carried out the visual examination but also carried out a microscopic examination and histology. In respect of Mrs. Melia he attempted histology but found that decomposition was such that a full assessment could not be made. In respect of his overall examination he said all internal organs were affected by moderate decomposition with associated shrinking of organs. Now again would that be consistent with that low liver reading in Mrs. Melia of 332 grams?
A. It could be but I would suggest that would be better directed at Dr. Rutherford.

Q. In this particular case, as in others, that is Mrs. Melia, you found the amphetamine type substance which you attributed, in fact, to the process of putrefaction?

A. Yes.

Q. In other words the rotting process?
A. Yes.

Q. So what there appears to be in this case on your chemical findings the rotting process has produced results?
A. Yes.

Q. And on Dr. Rutherford’s visual findings the decomposition has resulted in shrinking of organs?
A. Yes.

Q. To be fair to you, Mrs. Evans, when you were giving the figures in Melia you put it this way, that the levels are a reasonable estimate but do not necessarily represent an accurate figure?
A. Yes.

Q. Is that because of that four-fold variation between the thigh reading and the liver reading?
A. It wasn’t because of that, it was that there was evidence of decay. You can get considerably higher levels in liver than in muscle tissue.

Q. Then just looking again at this table where we see quite clearly the different correlations, would you accept this, that Mrs. Grundy and Mrs. Melia, standing out as they do, this fourfold variability in reading, it is more likely than not that that variability is due to the process of decomposition?
A. It is certainly a probability.

Q. It being probably that it is due to that process, it must raise questions as to the reliability of any such reading?
A. In the livers, yes.

Q. And that is something which you have acknowledged in your answers?
A. Yes.

Q. Can I ask you this, you must have known having come to the end of those 4 cases that you had, certainly 2 out of 4, this fourfold variability. Was that a factor when you moved onto the next 5 which you took account in deciding, and I am not at the moment criticising you, in deciding that it wasn’t appropriate to attempt sampling in the liver?
A. Yes, it was part of the consideration.

Q. So was it really then a twofold consideration, one you had decomposed livers because in fact the liver in the next lady, Mrs. Lomas, was of very much the weight of Mrs. Melia, it was just in the 300 grams, was it a twofold consideration, one you had the decomposed organ and, secondly, you knew from your previous experience such decomposed organs were giving you difficulties in reliability of your analysis?
A. Yes.

Q. Right. So then you are left in effect with the thigh muscle?
A. Yes.

Q. Again this is not remotely a criticism, Mrs. Evans, you have tried the first line which is blood and have not been able to succeed. You have tried the second line which is liver and you have found, and properly found, it wasn’t reliable, and you have no choice but to rely on the third, which is the thigh muscle?
A. Yes. There were alternative samples, as I said earlier, but again I felt we would have had the same problems as we were encountering with the liver and given that data had been published on thigh muscle I felt that was the best course of action at this stage.

Q. Probably the greatest difficulty you faced in carrying out this analysis was the length of time that these bodies had been in the ground?
A. Yes.

Q. Because again if we just look at the longer table, the very first table, the shortest was the very first exhumation which was Mrs. Grundy. That was 38 days. In respect of Mrs. Pomfret it was 287 days; in respect of Mrs. Mellor it was 134 days; Mrs. Melia 101 days; Mrs. Lomas 501 days; Mrs. Quinn 332 days; Mrs. Turner 852 days; Mrs. Lilley 566 days; and Mrs. Grimshaw 512 days?
A. Yes.

Q. You were embarking on somewhat novel territory, weren’t you, in having to carry out this analysis on bodies exhumed for this period of time?
A. Yes. There has been very little done in terms of studies on exhumed bodies. There are relatively few exhumations for toxicology purposes anyway.

Q. And that did not make your considerable task any easier?
A. No.

Q. Because as a matter of fact morphine levels in dead bodies are generally taken from the blood if that is possible?

A. Yes. The majority of research would give you a blood level as opposed to a tissue level.

Q. That is why at first try you go for the blood because that is where the research has been done, that is where comparable levels have been produced as a result of studies and research?
A. In fairness I wouldn’t expect blood from an exhumed body to give reliable results anyway.

Q. Is that because of postmortem redistribution?
A. Yes.

Q. But in fact the whole issue of postmortem redistribution really was being talked about in the late 80s and it was only at that point there was this realisation that the readings in blood in exhumed bodies was difficult if not impossible to interpret, is that right?
A. There are great difficulties if the means of sampling is not known and a lot of the data published can now be actually deemed to be unreliable.

Q. And so for scientists like yourself working in the field, let’s take it from the late 80s, there has been this growing realisation, certainly over the last 10 years, of the unreliability of blood readings and indeed research is going on even as of now, isn’t it?
A. Yes.

Q. Were you present in Dublin when Gisela Scopp presented her paper in the summer of this year?
A. No I wasn’t.

Q. You have read it haven’t you?
A. I am aware of it.

Q. It is yet another paper that highlights the difficulty of postmortem redistribution in blood levels and morphine readings thereafter?
A. Yes.

Q. By reason of this case, Mrs. Evans, I have had to learn about postmortem redistribution but it may not be the first phrase on everybody’s lips. Could you tell us quite shortly what is meant by postmortem redistribution process?

A. In very simple terms it is the way in which drugs move around the body after death. Although the heart has stopped pumping that does not mean that everything within the body has stopped. In the same way as you can have a liquid where you have a concentrated area at the bottom, leave that to stand and it can diffuse around so that you end with a more even distribution. That can happen in a body, particularly if there is an organ close to a blood vessel that carries a high concentration such as the liver. If you were to take a blood sample close to that there is a possibility that you are not only going to draw blood from the liver but are also have an elevation of drug levels if only by simple diffusion, but that is not the whole story.

Q. It is a pretty complicated story isn’t it?
A. Yes.

Q. And it is a story in which research is going on and if anything it is throwing up more problems as to the difficulty with interpretation?
A. Yes.

Q. Notwithstanding those difficulties of interpretation, blood is still the first sample of choice?
A. It is, especially if you know the site from which blood was taken.

Q. But as we know that was a choice that simply wasn’t available to you?
A. That’s correct.

Q. So you had to move forward on the muscle tissues. The particular difficulty you faced was the absence of scientific studies on morphine levels in muscle tissue?
A. There was relatively little data on any tissue samples.

Q. And indeed such data as existed was not the result of controlled scientific studies, it was purely anecdotal?
A. That’s correct. There have been no controlled studies into this phenomenon.

Q. Because they cannot be done?
A. That’s correct.

Q. So the most one is left with is anecdotal reports of fatalities?
A. Yes.

Q. You yesterday cited the paper produced by Phelby. I think that was 1974, wasn’t it?
A. Yes, Soren Phelby.

Q. And that cited 10 cases where there was death which was attributed to morphine?
A. Yes.

Q. You told the Court yesterday that there was no report of the route of administration?

A. In the work of Phelby it says there it is intravenous, but because it is purely anecdotal I don’t think you can have 100 percent confidence in that as being the route of administration. It is the suggested route.

Q. Indeed, and that is the difficulty, isn’t it, it is anecdotal, it is not in a controlled study?
A. Yes.

Q. And in fact in the Phelby study, although there were 10 cases cited only 6 muscle readings were given of the 10 cases relied on?
A. I think you will find there were 7.

Q. I don’t doubt you are right, Mrs. Evans?
A. It wasn’t in all 10 the muscles were measured.

Q. Of the 10 cases relied upon, because some were not relied upon because other drugs were found, of the 10 cases relied upon, 6 of them gave muscle readings. There was a 7th muscle reading but there was evidence there of another drug being found?
A. That’s true, yes, there was another drug present.

Q. So confining it, because there were 14 cases in all weren’t there?
A. Yes.

Q. 4 were eliminated because other drugs were found in the blood?
A. Yes.

Q. Of the 10 cases remaining, only in 6 of those were there muscle readings given?
A. Yes.

Q. And as you told the Court yesterday the most that one can extrapolate from that is that it was a muscle but there is no information as to which muscle in the body it was?
A. That’s correct.

Q. Is it fair to say this, Mrs. Evans, that by reason of reliance on literature such as Phelby’s article, the most one can do is to make broad generalisations?
A. That’s correct, but my conclusions weren’t just based on the work of Phelby.

Q. But notwithstanding, I am willing to broaden it but is it fair to say that by reason of reliance on literature the most when it comes to levels one can do is to make broad generalisations?
A. Yes.

Q. And indeed yesterday you gave us a range, did you not, and that is extrapolated from the literature?
A. Yes.

Q. Specifically in respect of morphine levels found in muscle there is no good scientific evidence upon the interpretation of morphine levels found in muscle postmortem in an exhumed body?
A. Not under controlled conditions, no.

Q. The science behind the finding is not known, and by that I mean what is not known is the process both in the drug and the muscle which leads to the final conclusion?
A. I don’t understand.

Q. Processes go on in the dead body notwithstanding the fact that it is dead?
A. Yes.

Q. You come to a body days, weeks, months, in this case years, after the death?
A. Yes.

Q. As a scientist you will be aware of processes which can go on?
A. Yes.

Q. As a matter of fact in each of those bodies you cannot say what process and to what extent it went on?
A. That’s correct, yes.

Q. So therefore in respect of any finding of yours, although you can recognise as a scientist the processes exist, you cannot say whether that particular process went on and if it went on to what extent it went on?
A. That’s correct, yes.

Q. Another difficulty which you faced is that because no studies, scientific studies I am talking about now, have been carried out, you do not have a control group and therefore no scientific comparators against which you can interpret the levels you found?
A. No. The only interpretation that can be placed is on levels that have been found in previous muscle tissues.

Q. There is no data available on the disposition of diamorphine or morphine and their metabolites in tissues from experimental studies in controlled conditions, that’s right isn’t it?
A. That’s correct.

Q. There is no data available on the stability of morphine and morphine glucuronide in muscle tissues?
A. That’s correct.

Q. There are no studies available on residual glucuronide activities in postmortem muscle tissues?
A. There are some limited studies.

Q. And insofar as, are those the studies you referred to as Stephen studies which refer to 28 days?
A. Yes. That is the one that does some morphine in livers.

Q. That is morphine in livers?
A. Yes.

Q. So it is not even in muscle tissue?
A. No.

Q. And in fact it is outside the period in all these cases because the shortest period we have here is 38 days?
A. Yes.

Q. So as a matter of fact there are no studies on residual glucuronide activities in postmortem muscle tissues?
A. Yes, in glucuronides, yes.

Q. I have just been asked if I would ask you to explain what a residual glucuronide is?
A. Glucuronides are these breakdown products that the morphine goes to. In getting the total you are measuring morphine glucuronides and morphine.

Q. As a matter of fact the long-term stability of morphine and diamorphine in postmortem muscle tissue has not been scientifically investigated?
A. Not adequately.

Q. There is no data available on the effect of embalming and specifically the effect of formaldehyde on muscle tissue and/or morphine?
A. That’s correct, yes.

Q. There is no data available on the taking of morphine in life and how it is converted into levels subsequently found in muscle?
A. That’s correct.

Q. Crucially there is no data available as to the muscle morphine concentration produced by a therapeutic dose of morphine in life?
A. That’s correct. You could not take tissue, muscle tissues from someone in life.

Q. You, to be fair Mrs. Evans, have acknowledged the difficulties you faced in attempting to interpret such levels and you said in your report, at pages 1187 FR, that caution must be used in interpreting the levels found. Is that something you stand by now?
A. Yes.

Q. And you also added a further caveat to that in respect of the caution because you said that in respect of the data at which you had looked on which some conclusions were based, that data was in the main from relatively fresh samples?
A. Yes.

Q. As matter of fact as a scientific, Mrs. Evans, you have actually been breaking pretty new grounds in this analysis that you have been carrying out, haven’t you?
A. Yes.

Q. So you are left with some anecdotal studies which do not give you evidence upon which you can safely rely as to the route of administration?
A. Yes.

Q. You are left with anecdotal studies which at best tell you it is muscle tissue?
A. Yes. They say it is skeletal muscle tissue.

Q. And you are left, and it was a phrase you used a number of times yesterday, that it was the opinion or that the cause of death was attributed to the use of morphine?
A. No, that the levels fell within a fatal, within the range previously reported. I haven’t speculated it is actually the cause of death.

Q. I was going to the actual anecdotal studies. In respect of the anecdotal studies you said that the cause death was attributed?
A. Yes, in the studies it has been attributed.

Q. And you used that word a number of times yesterday, attributed. What one was left with as a result of reading those studies was in effect relying on the opinion of those who had played a part in the investigation?
A. Yes.

Q. Another word you used yesterday was excessive in terms of dose?
A. Yes.

Q. Would the position be this, that looking at those anecdotal studies you are inferring that the levels you have found here relate to an excessive dose because in those studies those levels have been attributed to death?
A. Not just in doing that. In those studies they also did comparisons to blood levels which given, we do have doubts on the reliability of blood levels anyway, so we have the first pointer that these were fatalities so they were indicating excessive doses from the anecdotal information. In addition to that the studies tended to show that thigh muscle tissues, muscle, skeletal muscle tissues, are generally in reasonable agreement with what you might expect from a blood level. Though they are not exact, the range could take them up to give you around 3 to 4 times actual level. Basing some very loose calculations on that it would suggest that these are not the sort of levels that you could get from somebody taking a normal over the counter preparation in a normal dosage regime.

Q. Which was evidence you gave later?
A. Yes.

Q. Can I move on now please to the way in which you calculate or the basis of your calculation because your unit of measurement is the mass of drug per unit mass of muscle, is that right?
A. Yes.

Q. There is no criticism as to your method of measuring and analysing but you are having to contemplate certainly 3 possibilities, because in all of these cases there is a significant period between death and your sampling procedure?
A. Yes.

Q. You have to contemplate what if anything could have changed between death and when you carry out your analysis?
A. Yes.

Q. The first thing that could have changed is the drug?
A. Yes.

Q. The second thing that could have changed is the muscle mass?
A. Yes.

Q. And the third are factors which could alter the concentration as between drug and muscle mass?
A. Yes.

Q. Let’s deal with the very first decomposition. You have already alluded to it, it being one the reasons you did not in fact proceed with your liver sampling. Can I ask you this, have you ever seen a decomposed exhumed body?

A. Yes.

Q. Frequently?
A. Not frequently, no.

Q. All these bodies showed some signs to a greater or lesser extent of decomposition?
A. Yes.

Q. In Mrs. Grundy the liver, and can I tell you I am obtaining this from Dr. Rutherford’s report, in Mrs. Grundy the liver showed some signs of the effects of embalming?
A. Yes.

Q. In Mrs. Pomfret decomposition had taken place and the liver showed signs of significant decomposition?
A. Yes.

Q. In Mrs. Mellor there was decomposition, the liver demonstrated significant decomposition. In Mrs. Melia exactly the same thing, decomposition, the liver demonstrating significant decomposition?
A. Yes.

Q. In Mrs. Lomas in respect of the thigh there was extensive decomposition. That is Dr. Rutherford’s finding?
A. I haven’t actually seen Dr. Rutherford’s finding in relation to that.

Q. In Mrs. Quinn there was some decomposition and there was decomposition in the left thigh muscle, were you aware of that?
A. I wasn’t aware but my visual examination suggested decomposition.

Q. In that particular body, Mrs. Quinn, Dr. Rutherford said the body was in a state of poor preservation and disintegration and in fact the disintegration of soft tissue was most marked in the left thigh, skin, ankle and foot?
A. As I say, I have not seen that.

Q. In Mrs. Turner and indeed Mrs. Lilley there was extensive decomposition and in Mrs. Grimshaw there was some. Now, as you have earlier accepted, the effect of decomposition is not just the loss of water, it is also a reduction in mass?
A. A loss or reduction in mass is due to dehydration of tissues and rotting but if you are rotting it, the mass that you take would still be the same. If you have got a hole there and you took one gram of it you would still have one gram. The hole wouldn’t weight anything. It is dehydration that accounts for a lot of the shrinkage of these organs.

Q. But it does not account for all of them, does it?
A. No it doesn’t account for all.

Q. So what you have is the loss of water, you have a chemical process going on which breaks down low volatile compounds?
A. Yes.

Q. You have loss of low volatile compounds?
A. Yes.

Q. And you have just a loss of mass?
A. Yes.

Q. Can I take the sort of example that I suspect I can more easily understand, a piece of meat. Just look at the times these bodies have been in the ground. If one put a piece of meat in the fridge, take Mrs. Grundy, for 38 days, I am sure in this Court we would all be able to, if not visualise, understand that the rotting process is not just water, it affects the whole piece, doesn’t it?
A. Yes, microbial activity breaks tissues down.

Q. And so what you are having is a shrinkage to a greater or lesser extent of that piece of meat?
A. Yes.

Q. So if there was something in that piece of meat, let’s say a drug, and there was that shrinkage, that concentration of that mass, that would increase the level of the drug wouldn’t it?
A. Only if, only in terms of, in taking one gram the area might be a bigger area if there was holes in it. You don’t actually get a shrinkage in weight. I actually have measured out one gram.

Q. But one gram might have been 2 grams but you don’t know because that shrinkage process has gone on?
A. Some shrinkage could have gone on.

Q. And the effect of shrinkage is to concentrate the mass isn’t it?
A. Parts of it, but given the water content of these, whether it was purely water or putrefactives, amounted to around what I would have expected in life. It didn’t suggest to me that there was significant shrinkage in terms of increasing that, the concentration of drug from the experiments I carried out. I can’t exclude it completely but—

Q. The other difficulty you have is that none of these bodies were weighed?

A. That’s true, yes.

Q. It is known that there is loss of weight from skeletal muscle?
A. Yes.

Q. So you have no in life comparator do you?
A. That’s correct.

Q. And you have no at time of death comparator have you?
A. No.

Q. So you acknowledge there would be loss of water you have attempted to quantify?
A. Yes.

Q. But in addition to that loss of water there has to be some loss of mass due to the process of decomposition?
A. Yes.

Q. The problem you have is you cannot quantify it can you?
A. That’s correct.

Q. And what that process of concentration will do is to increase any drug in that mass, the level of the drug in that mass?
A. To some extent, but from my visual examination I wouldn’t, it would suggest to me there wasn’t extensive concentrations. There could have been some concentration I will accept.

Q. And you also accept that if there has been some concentration the very fact of concentration would elevate the drug level in that mass of muscle it?
A. Could elevate it, yes.

Q. And whatever calculation you have done on loss of water is not the complete answer to that concentration of muscle and the resultant level of drug rising?
A. Yes.

Q. Have you also, speaking of decomposition I hope, because I did actually ask it be given to you yesterday, Mrs. Evans, have you been given an article headed Time Since Death and Decomposition of the Human Body, Variables and Observations in Case and Experimental Field Studies by Mann et al?
A. Yes I have.

Q. Have you had an opportunity to read that?
A. I have had an opportunity to read the majority of it, yes.

Q. Can I give you a copy. My Lord, I am more than happy that this be circulated. It is a short point and unless anyone wants me to for the time being I won’t. What in fact that was looking at was the findings and observation of 8 years of research which may clarify some of the questions concerning bodily decay, yes?
A. Yes.

Q. Turning to page 108 of that paper, in fact Mrs. Evans, quite inadvertently it has been marked so you probably can see the point I am going get to anyway, it is under embalming?
A. Yes.

Q. “Embalming does greatly slow the decay rate of the body Further, the pattern of decay is different in an embalmed body from one that decays naturally. For example, unembalmed bodies usually show the first signs of decay in the face whereas embalmed bodies first show decay in the buttocks and legs perhaps as a result of insufficient penetration of the embalming fluid in these areas.” Yes?
A. Yes.

Q. Do you have any reason to disagree with this article, which I know has subsequently been taken up in other textbooks, as a proposition as to the process and areas of decomposition?
A. Certainly it is a proposition. I would question just how reliable it is seeing as it is based on a single body buried, it would appear, directly into soil, but yes, I would accept that this is published and has been accepted in other works.

Q. So you accept that this has been published and accepted in other works and following from this it certainly suggests that in embalmed bodies the first sign of decay is in the buttocks and legs?
A. Yes.

Q. And we know, because you have told the Court, that in respect of the muscle that came from the thigh, ie the leg?
A. Yes.

Q. And if again we look at our chart again we can see that of the 9 bodies that were exhumed 6 of them were embalmed, Mrs. Grundy, Mrs. Pomfret, Mrs. Mellor, Mrs. Lomas, Mrs. Quinn, Mrs. Turner and Mrs. Grimshaw. I don’t think there is any dispute about that, is there Mrs. Evans?
A. There is no dispute, only that in some of the cases I didn’t have the full details about the embalming.

Q. Very well. My Lord, I am entirely in the hands of the Court. I am conscious these are not the easiest of topics, and you indicated yesterday that we would stop at appropriate moments. I am going on to a separate topic now. I am more than happy to continue with but if it is appropriate I should stop now I will do that.

MR. JUSTICE FORBES: It is a matter for you, Miss Davies, really. How long is this next topic going to take roughly?

MISS DAVIES: I can take this in about 5 minutes.

MR. JUSTICE FORBES: Right.

MISS DAVIES: Let’s just deal now please with embalming, because you told the Court yesterday that embalming fluid contains as its main active ingredient the chemical formaldehyde?
A. Formaldehyde and methanol, yes.

Q. Forgive me, you gave both. And you have already accepted that there is no research on the effect of formaldehyde on morphine levels found in muscle tissues?
A. That’s correct.

Q. The effect of formaldehyde is that it may chemically change one drug to another and by reason of that affect the concentration of the drug ultimately detected?
A. With some drugs yes, that does happen.

Q. A drug concentration determined in formaldehyde affected tissue cannot be taken at face value as the real level of the drug in the tissue before formaldehyde was added is not actually known?
A. That’s correct.

Q. The effect of formaldehyde can be different depending on whether it is in the tissue itself or in the surrounding tissue?
A. Yes.

Q. If the formaldehyde is in the tissue it can increase the mass of the tissue because basically it is adding liquid?
A. Yes, diluting out effects.

Q. However, if it is in the surrounding tissue it has a dehydrating effect doesn’t it?
A. Yes.

Q. And what it can do is extract the water into the surrounding tissue?
A. Yes it can.

Q. And therefore it would increase the concentration of the muscle mass?
A. That is the theoretical possibility. However, of the works that I have seen done with embalming fluid the majority suggest that embalming has a dilution effect, it actually is increasing mass more than decreasing it. But I would accept that if it is not actually penetrating that tissue there is a possibility that formaldehyde could draw water away.

Q. As a matter of fact in the 6 bodies that were embalmed the most you can say is that formaldehyde was used as part of the embalming process but you cannot say in any one of those samples what effect formaldehyde had on the sample you tested?
A. That’s correct.

MISS DAVIES: My Lord, could I stop there now please?

MR. JUSTICE FORBES: If that is convenient?

MISS DAVIES: Yes.

MR. JUSTICE FORBES: Very well, members of the jury, I will give you a short break for 10 minutes before we move on to the next part of the evidence.

Short adjournment

MR. JUSTICE FORBES: Yes, Miss Davies.

MISS DAVIES: Mrs. Evans, we have insofar as some questioning is concerned come thus far, it is accepted that in all of these bodies there is a greater or lesser degree of decomposition?
A. Yes.

Q. Which is wholly to be expected given the period of time between death and exhumation?
A. Yes.

Q. The process of decomposition brings about changes in the deceased’s body affecting various parts of it, including muscle, tissue and levels that can be found therein?
A. Yes.

Q. In respect of a muscle, that muscle can become more concentrated, ie can shrink down, by reason of rotting, putrefaction, call it what you will?
A. Yes.

Q. And the process of that concentration can elevate any subsequent drug level found in that piece of muscle?
A. To some degree, yes.

Q. And the difficulty that you and any other scientists like yourself have is you cannot quantify the degree to which that elevation has occurred?
A. No. Other than measuring water content there is no other means to determine that.

Q. But the water content only tells part of the story because what you cannot quantify is the loss of other compounds, materials, whatever?
A. Yes.

Q. So that for example you could have that 2 gram piece of tissue that would have been present at the time of death but when you go to carry out your sampling, by reason of this process of rotting or decomposition that 2 gram piece of tissue has shrunk down to a one gram piece of tissue?
A. That could happen, yes, but what must be remembered is that the drug isn’t just distributed in the tissue area, it is also distributed in the water content as well.

Q. But the problem that you have is that because you do not know the weight of the original tissue, and by no proper means could you know that, you have to deal with the tissue as you find it at sampling?
A. That’s correct.

Q. And you have to deal with it and you really did have to deal with these in quite difficult circumstances didn’t you, given the decomposition?
A. Yes.

Q. So we are left with this, that you are doing your professional best to analyse decomposed material and produce a level when by reason of the processes which have occurred in that tissue you do not know whether the level accurately reflects the level it would have obtained at the time of death?
A. That’s correct.

Q. Can I now please just deal with one example and it is the longest period, it is Mrs. Turner. If we look at our chart Mrs. Turner died on the 11th July 1996. The postmortem interval was 852 days and in fact it was in, I am sorry?
A. It is okay. I have my own table anyway.

Q. In respect of Mrs. Turner that gave the highest level of all your morphine readings, the reading in the thigh muscle being 1.4 to 1.6?
A. Yes.

Q. When you carried out your analysis of water content Mrs. Turner was the lowest, wasn’t she?
A. Yes, she was. There was around about a 7 percent reduction from what you would normally expect.

Q. I think it was 67 percent when you gave the average reading as being 74 percent?
A. Yes.

Q. Insofar as autopsy findings were concerned, I am now going to Dr. Rutherford’s report again Mrs. Evans, he describes the decomposition there as moderate and characterised by fatty tissue turning to soap. There is in fact a particular description of that, is there not?
A. There is. I am afraid I can’t recall exactly the term at the moment.

Q. I think it is adiposae but I may not be pronouncing it correctly?
A. Yes.

Q. He also found patchy parchmentation affecting the skin and subcutaneous tissue and the internal tissue?
A. Yes.

Q. Were you aware of that?
A. I was aware of that.

Q. And another word for patchy parchmentation would be drying?
A. Yes.

Q. He found drying of the skin, subcutaneous and internal tissue?
A. Yes.

Q. Were you aware that when Dr. Rutherford attempted histology on the body of Mrs. Turner he found that the degree of post mortem degenerative changes precluded meaningful interpretation?
A. Yes.

Q. In toxicological terms it was found that it was suggestive of extensive decomposition?
A. Yes.

Q. Given that in Mrs. Turner’s case we have one of the longest intervals between death and exhumation, on your analysis of water content it is 7 percent below normal, on Dr. Rutherford’s findings there is decomposition, there is drying affecting internal tissue and degenerative changes precluding histological interpretation, do you think it is simply coincidence that the reading you have there found is the highest morphine reading?
A. I think in part there was dehydration to account, so that is going to have devaluated it possibly by some 10 percent but I would still put it above 1, especially given that I took the areas deep within the muscle tissue where there was some reddening so I deliberately targeted where there was less decomposition. There obviously is going to be some contribution from the decomposition, the extent of which I can’t measure, but I couldn’t say that entirely accounted for that being the highest level.

Q. And we have this don’t we, we have the highest level which you say firstly is likely to be affected by the reduced water content?
A. Yes.

Q. You accept that decomposition would affect that reading but you cannot quantify the extent?
A. Yes.

Q. And can I just deal please with your point on the decomposition. You went in to try and find a deeper level of tissue, is that right?
A. Yes I did.

Q. The process of decomposition is caused by bacteria, is it not?
A. That is one of means of decomposition, yes, bacterial invasion.

Q. And the bacteria would come from the lower abdomen?
A. Yes.

Q. It would work from the inside out?
A. Assuming that the skin surface was intact. We know that some of the skin surface was not intact, therefore you would get microbial invasion from the surface as well, but yes.

Q. Therefore when you are going into that deeper tissue you are actually going deeper to the path of bacteria that is coming out, aren’t you?

A. Only if you are also tracking upwards. If we were just tracking down, all I looked for was the areas that looked most like you would normally expect to encounter in a fresh sample, so yes, they went deeper into it in that I have a skin surface and then I just tracked down. That does not necessarily mean that it was closer to the abdominal cavity.

Q. You cannot say?
A. I can’t say.

Q. And to be fair to you again you are trying to do your professional best but this wasn’t a scientific finding, it was a visual finding?
A. It was.

Q. But you accept the process of bacteria would be working from that lower gut out?
A. Yes.

Q. Insofar as you carried out again your water content calculations, the two where you found reduction in the heart were Lomas and Quinn, were they not? I think you found a 29 percent reduction in each?
A. Yes.

Q. Mrs. Quinn, together with Mrs. Grimshaw, was the lowest morphine reading, it was 0.3 to 0.4?
A. Yes.

Q. Given that you had found reduced water content in the heart which again can affect the concentration of an organ, can’t it?
A. It can affect?

Q. The concentration of an organ, the reduced water content?
A. In the heart, yes.

Q. The only other sampling that you dealt with in Mrs. Quinn was that of the thigh?
A. Yes.

Q. Insofar as you carried out this analysis of water content you said in your report, page 1187 FK, it was the paragraph after you cited your percentage findings, you said, “The water content of muscle tissue is generally regarded as approximately 74 percent. Thus my findings suggest that little dehydration had taken place in the tissues used in the morphine determination in these 9 women. It is, however, by no means certain that the water present in the muscles was that present at the time of death. It may be that some exchange has occurred.” What has happened, Mrs. Evans, in that process?

A. In that a lot of these were in very watery ground, some of the coffins were actually water filled. I can’t be sure that the water I was determining was the water that was present at the time of death. It is, of course, possible there was some dehydration but then you have tissues sat in a watery solution and rehydrating from the water surrounding the body.

Q. So if we have one fluid coming in and moving around, yes?
A. Yes.

Q. Drug would be in fluid form, wouldn’t it?
A. The drug from the body could have gone out into the liquid in the coffin and then subsequently been reabsorbed, yes.

Q. So as you have this exchange of water fluid there could also be movement of drug fluid, couldn’t there?
A. There could if the drug has gone out into this solution, which is a distinct possibility. It could then be reabsorbed in the muscle tissue. But it had to have come out of the body in the first place to be reabsorbed.

Q. That creates another uncertainty as to the level of drug subsequently found?
A. Yes.

Q. And within the fatty tissues in the muscle there can be pooling of blood, can there not?
A. Yes.

Q. It can drain muscle of blood?
A. As I understand it, yes.

Q. And it can go the other way and congest it by adding to the blood in the tissue?
A. Yes.

Q. Because all the time a body is in the ground there is this physical process of diffusion going on?
A. Yes.

Q. So again that can effect any subsequent reading in muscle?
A. Yes.

Q. Within the muscle is fat, isn’t there?
A. Yes.

Q. The morphine is a highly fat soluble drug?
A. Relatively speaking it is fat soluble, yes.

Q. As a matter of common sense the amount of fat in any one person varies?

A. Yes.

Q. And therefore the amount of the fatty streaks in the muscle is going to vary person to person?
A. Yes.

Q. And therefore in those fatty streaks there could be different concentrations of a drug?
A. That is a possibility, yes.

Q. It is accepted, isn’t it, that within one person, taking drug levels in muscle there is muscle variability?
A. From one muscle to the next yes there is. There don’t appear to be significant variations within the same muscle as long as it is a remote skeletal muscle, such as the thigh muscle.

Q. There are some variations?
A. There are some variations, I think as much as a fourfold variation has been reported, but I did take 2 different areas and did have good correlation suggesting there wasn’t significant variation within the muscle tissue I was sampling.

Q. You took two samples?
A. In the cases, yes, I took two samples of muscle tissue.

Q. But the difficulty is this, isn’t it, that within that sample procedure, and I am not criticising you Mrs. Evans, please don’t think that, accepting that there is this muscle variability even within one piece of muscle, you cannot be confident that a third or fourth reading would have produced a different result?
A. I would doubt that it would within the muscle tissues I had. I suspect partly as a result of the fact they had been deep, they had been in the ground so long that an equilibrium had been established. It may be a factor that these bodies had been in the ground so far that we weren’t seeing significant variation across the muscle tissue, as opposed to some of the studies where they have seen these differences which were in relatively fresh samples.

Q. This issue of variability, the muscle variability, is another aspect of the process which can be affected by postmortem redistribution, isn’t it?
A. Yes.

Q. And the most you can proffer, and properly proffer, is an opinion that the muscle tissue is less likely than blood to be affected by post mortem redistribution, but it is still susceptible to it?
A. Yes.

Q. And the difficulty that you encounter is that, accepting that a postmortem redistribution will affect that tissue, you do not know to what extent because you have not been able to carry out any trials prior to your sampling?
A. Correct, in the same way as the people who conducted the original studies couldn’t know that.

Q. That is a difficulty which any scientist in your position would face?
A. Yes.

Q. Can I now please deal with the drug. We have already seen that within the body. Let’s just take the first 4 cases. There are differences in levels. I mean the starkest example are two of those cases where there is a fourfold difference?
A. Yes.

Q. As you have already accepted, notwithstanding the fact that a body is dead and indeed buried, there is still diffusion within that body?
A. Yes.

Q. And as you have accepted there is, for example, diffusion of blood, there is also diffusion of drug?
A. Yes.

Q. And again one of the difficulties that you would have encountered is that although as a scientific you know that that diffusion will have taken place, in respect of any specific body you do not know the nature or the extent of that procedure in any one body?
A. That’s correct.

Q. Putting it very shortly, Mrs. Evans, you do not know as a matter of fact where and at what level any drug was in the body at the time of death?
A. That’s correct.

Q. The most you have been able to do, and properly been able to do, is achieve a level which you believe to be, as you described it yesterday, representative?
A. The most representative level that we would expect in tissues of these types.

Q. But the major difficulty is you cannot say as a scientist that it accurately reflects the level of the drug at the time of death?
A. That’s correct.

Q. Would you just allow me one moment. One of the other difficulties that you encounter, or it may be you don’t even have to apply your mind to this, tell me if that is the case, is that although you find a level you are not able to say whether that represents one dose or more than one dose?
A. I can’t say.

Q. What I would like to do now, Mrs. Evans, is just move on to the individual cases please and just deal with some of the factors that arose within them. If at any time you want to look at any more documentation please don’t hesitate to say so?
A. Thank you.

Q. In respect of Mrs. Grundy, I am going to take them in the order that you gave evidence to the Court, in respect of Mrs. Grundy you were aware, were you, that according to the pathologist the liver showed some of the effects of embalming?
A. I was not aware at the time of the analysis but I have subsequently been made aware of that.

Q. And we have already dealt with the effect of formaldehyde and I am not going to go through that again. You said in this case, as you did in others, that you did not undertake testing for all drugs?
A. That’s correct. It is impossible to test for every drug anyway.

Q. And again, I am not putting that as a criticism, it is a fact you go so far and you stop?
A. Yes.

Q. It was a further finding by Dr. Rutherford that in respect of the internal organs of Mrs. Grundy all were affected to a greater or lesser degree by embalming. Were you aware of that?
A. Yes I was.

Q. Now after you carried out the analysis of the samples obtained from the body of Mrs. Grundy you were asked then to analyse one particular tablet which was found near a bedside table?
A. Yes.

Q. And you found that in fact to be nitrazepam?
A. Yes, a 5 milligram nitrazepam tablet.

Q. Which is a sleeping tablet?
A. Yes.

Q. And you were asked about that and about the overdose produced by the taking of too many of those tablets and you described certain symptoms. As a matter of fact have you ever had to treat or deal with anyone suffering from nitrazepam overdose?
A. No, my comments were based on literature reports.

Q. In other words you went to the textbooks?
A. Yes.

Q. Because your field is that of science, you are a chemist you are not a doctor?
A. Correct.

Q. In your report, and indeed in the evidence that you gave to the Court yesterday, you said that in respect of nitrazepam it is not stable in biological specimens which are not stored under refrigerated conditions?
A. That’s correct, yes.

Q. As a matter of fact Mrs. Grundy, obviously her body was not stored in refrigerated conditions. You accepted in the report that you made to the Court the possibility that any nitrazepam present at the time of death may have been lost?
A. Yes.

Q. That is because of the basic instability of the drug in unrefrigerated conditions?
A. Yes.

Q. In respect of Mrs. Pomfret there decomposition had taken place. In respect of Mrs. Pomfret’s liver there were signs of significant decomposition. In respect of Mrs. Pomfret your finding was positive for opiates, benzodiazepine and amphetamine type substance, and this was probably the first of the cases, wasn’t it, where you attribute the initial finding of the amphetamine type substance to the process of putrefaction?
A. Yes.

Q. Rotting?
A. Yes.

Q. You were subsequently asked in the case of Mrs. Pomfret to consider the issue of lithium?
A. Yes.

Q. I don’t know how much you know about this lady’s medical history. Were you aware there was a rather lengthy psychiatric history and she been in receipt of medication?
A. I was aware of medicines she was in receipt of over a period. In terms of her actual medical conditions I could only surmise from the medicines prescribed that that was the case.

Q. Were you aware that when this lady died her treating psychiatrist, Dr. Tait, got in touch with Dr. Shipman because he had a fear that she may have committed suicide?
A. I have only recently been made aware of that, yes.

Q. And you were asked to consider whether or not this lady had died from a lithium overdose?
A. Yes.

Q. Does it follow from the answer you gave in respect of nitrazepam that you have never seen nor indeed had to treat any person suffering from a lithium overdose?
A. That’s correct.

Q. Does it follow that any evidence that you gave as to any such symptoms comes, as in the previous case, from textbooks or medical literature?
A. Yes it does.

Q. As a matter of fact you did not analyse to see if lithium was present, did you?
A. I didn’t, no.

Q. Lithium is an element, one of the most basic forms of chemical, isn’t it?
A. Yes.

Q. It would not have deteriorated so if you so tested you would have been able to discern whether it was there or not?
A. Yes, but the levels wouldn’t have been interpretable given that we were looking at thigh muscles. Again we are back to how do you interpret what you find anyway.

Q. Is that why you did not carry out that particular procedure?
A. Yes.

Q. Can I turn please to Mrs. Mellor. Again the liver, significant decomposition, again here was another body where you found the putrefaction, the chemical evidence of putrefaction on that initial screening of an amphetamine type suggestion?
A. Yes.

Q. And again, like Mrs. Grundy, again not a criticism, such testing as you carried out was not exhaustive, not all drugs were excluded?
A. That’s correct.

Q. Mrs. Melia. We can probably do it this way, Mrs. Evans, do you have pages 423 and 424 in our bundle of your statement of the 26th October 1998? If it is easier for you to deal with it in this way it is pages 4 and 5 of your statement of the 26th October 1998?
A. I don’t actually have your bundle at all. This is my own.

Q. Let’s make sure you have those 2 pages. I will tell you at once it is to do with the medication found in respect of this lady. Do you have your statement in respect of Mrs. Melia of the 26th October 1998?
A. I do.

Q. Then let’s just turn to that. Have you got it in front of you?
A. I have.

Q. Do you have pages 4 and 5?
A. Yes.

Q. At page 4 of your statement, page 423 of our bundle, you there set out the medication which you were given, your understanding being it was medication found at the home of Mrs. Melia at the time of her death?
A. All I knew it was passed to the police by a relative.

Q. I see, and then it was subsequently passed to you?
A. Yes.

Q. And there you list the medication. The first is amoxicillin?
A. Yes.

Q. And you there say, “This bottle contained 6 small red tablets whose appearance was not consistent with that of amoxicillin tablets. Preliminary testing of these tablets suggested them to be prednisolone and their appearance was consistent with this identification.” Amoxicillin is an antibiotic isn’t it?
A. Yes?
A. What is prednisolone?
A. It is a steroid type drug.

Q. Used for what?
A. I am afraid I am not exactly sure without just checking.

Q. Very well. Putting it very shortly, the wrong tablets were in the wrong bottle?
A. Yes.

Q. And when you did your preliminary testing what testing did you do?
A. They were identified on the basis of their appearance and their markings.

Q. The sort of markings that we all of us have seen on tablets?
A. Yes.

Q. What were the next tablets you found or were given to you?
A. It was a bottle labelled as being metronidazole.

Q. Do you know what they are?
A. There are an antimicrobial drug.

Q. And you did not carry out any specific testing, you worked on the basis of similar markings, is that right?
A. Yes.

Q. And then some more amoxicillin was given in a bottle and again you dealt with appearance without specific testing and you found those to be amoxicillin?
A. Yes.

Q. Then penicillin was found in a bottle and again you dealt with appearance but not specific testing?
A. Yes.

Q. Quiet life, I think these are probably herbal preparations, aren’t they?
A. Yes they are.

Q. And again you dealt with appearance but not specific testing?
A. Yes.

Q. Calms, that is a natural plant remedy, yes?
A. Yes.

Q. You found 94 white tablets there. You did not test them, again you went on appearance?
A. Yes.

Q. And what was the next one please, Mrs. Evans?
A. It was a box has was labelled theophylline.

Q. What exactly is theophylline?
A. It is a bronchodilator. It can be used in the treatment of things like asthma.

Q. You found tablets in foil blister packs. Again no testing, you went on the appearance?
A. Yes.

Q. And the final box was ferrograd. Do you know what that is?

A. Ferrous sulphate used in the treatment of iron deficiency.

Q. Again you went on appearance, no specific testing?
A. Yes.

Q. That is all I want to deal with. I just wanted to identify the drugs that certainly had been handed to you. Now in respect of Mrs. Melia this was the one body where you found morphine in the stomach?
A. It was the only one we actually had stomach contents.

Q. I see, it was the only one where you had stomach contents?
A. Yes.

Q. Because what in fact you found in Mrs. Melia, just allow me one moment, you found in the stomach a viscose green brown liquid, yes?
A. Yes.

Q. Does it follow from the answer that you have given that in respect of the other bodies you examined the stomach contents but there are none?
A. In the majority no stomach contents were submitted to the laboratory. Presumably the stomachs had been washed anyway in the embalming process.

Q. I see. So insofar as you have been able to carry out an analysis of these stomach contents, you were precluded from doing any other cases because none were for, warded to you?
A. Yes, presumably none being available.

Q. In respect of those stomach contents you said that they were a viscose green brown liquid. There was no obvious tablets or is it particulate matter?
A. Particulate matter.

Q. And what is particulate matter?
A. Any sort of solid material, whether it being just granules as opposed to whole tablets, so it could be a tablet that had broken down or even a granular preparation of drug.

Q. So what you were analysing was this viscose liquid?
A. Yes. There wasn’t a lot of it and it did actually resemble bile.

Q. Because of the colour?
A. Yes.

Q. Greeny brown?

A. Yes, but at the same time it could just have been some food that had putrefied in the stomach.

Q. On your finding you found 2 milligrams of morphine, yes?
A. Very approximately. It wasn’t accurately determined but yes, approximately 2 milligrams.

Q. 2 milligrams of morphine in this greeny brown liquid?
A. Yes.

Q. Are you aware of the colour of certain forms of oral morphine?
A. I am not exactly sure in terms of what they would look like once they have reacted with stomach acid.

Q. Are you aware of a form of morphine known as cervadol?
A. I have not actually seen that preparation no.

Q. Are you aware of its existence?
A. Yes.

Q. Are you aware that it is pale green?
A. I have seen in the literature there are reports of it being pale green. How pale that green is I don’t know.

Q. This Court has heard on more than one occasion of MST tablets. They are used certainly for pain relief and certainly for those suffering from particularly painful illness?
A. Yes.

Q. Are you aware that MST tablets are green?
A. I think some of them can be green, yes.

Q. Are you aware of capsules known as MXL capsules, oral morphine, particularly high dosage, 120 milligram capsules?
A. I am not actually aware. I have never actually seen one of those preparations.

Q. Are you aware of their existence?
A. Yes.

Q. Are you aware that they are green?
A. I wasn’t, no.

Q. In respect of this finding of morphine in the stomach you postulated two scenarios, one was that it was the result of what you describe as enterohepatic recirculation?
A. Yes.

Q. But you also said you could not entirely exclude the possibility of it being residual from an orally administered dose of morphine?
A. That’s correct, yes.

Q. Can we in the first instance please deal with this procedure, that is the wrong word, this concept of enterohepatic recirculation?
A. Yes.

Q. Could you please explain to the Court what that procedure entails?
A. In part it is as blood goes round the body it goes to the liver and from the liver you have the gall bladder, inside the liver there is the gall bladder. Any blood that is circulating within the system can subsequently go into the bile that is contained in the gall bladder and subsequently back into the stomach. Alternatively you can get reabsorption of drug from blood vessels surrounding the stomach back into the—

THE SHORTHAND WRITER: Sorry, can you slow down a little please?

MISS DAVIES: If I were you, Mrs. Evans, I would start again. I think we are giving the shorthand writer quite a difficult time and I hold myself responsible.

MR. JUSTICE FORBES: Start that answer again if you would please, Mrs. Evans?
A. As the blood goes around the body and a drug has been absorbed into it, whether it be from the stomach itself, from intravenous administration, or an intramuscular administration or any other route, to have an effect it must go into the blood. Then the blood in circulating around the body calls into the liver and the liver has within it the gall bladder and the gall bladder contains bile. This bile can then subsequently have drug within it and bile feeds back into the stomach. There is, also there are vessels surrounding the stomach itself. These leak back into the stomach and thus put drug back into the stomach. Drug that may not ever have been in the stomach originally just as a result of circulation can end up in the stomach.

MISS DAVIES: So what you are saying is that for this process of enterohepatic recirculation to have taken place the drug in question has to move from the blood, it moves into the gall bladder, yes?
A. Yes, that is one route, yes.

Q. It concentrates in the gall bladder, yes?
A. Yes.

Q. And it then has to move from the gall bladder into the small intestine, yes?
A. The gall bladder can actually by means of the hepatic portal vein feed back into the stomach or into the small intestine.

Q. And then from the small intestine it can go back into the stomach?
A. Yes.

Q. Are you aware of the effect of morphine and the sphincter in the gall bladder?
A. No.

Q. You don’t know that one effect of morphine on that sphincter is to constrict it?
A. No I didn’t.

Q. If you would accept from me that that effect is one of constriction, that would slow up such a process, would it not?
A. Yes it would.

Q. If you cannot answer this next question because it is simply beyond your expertise please don’t hesitate to tell me. On this process of recirculation as you describe it, how long are we talking about?
A. I couldn’t accurately determine that. It is outside my field.

Q. In respect of the quantity that you found, 2 milligrams, that is a not insignificant quantity, is it?
A. It is not insignificant. It could amount to a therapeutic dose of a drug.

Q. Can I move on then please to Mrs. Lomas. Mrs. Lomas, by reason no doubt of the period between death and exhumation, her body was decomposed and in respect of the thigh there was extensive decomposition, is that correct?
A. Yes.

Q. Again this was one of these occasions where you found chemical evidence of the putrefactive process?
A. Yes.

Q. This was a case where you tested positive for opiates, benzodiazepine and what was found to be the chemical evidence of the putrefactive process?
A. Yes.

Q. You, as I understand it, did not attempt to identify the benzodiazepines which led to the positive testing, am I correct as to that?
A. That’s correct.

Q. Insofar as the other findings were concerned you mentioned that pholcodine had been prescribed. We know in fact it had been prescribed on the 16th May 1997 and Mrs. Lomas had died on the 29th May of that year so it had been prescribed in the month of her death?
A. Yes.

Q. As a matter of common sense, and I put it no higher Mrs. Evans, although you were working out the supply of pholcodine no-one in this Court knows to what extent and when Mrs. Lomas took the pholcodine tablets?
A. That’s correct, and it is also available over the counter as well.

Q. You are aware that pholcodine can break down?
A. Yes.

Q. And it can break down into morphine?
A. Under extreme conditions, yes.

Q. As a matter of fact morphine can, I beg your pardon, as a matter of fact pholcodine can break down totally into morphine?
A. Under very extreme conditions yes, but not under the conditions I would expect within the bodies.

Q. In the case of Mrs. Lomas your finding in the thigh muscle was 0.9 percent, yes – 0.9, I beg your pardon.
A. Yes.

Q. As a matter of fact you are unable to say whether that level represents in part or in whole any of the breakdown of pholcodine?
A. There may be a very small contribution from pholcodine. Testing that I have done as a result of this case, I have actually had samples that have been spiked up with pholcodine and have been allowed to putrefy for the last 12 months and in that 12 month period no detectable morphine has been detected under naturally occurring conditions. If we treat those samples with a concentrated acid then we can get conversion.

Q. Acid can be produced in the body, can’t it, when the body is in the ground?
A. It can, yes, same as with any decomposing tissues, and these tissues have been left to decompose.

Q. So therefore there would have been this agent present which could in whole or in part have broken down pholcodine to pure morphine?
A. I would not expect it to go entirely to morphine, I would expect to find some pholcodine.

Q. As a matter of fact the agent was present which could convert some of the pholcodine to morphine?
A. Acidic conditions do exist in these bodies, yes.

Q. As a matter of fact those acidic conditions could have broken down the morphine in whole or in part and converted the pholcodine into morphine?
A. I would expect in part. In my opinion I would not expect it to go to completion.

Q. If you accept in part that there could have been this conversion process, it follows doesn’t it that of that finding you have made of 0.9 you cannot say what part of that represents the breakdown of pholcodine to morphine?
A. I would say there could be some contribution to that from pholcodine, yes.

Q. But as a matter of fact you cannot quantify that contribution?
A. From the experiments I have done I would suggest it is a small part.

Q. But as a matter of scientific fact you cannot say of that 0.9 level what is represented by the break down of pholcodine to morphine?
A. That’s correct.

Q. The next lady please, Mrs. Quinn. This was a body described by Dr. Rutherford as being in a state of poor preservation. The disintegration of the soft tissues was most marked in the left thigh, skin, ankle and foot. As a matter of fact, Mrs. Evans, your sample came from the left thigh muscle?
A. Yes.

Q. And therefore the area identified by Dr. Rutherford as demonstrating the most marked disintegration?
A. Yes.

Q. Therefore we have decomposition probably at its most active in this particular part of Mrs. Quinn’s body?
A. With the exception that again I sampled the areas where there was still considerable reddening so therefore it was minimal.

Q. You say that, but one, that is only reddening to your eye isn’t it?
A. Yes.

Q. And you have accepted that in going in you are moving further into that area where bacteria are moving inside out?
A. I am moving deeper, I am not necessarily moving closer to the abdomen, but yes, the decomposition process is where they were present.

Q. They were more than present, the decomposition processes rendered this body in a state of poor preservation according to Dr. Rutherford?
A. Yes.

Q. Mrs. Quinn represents, together with Mrs. Grimshaw, the lowest of the levels that you found, 0.3 to 0.4?
A. Yes.

Q. And this is a body where the effects of decomposition appear certainly on the face of it to be at their highest?
A. Yes.

Q. You simply cannot say in that badly decomposed sample that you were doing your best to analyse what the state of that sample was at the time of death?
A. No.

Q. It follows, doesn’t it, that from the very low reading that you have obtained there, and I am saying low in the range that you have told the Court of, you simply cannot say what any such reading would have been at the time of death?
A. No.

Q. This was a lady who 11 months prior to her death had been prescribed co-codamol?
A. Yes.

Q. In respect of the next lady, Mrs. Turner we have dealt with when I was dealing specifically with the liver and I don’t need to take up your time or this Court’s time any further on that particular case. Can I move on then please to Mrs. Lilley. ere again was a body where there was extensive decomposition noted by Dr. Rutherford. This was where you found chemical evidence of the process of putrefaction, yes?
A. Yes.

Q. And by reason of such findings you said that the levels do not – I won’t pursue that. I am concerned I have not accurately recorded what you said. It was a case insofar as Dr. Rutherford was concerned where the liver was too degenerate for meaningful appraisal?
A. Yes.

Q. And there was obvious degradation apparent in the tissues?
A. Yes, even on my visual examination.

Q. Even on your visual examination?
A. Yes.

Q. And in the case of Mrs. Grimshaw again we have decomposition present?
A. Yes.

Q. And this again, like Mrs. Quinn, was the lowest of the readings produced by yourself, 0.3 to 0.4?
A. Yes.

MISS DAVIES: Mrs. Evans, would you allow me just one moment please. I have no further questions thank you.

Re-examined by MR. WRIGHT

Q. So far as you are concerned is there any problem in the reliability of the evidence that you have given as to the finding of morphine within the body by the fact that the sample has been obtained and analysed from the thigh?
A. No, morphine is definitely present in these samples.

Q. So far as the choice of the thigh muscle in order to perform your analysis in each of these 9 cases, was there a distinct preference or order of preference that you undertook?
A. Yes.

Q. And which, please, is the preferred site of sample in each of these cases?
A. Preferred site would still be the thigh muscle. It is a peripheral muscle.

Q. And in general please, so far as the body is concerned and the preference by way of sample site generally, what would be the preferred site?
A. In cases of exhumed material I would still say the thigh muscle.

Q. Is there anything in the literature that causes you to consider that that may be wrong?
A. No.

Q. In fact, is there anything in the literature that may confirm your opinion?
A. The reported levels in terms of stability, the reported stability suggests that thigh muscle is the one least susceptible to microbial invasion and therefore the best specimen of choice.

Q. Is there any dissent among this field of expertise?
A. Not that I have come across.

Q. Is there any dissent in the material that you have considered in relation to this enquiry?
A. Not that I am aware of.

Q. Has any report of any form been drawn to your attention that may seek you to cause to reconsider your view?
A. No.

Q. Is it so far as you are concerned appropriate to infer that the thigh was the third option?
A. The third option?

Q. The least favourable of the 3, blood, liver, thigh?
A. In an exhumed body, no, I wouldn’t say it was the third option. I would still say it would have been a sample of choice.

Q. And so what is the purpose in seeking to analyse liver and blood?
A. Just to show that there was additional support for its presence in the thigh muscle, that it was in the general circulation and in other areas of the body, and that what we were looking at was maybe an injection had been given into a thigh muscle after death and therefore this was just present there for no other reason.

Q. So how many different areas of the thigh did you then seek to obtain samples from?
A. 2.

Q. How deep within the thigh did you seek to obtain the sample?
A. Until I found areas of reddening. In most cases that was quite deep. We were looking at a few inches below the surface.

Q. A few inches below the surface?
A. Yes.

Q. Were you aware of the concept of postmortem redistribution in blood at the time that you performed these tests?

A. Yes I was.

Q. And therefore did the concept of postmortem redistribution in blood affect your preferred source of sample?
A. No.

Q. Why is that?
A. The only reason that affected the decision was that of the reports that are available concerning postmortem redistribution. These suggest that the femoral, which is the vessel in the leg, is the one least susceptible to change.

Q. Do continue?
A. Thus in deciding on a skeletal muscle to choose I chose the one that was nearest to a vessel that would give the representation if we were looking at a fresh autopsy.

Q. Does the concept of postmortem redistribution in blood effect the total level of morphine?
A. If we were looking at blood, yes.

Q. Does it affect the total level in the sample of thigh tissue?
A. Theoretically yes it could, because it depends on how reliable data is but as I am comparing like with like, I was comparing muscle to muscle, I take those to be minimal considerations.

Q. So far as the total level is concerned, is it possible by postmortem redistribution to increase the total level?
A. Only by—

Q. Sorry?
A. Only by way of concentration and in my opinion there was no significant concentration effects evident in these muscles.

Q. So consequently the converse of that is whether it may effect a decrease in the total level?
A. There is a possibility of a decrease, yes.

Q. So there may be a decrease from death but the increase is in the terms, the potential for increase is in the terms in which you have explained?
A. Yes.

Q. And that is of what extent?
A. That is a negligible consideration.

Q. So is the problem of postmortem redistribution a problem with the reliability of the findings of morphine or with an interpretation of the level found?
A. The problems are with the interpretation of the level found. Morphine was present.

Q. So far as the deep thigh is concerned and postmortem redistribution being by blood, yes?
A. Yes.

Q. Then in the deep thigh muscle itself, how approximate is that to the major blood vessels?
A. In all the reported literature on comparisons of muscle to blood they give an average of 1, ie that the blood is approximately equal to that in the tissues. The range goes from .4 to 3.3. But I didn’t seek to do a comparison to blood because of the problems of postmortem redistribution and the unreliability of data. I merely looked to compare thigh muscle tissue to other muscle tissue.

Q. It is put that by the process of decay you can get considerably higher levels in liver to muscle tissue?
A. Yes.

Q. And you would accept that?
A. Not just because of the decay, you can get higher liver levels than muscle tissue.

Q. Tell us why that is please?
A. The liver is effective a storage organ. Drugs can actually accumulate within the liver?

Q. Is the thigh muscle a storage organ?
A. It is not a storage organ for drugs.

Q. Is it really an organ?
A. No.

Q. You were asked to consider the report of Phelby, yes?
A. Yes.

Q. Soren Phelby. Morphine Concentrations in Blood and Organs in Cases of Fatal Poisoning?
A. Yes.

Q. Is that an article with which you are familiar?
A. Yes.

Q. It was put to you that that was anecdotal by way of study?

A. It is anecdotal in terms of these were people that died but they were not under controlled conditions, therefore they were reliant on information provided to them either by the police or witnesses to the death that the mode of death was from morphine.

Q. Does the literature also include the range indicating whether these deaths were in the morphine naïve or in the morphine user?
A. In the study by Phelby he suggests that most of them had some degree of addiction.

Q. And that the range incorporating that detail was one within which these individual deceased with which we are dealing fell?
A. Yes.

Q. And the lowest end of the scale, the end of the range was what please?
A. 0.1.

Q. And so in dealing with a figure of 0.3 as being the lowest here in the cases of Mrs. Grimshaw and Mrs. Quinn, what number fold increase in the level of morphine does that actually indicate?
A. Threefold.

Q. A threefold increase in the level?
A. Yes.

Q. Would it be fair to deal with that in terms of percentage as being a 300 percent increase?
A. Yes.

Q. In the actual level of morphine?
A. Yes.

Q. And this is in an anecdotal report of the deaths of intravenous morphine users?
A. Yes.

Q. Whilst you were asked about the anecdotal nature of that particular report, have there been any animal studies into this particular field?
A. There have but most of those have been on rats and they are not reliable results for a small animal.

Q. So far as the long-term stability of diamorphine or morphine in muscle tissue is concerned, have you yourself performed any control tests in that regard?

A. I have for the preceding 12 months had samples spiked not with diamorphine or morphine but with other drugs that could be considered potential drugs that morphine could be produce from, ie pholcodine, codeine, and in that 12 month period I have found no measurable morphine, just the parent drug. I have also spiked those same things with embalming fluid as well and I have still not detected any free morphine from those.

Q. Did you spike them with the embalming fluid of the type used in each of these individual cases?
A. Yes I did.

Q. In which the deceased were embalmed?
A. Samples that were submitted that were of the type used in some of these, yes.

Q. Any morphine?
A. No.

Q. Dealing with the pholcodine point and the conversion of pholcodine to morphine, you accept as a proposition that pholcodine may in certain circumstances be converted to morphine?
A. Yes.

Q. And converted in its entirety?
A. In laboratory conditions, yes.

Q. That is what I wanted to ask you about, laboratory conditions. Firstly, what does that involve?
A. It involves adding a strong acid, such as hydrochloric acid, at a very low pH to those samples and allowing them to stand in the presence of that acid for a period of time.

Q. Now hydrochloric acid, very strong acid, for a very long period of time?
A. Yes.

Q. You were asked specifically in relation to Ivy Lomas about the pholcodine point?
A. Yes.

Q. Firstly, does embalming fluid contain hydrochloric acid?
A. No.

Q. Secondly, was Ivy Lomas even embalmed?
A. From the records I have then, no.

Q. From our schedule, no. Therefore, so far as the presence of hydrochloric may be concerned, or an acid of similar strength, is there anything to indicate from your analysis of the tissue in the case of Ivy Lomas that there was present hydrochloric acid?
A. No.

Q. You say that pholcodine may be so converted over a lengthy period of time?
A. Yes.

Q. What sort of length of time are you talking about?
A. We are only talking about a few hours in the presence of that under laboratory conditions.

Q. In hydrochloric acid?
A. Yes.

Q. Insofar as acids produced by any putrefactive process post death, are there any acids produced by that process that are akin to hydrochloric acid?
A. Not within the putrefactive process. Hydrochloric is present in the stomach, so if that was to come into context then there is a possibility, but as the stomach does not directly contact the thigh muscle….

Q. It was a point I was going to investigate with you. Hydrochloric acid in the stomach, your sample was from the thigh?
A. Yes.

Q. Furthermore, so far as pholcodine is concerned what percentage, if you can deal with it in those terms, is the active ingredient of codeine, sorry morphine?
A. Of pholcodine.

Q. Yes?
A. Zero.

Q. How then does pholcodine convert to morphine?
A. It is by processes involving acidic breakdown.

Q. In your view how likely is the prospect of pholcodine converting entirely to morphine?
A. Extremely unlikely. In my experience you cannot actually get the tissues to degrade pholcodine to morphine.

Q. Why is that?
A. Because the acidic conditions developed during the decomposition are not strong enough to convert it.

Q. Did you find any pholcodine by way of parent drug?
A. No.

Q. As far as the levels that you found of total morphine within the tissue samples analysed by yourself, you said this, these are not the sort of levels you could get from an over the counter regime?
A. Yes.

Q. Could you explain what you mean by that please?
A. If someone was to purchase for instance kaolin and morphine or any of the over the counter preparations and take them as the dosage indicated on the bottles, then you could not achieve levels like this.

Q. I will return to that topic briefly when asking you about an analysis of the stomach content a little later, but dealing with analysis of the thigh tissue and the state of decomposition of the bodies, what please was the state of decomposition of the samples taken from the thigh of these 9 respective deceased?
A. There was some evidence of decomposition in the majority of them but the samples I actually took were the ones where there was reddening and the least amount of degradation, although there would be some degradation.

Q. Where does the decomposition manifest itself?
A. In the ones I examined the greatest amount of decomposition was closest to the skin.

Q. Your sample was, as you told us, that number of inches away from?
A. Yes.

Q. Having regard to the matters brought to your attention so far as decomposition is concerned and the analysis that you undertook upon the thigh muscle, thigh muscle that you obtained, have you any cause to reconsider your opinion?
A. No.

Q. Does anyone suggest that morphine occurs naturally as a decomposing product?
A. No.

Q. Have you considered the literature available in this case?
A. I have, yes.

Q. And have you considered various reports served for your consideration?
A. I have, yes.

Q. Is there anything that causes you to reconsider that particular expressed opinion?
A. No.

Q. Dehydration. On the tests that you performed a degree of dehydration in the organs was revealed?
A. In the heart and lung, yes, negligible in the muscle tissue.

Q. Negligible in muscle tissue?
A. Yes.

Q. Therefore, does that factor of dehydration cause you at all to review your opinion?
A. No.

Q. Or to reconsider it?
A. No.

Q. Does the concentration of morphine, total morphine, in the thigh tissue by dint of any dehydration, negligible or otherwise, does the fact of dehydration affect the concentration of total morphine?
A. If the tissue was dehydrated then yes, it would raise the level, but I found no evidence of dehydration.

Q. So you accept the principle?
A. Yes.

Q. And did you apply it in practice?
A. Yes.

Q. And are you therefore able to consider and reject the prospect of that having affected the calculation?
A. I did consider it in drawing my conclusions and I did reject it.

Q. Now you were also referred to the literature from the Journal of Forensic Sciences, a report by Robert Mann and others, Time Since Death and Decomposition of Human Body, Variables and Observations in Case and Experimental Field Studies?
A. Yes.

Q. And you were asked to consider paragraph 12 of that particular report at page 108?
A. Yes.

Q. And the effect of embalming?
A. Yes.

Q. Firstly, that particular paragraph and the report upon embalming, how many bodies were involved in that particular study?
A. It would appear one.

Q. Do we know anything about the circumstances in which the embalming took place?
A. No.

Q. Do we know how that embalming was undertaken?

A. No.

Q. Was the body of the deceased in that particular case buried in a coffin?
A. On the basis of what is here it would appear that it wasn’t.

Q. Was the body of the deceased in that case buried to any noticeable or considerable depth?
A. No, it says it was in a shallow depression.

Q. Is that particular anecdotal report so far as you are concerned of any assistance in the matters that were undertaken by you?
A. No.

Q. Or in the considerations that you have in giving your opinion?
A. No.

Q. Formaldehyde and embalming. Does morphine, forgive me, does formaldehyde have any component constituent chemical that is susceptible to conversion to morphine?
A. No.

Q. So far as the levels of total morphine ascertained by yourself as being present in the thigh muscle of each of the deceased is concerned, insofar as there may be any variable or any variation from the matters that have been drawn to your attention, could the total level at death have been higher?
A. Yes, it is a possibility that it was higher at the time of death than that I found during my analysis.

Q. Could the level have been lower?
A. I think it unlikely.

Q. Why is that?
A. Because if a drug is unstable it is going to breakdown, it is going to be lost, but there is no reports of spontaneous production of morphine in tissues so it is not being produced within the body, there was no measurable dehydration in these muscle tissues to suggest that we were getting a concentration effect. So in my opinion there is nothing to suggest that these levels may have been lower, though it is conceivable that they were higher.

Q. Muscle variability please. You are aware of the literature in relation to that particular concept?
A. Yes.

Q. And also the tests reported by, is it Professor Pounder?

A. Yes.

Q. Did he test for morphine when dealing with muscle variability?
A. No.

Q. So far as the first 4 cases are concerned, Grundy, Pomfret, Mellor, Melia, you were asked to consider the difference in levels present in the thigh?
A. Yes.

Q. What may explain the difference in levels?
A. It may be that different doses were administered, it may be that because the older bodies were showing the lower levels that, as I suggested, maybe the drug does become unstable after very prolonged periods and therefore you get a reduction.

Q. A reduction?
A. Yes.

Q. But not an increase?
A. No.

Q. You can go down but you cannot go up?
A. In my opinion, yes.

Q. Speaking of those that had been buried for longer of course, and looking at our schedule briefly, Mrs. Turner was 852 days, the longest?
A. Yes.

Q. Yet her reading in the thigh was 1.4 to 1.6?
A. Yes.

Q. How many fold is that increase from the level of 0.1 referred to in Phelby?
A. A 15 fold increase.

Q. 15 fold increase?
A. Yes.

Q. Is that 1,500 percent increase?
A. Yes.

Q. Nitrazepam please. I am going to turn, and I hope very briefly my Lord to the individual cases. Nitrazepam, Mrs. Grundy, sleeping tablet?
A. Yes.

Q. Morphine?

A. Not present within nitrazepam and wouldn’t break down to give morphine.

Q. Mrs. Pomfret, benzodiazepine, susceptible to conversion to morphine?
A. No.

Q. Lithium, susceptible to conversion to morphine?
A. No.

Q. Mrs. Melia, amoxicillin, susceptible to conversion to morphine?
A. No.

Q. Any of the tablets or the capsules that you were supplied with and asked about by my learned friend susceptible to conversion to morphine?
A. No.

Q. Stomach content analysis please of Mrs. Melia. Viscose liquid that resembled bile?
A. Yes.

Q. Did you find any tablets or particulates within that liquid?
A. No.

Q. Enterohepatic recirculation. From the material that you have considered in the case of Mrs. Melia is there anything that leads you to conclude that the residue, that the liquid found within the stomach and containing 2 milligrams of morphine, was the residue of morphine tablets, capsules or syrup?
A. I can’t exclude the possibility.

Q. Is there anything that has been brought to your attention by way of report or document that leads you that conclusion?
A. The only thing I can say is that I found nothing in the medical records to suggest that she was on anything morphine related.

Q. Furthermore, you say that the 2 milligrams is not insignificant, it could amount to a therapeutic dose of the drug?
A. Yes.

Q. That would be the 2 milligrams found in the stomach content?
A. Yes.

Q. Of Mrs. Melia?

A. Yes.

Q. Then what please of the 0.7 to 0.9 total morphine found in the thigh?
A. They are greatly in excess of what would be expected from therapy.

Q. If there are 2 milligrams in the stomach how does the total morphine get to the thigh?
A. Could be from another route of administration, from injection.

Q. Mrs. Lomas, I have dealt with, touched upon, the pholcodine point. Just one matter. We know that she was not embalmed in any event and the acidic conditions that are required you have dealt with so far as hydrochloric is concerned?
A. Yes.

Q. Are you also aware of any report by a Professor Forest?
A. I am aware of a number of reports by Professor Forest.

Q. And as to the alkaline or acidic state of any cadaver?
A. Yes.

Q. What please is the situation so far as the alkaline or acidic state of a cadaver is concerned?
A. In terms of Professor Forest’s reports I would prefer if I could actually relate to that report as opposed to doing it from memory.

Q. Whether I need to pursue it further, may I at 2.15. Otherwise that concludes the matters I would seek to raise by way of re-examination.

MR. JUSTICE FORBES: Subject to that then we will break off now, members of the jury, and resume again at 2.15. Mrs. Evans, you still remain giving your evidence until after the lunch break. If you would like to go with your usher, members of the jury.

Lunch adjournment

MR. JUSTICE FORBES: Yes, Mr. Wright.

MR. WRIGHT: I am sorry, forgive me, I did convey the message that it is not a point I wish to explore further. There is no re-examination of Mrs. Evans, I have no further questions thank you.

MR. JUSTICE FORBES: Thank you very much. Thank you, Mrs. Evans. You are free to go. Thank you very much.

MR. WRIGHT: Would you forgive me just for a moment whilst I just confirm something. May we now turn to computer evidence by the calling for cross-examination of Detective Sergeant Ashley. I acknowledge that it is interposed during what is a complex area, but there are reasons why it is not possible for Detective Sergeant Ashley, or indeed anyone representing the interests of the defendant so far as this field is concerned, to be both here at court on any other day.

MR. JUSTICE FORBES: Yes very well. Let Detective Sergeant Ashley be brought into court.

JOHN FREDERICK ASHLEY, recalled

MR. JUSTICE FORBES: You are still under oath you understand?
A. Yes my Lord.

MR. WRIGHT: Would you wait there, there may be some questions for you.

Cross-examined by MR. WINTER

Q. Detective Sergeant, before I ask you some questions might I just explain, my Lord, the device that has appeared in the right hand corner of the court, so that the witness understands what has happened and so that your Lordship and the members of the jury can follow. Detective Sergeant, what you see to your right is, as you will probably immediately recognise, a lap top computer. It is connected to a projector just to the side of his Lordship which is projecting upon that screen what you would ordinarily see appear on the screen of the computer. The screen of the computer is in fact blank and you will therefore be asked to look at the screen in due course rather than the screen of the computer. And the programme that has been loaded on that lap top is the programme and the patient histories that was seized by you, in other words copied from the surgery computer, in the way in which you described when you gave your evidence. Do you follow? So a copy of what you removed has been placed upon that computer and we now have access here to the same Microdoc programme?
A. So this is the record on the day that I seized it?

Q. That’s correct. Do you follow that?
A. Yes.

Q. Before I ask you to access that programme I would like to ask you one or two questions about the nature of Microdoc because you have given evidence both orally and the jury has heard a number of statements of yours read to them, wherein you describe the finding upon the computer in relation to the specific patients with which we are concerned, entries which appear to have been backdated?
A. Yes.

Q. Now the Microdoc programme is designed, is it not, specifically to enable that to take place?
A. The Microdot programme is designed as a computerised medical records data base.

Q. But intrinsic with it is an ability to make an entry at any time within a patient’s history details?
A. Yes.

Q. And it carries with it what is known as an audit trail whereby it records the time at which that particular entry was made?
A. That is attached to each record, yes.

Q. And that is an intrinsic feature, isn’t it, of the programme?
A. Yes.

Q. Details of how one does that and how one would view the audit trail are included within the manual to the programme?
A. Yes.

Q. So, for example, if one makes an addition, we will do this shortly, to a patient’s record, and dates that addition some years previously or sometime previously, let’s say a year previous to the time it is being entered, the entry itself becomes part of the patient history chronologically. In other words if you make it for the 10th December 1997 it would work its way into the patient’s history at that time?
A. Yes.

Q. And you would then by simple procedure be able to analyse the audit trail part of the programme in order to be able to establish when that entry was placed upon the computer?
A. Yes.

Q. Have you seen a copy of a report prepared by Mr. Jonathan Beck?
A. I would need to see the report. I have seen a report.

Q. I am just going to ask you one short question, I hope, about it. Did you also receive with that a rather large volume of printout patient codes?
A. Yes.

Q. Which was a print out of the total number of backdated entries for whatever patient that were recorded within that computer?
A. I believe that was what it was supposed to be, yes.

Q. Did you perform any checks on it?
A. No.

Q. Do you have any reason to believe other than, as Mr. Beck states, that that is a printout of every backdated entry on the computer?
A. No.

Q. It does not matter as to specifics but there are a very large number of those entries, aren’t there?
A. Yes.

Q. Probably in excess of 20,000?
A. Possibly yes.

Q. I am grateful to my learned friend, just over 19,000, 19,206. The programme has to be entered by way of a code?
A. Yes.

Q. And perhaps if you would turn to the computer now and assist us because do we see on the screen that the very first screen that one finds when one has logged into the Microdoc one is about to embark upon entering patient histories?
A. That is a screen, when the computer, the server, has been powered up that is the screen that, when it has gone through power up process you are faced with. You are not actually into the Microdoc system as yet, that is the menu that allows you to go into it.

Q. This is the menu to gain access and one can see the third entry Microdoc, so would you be kind enough to enter that. It tells us it is loading Microdoc and appears, there two spaces with the flashing cursor. That is where one needs to enter the code?
A. Yes.

Q. There was in fact, do you understand, in effect only one code used by all the staff in the surgery?
A. I believe so but that is not a matter of fact to me. I have not spoken to anybody about that.

Q. That is from your understanding, it is not something you have been able to understand from the computer itself?
A. No.

Q. That is agreed. I am very grateful. And I hope this will work, if you enter HFS ACP222?
A. The way I normally enter the system is by a super user pass word, not his way.

Q. There are two ways of gaining entry, that is the way the normal user would gain entry but there is a super user which is the word “Bowls?”
A. Yes.

Q. Whichever route you prefer. Having therefore entered Microdoc, entered the user code, the first page that you see is a page that states in the centre of it the date?
A. Today’s date as picked up from the computer.

Q. I am going to come back to this in a little more detail but the way that computers work is that they don’t have an understanding of what today’s actual date is, they are told by the user what the date is?
A. I can enter any time and date on there I wish. The date and the time we are seeing is actually picked up from the computer itself. So there is a record within the computer of what today’s time and date is now.

Q. But that has come from it having been entered into the computer at some earlier stage?
A. Probably at manufacturer.

Q. Quite possibly. But the computer will calculate today’s date from the date that has been entered into it either by the manufacturer or by some other person?
A. Yes.

Q. In other words, if the manufacturer entered the wrong date for some reason, we would not be seeing today’s date, we would be seeing a different date?
A. Correct.

Q. At the bottom of that it clearly states, does it not, an ability to change the date by using D, to change the time by using T, and once having done that to confirm that it is correct by pressing enter?
A. Yes.

Q. Would you for the moment confirm we are at the 10th November and move to the next page. The next page is the main menu?
A. Yes.

Q. For the particular part of the programme in Microdoc that would be of use to a doctor in a general medical practitioner’s surgery?

A. Yes.

Q. And one can see there a list of the various possibilities available. If one goes to M?
A. M.

Q. M, one sees Medical Summaries. Would you press that please. And comes up a refined menu so one is narrowing the field, is that correct?
A. Yes.

Q. And on that summary menu there are 4 choices on the left and a cohort histories choice on the right, but of the 4 one can see there is Histories, Medical, Summary, and then an entry for removing summary. Do you understand, don’t press this button because it takes a very long time to do it but do you understand if you were to press R you would remove a particular patient’s summary completely from the programme?
A. Yes. You would be required to input the patient’s registration number or identity and then you could remove that patient’s whole summary.

Q. Exactly. So that would be a way of going about removing someone completely from the practice, for example if they left the practice?
A. Yes.

Q. Could you, however, press M again please for medical summaries. I am sorry, I have gone wrong already, I knew this was going to happen. Could you press escape to go back and press H for Histories. We need the full histories. This is now inviting the user to enter a particular patient’s history and obtain access to that set of records?
A. The patient’s registration number, that is what it is waiting for.

Q. Would you please enter the registration number for Mrs. Pomfret which I shall tell you is number 31082. It immediately comes into her record and also flashes that she is deceased?
A. Yes.

Q. So would you please press escape to enter her full history. Then do we see access as you have described, and we have seen photocopies of these records in our bundle. We have entered the particular history of Bianka Pomfret?
A. It is. This is not the way that I normally enter by reference to my statements.

Q. I appreciate that but as a user following simple steps through the operation of the Microdoc programme this is a route to gain access to the summary?

A. Yes obviously, yes.

Q. It has highlighted, has it not, in fact for the 11th December a particular entry?
A. That will be the last entry, I presume, of the record, yes.

Q. If you press the arrow keys you can go up to select a particular entry so would you perhaps select the first one for the 10th December. In order to look in greater detail as to that entry one goes simply to Display, doesn’t one?
A. F6.

Q. Or F6 makes the same route. Just before you do that can I point out through you that at the top of the page just under where it has the patient number and Mrs. Bianka Pomfret there is a box under the heading “Patient history” which has various possibilities listed horizontally?
A. Yes.

Q. The first is Add, by which one would simply add an entry. The second is Display, by which one enters a specific entry in order to analyse it further. The third is Correct, if one wishes to make amendment to an entry. The fourth is Remove if one wished to remove a specific entry. Do you agree that here set out in very easily understandable terms intrinsic to the programme is the ability to amend, to add, to remove, to deal with as you see fit entries in that patient’s history?
A. What you are referring to there is a drop down menu system. We can actually go to that menu and display all the options that appear under each of those words. So yes, basically what you have said is correct. There may be other functionality available within that drop down menu.

Q. Precisely. That is the route in to remove an item, for example?
A. That is one way, yes, definitely.

Q. Would you kindly enter the display part of that. I think that is F6. So by pressing that button one then gets the full entry in this case for the 10th December?
A. The Display History Details yes, in that central box.

Q. And would you confirm, I will show you the manual if you need to but it may be that you know this in any event, all of this is set out in the user manual?
A. Yes.

Q. If the user wanted to know when that particular entry had been made one can see that it is dated on the left the 10th December 1997, but if one wished to discover when that particular entry had been made, it is a very simple step isn’t it?
A. Yes.

Q. One simply goes into Info that we see on the second box down under Display History Details?
A. Yes.

Q. So would you perhaps do that please. You pressed, did you press “I” for Info?
A. Yes I did.

Q. And we can see that was created, as we see there, on the 10th December at 15.52. So do you agree with this suggestion, not only is it very straightforward to analyse a particular entry, it is equally straightforward and an intrinsic part of the programme to discover when that entry was made?
A. Yes.

Q. Would you please return to the main history menu by pressing escape. I am grateful. Could you please be shown the first volume of the jury’s bundle and might I invite your Lordship and the members of the jury’s attention to the first bundle. Under the flag for Mrs. Pomfret, maybe you have got the second, may I invite attention under the divider for Mrs. Pomfret to page 721.

MR. JUSTICE FORBES: Can I have the reference again?

MR. WINTER: Page 721 which is towards the rear of the divider labelled “Pomfret.” Before we come to refresh our memory of this and another related document, can I just ask you this. You said when you gave your evidence to my learned friends who prosecute that it was quite possible in your view that the user of the computer would not know that a particular entry was being timed. Can you remember? It is a long time ago. Can you remember saying that?
A. Yes.

Q. Well, that might be the case but it would only be the case of a user who had not (a) read the manual and (b) looked in Info as we just did on the computer?
A. The manual being, I would estimate, in excess of 300 pages.

Q. It is a very very lengthy, I agree?
A. Not the easiest thing to read.

Q. And not the easiest thing to read, but in the paragraph that tells you how to make an entry, that very paragraph goes on to explain how you can examine through the Info button when that entry was in fact created?
A. Yes.

Q. So you might not read the entire 300 pages but if you looked in order to discover how to make an entry, all of this information is included at that part of the manual?
A. It exists in the manual.

Q. And as we have just seen even a mildly curious user would be able to access that information?
A. If you looked in that section you would find the answer, yes.

Q. Can I just refresh the memory of the ladies and gentlemen of the jury. At page 721, do you have that there?
A. I do.

Q. We have an entry dated 28th April 1997 with an end date of the 10th December and if you look at the previous page that was created on the 28th April but removed on the 10th December. It is page 721 and 720?
A. Yes.

Q. If you turn now to page 691?
A. Yes.

Q. We see an entry again for the 28th April 1997, this time with no end date, which over the page is said to have been created on the 10th December 1997?
A. Yes.

Q. And what is said by the prosecution is that page 721 was removed on the 10th December and in its place page 691 was put on the machine?
A. Yes.

Q. If you look please at the times involved, so at page 691 the time of that entry if you move over the page is 15.59 and 8 seconds on the 10th December?
A. Yes.

Q. That is precisely the same time, is it not?
A. Yes.

Q. At which the entry for page 721 was removed?
A. Yes.

Q. You find that at page 720, 15.59 and 8 seconds. What happens is this, if a correction of any form is made to an entry the computer regards the process that has taken place as the removal of one entry and the replacement of it by a new entry?
A. Yes, I am aware of that.

Q. Do you agree with that?
A. Yes I am aware of it, I agree with it.

Q. In effect what is happening is that an entry is simply replacing another entry?
A. In this case the entry on the 28th of the 4th existed within the record and on the 10th December at 15.59.08 that entry was altered. The original entry was placed into the removed section of the data base and it was replaced with the entry that was created at that time on the 10th of the 12th.

Q. Exactly. The point being this, that even if you were to go in and correct a spelling mistake, for example, the computer regards the entry which was corrected as having been removed and a new entry as having been put in its place?
A. That is correct.

Q. The previous entry, as you say, goes into a list of entries that have been removed from the computer and can be accessed as we will see in due course?
A. Yes.

Q. And that explains, doesn’t it, why on the occasions when the date and time are precisely the same, what has happened is that some form of amendment has taken place to an entry?
A. Yes, definitely.

Q. For example, the top of the page you see the word filters?
A. This page.

Q. Yes, forgive me, top of the screen?
A. Yes.

Q. You see the entry for filters immediately under Histories in the top box?
A. Yes.

Q. Would you be kind enough to enter Filters. By going into that entry do you see the 4th entry down you have got, Read, Code, Date, Range, Context, Show, Remove. If you access that you go into a list of entries that have been removed. So do you agree again with this proposition, that it is an intrinsic function of this computer that when an entry is amended the previous entry is there stored in a list of entries that have been at some point either removed or amended?
A. Yes.

Q. And we can see there the relevant entry, it is the second one down, “28th April 1997, Seen in GP’s surgery.” That is the entry which we saw at page 721 as being amended in some way and therefore the original entry has simply been placed in a list of entries that have been amended or removed? You agree with that?
A. Yes, I agree.

Q. Yes. Would you return please to the main menue. Escape I believe. Sorry, I didn’t mean you to do that. Can you enter Mrs. Pomfret’s number again, 31082. Right. Can you now show us what happens please when one wants to remove an entry. So one accesses Remove. The entry which has been previously highlighted is there, and it is thereby possible simply by pressing the Remove word on the left of that box – do you want to do that please? Have you done that?
A. Yes. I presume you want to go to the Filters menu.

Q. Now we need to go to the Filters to see that it has been removed and you can see there the entry which you have just removed. So in pretty much two very simple steps you can remove any entry of your choice?
A. Yes.

Q. Could you now please press the Add function.
A. You can’t from this screen. You have to go back to the Main History.

Q. I think if you go back to Filters. It is 31082. Now can we go to Add please. So if somebody has, for example, come into the surgery and it is necessary to make an entry, by pressing Add this box appears. And this is the box that prints out in the form that we have seen for example at page 721, when it is completed, the printout, the information is coming from this box?
A. The information probably is coming from there. This isn’t any function I have ever done with this data base. I wasn’t required to add records to it.

Q. Can we just have a look at it please. Now the first that is highlighted is Term keys. Do you understand within the programme there are a very large number of short cut routes into making an entry?
A. Yes. We can list them at this point if you wish to.

Q. Would you just do that so that we can see. There are various headings under which you might want to have a look. So would you go to one of those, it does not matter which. And you have got Administrations at the bottom. Can you then display a list of possibilities under Administration Detail?
A. I am not sure.

Q. It is easier if I do it this way, type in the word “seen,”
S-E-E-N, and enter that. Right. Different form?
A. I can’t understand why that is.

Q. Try if you would 9N1?
A. Do you want me to try something else?

Q. Try 9N1. Sorry, forgive me, you have to press F9 first to show the Read codes.

MR. JUSTICE FORBES: Have you read the manual?

MR. WINTER: I have my Lord?
A. It is complex.

Q. It is very complex. Just F9. Yes. Can I just summarise it in this way?
A. Please do.

Q. There are an awful lot of Term keys like 9N1?
A. I believe you.

Q. Which will come out at the end of the day as saying things like “Seen in own home,” “Seen in surgery,” “At hospital?”
A. Abbreviations would be a better word.

Q. Which are short cuts into placing for example “Seen in GP’s surgery” into the computer?
A. Time saving lists.

Q. Precisely. The Comment, which is the next box down, is a box which must be completed by the user. It is very faint at the moment. Can you go down to it. Don’t worry about entering it?
A. You have got to put something in the Code field.

Q. Precisely, but under comment the user simply makes whatever comment is appropriate and there he has to make an entry if he wants anything to be recorded?
A. I don’t know.

Q. Right. The next entry down is Date and again any particular date can be entered by the user?
A. Yes.

Q. The next entry down is End Date and again the user can place a date there, for example if someone has had an illness for a specific period of time but has come to an end, that particular part of the entry can be concluded by putting a date in at that point. Review is simply you might want to ask the computer to pull up this patient in the future if she needs to come back, for example, for a 3 monthly check, is that right?
A. I don’t know.

Q. You don’t know. But Where, is the point I am getting to, you told the jury when you gave evidence earlier that Where related to where the entry had been made. Do you recall giving that evidence?
A. No.

Q. What do you understand the Where to mean?
A. I understand that by default in this data base, as we see there, every record will have “Here (this practice)” unless anything else is entered there instead of.

Q. Precisely. The default entry means this, does it not, that unless you enter something specifically for that entry the computer automatically records “Here (this practice)?”
A. Yes.

Q. So where we see for example on page 721 the words “Here (this practice),” that may specifically have been entered by the user or the computer may have entered it as its default entry because no other entry was put there?
A. I would suspect the computer has done it because it is identical to what we see on the screen now.

Q. Yes. It is therefore impossible from an analysis of the computer to know whether that entry was deliberately and specifically placed in or is simply there as a result of the functioning of the machine?
A. I think it is more important to look at the difference between the two entries as opposed to the timings perhaps. We know that the entry on the 28th April existed in the data base and on the 10th of the 12th was amended. So if we examine the contents of the 10th of the 12th as amended, we will see the alterations from the 28th April’s original record.

Q. Precisely. I am merely using this page as an example. You cannot say, can you, from this machine whether the entry “Here (this practice)” was specifically and deliberately entered in at the time the entry was made?
A. No, I suspect that is put in automatically by the system.

Q. Precisely. Now finally I hope, this, if I wanted to make an entry for the 10th December, for example today I want to make an entry for the 10th December, but I do not want the computer to record that I have made it today on the 10th November, there is a very simple way of going about that, isn’t there?
A. I don’t think so, no. Try and enlighten me.

Q. Would you go back please to the front of the computer where we saw the time page?

MR. JUSTICE FORBES: Do I understand this is a way of avoiding the audit trail?

MR. WINTER: Yes.

MR. JUSTICE FORBES: Thank you.

MR. WINTER: Would you enter your code please. Would you apply Change the Date, so press D, and put the date the 10th December 1997. Leave the day of the week, it doesn’t matter. Now apply please to change the time. Would you please type in 15.59. Would you confirm that please? Enter again the medical Summaries, the Histories, and the code 31082. Would you please apply now to Add an entry. Now press F9 please for the Read code and put in please 6144, just an example of a particular code. I promise you I wasn’t aware that was coming. Can you put a Comment now please, perhaps you would write “Test” and the date 10th December 1997. And save that as an added entry. So you press Add. Would you please return to the previous page. Do you see there that we have the entry you have just made for the 10th highlighted for the 10th December 1997 with the details and your word Test?
A. Yes.

Q. Now please analyse to see when the computer thinks that entry was made. The computer thinks that entry was made on the 10th December 1997. Do we understand therefore by that, by the simple changing of the internal computer clock at the outset of the programme, one can completely alter the effective operation of the computer?
A. This data base was held on a separate server. The actual data base manipulation would take place at work stations throughout the surgery.

Q. Although it has a central server?

A. It could be done in the manner in which we have done it, but obviously all entries made thereafter would be incorrect. One would have to come back out of the data base and reenter the correct time for all the other entries then to pick up the right time. Quite in overall a lengthy operation.

Q. In order to put it back to where it was before one simply changes the date at the outset?
A. One comes back to the screen we were in, changes it back to the correct, and then, yes.

Q. If one wanted to create computerised records that purported to show that they were created at the time and date which is entered upon the patient’s history, that is, is it not, a very simple way of doing it?
A. That is a way to do it deceptively, yes.

MR. WINTER: Thank you very much.

Re-examined by MR. WRIGHT

Q. Using that particular illustration, what would happen thereafter whenever you then made a further entry?
A. Without going back and changing the time and date all further entries would follow on chronologically. That clock is now ticking. It is probably, at the moment it is 16.03 so any further additions would also be incorrect.

Q. So the clock on the computer would think that it is now the 10th December 1997 and it is 42 seconds past 4 o’clock?
A. Yes.

Q. And so if then anybody within the practice was then to use the computer?
A. From any of the other work stations.

Q. From any other work station and enter in any details in relation to any other patient?
A. Yes.

Q. Then the date and time that would be displayed upon that entry would be what?
A. Incorrect by the number of days we are amending it or whoever is amending it.

Q. And just to remind us, how many work stations were there please in this surgery?
A. Excluding the actual server there were 5 work stations.

Q. And including the server?
A. 6.

Q. What about if there are 3 successive late entries, each of different dates for example. How could that be done?
A. In an individual record?

Q. Yes?
A. It means that by that methodology one would have to go and change the clock 3 times.

Q. And then put it back to the correct time?
A. Yes.

Q. In other words, once you have put in 3 entries for December 97, September 97 or April 98, you would then have to return to the correct time being the 10th November 1999?
A. Yes.

Q. The user manual that you were asked about, the Microdoc programme user manual, does that set out how you are able to perform that exercise?
A. I would think it probably does. I can’t say specifically. I would think the user is probably explained the relevance of that screen where you are able to change the actual time and date. I am sure it is included in the software to provide the facilities to put it to the correct time and date should your computer’s clock be faulty, which does occur. I am sure it is not designed to be put in there to allow users to use it for this subterfuge.

Q. Furthermore, if we look please at the Bianka Pomfret entries for a moment, and using the schedule as we have it please ladies and gentlemen in our volume 1.

MR. JUSTICE FORBES: The A3 schedule?

MR. WRIGHT: The A3 schedule my Lord, yes thank you. And using the examples that were given to us earlier, so we look at the deletion and creation of the entry dated 28th April of 1997, yes?
A. Yes.

Q. You were able to ascertain from an interrogation of the record information held within the computer the time of the creation of that entry and the deletion of the previous entry?
A. Yes.

Q. At 15.59.08?
A. Yes.

Q. We know that the body was found at 5 pm, that is 17.00 on that day. Now insofar as those entries are concerned is the time of the 15.59.08 a manual creation by the process that we have been having described to us?
A. I can’t say whether it was or it wasn’t. It could have been. The data base can be used in that fashion.

Q. So either the time that was ticking on the clock was the time that day, namely 2 hours, an hour and a half, no, an hour before the discovery of the body, or it was a time deliberately selected by manual entry in the way that we have just undertaken here?
A. One of the two, yes.

Q. And after that the computer itself was then reset?
A. Yes.

Q. Does the user manual explain also that if the date is changed then the audit trail is also necessarily changed?
A. I don’t know. I think the computer manual is so lengthy, computer manuals are generally not anything that anybody particularly likes to read, particularly if one is not overly computer literate. And it may well be that even a regular user of this system would not be aware of all the facilities of the software and all that was contained in the manual.

Q. That with respect does not answer my question. It is more a comment really, isn’t it?
A. It is.

Q. What I am seeking to explore with you is whether or not, whilst the facility may be explained within the manual, is the consequence also likely to be explained within the manual so far as the audit trail is concerned?
A. I would doubt it is because that is not what it is intended to be used for.

MR. WRIGHT: I have no further questions.

MR. JUSTICE FORBES: Thank you very much Detective Sergeant Ashley, you are free to go.

MR. WRIGHT: My Lord, before return to t, oxicology is that a convenient moment?

MR. JUSTICE FORBES: Yes.

MR. WRIGHT: At that stage we can remove the screen and remove the various pieces of equipment.

MR. JUSTICE FORBES: That sounds like a very good idea.

MR. WRIGHT: And resume transmission, as it were.

MR. JUSTICE FORBES: Members of the jury, if you would like to go with your usher for ten minutes we will dismantle all this technology.

(Short adjournment)

ROBIN ADRIAN BRAITHWAITE, sworn
Examined by MR. WRIGHT

Q. What is your full name please?
A. Robin Adrian Braithwaite.

Q. And what is your occupation?
A. I am a Consultant in Toxicology and Head of the Regional Laboratory for Toxicology which is based at City Hospital in Birmingham.

Q. Are you a Consultant Clinical Scientist in Toxicologist?
A. Yes.

Q. And Director of the Regional Laboratory for Toxicology and Super Regional Assay Service?
A. Yes I am.

Q. Honorary Senior Clinical Lecturer in the Division of Medical Sciences at the University of Birmingham?
A. Yes.

Q. Senior Research Fellow at the Institute of Occupational and Environmental Health?
A. Yes I am.

Q. Were you also trained in analytical, clinical and forensic toxicology at Guy’s Hospital, London?
A. Yes.

Q. Do you have over 25 years’ experience in this field?
A. Yes I do.

Q. And have you held a variety of appointments involving medical toxicology, clinical pharmacology, clinical research both here and abroad?
A. Yes I have.

Q. And is an area of particular interest analytical and forensic toxicology and drug and substance abuse?
A. Yes it is.

Q. Have you also published a large number of papers concerning various aspects of human pharmacology and toxicology?
A. Yes I have.

Q. Is that something in the region of 160 such papers?
A. Yes I have.

Q. Senior adviser to the World Health Organisation?
A. Yes I am.

Q. Amongst other particular positions that you hold?
A. Yes that’s correct, yes.

Q. I want to ask you please firstly, and this is page 1187 GH, 1 is the starting point, my Lord.

MR. JUSTICE FORBES: I have it thank you.

MR. WRIGHT: I want to ask you please firstly general matters concerning the metabolism of diamorphine and morphine. This is little 4 within that section. GH(iv).

MR. JUSTICE FORBES: Thank you.

MR. WRIGHT: We heard described by Professor McQuay the arterial road map of the body?
A. Yes.

Q. The motorway of the body?
A. Yes.

Q. And using that as the description of the blood the system together with the approaches to the brain being the big city?
A. Yes.

Q. Is that a particular analogy that you would accept?
A. Yes, I think it is attractive analogy to use.

Q. Diamorphine may enter the blood circulation by a variety of routes, may it not?
A. Yes, that’s correct, either by intravenous injection into a vein or injection into a muscle or by mouth, a variety of routes.

Q. Once it has entered into the body thereafter is diamorphine then rapidly converted?
A. Yes it is. It is rapidly converted to another product which has a long name of 6 monoacetyl morphine, or 6 MAM for short, which is then further converted relatively rapidly to morphine.

Q. That was the halfway stage that Professor McQuay spoke of?
A. That’s correct.

Q. And the time over which such a metabolism or conversion takes place?

A. Yes. Diamorphine will convert to 6 monoacetyl morphine within minutes and this intermediate product is relatively unstable and further converts to morphine in a period of maybe half an hour to an hour.

Q. Now we have heard reference to in this case on a number of occasions both what is called free and total morphine. I don’t propose to spend a great deal of time dealing with the distinction but could you just explain to us please what happens to morphine within the body as to how it is metabolised or conjugated?
A. Right. Morphine continues to be metabolised in the body so morphine is converted to what is called glucuronide metabolite and this largely takes place in the liver and—

Q. Just pause for a moment. Glucuronide metabolite?
A. Yes.

Q. In other words that is morphine and its metabolites?
A. Yes, well the glucuronide is the metabolite so morphine is converted to another product which we know as morphine glucuronide. There are two different, slightly different forms of this but this is the next product which we call glucuronide metabolite. When we talk about total morphine generally this means morphine plus that morphine which is present as its glucuronide metabolite. So it is the total amount of drug that is present that is either as morphine or its metabolite.

Q. So would it be fair to put it in these terms, it is the total amount of morphine together with that part of the morphine that has been metabolised?
A. That’s correct, yes.

Q. What then please is free morphine?
A. Morphine, sorry, free morphine is the unmetabolised morphine so it is actually morphine itself. The molecule has not undergone that change so it is morphine which, as I say, is termed free morphine. It is the unmetabolised part of morphine before it is converted into this glucuronide metabolite.

Q. So putting it another way, squaring the circle, free plus metabolite?
A. Equals total.

Q. Equals total?
A. Yes.

Q. You heard the evidence of Professor McQuay so far as the administration and the effect of various quantities of diamorphine and morphine administered either intramuscularly or intravenously?
A. Yes I did.

Q. Do you seek to dissent in any way from that?
A. No, I would fully support what he said.

Q. May I turn please to codeine, because we have had reference to codeine in this case. What is codeine?
A. Codeine is the sort of 3-methyl derivative of morphine so it is a chemical derivative of morphine that is commonly used in many over the counter preparations combined with paracetamol or aspirin. It is a well known over the counter pain-killer.

Q. But is combined with other chemical substances?
A. Very often. I mean, it can be used on its own but it is most commonly in medicines which are bought over the counter in a pharmacy. It is often combined with either paracetamol or codeine or it may be in other medicines where it is combined with other products.

Q. Is codeine known to convert to morphine in the body?
A. Yes, it is well known that codeine or part of the codeine will be metabolised in the body to produce morphine.

Q. But does it metabolise entirely into morphine?
A. No, it will go through other routes to produce other products, so part of its route is to produce morphine.

Q. And so as part of it produces morphine would you expect to find if codeine were administered and part converts into morphine, the presence of other substances?
A. Yes.

Q. Within the tissue?
A. One would expect to find codeine and a smaller quantity of morphine.

Q. Pholcodine please?
A. Is a morphine like drug, sorry, it is a derivative of morphine that is used in cough medicines, so it is a chemical derivative of morphine that is widely used in a lot of over the counter preparations, particularly for treatment of coughs.

Q. When you say derivative, is it thought to convert to morphine in the body?
A. No, there is no good evidence to show that it is converted. It seems to be remarkably resistant to conversion to morphine in the body.

Q. So is the high water mark that it may convert?
A. It may convert.

Q. Is there any evidence of that?
A. There is no real evidence that it does actually convert to any significant degree.

Q. Dealing with conversion to any significant degree, what would you expect to find if there had been some conversion of pholcodine to morphine?
A. One would expect maybe to find a small trace quantity of morphine but a much larger quantity of the parent drug pholcodine also present.

Q. And why is that?
A. Because very little, from what we know of pholcodine, virtually none of it is converted to morphine. One would expect because it is really metabolised so little in the body that you would largely find unchanged drug pholcodine there in samples of tissue and other tissues and fluids.

Q. I am going to turn to page 1187 F X my Lord.

JUSTICE FORBES: It occurs to me, Mr. Wright, that the members of the jury may have a little difficulty from time to time understanding the names of the various drugs to which reference is made. I merely cast out the thought. Is that so, members of the jury, or are you following the names of these drugs? Very well, I was going to suggest perhaps just a list of the names.

MR. WRIGHT: We could provide a glossary of those terms.

MR. JUSTICE FORBES: Would that help?

MISS DAVIES: Certainly, my Lord.

MR. JUSTICE FORBES: Members of the jury, we will take steps to provide you with a glossary of the names of the drugs. Yes, Mr. Wright.

MR. WRIGHT: Did you receive a bundle of documents in July of this year concerning the forensic investigations carried out by Julie Evans?
A. Yes I did.

Q. And also by Dr. Rutherford?
A. Yes I did.

Q. And also various reports prepared by Dr. Grenville?
A. Yes I did.

Q. We also are aware of documentation concerning a Dr. Karch, the gentleman seated in the middle of the middle row here, from the United States, and also from Julie Evans?
A. Yes I did.

Q. And as a consequence of considering those particular documents did you then review these findings?
A. Yes I did.

Q. And did you prepare a report to that effect?
A. Yes I did.

Q. And from that report was a statement prepared?
A. Yes it was.

Q. And would you wish to refer to that statement whilst giving your evidence?
A. I can do, yes.

MR. JUSTICE FORBES: There is no objection so yes, Dr. Braithwaite, you may refer to it.
A. Thank you.

MR. WRIGHT: We are at page FY. It may assist if you turn, as it were, towards the ladies and gentlemen of the jury, Dr. Braithwaite, and use that part of witness box. Do you have it?
A. Yes. I will just find it.

Q. That should have been done for you by me. I am sorry about that. You have consider the conclusions drawn by Julie Evans and also Dr. Rutherford concerning the cause of death in each of those 9 cases?
A. Yes.

Q. And do you dissent at all from the considered opinion of those two individuals?
A. No, I would support what they have said.

Q. Does there appear to be any other rational or feasible explanation?
A. Not that I know of.

Q. On the material that you have considered does there appear to be any other rational or feasible explanation?
A. No, I am not aware of any.

Q. You have been seated in court whilst Julie Evans gave her evidence?
A. Yes.

Q. Matters were raised by way of cross-examination?

A. No, I would still agree with what I have written in the report and what other experts have said.

MR. JUSTICE FORBES: Can I just be sure, rational or feasible explanation for what, Mr. Wright?

MR. WRIGHT: For the death of the 9 individuals in this case?
A. Yes they, that they probably took or were administered a substantial dose of morphine or diamorphine shortly before death, which is what I wrote.

MR. JUSTICE FORBES: Thank you.

MR. WRIGHT: So far as dosage may be concerned, would it be fair to say this, it is not possible to seek to extrapolate any precise form of measurement from the figures that have been obtained and considered?
A. Yes, it is unwise to do that.

Q. But is there any general conclusion that you are able to give so far as dose is concerned from the figures that you have been made aware of?
A. From the postmortem tissue measurements one would surmise that a substantial dose of morphine or diamorphine had been given or had been taken by the deceased.

Q. And insofar as the range, the bracket that we are aware of the Phelby paper?
A. Yes.

Q. Of deaths from morphine poisoning?
A. Yes.

Q. Are you satisfied that these particular deaths fall within that bracket?
A. Yes, they fall within that range reported in that particular paper.

Q. And so in considering the nature and terms of the dose, what is your opinion so far as that is concerned?
A. Again a large dose, potentially fatal dose of morphine or diamorphine.

Q. Have you considered the method by which the samples were extracted by Julie Evans?
A. Yes. I have seen copy of her report and the methods which she has used and they are acceptable.

Q. And insofar as the, paragraph 7 my Lord.

MR. JUSTICE FORBES: Yes.

MR. WRIGHT: So far as the use of the thigh tissue is concerned, what is your considered opinion as to the use of that particular tissue above any other?
A. I think one would regard it as a recommended specimen to take in many cases and that it has many advantages over other specimen types such as liver or even blood.

Q. Does the fact of the taking of simply thigh tissue, albeit from two separate areas, two separate sites?
A. Yes.

Q. In any way cause you to express any concern as to the reliability of the findings?
A. Well, I think samples were taken from separate sites and showed remarkably good agreement, so one draws the conclusion that what was measured was measured reproducibly and an accurate estimate of the amount of drug in that sample.

Q. Paragraph 11 of the report.

MR. JUSTICE FORBES: Thank you.

MR. WRIGHT: Postmortem redistribution. Is this a concept with which you are familiar?
A. Yes indeed.

Q. Is also a concept of the problems that are attached to it, also matters with which you are familiar?
A. Yes.

Q. Is there in any way any restriction or confinement to the problems of postmortem redistribution that you are aware of?
A. In what respect?

Q. Do they apply equally on blood as they may do to thigh tissue across the gamut of specimens that may be obtained from the deceased?
A. They are a far greater problem with specimens of blood and this is widely discussed in the scientific and forensic literature about those problems. Problems can occur with other tissues but probably muscle tissue, to some extent the postmortem redistribution changes one has mentioned, are probably minimised or least effected in the case of muscle tissue in comparison certainly with blood specimens.

Q. How does the absence of any good in-house data or research on muscle with which to compare these case findings affect your conclusions?

A. It does not affect them substantially. I think one would, it is very difficult to do such studies. Perhaps in a perfect world one might have the opportunity to do those sorts of studies but it does not affect the conclusions which I draw in terms of the significance of those values.

Q. So far as those values are concerned, acknowledging the limitations that may apply to them or attach to them, how do you view the calculations themselves and the figures obtained in relation to thigh muscle?
A. In what respect? The value, the magnitude of the values?

Q. Yes?
A. They are substantial, they are significant toxicologically and one would associate them with, as has been done in the Phelby set of data and other data sets, that they are consistent with the administration of a substantial dose of morphine or diamorphine and not inconsistent with death.

Q. We heard some evidence of the stomach content of Mrs. Turner?
A. Yes.

Q. And a therapeutic dose of morphine?
A. Yes.

Q. 2 milligrams. How do these compare at all with a normal therapeutic dose of morphine?
A. Probably on the low side. I mean 2 milligrams perhaps as compared with a therapeutic dose of morphine maybe of 5 milligrams to 10 milligrams.

Q. How do the figures by way of thigh tissue in relation to the deceased compare?
A. That the values from the thigh measurements would indicate a substantially greater dose than that.

Q. You considered the evidence of dehydration?
A. Yes, yes.

Q. In the various organs with which we have been concerned?
A. Yes.

Q. And you have listened and considered the matters raised this morning?
A. Yes.

Q. Do they cause you any concern?
A. No, I don’t think they are a substantial factor.

Q. Stability of morphine in postmortem material, that too is something that has been reviewed?

A. Yes.

Q. In the evidence thus far?
A. Yes.

Q. And was that also reviewed by you?
A. Yes. There is perhaps limitations on the amount of data available for thigh tissue. There is data available on blood and other materials, and broadly it appears to be relatively stable in postmortem material.

Q. So far as total morphine is concerned is there any observation you would wish to make on that particular topic?
A. As regards total morphine it would seem to be quite stable.

MR. WRIGHT: Thank you. Would you wait there.

Cross-examined by MISS DAVIES

Q. Dr. Braithwaite, your experience, and if I may say so looking at your statement your considerable experience, is in the field of toxicology?
A. It is, yes.

Q. And you have held a number of positions in that field at specialist centres?
A. Yes.

Q. In the course of this case it is clear from your statement that you were asked to look at the reports of Dr. Rutherford, the pathologist?
A. Yes.

Q. And you appear to have been asked to consider those reports. Would you hold yourself out as an expert in the field of pathologist?
A. Not forensic pathologist, no. I was aware of the reports and tried to take from them the major conclusions.

Q. Yes, and that is in effect what you were doing?
A. Yes.

Q. Please don’t think for one moment I am seeking to minimise your expertise in your specialist field, but you were relying on the conclusions of another specialist in another field?
A. Yes.

Q. And for reasons I am sure everybody in this court will understand you did not seek to challenge those conclusions, his experience being wholly different to your own?

A. Absolutely.

Q. As no doubt he would defer to your conclusions in the field of toxicology?
A. Yes.

Q. So far as Dr. Rutherford is concerned you relied on his conclusions in coming to the views you have expressed to the Court today?
A. Yes.

Q. Can I please turn not at great length to your own field, that of toxicology. The greatest, I beg your pardon, one of the major difficulties of dealing with levels in muscle tissue is that there is no good scientific data to assist the interpretation of such levels?
A. I think it is very limited, it is limited should I say.

Q. By all means, limited. It is ground I went over this morning, I am not going to go through it at length now. The fact is that there are no controlled scientific studies, the best literature that can be produced is anecdotal?
A. Not necessarily anecdotal. I think in all of toxicology, particularly forensic toxicology, it is almost impossible to do controlled studies by the very nature of the subject.

Q. Indeed?
A. One perhaps can only do control studies in animal studies.

Q. And therefore insofar as there is any attempt to interpret the findings in this case with anything in published literature, I think you have used on one occasion the word “consistent,” on another in your statement you have used the phrase “broadly comparable?”
A. Yes.

Q. That really is as far as one can go?
A. Yes.

Q. The other difficulty is this, that by reason of the period between death and exhumation in all of these cases, and by reason of the processes which would have continued in each of the 9 bodies, although there is a level that has been subsequently analysed by Mrs. Evans, one cannot say that level accurately reflects the level of the drug at the date of death?
A. No. I wouldn’t wish to state that it is inaccurate. It is an index of.

Q. It is an index of. And can I please deal just with one other separate point. You have raised the issue of dehydration, namely the loss of water content. You have heard me no doubt deal at some length this morning with the issue of concentration of the mass?
A. Yes.

Q. Would you accept the proposition that during any process of decomposition there is a concentration of mass which is due not simply just to loss of water but, for example, to the low volatile compounds and other factors?
A. There may be loss of some volatile compounds but the actual concentration of the drug is perhaps not changed. If the water contents is broadly the same, one is still measuring the amount of drug in one gram of material. It is still one gram of material that one is taking.

Q. But the real difficulty is one does not know at the date of sampling what that one gram of material represented at the date of death?
A. There is some, there is likely to be change due to putrefaction within that tissue and, as you say, it may not be exactly the same gram of material, but it is again a representative amount of material—

Q. It is a, I do beg your pardon?
A. …that one is comparing with.

Q. It is a representative sample but as a matter of fact the person carrying out that analysis does not know if that sample represents the same weight as at the date of death?
A. I think the biggest problem is the loss of water and dehydration rather than loss of other materials.

Q. There is the loss of other materials as well isn’t there?
A. I think that is not quite so well documented as loss of water which would be the major factor that one would perhaps be concerned with.

Q. Can I please deal with something that arose this morning which you touched on briefly in your evidence, namely the finding of morphine in the stomach of one of the ladies, Mrs. Melia, where something in the order of 2 milligrams was found?
A. Yes.

Q. Two propositions were put forward. One is it was the result of enterohepatic recirculation?
A. Yes.

Q. Could you explain that please?

A. This is where a drug and metabolites is excreted in the bile from the liver and enters the small intestine. Then it can be converted by microorganisms in the gut, so in the case of the morphine metabolites that might release some free morphine which then can be reabsorbed back into the body. So it is a sort of recirculation, recycling process.

Q. Are you able to say over what period of time such a process would take?
A. Maybe over some hours.

Q. And that is what we are talking about, a period of some hours?
A. Yes.

Q. And it would be a period of some hours in a living person?
A. Yes, yes.

Q. So that in order for the two milligrams of morphine to be subsequently found in the stomach of Mrs. Melia, for that process of recirculation to have taken place there would have had to have been a period of some hours in life during which that morphine could have been recirculated for it to result in being in the stomach?
A. It would also depend on the validity of that stomach sample and whether it is contaminated in some way or, you know, within the body.

Q. But if one explanation, and in fairness to Mrs. Evans she allowed for two, if one interpretation is the presence of the morphine in the stomach is enterohepatic recirculation, that has to take account of morphine in the body in life for some hours?
A. I wouldn’t want to put a very precise time scale on it. I am saying it is some hours.

Q. Indeed. The point I was seeking to make is we are dealing with hours as opposed to minutes?
A. Yes.

Q. Dr. Braithwaite, as you were giving your evidence I was handed a tone which is entitled, The Disposition of Toxic Drugs and Chemicals in Man. It may be a tone well known to yourself and it is to do with the point on pholcodine and the breaking down into morphine?
A. Yes.

Q. I have not had an opportunity to give you a copy of it, not at least because the evidence you have given is not in your report. I wonder in those circumstances it is probably much easier if I hand the book to you for one simple passage in it. I apologise to yourself and the members of the jury, it wouldn’t be the way I would normally do it?
A. Thank you very much.

Q. If I can hand this out on a limited basis. It is a short point. Is the book known to you?
A. Oh, yes indeed. It is probably the very latest edition. I haven’t actually seen it yet.

Q. And if we turn to page 705 of it we find the part that deals with pholcodine, yes?
A. Yes indeed.

Q. It deals with the occurrence and usage, blood concentrations and page 706 at the beginning of the second paragraph deals with metabolism and excretion and there are various diagrams which replicate diagrams you have produced for the Court?
A. Yes.

Q. It would seem, would it not, that that certainly contemplates the breaking down or conjugation of pholcodine into morphine?
A. Yes, it does, it shows the structure of morphine down at the bottom left-hand side, yes.

Q. And the book to which I have referred you, it is very much one of the recognised books in the particular field of toxicology?
A. Yes. I mean, it is very much a review book and so the author takes, reviews work from all sorts of sources, so the original work might have been done by the somebody else, not the editor of the book himself. So I am not sure without reading it in more detail who he is citing there as the author of this metabolic plan.

Q. Dr. Braithwaite, I have literally shown it to you. If you want any more time to look at it—
A. No, no, it is fine.

MISS DAVIES: That being the case I have no further questions thank you.

Re-examined by MR. WRIGHT

Q. Does it necessarily mean when dealing with the stomach contents, this was Mrs. Melia?
A. Yes.

Q. And the two milligrams of morphine found within the liquid within the stomach, does it necessarily mean that the patient was alive for that period of time, a couple of hours?
A. No, I wouldn’t want one to be categorical about that. I think it is very difficult to be precise.

Q. And this is considering the concept enterohepatic recirculation?
A. Yes.

Q. Is that the only route by which the morphine may actually have been eventually distributed into the stomach?
A. No, it might have diffused from the blood.

Q. And—
A. And been trapped in that sort of fluid in the stomach.

Q. So it may have diffused from the blood. Would that involve also the problems or the problem area of postmortem redistribution?
A. It is part and parcel of that problem.

Q. So the quantity found within the stomach could be quantitatively identified through a process postmortem as opposed to premortem?
A. Yes.

Q. In other words it could have occurred after death rather than before it?
A. Either, yes.

Q. Could it also be in the stomach from contact with the liver?
A. Yes. Again part of postmortem diffusion.

Q. So we have leakage from blood vessels, postmortem redistribution from the liver?
A. Yes.

Q. As well as enterohepatic recirculation?
A. All those potentially.

Q. All of the above really?
A. Yes.

Q. So is it possible say precisely how this morphine within the stomach may actually have arisen?
A. In honesty no.

Q. In terms of quantity is it of significance?
A. It is a small quantity.

Q. You were asked a few points on the factor of dehydration. Does that particular factor and the matters that have been raised cause you to review in any way your stated considered opinion?
A. Not at all.

Q. As to the cause of death in each of those cases?
A. No.

MR. WRIGHT: I have no further questions.

MR. JUSTICE FORBES: Thank you, Dr. Braithwaite. You are free to go. Thank you very much.

MR. WRIGHT: I can’t now remember just precisely how many breaks we have had this afternoon. It has been one of those days I am afraid. The next witness I propose it call is Dr. Karch. It is a little different by topic although still essentially toxicological, but there are also clinical findings to be dealt with. Might we have a few moments just to stretch our legs?

MR. JUSTICE FORBES: Of course you may. Members of the jury, we will break off for a short while whilst Mr. Wright regroups and then resume again as soon as he is ready. I imagine 5 minutes.

MR. WRIGHT: No more than that.

In the absence of the jury

MR. JUSTICE FORBES: Yes I gather you want….

MISS DAVIES: Thank you for giving me time to address you. Tomorrow the prosecution propose to recall Dr. Rutherford for cross-examination.

MR. JUSTICE FORBES: Yes.

MISS DAVIES: As, my Lord, you know my learned friend Mr. Winter and I have effectively split the cases factually between us. I am conscious this is a somewhat unusual course but insofar as individual cases are concerning cross-examination of Dr. Rutherford, would you permit us to each deal with our individual cases each so that I would, for example, deal with those cases where I have cross-examined.

MR. JUSTICE FORBES: Of course.

MISS DAVIES: Thank you very much indeed.

MR. JUSTICE FORBES: Whatever is the way which most assists you in the conduct of the defence entirely meets with my approval.

MISS DAVIES: Thank you very much. Can I also say this, I would also be seeking your leave to do exactly the same thing with Dr. Grenville.

MR. JUSTICE FORBES: You need not ask me again.

MR. WRIGHT: May I raise one matter in the absence of the jury, that in the examination-in-chief of Dr. Braithwaite I elicited, in fact it had not sunk in with me at the time I elicited it, I had a discussion with my learned friend Miss Davies about it, I elicited a response from Dr. Braithwaite as to the administration of a substantial dose of morphine.

MR. JUSTICE FORBES: Yes.

MR. WRIGHT: Which he then went on to remark was shortly before death.

MR. JUSTICE FORBES: Did he?

MR. WRIGHT: Well, there we are. It is not our case that that is asserted by the Crown. It is a matter that there was discussion on and we have considered the reports of experts that have been served upon us. We have been steadfast in our approach to the calculations in this case and the use merely of total morphine as opposed to any ratio between free and total, and we do not in any way seek to elicit evidence as to rapidity of death. That remark, of course, is entirely on the point of rapidity of death. It is not the way the Crown put their case. It was elicited by way of a question to which the response itself was not anticipated would incorporate that particular phrase and I thought I had better raise it at this stage so that in due course your Lordship in summing up the case, when you will remind them of the evidence of Dr. Braithwaite, that particular factor is not a factor in this case the Crown seek to rely upon.

MR. JUSTICE FORBES: Thank you for drawing it to my attention so that I should not repeat the error in the course of the summing up. Do you require me to take any other action?

MR. WRIGHT: No. We thought it preferable to deal with it in open court because the press also have interest in the evidence as it has been elicited in this case. But may I say, for the avoidance of any doubt, that that particular feature is not a feature of this case that the Crown in any way seek to rely upon. There is clear authority upon the point from the experts that rapidity is a most unreliable topic and is not one upon which there ought to be any faith at all.

MR. JUSTICE FORBES: By rapidity you mean the speed with which or the duration of the time interval between the administration of the substantial dose of diamorphine by whatever means and ensuing death?

MR. WRIGHT: Yes, by any calculation from the figures so far as the total morphine within the thigh is concerned one cannot – we have the evidence of Professor McQuay as to the effects of the administration of morphine, that is the Crown’s case, and as to the on-set of any stupor, any sleep, any sleepiness on the part of the patient and thereafter death, but what we cannot do is seek to extrapolate from the figures that in any particular case there was from the figures alone such a rapid death.

MR. JUSTICE FORBES: Yes, I understand. Thank you for drawing it to my attention. I shall take appropriate steps to ensure I make no reference to it myself. Are you content that the matter should be left on that basis?

MISS DAVIES: My Lord, yes.

MR. JUSTICE FORBES: Very well. Thank you very much.

MR. JUSTICE FORBES: Let the jury come back.

MR. WRIGHT: Would your Lordship permit one other matter? Would your Lordship consider going one stage further and directing there be no reporting of that particular facet of the evidence of Dr. Braithwaite.

MR. JUSTICE FORBES: Pursuant to what power, exhortation to the press?

MR. WRIGHT: It would have to be exhortation to the press because I don’t consider that section 4 of the Contempt of Court Act would cover the situation.

MR. JUSTICE FORBES: I am sure the press have heard what you have said. They know what I am going to do or rather what I am not going to do in the course of my summing up with regard to this particular part of Dr. Braithwaite’s answer to a question and I am sure that they will be very co-operative and make no reference to it in any report of today’s proc, eedings which they intend to publish. And I would simply ask all representatives of the press to oblige me and oblige the process of the proper conduct of this trial by co-operating in that regard.

MR. WRIGHT: Thank you.

Members of the jury returned

STEVEN BERNARD KARCH, sworn
Examined by MR. WRIGHT

Q. My Lord, this witness’s evidence is to be found at page 1187 GI which is volume 2 of 2 of the expert evidence.

MR. JUSTICE FORBES: Thank you.

MR. WRIGHT: What is your full name please?
A. Stephen Bernard Karch.

Q. Dr. Karch, what are your qualifications please?
A. I have an MD from Tulane University.

Q. And are you then a Doctor of Medicine?
A. I am a Doctor of Medicine, yes.

Q. In the United States?
A. In the United States.

Q. Do you have other further qualifications?
A. I received my Bachelors degree in Philosophy from Brown University in Providence, Rhode Island. I did graduate work in cell biology at Stamford University. I was a fellow in neuropathology at the London hospital in London. I was a resident in Neurology at Stanford University. I did an internship in general medicine at Kaiser Foundation in Oakland, California and worked for 7 years in the cardiac pathology Laboratory at Stanford University doing resuscitation research and research on the effects of drugs on the heart.

Q. Are you also the author of a considerable number of publications?
A. Yes

Q. Including publications on drug abuse?
A. Primarily on drug abuse.

Q. Are you also involved in funded investigations, including the position of investigator in the World Health Organisation in a collaborative project for sudden cardiac death?

A. Yes. I just came here from the organisational meeting. We will be starting an international project to see if we can determine risk factors from analysis of hearts of individuals who died suddenly.

Q. And do your publications also include the pathology of drug abuse?
A. Yes.

Q. Have you prepared a report in this particular case concerning the deaths of the 9 deceased exhumed in relation to this enquiry?
A. Yes.

Q. And have you also considered the post mortem reports of Dr. Rutherford?
A. Yes.

Q. The laboratory reports of Mrs. Evans?
A. Yes.

Q. Also the report of Dr. Braithwaite?
A. Yes.

Q. And of Dr. Grenville?
A. Yes.

Q. And have you also considered the report of a consultant toxicologist from whom we will hear in due course Dr. Sachs?
A. Yes I have.

Q. Dr. Hans Sachs?
A. Yes.

Q. Have you also considered a number of reports from other experts in the field concerned with this particular enquiry?
A. Yes. I received a packet of reports from experts for the defence.

Q. Have you examined any of the microscopic sections of any of the specimens from the deceased?
A. No, I have not had that opportunity.

Q. But have you considered the records of those particular histological findings?
A. Yes. My conclusions are based on Dr. Rutherford’s interpretations of the slides.

Q. I want to ask you this please, the very bottom of page GJ my Lord. In your opinion are the anatomic findings elicited by Dr. Rutherford, taken together with the findings of Julie Evans and of Professor Sachs, in your opinion sufficient to explain the deaths of the 9 deceased in question?
A. Yes, I believe they are.

Q. Have you also considered various matters drawn to your attention by way of the reports submitted to you from the defence?
A. Yes I have.

Q. Have you taken into account any abnormality as identified at postmortem examination in the hearts of any of the deceased?
A. Indeed yes.

Q. And considered whether they were sufficient to cause sudden cardiac death at any time?
A. Yes.

MR. JUSTICE FORBES: Dr. Karch, would you be assisted by referring to your report whilst giving evidence?
A. Yes sir, my Lord.

MR. JUSTICE FORBES: Have you any objection?

MISS DAVIES: No.

MR. JUSTICE FORBES: Very well, you may.

MR. WRIGHT: May I ask then please a general point so far as any abnormality of the heart is concerned. What in your opinion please is the effect of the administration of morphine to an individual suffering such a defect?
A. Well, there are a number of different effects exerted by morphine and it would be very difficult at this stage to say which effect exerted, which property of the morphine exerted the greatest effect, but morphine does two things that would exacerbate the sort of heart disease that we see in several of these individuals. The first thing that happens is that, and some of you may have had experience with seeing drug addicts, seeing train spotting, that drug addicts, particularly heroin addicts, often have scratches and it is not because of bad hygiene but it is because when you inject heroin that releases histamine and histamine causes the skin to itch and addicts are often itchy and have scratches. One of the other things that happens when the histamine is released is that it can affect the heart beats and it can also dilate blood vessels. People who have a histamine reaction get red faced and that reflects dilation of blood vessels throughout the body. If the blood vessels in the body dilate, less blood goes back to the heart and if there is less blood going back to the heart that means that less blood is available to go through the partial obstructions that were present in a number of these patients.

Q. So please how would be administration of a significant dose of morphine, diamorphine, affect an individual with any, with a heart condition?

A. Even without a heart condition we know from studies, controlled studies in humans at surgery, that their blood pressure would likely go down, histamine levels would go up, blood pressure would go down. If blood pressure goes down then the heart is not profused. Not enough blood going to the heart muscle means the heart muscle becomes irritable and may fail either electrically, in other words have an arrythmia, cardiac arrest, or may fail pump wise, in other words not pump adequately or both.

Q. You see the lady with her eyes closed here trying to keep pace with what you are saying. If you could show down a little. I am the one that gets the look that tells me that you are going too fast. Any other effect so far as the administration of morphine, diamorphine is concerned? We have dealt with the effect on the heart or on the blood vessels please, any other area, any other topic?
A. Well, there is a very big one and that is that morphine given to individuals who are not tolerant will stop them from breathing and cause respiratory arrest and subsequently death. In this particular case we are very fortunate because we have hair to look at and hair is an indicator, as we have only known for the last year, of the degree of drug use. And in the cases of the individuals here analysis of their hair shows very low levels based on Dr. Sachs’s analysis, shows very low levels of heroin. In fact the levels are comparable to the levels that are seen in people that die of heroin overdose and this is information that only was published last year in Lancet.

Q. If I can just stop you for a moment, Dr. Sachs will be called in due course to give evidence of the hair findings, but insofar as your own opinion is concerned have you taken into account the hair findings of Dr. Sachs?
A. The hair.

Q. Professor Sachs?
A. Professor, the findings of Professor Sachs in my mind are extremely important because they establish drug naïvety.

Q. In whose cases?
A. Well, one case had a level of 11 nanograms.

Q. I am not going to ask you about precise figures of each of them but so far as each of these deceased are concerned have you considered the question as to whether these individuals may or may not have been morphine naïve?
A. Yes, and I think in every single case they were. One of the individuals had somewhat more morphine in the hair than all the others but compared to known heroin addicts the levels were generally very very low.

Q. Is there an explanation for that, an innocent explanation for it?
A. No, there is no innocent explanation, except they had not taken morphine in the past.

Q. They had not taken morphine in the past?
A. No.

Q. Final general topic before turning to rather more specific findings. Any diagnosis of a stroke in the deaths here, for example in the case of Mrs. Quinn and Mrs. Grimshaw as entered on the death certificate? Can you help us please as to what the effect may be of the administration of a significant dose of morphine upon—
A. There are two kinds of strokes that people can have, one is a haemorrhagic stroke where there is bleeding into the brain and that is almost always associated with the either malformation you are born with or high blood pressure. Morphine would not raise the blood pressure so would not be associated with a haemorrhagic stroke. It seems extremely unlikely that could ever be the case. On the other hand, someone who is elderly and has atherosclerosis, furring up if you will, of the blood vessels in the brain, who has a large dose of morphine but sufficient to drop their blood pressure, might well sustain a stroke.

Q. So I would just like to ask about cause and effect really. Is the administration of morphine then necessarily connected if there were a stroke to such a stroke?
A. It might be connected to an infarction, a non-haemorrhagic stroke, but not to haemorrhagic stroke.

Q. Hydration within the organs, dehydration within the organs. You have considered evidence that has been elicited on that particular topic?
A. Yes.

Q. Do you seek in any way to disagree with the expressed opinion of Julie Evans and Dr. Braithwaite?
A. No.

Q. Do you consider that the total morphine concentration measured in each of these cases would be significantly altered by the degree of dehydration?
A. The total amount measured would be affected by the degree of hydration.

Q. To what extent?
A. Well, if dehydration were present the levels would go up but there is no evidence of dehydration, or only negligible changes.

Q. So far as the morphine levels found in the hair samples of the deceased, of which we can ask Professor Sachs in due course, do you find those levels at all an unexpected finding?

A. No. This is not a very well studied field, or as well studied as we would like it to be, but we do know that drugs end up in hair via several different routes. One way is through the little follicle that attaches the hair to your scalp but another way is from sebum and sweat secreted from your scalp. And the low levels seen here could be consistent with sweat and sebum containing drug because morphine appears very rapidly in the sweat and could have accumulated between the time the drug was given and the time the patient died. The other possibility that also exists, particularly in the one patient who has a slightly higher level—

MISS DAVIES: My Lord, I have great unease about this evidence because the primary evidence is not before the Court.

MR. JUSTICE FORBES: Sorry, I didn’t quite hear.

MISS DAVIES: I have an unease about this witness commenting on evidence when the primary evidence is not before the Court and has not yet been subject to any scrutiny.

MR. JUSTICE FORBES: How do we deal with that? There is a point there but on the other hand…

MR. WRIGHT: There is, but there ought to be, in my respectful submission, no bar to this witness giving evidence, considered as expert evidence, having regard to the reports that he has read in the case and the matters that are to be elicited by way of evidence. The mere fact that Professor Sachs has not given evidence in advance of this witness does not make his evidence on the topic inadmissible. But may I put it a different way, I don’t propose to explore it at any—

MR. JUSTICE FORBES: You are perfectly correct and in the ordinary way if I were sitting as a judge alone I would hear the evidence de bene esse and look at it again in the light of the way in which the later evidence develops, but I can’t have that luxury at the moment, so is there a way you can deal with this without asking Dr. Karch to develop his evidence too extensively on the basis of what he has read in a report of a witness who has not yet given evidence?

MR. WRIGHT: Yes.

MR. JUSTICE FORBES: If this causes any difficulty I will be sympathetic to you recalling Dr. Karch after Professor Sachs has given his evidence to give further evidence about it.

MR. WRIGHT: Thank you. There may be logistical difficulties in this regard, I think he is next headed to Sydney amongst other places, but I think it can be resolved by discussion between us as opposed to by ruling or by at this stage taking the matter any further.

MR. JUSTICE FORBES: Would you like opportunity to consider it overnight?

MR. WRIGHT: Please?

MR. JUSTICE FORBES: Does that meet with your approval, Miss Davies?

MISS DAVIES: My Lord, yes.

MR. JUSTICE FORBES: Members of the jury we will break off now and resume again at 10.30 tomorrow morning. Can I just check with you that you find the morning and afternoon, mid morning and mid afternoon breaks of assistance to you in concentrating on the evidence? I see you nodding. You don’t find it disruptive to your ability to follow the evidence in this case. Very well.

Members of the jury retired

MR. JUSTICE FORBES: Dr. Karch, I am sure I don’t have to tell you this but I must warn you that while you are still giving your evidence you must not discuss any aspect of this case with anybody at all without my permission do you understand?
A. Yes.

MR. JUSTICE FORBES: Very well. 10.30 tomorrow morning.

[COMMENT1]
354 folios

94

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R v Harris [2006] 1 Cr App Rep 55:

[2005] EWCA Crim 1980; [2006] 1 Cr App Rep 55; 85 BMLR 75

R v Harris

COURT OF APPEAL, CRIMINAL DIVISION

[2005] EWCA Crim 1980; [2006] 1 Cr App Rep 55; 85 BMLR 75

HEARING-DATES: 21 JULY 2005

21 JULY 2005

CATCHWORDS:
Expert witnesses – Medical evidence – Fresh evidence on appeal – Non accidental head injury in infants – Shaken baby syndrome – Carers convicted of murder, manslaughter and grievous bodily harm – Triad of intracranial injuries consisting encephalopathy, subdural haemorrhages and retinal haemorrhages – Whether triad diagnostic of non accidental head injury – Whether alternative cause of injuries credible – Level of force necessary to cause injuries – Whether convictions safe – Offences Against the Person Act 1861, s 20 – Criminal Procedure Rules, SI 2005/384, r 24.

HEADNOTE:
The four appellants, Lorraine Harris, Raymond Charles Rock, Alan Barry Joseph Cherry and Michael Ian Faulder, appealed against their convictions for respectively manslaughter, murder, manslaughter and inflicting grievous bodily harm. All four cases involved allegations of ‘shaken baby syndrome’ (SBS) now more properly referred to as non accidental head injury (NAHI) and all of the appellants had been convicted following trials. The common thread running through each of the four appeals was a submission that since the convictions, medical research had developed to the extent that there was ‘fresh evidence’ which threw doubt on the safety of each conviction. For many years the accepted hypothesis depended on findings of a triad of intracranial injuries in infants (babies aged between 1 month and 2 years). The triad consisted of encephalopathy (defined as disease of the brain affecting the brain’s function), subdural haemorrhages (SDH) and retinal haemorrhages (RH). The triad was considered to be a hallmark of NAHI as the mechanism of the injuries was said to be shaking of the infant, with or without impact on a solid surface. Between 2000 and 2004 a team of doctors led by Dr Geddes, a neuropathologist, produced three papers setting out the results of their research into the triad. In the third paper (Geddes III) the team put forward a new hypothesis, the ‘unified hypothesis’ which challenged the supposed infallibility of the triad. It was called the unified hypothesis because it relied on the proposal that there was one unified cause of the three intracranial injuries constituting the triad and that cause was not necessarily trauma but hypoxia (lack of oxygen in the tissues), both alone and in combination with infection. The unified hypothesis did not seek to show that the triad was inconsistent with NAHI, merely that it was not diagnostic. The criticism of Geddes III was that it was trauma which caused SDH and RH, not hypoxia and/or brain swelling.

Held – The unified hypothesis could no longer be regarded as a credible or alternative cause of the triad of injuries. In cross-examination Dr Geddes had accepted that she could no longer support the hypothesis that brain swelling was the cause of SDH and RH. However, this conclusion was not

determinative of the four appeals before the Court as many other medical issues were involved in cases of alleged NAHI and there remained a body of medical opinion which did not accept that the triad was an infallible tool for diagnosis. On the evidence before the Court, the triad did not automatically and necessarily lead to a diagnosis of NAHI and all the circumstances, including the clinical picture, should be taken into account. Cases of NAHI were fact-specific and would be determined on their individual facts.

Harris: In relation to the appeal in the case of Harris, the evidence relating to an alternative cause of death based on a possible infection did not form any basis for holding that the conviction was unsafe. The triad stood alone and the clinical evidence pointed away from NAHI. In this case the triad itself was uncertain. New evidence threw doubt on the significance of such SDH as there were and it threw doubt on the evidence of injuries to the brain. Although evidence of the findings of RH was powerful supporting evidence of shaking, on its own it was not diagnostic of shaking. The fresh evidence as to the cause of death and the amount of force necessary to cause the triad might reasonably have affected the jury’s decision to convict. Accordingly the conviction was unsafe, the appeal would be allowed and the conviction quashed.

Rock: This was not a case where the expert medical evidence and the presence of the triad stood alone. There was evidence that the appellant had shown some hostility towards the victim and there was no dispute that he had shaken the victim and that the victim had suffered an impact to the back of her head. On all the evidence the appellant’s conviction for unlawful killing was safe. However, a brief period of violence (going beyond even rough play) was all that was required to cause the victim’s fatal injuries and whilst such violence undoubtedly furnished the mental element necessary for a conviction of manslaughter, it did not necessarily demonstrate the intention to cause grievous bodily harm which was necessary for a conviction of murder. Accordingly the appellant’s conviction for murder would be set aside and a conviction for manslaughter substituted.

Cherry: The decision for the jury in this case was whether they could be sure that victim’s death was caused by an unlawful act on the part of the appellant, or whether her death might have been attributable to an accidental fall from a chair some 6-8 inches high. Two elements of the triad (encephalopathy and SDH) were present and the appellant’s factual account could not explain the victim’s injuries and death as the postulated fall was not a credible cause or contributory cause of death. On any realistic view the force must have been such that the risk of some harm to the victim would have been foreseeable to all sober and reasonable people. Furthermore there was evidence of up to 22 bruises on the victim’s body. In the circumstances the appellant’s conviction for manslaughter was safe and the appeal would be dismissed.

Faulder: In this case the appellant had claimed that he had dropped the victim by accident when placing him in his pushchair. On appeal, the introduction of potentially credible alternative explanations presented by defence expert witnesses and the fact that the Prosecution’s case had had to change from allegations of ‘very severe shaking’ to allegations of multiple blows to the head led to the conclusion that, despite the number of bruises

found on the victim’s body the appellant’s conviction had to be considered unsafe. The appeal allowed would be allowed and the conviction quashed.

CASES-REF-TO:
AB (child abuse: expert witnesses), Re [1995] 1 FCR 280.

Dial v State of Trinidad and Tobago [2005] UKPC 4, [2005] 1 WLR 1660.

Lillie v Newcastle City Council [2002] EWHC 1600 (QBD), [2002] All ER (D) 140 (Jan).

National Justice Cia Naviera SA v Prudential Assurance Co Ltd, The Ikarian Reefer [1993] 2 Lloyd’s Rep 68; rvsd [1995] 1 Lloyd’s Rep 455, CA.

R v Bonython (1984) 38 SASR 45, S Aus SC.

R v Cannings [2004] EWCA Crim 1, [2004] 1 All ER 725, [2004] 1 WLR 2607.

R v Clarke (RL) [1995] 2 Cr App R 425.

R v Hakala [2002] EWCA Crim 730, [2002] All ER (D) 277 (Mar).

R v Hanratty [2002] EWCA Crim 1141, [2002] 3 All ER 534.

R v Ishtiaq Ahmed [2002] EWCA Crim 2781, [2002] All ER (D) 80 (Dec).

R v Kai-Whitewind [2005] EWCA Crim 1092, [2005] All ER (D) 14 (May).

R v Pendleton [2001] UKHL 65, [2002] 1 All ER 524, [2002] 1 WLR 72.

R v Stacey [2001] EWCA Crim 2031, (2001) 64 BMLR 115.

Stafford v DPP [1973] 3 All ER 762, [1974] AC 878, [1973] 3 WLR 719, HL.

INTRODUCTION:
Appeals

The first appellant, Lorraine Harris, appealed against her conviction for manslaughter at Nottingham Crown Court on 7 September 2000. The second appellant, Raymond Charles Rock, appealed against his conviction for murder at Chelmsford Crown Court on 21 September 1999. The third appellant, Alan Barry Joseph Cherry, appealed against his conviction for manslaughter at Birmingham Crown Court on 9 October 1995. The fourth appellant, Michael Ian Faulder, appealed against his conviction for inflicting grievous bodily harm at Teeside Crown Court on 28 April 1999. The facts are set out in the judgment of the court.

COUNSEL:
Richard Horwell and Zoe Johnson for the Crown.; Michael Mansfield QC and Peter Wilcock for Lorraine Harris and Alan Barry Joseph Cherry.; Michael Mansfield QC and James Gregory for Raymond Charles Rock.; Michael Mansfield QC and Robert Woodcock for Michael Ian Faulder.

PANEL: GAGE LJ, GROSS AND MCFARLANE JJ

JUDGMENTBY-1: GAGE J.

JUDGMENT-1:
GAGE J.

[1] In these four appeals, which have been heard together, four carers, as they have been described, appeal against convictions for manslaughter, Lorraine Harris; murder, Raymond Charles Rock; manslaughter, Alan Barry Joseph Cherry; and s 20 inflicting grievous bodily harm, Michael Ian Faulder. The victims were Patrick McGuire, aged four months, in the case of Harris; Heidi Smith, aged 13 months, in the case of Rock; Sarah Eburne-Day, aged 21 months, in the case of Cherry; and N, aged seven weeks, in the case of Faulder. Throughout this judgment we shall refer to the victims by their christian names and to the appellants by their surnames. Patrick was the son of Harris; Heidi was the daughter of Rock’s partner; Sarah was the daughter of Cherry’s partner; and N was Faulder’s son. At the time immediately before each of the victims became seriously ill each was in the sole care respectively of Harris, Rock, Cherry and Faulder.

[2] All of the appellants were convicted following trials. On 7 September 2000 at Nottingham Crown Court Harris was convicted of manslaughter and sentenced to three years’ imprisonment. On 21 September 1999 at Chelmsford Crown Court Rock was convicted of murder and sentenced to imprisonment for life. On 9 October 1995 at Birmingham Crown Court Cherry was convicted of manslaughter and sentenced to two years’ imprisonment. On 28 April 1999 at Teesside Crown Court Faulder was convicted of s.20 inflicting grievous bodily harm and sentenced to 30 months imprisonment.

[3] The common thread running through each of these four appeals is a submission that since these convictions medical research has developed to the extent that there is now ‘fresh evidence’ which throws doubt on the safety of each conviction.

[4] Following the judgment of this court in R v Cannings [2004] EWCA Crim 1, [2004] 1 All ER 725, [2004] 1 WLR 2607 the law officers set up an Interdepartmental Group to review convictions of defendants in alleged ‘battered babies’ cases. As a result of that review letters were sent to Harris and Cherry advising that each might feel it appropriate for the safety of her or his conviction to be considered further by the Court of Appeal. Each lodged notices of appeal and sought extensions of time in which to apply for leave. Each has been granted an extension of time and leave to appeal. Rock had already lodged a notice of appeal. He appeals with the leave of the Court. In the case of Faulder his appeal comes to this court by way of a reference from the Criminal Cases Review Commission. Mr Michael Mansfield QC is leading counsel for all four appellants. Mr Richard Horwell leads for the Crown in each appeal.

[5] These appeals have involved the court receiving (by agreement of the parties) evidence from ten medical expert witnesses called on behalf of the appellants and eleven called on behalf the Crown. We also received the written evidence of four further witnesses. In general terms the issues between the two sets of medical expert witnesses are as follows. First, the evidence called on behalf of the appellants relied on recent research which it is said demonstrated that long held medical opinion of the conventional signs giving rise to inferences of unlawful assaults on infants and very young children is unreliable. The basis of this challenge was a hypothesis based on recent research. However there were also other associated medical issues. The Crown’s medical witnesses do not accept that the hypothesis is correct or that it is supported by the new research.

[6] Secondly the Crown do not accept that the fresh evidence in relation to other specific issues in any way renders the convictions of these appellants unsafe.

The trials

Harris

[7] Harris faced a single count of manslaughter. In summary the evidence was as follows. Patrick was born on 13 August 1998. He was the son of

Lorraine Harris and Sean Maguire all of whom lived in the same house with two daughters of Harris from a previous relationship. The evidence showed that, although the pregnancy was not planned, both Harris and Maguire were happy about the impending birth. After his birth, Patrick gave every indication of being a thriving and much loved baby. Maguire described Harris as being as happy as he had ever known her. Harris received support from Maguire’s mother and her own mother. There were no financial difficulties and health professionals said that the family gave the impression of perfection.

[8] On 4 December 1999 Harris took Patrick for his third immunisation. The rest of the day passed without any significant event. Maguire was on night shift and Harris remained in the house with Patrick. Shortly before 1.00 a.m. on 5 December 1999 Harris noticed that Patrick was having difficulty breathing and called Dr Barber, the general practitioner. Whether or not this was in evidence at the trial, it is agreed that in the telephone call Harris said to Dr Barber:

‘I woke up to give him his feed and he wasn’t breathing. Not until I picked him up and sort of shook him. He seems as right as rain now.’

[9] Dr Barber stated that on arrival Harris appeared calm and controlled. Dr Barber had formed the opinion that Harris was an experienced and sensible mother. He examined Patrick. Patrick’s eyes were normal and he had all the appropriate reflexes. He recorded Patrick’s temperature as 38.2, mildly raised. There were no signs of abuse or bruising. Patrick’s chest was clear and although he was a little ‘snuffly’ Dr Barber concluded that there was nothing wrong with him. He left the house at 1.30a.m.

[10] At 2.34am Harris made a 999 call to the emergency services and reported that Patrick would not wake up. An ambulance arrived seven minutes later. The crew endeavoured to resuscitate Patrick. They recorded that Patrick did not have a pulse and was making no respiratory effort although he was still warm. Patrick and Harris were taken to Derby Children’s Hospital arriving at 3.15am Patrick was put on a life support machine. The evidence was that Harris was ‘plainly in considerable stress and crying.’ Patrick was noted as having fixed and dilated pupils and retinal haemorrhages.

[11] Patrick was seen by Dr Dodd a consultant paediatrician, who examined him at approximately 4.30am He described Patrick as having widely dilated pupils enabling him to make a clear examination of the retina. He found gross preretinal haemorrhages which were so extensive that he could not recall seeing any that were worse. There were no external injuries. He was so concerned about Patrick’s condition that he arranged for him to be transferred to the specialist unit at Nottingham. In Nottingham a blood sample test was taken. The test showed that there was marked hypofibronogenemia. Despite the best efforts of the medical team caring for him Patrick died on 6 December 1999.

[12] In late March 2000 Harris was arrested and interviewed about these events. In the summing-up the judge described Harris’ answers at interview as entirely consistent with the evidence which she gave at her trial.

[13] The prosecution called a number of expert medical witnesses both as to fact and also opinion evidence. Those witnesses were Dr Bouch, a Pathologist, who had conducted a post mortem on Patrick. He concluded that Patrick had died as a result of a shake which caused bleeding into the skull around the brain. He described what he meant by a ‘shake’ as much more than rough handling. Professor Green, a paediatric pathologist, with a special interest in ophthalmic pathology gave evidence that there was extensive bleeding in the vitreous of the left eye and extensive haemorrhaging of the retina. The bleeding in the right eye was less extensive. His conclusion was that his findings were those typically seen when shaking or, shaking and an impact had occurred. A consultant haematologist, Dr Giangrande, who specialised in blood diseases, gave evidence to the effect that the low level of fibrinogen in the Patrick’s blood system, in his opinion, was the result of an injury sustained by Patrick and not a pre-existing condition. However he was unable to rule out the possibility that that condition was present before the brain injury was caused. Finally, the prosecution called Mr Punt, a consultant paediatric brain surgeon. His evidence was that the amount of blood over the surface of the brain shown on the scan and the description of the amount of blood over the surface of the brain at post mortem was not sufficient to cause Patrick’s death. In his opinion it was injury to the brain itself which caused death; and that the brain injury was caused either by shaking or an impact or a combination of both. In his opinion whatever caused the injury to the brain was likely to have been in consequence of an incident after Dr Barber had left the home at 1.30a.m. In his view it was extremely improbable that the injuries were the result of a bleeding disorder.

[14] Harris, a woman of good character, gave evidence in her own defence. Her evidence was that on the evening of 4 December 1998 Patrick became ‘chesty and grunty’. Because he had difficulty in breathing she called out Dr Barber. After his visit she put Patrick in his cot. He seemed to have settled a bit. When she awoke approximately an hour later she checked him. His arms were on the top of the covers; he was a bit pale and cold. When she picked him up he was floppy. She said that she panicked and put him down in the cot. She telephoned her mother and then the ambulance. She vaguely remembered bouncing him on her knee whilst she was on the telephone. At interview she had said that she had Patrick on her knee when she telephoned the ambulance and that she remembered her knees ‘were going ten to the dozen.’ In evidence she said that she found it difficult to remember the sequence of events because she had tried to put it out of her mind. She accepted that she had told the doctor on the telephone that Patrick had stopped breathing in order to make him hurry. She said she was unable to offer any explanation for his injuries.

[15] On her behalf three expert medical witnesses gave evidence. They were Dr Batman, a consultant histopathologist; Dr Jones, a consultant paediatrician; and Dr Macdonald, a consultant neuropathologist. Dr Batman thought that there were three possible causes of Patrick’s death. They were (a) natural causes such as bleeding from a blood disorder; (b) shaking with or without impact; and (c) re-bleeding of an old blood clot. He regarded the latter as the least likely of three. In evidence, Dr Jones stated that his conclusion was that the findings were entirely consistent with a bleeding disorder. However he conceded that one would have expected more blood than was present if there was a blood disorder. He accepted that the findings were consistent with Patrick having been shaken and he agreed that he had never seen a child with fibrinogen deficiency which had died. Dr Macdonald concluded that Patrick’s injuries were not the result of a severe non-accidental injury although he conceded that the extent of the haemorrhages inside the vitreous jelly of his eye equated to a quite severe shaking. But the fact that there was no bleeding on the optic nerve of the right eye was a contra-indication.

[16] In a summing-up, about which there is and can be no criticism, the judge described the issue for the jury as follows:

‘The prosecution assert that she killed Patrick by deliberately shaking him violently or by shaking him violently and then throwing him down in his cot so as to cause bleeding inside his skull, thus leading to his collapse and death. The defendant denies that she did any such thing. She cannot explain her son’s collapse and death, but maintains that she did nothing which might have brought about that death. If you are not sure that the defendant killed Patrick, then you find her not guilty.’

After deliberating for just short of three hours the jury returned a verdict of guilty of manslaughter.

Rock

[17] Rock faced an indictment charging him with the murder of Heidi Smith. Heidi Jane Smith was born on 10 May 1997 and was the daughter of Lisa Hudson and James Smith. Lisa Hudson’s relationship with James Smith did not last long and by March 1998 she was living at the home of Rock. Rock was aged 26 and had previously been married with two children of his own. His children lived with their mother.

[18] The evidence was that Heidi was a happy, healthy baby and hardly ever cried. In general Rock was very good with and doted on Heidi. There was evidence that he was concerned about her well-being and showed no hostility towards her. However, Lisa Hudson said in evidence that Rock had a temper. She spoke of an incident about two weeks before Heidi’s death when Heidi was grizzly and would not settle. She said that on that occasion Rock held Heidi to his face and said ‘shut up’ in what she thought was a nasty fashion. On another occasion Rock complained that ‘Its Heidi this and Heidi that’.

[19] On 2 June 1998, Lisa’s mother, Thelma Hudson, was looking after Heidi. At 6.30pm Thelma took Heidi back to Rock’s home after he had returned from work. Lisa Hudson was still at work. Thelma Hudson placed Heidi in her cot at 6.35pm. She said that when she left Heidi was asleep and breathing normally. At 7.08pm Thelma Hudson telephoned Rock and spoke to him. From approximately 7.00pm Lisa Hudson could not get a response from the telephone at Rock’s home. A next door neighbour, Gail Banham, said that some time between 7.05pm and 7.10pm, from her kitchen, she could hear screaming coming from one of the homes at the back of her house. She said that the screaming sounded like a very sustained temper tantrum of a child aged between nine months to eighteen months. She also heard someone shouting at the child. It was a male and youngish. He was swearing and told the child to ‘fucking shut up’. The screaming did not stop. She went to the front of her house where she could hear nothing but then returned to her back kitchen. The screaming continued and she heard the same voice telling the child to shut up. The screaming continued but as she finished dishing up a meal it stopped and went completely silent. Her evidence was that this occurred at 7.20pm. In the unused material there were statements from police officers concerning an experiment conducted by them to see if shouting in one house could be heard in the other. The result of this experiment was inconclusive.

[20] However, Rock, in evidence, agreed that he had told Heidi to shut up but it was in the context of a longer sentence in which he said ‘you heard your mum, you’ve got to shut up’. He said that after Thelma Hudson had telephoned him he checked that Heidi was asleep and went downstairs to watch a video. During this time he heard loud crying. He went upstairs and found Heidi sitting up in her cot, red-faced and very upset. He said that he picked her up by her armpits and placed her in the crook of his right arm with his left hand under her bottom. He then rocked her from side to side at the same time trying to wind up the mobile on the top of the wardrobe. Heidi slipped through his arms onto the floor. He said that he saw Heidi hit the floor; she did not bang her head but did not stop crying. He immediately picked her up. She was completely still and not breathing. He patted her on the back saying ‘come on Heidi sweetheart’. He then held her in front of him but did not violently shake her. He shook her lightly by placing her on the floor where she was having the occasional spasm. He tried to give her mouth to mouth resuscitation but on the fourth occasion she began to vomit. He took her to the bathroom, held her face down over the sink and banged her back to allow the sick to come out. His evidence was that she began vomiting again. Seeing this he ran downstairs with Heidi and dialled 999. His telephone call was timed at 7.27pm. The paramedics arrived at 7.37pm. They found Heidi lying on the floor in a dimly lit room. Rock told them that he had dropped Heidi onto her bottom whilst he had been trying to wind up a clockwork toy. He told them that Heidi had not hit her head on the floor as he had been able to catch and support her head before it hit the floor. He then picked her up and she had gone limp and stopped breathing. He told them that he had tried mouth-to-mouth resuscitation and Heidi had vomited. One of the paramedics saw signs of vomit around Heidi’s mouth. He said that on the way to the hospital in the ambulance Rock had asked questions such as ‘has she got brain damage?’ ‘Has she got lung damage?’ On arrival at the hospital Heidi was taken straight to the resuscitation room. She was subsequently transferred to the Intensive Treatment Unit as she was having spasmodic fits; both her eyes were rolling to the left; she was pale but breathing and unconscious.

[21] At the hospital, Rock gave an account of events to both Lisa and Thelma Hudson and all of the medical staff. His explanation of the incident was much the same as that which he gave in evidence. He maintained that Heidi did not bang her head when she fell and he told no one that he had shaken her. To Lisa Hudson he said ‘I am so sorry, I dropped her on her bum’. And later in the hospital chapel, ‘I killed her, I killed her. Please God let her live, save her.’

[22] The prosecution called a number of medical witnesses including expert witnesses. A consultant ophthalmic surgeon said that he examined Heidi’s eyes when she was comatose and on a ventilator. He found massive retinal haemorrhaging at all layers on both retinas. There was also tenting/pulling forward of the major retinal vessels or folds. He concluded that in the absence of any specific medical condition the haemorrhages and tenting were the result of severe acceleration and deceleration forces. He said that he had never seen such severe damage to a person’s retina. Dr Jaspan, a consultant neuroradiologist (one of the expert witnesses called by the Crown in these appeals) examined a CT scan taken at 10.25pm on 2 June 1997. He found a thin layer of blood lying along the falx and within the brain at the back of the head. In his opinion these findings were consistent with trauma. In his view the disrupted delicate blood vessels in the brain had been damaged and the damage was profound and irreversible. He concluded that the trauma was so severe as to render Heidi immediately unconscious and that the injuries were highly characteristic of violent shaking. In his opinion dropping a child on its bottom was inconsistent with Heidi’s injuries.

[23] Mr Jonathan Punt, a consultant paediatric neurosurgeon, also examined the first CT scan of 2 June and agreed with Dr Jaspan’s conclusions. He concluded that the degree of violence required to cause the injuries to Heidi was ‘extreme; grossly in excess of any vigorous handling, even rough handling.’

[24] Dr Cary, a pathologist, conducted the post mortem on the same day as the life support machine had been discontinued. He found a number of superficial bruises over Heidi’s body. In addition there was bruising within the scalp over the back of head and bleeding around the optic nerve. The brain was swollen and there was bleeding on the surface of the brain. There was no skull fracture. He said that in his opinion the head injuries in conjunction with the retinal detachment in both eyes were consistent with shaken baby syndrome (SBS). In his view the cause was shaking or shaking plus an impact which caused injuries to the brain. He said that the force required was ‘shaking as hard as you can’. Further, he concluded that the changes which had occurred to Heidi’s eyes meant that there must have been several shakes back and forth with acceleration and deceleration.

[25] A professor of forensic pathology, Professor Michael Green, gave evidence that there were haemorrhages around both optic nerve roots and that the retina had started to pull away. There was a detachment between the sclera and the retina and extensive bleeding around the optic nerve. In his view the injuries were typical of a serious shaking plus impact.

[26] Finally, Dr Christine Smith, a consultant neuropathologist, called by the prosecution, described the brain as swollen and said that she had found on the inner surface of the dura remnants of blood. There was also widespread damage to nerve cells. She concluded that the injuries to the brain were consistent with trauma which had caused the brain to move in relation to the skull. She said that the most likely cause of the haemorrhaging to the eyes was shaking. She said there was no evidence of natural diseases present which could have lead to Heidi’s death.

[27] Rock gave evidence in his own defence. We have already referred to his version as to how he came to drop Heidi on the floor. He denied shaking Heidi but accepted that as a father he knew the consequences of shaking a baby could be fatal. He accepted in cross-examination that he had not told the doctors or the police that Heidi had become floppy after he had shaken her. He said that feelings of guilt were the reason for him not telling the police. He confessed that at the hospital it was obvious to him that Heidi was suffering from brain damage but he did not tell the doctors about shaking Heidi.

[28] No expert witnesses were called on Rock’s behalf.

[29] In his summing-up the judge told the jury that Rock admitted shaking Heidi. He said:

‘It is for you to say, but you may think that, in the end, the defendant was bound to admit that he had shaken Heidi, and shaken her before she became floppy, because the evidence that she was shaken is so strong, so overwhelming. How else were those injuries caused to Heidi, if it were not by the defendant shaking her, and shaking her with considerably excessive force? That is a question you are entitled to ask yourself, obviously. There is no question of accident here. It is not suggested that what the defendant did was done otherwise than deliberately.’

[30] The judge went on to direct the jury that the difference between murder and manslaughter was one of intention. Further, he told them that there was a third possible verdict and that was not guilty of anything. He continued:

‘So, I must leave it open for you to say whether the defendant is not guilty of anything. I am allowed, however, to suggest to you that not guilty of anything is not a realistic verdict in this case. As I say, you decide this case. If you think that the defendant’s account that he did not shake Heidi violently so as to cause those injuries to Heidi from which she died, that his account is true or may be true, then he is entitled to be acquitted both of murder and manslaughter.’

After deliberating for a period of 40 minutes the jury returned a verdict of guilty of murder.

Cherry

[31] Cherry faced an indictment charging him with the manslaughter of his partner’s daughter Sarah. Sarah’s mother, Mrs Shirley Eburne-Day, and her children including Sarah and Cherry, at the time of the incident giving rise to the charge, were all living together at Mrs Eburne-Day’s home. Sarah was the youngest of Mrs Eburne-Day’s three children. Mrs Eburne-Day and Cherry had lived together for some months. The evidence suggested that he was a good step-father to the children. On Thursday, 3 February 1994, in the morning, Sarah was left in the sole care of Cherry. Earlier in the week she had developed a thumb infection for which a doctor had prescribed antibiotics. After taking some medicine on 2 February Sarah was sick so different antibiotics were prescribed.

[32] On the morning of 3 February 1994, at about 8.30am, Mrs Eburne-Day left Sarah at home with Cherry whilst she drove her two older children and a neighbour’s daughter to school. The plan was that Cherry would take Sarah to Mrs Eburne-Day’s father’s home where, in the course of the morning, Cherry and Mrs Eburne-Day would meet before both went to Birmingham for Cherry to attend a job interview.

[33] That morning Sarah was a little better than on the previous day and appeared to be behaving perfectly ordinarily. Mrs Eburne-Day said that she

had no concerns about leaving her. She said that she and Cherry had discussed Sarah’s health and decided that she was fit enough to be left with her grandparents. In evidence, Cherry said that he disagreed. He said that Sarah was not very well on Thursday morning. She was not in a bright condition and wanted to sleep and be cuddled by her mother. He denied that he had any conversation with Mrs Eburne-Day about Sarah’s health that morning.

[34] Lianne Osbourne, a next door neighbour, called that morning for a lift to school. Before leaving with Mrs Eburne-Day she said that she saw Cherry briefly. He was wearing dark trousers, a white striped shirt and a red brown paisley patterned tie. Apart from his jacket he appeared almost ready to go out. In evidence Cherry denied that when seen by Lianne Osbourne he had been fully dressed for work.

[35] There was evidence that Cherry was next seen in the street in a distressed state seeking assistance from various neighbours. Sarah’s grandfather, Mr Eburne-Day, received a telephone call from Cherry at precisely 8.55am asking him to call an ambulance, which he did. Mrs Redding, a neighbour and trained nurse, saw Sarah just before the ambulance arrived. She said that Sarah appeared to be dead or on the verge of death. She applied resuscitation techniques until the ambulance arrived at approximately 9.20am. Sarah was taken first to George Eliot Hospital in Nuneaton but was later transferred to the Intensive Therapy Unit at Birmingham Children’s Hospital. In spite of all medical efforts Sarah died about 48 hours later.

[36] On 4 February 1994 Cherry was arrested on suspicion of causing grievous bodily harm with intent. This was before Sarah had been pronounced dead. He was interviewed by police and explained that he had left Sarah standing on a small yellow chair whilst he went upstairs briefly to put on a shirt and tie. Apparently, it had been Sarah’s habit to stand on the yellow chair in order to look out of the window at the front of the house. He explained that when he returned he found Sarah lying on the floor motionless and making gurgling noises. He said that he picked her up and described her body feeling like a rag doll. She did not respond and therefore he telephoned her grandfather to ask him to telephone for an ambulance. He explained that she must have become suddenly ill and fallen from the chair. He denied shaking her or throwing her around but said that she had fallen out of her sister’s bed at the weekend. On 6 February 1994 he was charged with the murder of Sarah and after caution replied ‘I’m not guilty. I’ve committed no offence’. In the event, the Crown proceeded with a charge of manslaughter rather than murder.

[37] At trial, giving evidence in his own defence, Cherry repeated what he had said at interview. He said that after going upstairs to finish off dressing for ‘only a few minutes’ he returned to find Sarah ‘lying on the floor, obviously badly injured.’ He said that when he picked Sarah up and tried to pat her back he removed ‘some yellow stuff from her mouth’.

[38] At trial the prosecution called a number of medical witnesses. Doctor (now Professor) Whitwell conducted the post mortem upon Sarah. Her finding was that death had been caused by ‘cerebral swelling and subdural haematoma’. In addition, she found two bruises at the back of the head (3.5cms and 1.5cms in diameter and on opposite sides) and five small areas of bruising higher up. In her opinion the five smaller bruises were consistent with pressure from fingers. In cross-examination she did not accept that the injuries could have been caused by falling from the yellow chair. She said that the injuries were more consistent with Sarah’s head being forcibly put against something. In her opinion it was highly unlikely that Sarah could have injured herself by banging her head against the floor although that was not impossible. She said it was unlikely the injuries could have been caused by a single fall because there were two separate areas of impact and two separate bruises, although she could not exclude this absolutely.

[39] A radiologist, Dr Chapman, stated that it was very rare for a child to have this kind of bleeding from a domestic fall. In his opinion a fall from the yellow chair had not caused Sarah’s injuries. Dr Akuba, a neurological registrar, in a witness statement, said that she had inserted a tube into Sarah’s skull as part of her treatment and recorded that ‘Cerebral spinal fluid emerged under moderate pressure. It was yellow and looked like old blood. Query, query’.

[40] Dr Rylance, a consultant paediatrician, having seen Sarah at Birmingham Children’s Hospital, took the view that her injuries were non-accidental. He was asked about a previous statement which he had made and in which he stated that the injury giving rise to blood inside the skull occurred almost certainly more than 12 hours previously and probably more than 36 hours previously. He said in evidence that he had since changed his opinion and in fact it could have been 101/2 or 11 hours previously. He said that Sarah’s vomiting the day before was more likely to have been caused by the medicine than a previous brain injury because when she stopped taking the medicine she stopped vomiting.

[41] Finally, the prosecution called Mr Flint, a surgeon, who described the five small bruises on Sarah’s head which were, in his opinion, indicative of her having been held. The two bruises on the back of her head suggested at least two blows. In his opinion it was very unlikely that the bruises were caused by her slipping backwards from the chair and hitting her head on the floor. In his opinion a healthy child could not sustain such injuries revealed by the post mortem by falling the short distance from the chair onto the carpeted floor.

[42] In addition to his own evidence, there was called on Cherry’s behalf a neurologist Dr West and a consultant pathologist, Dr Ackland. Dr West had viewed films taken by Dr Whitwell. He said that what he saw was consistent with a child having aspirated liquid which was a frequent complication of head injuries. Dr Ackland did not rule out the possibility of abuse causing the injuries but was of the opinion that an accidental fall from the chair was a significant possibility. In his opinion there was a small possibility that Sarah [had] some earlier injury that was aggravated by the fall but he did not regard that as a high possibility. He said that the five marks on Sarah’s head may have been caused by a firm grip during the medical treatment.

[43] In his summing-up the judge described the issue for the jury to decide in the following terms:

‘The cause of her death was a swelling of the brain caused by an impact of one sort or another. It is the prosecution case that the impact was in consequence of an unlawful blow delivered by this defendant. Your task will be to decide whether that case is proved or not.’

After deliberating for just over two and a half hours the jury returned a unanimous verdict of guilty of manslaughter.

Faulder

[44] At trial Faulder faced an indictment containing two counts. They were count 1, a s 18 offence of causing grievous bodily harm with intent; and count 2 an alternative s.20 offence. He was convicted of the latter offence. The evidence showed that at 10.30pm on Friday 13 February 1998, N then aged seven weeks (but born two weeks premature) was admitted to the Dryburn Hospital with severe injuries. On the following day N was transferred to a specialist unit at the Newcastle General Hospital where his condition deteriorated over the following week. Although there was concern that he might not survive he recovered and was transferred back to Dryburn Hospital on 5 March 1998. On 16 March 1998 he was discharged from hospital.

[45] The event which led to N’s admission to hospital occurred at the home occupied by Faulder and his partner. It was common ground that at the time Faulder was the sole carer of N. His case was that N’s injuries were caused entirely accidentally. He said that he had dropped N and that in falling N struck and injured his head. The case for the prosecution was that Faulder had caused the injuries by a deliberate act or actions.

[46] The prosecution case was based on the assertion that the extensive brain injuries sustained by N and revealed on x-ray and brain scans could not have been occasioned in the manner described by Faulder. The prosecution relied on the evidence of three expert witnesses for the proposition that Faulder must have shaken N and thrown him onto the floor.

[47] Dr Camille de San Lazaro at the time a consultant paediatrician at the Royal Victoria Infirmary gave evidence that the injuries sustained by N were consistent with shaking and were not consistent with Faulder’s account. She said that his version of the events could not account for the subdural haemorrhages. She further stated that in relation to Faulder’s account of N making a sudden arching movement which caused him to drop N that at that age the child would have had insufficient muscle tone to achieve the movement described by Faulder. Further Faulder’s description of N falling onto a pushchair and then a highchair before hitting the floor would have had the effect of breaking N’s fall rather than exacerbating it.

[48] Dr Alexander, a consultant paediatrician at the Newcastle General Hospital, gave evidence that on examination of N on 14 February 1998 he found a triangular bruise on the top of N’s head and two bruises on the forehead over the right eye. He said that the child’s fontanelle was unusually tense, symptomatic of swelling of the brain due to brain damage. In his opinion the CT scan showed bilateral subdural haemorrhages. He conceded that the superficial marks on N’s face and head were consistent with Faulder’s account but asserted that this account did not provide an explanation for the bruise on the right side of the forehead or the severity of the brain injuries. In his opinion the brain injuries were such as were commonly caused by repeated shaking with considerable force, and the clinical findings were more consistent with non-accidental injury than with an accident.

[49] Mr Gholkar, a consultant neuroradiologist, having examined the brain scans concluded that the evident changes in the appearance of the brain were due to severe brain damage unlikely to have been occasioned in the manner described by Faulder and were characteristic of shaking injuries.

[50] There was no evidence of retinal haemorrhages and there was some dispute as to the extent to which retinal haemorrhages were to be found in babies with ‘shaking’ injuries. Dr de San Lazaro stated that her study showed that 53% of children believed to have been shaken, had retinal haemorrhages.

[51] Faulder gave evidence in his own defence. He said that he did not deliberately cause the injuries. He explained how he had dropped N by accident when attempting to place him into his pushchair. He said that he had been holding him along his arm with his hand supporting the baby’s head. The baby moved suddenly and fell on to the edge of the pushchair. This caused him to bounce off the pushchair and on to the concrete floor bouncing his head on the adjacent highchair as he fell. Faulder conceded that the baby had been crying for twenty minutes but said that he had not lost his temper. He maintained that he did not shake nor forcibly place N into his pushchair. His answers at interview were consistent with his evidence at trial.

[52] Dr Rushton a paediatric pathologist gave evidence for Faulder. He put forward the possibility that N’s contact with the pushchair and highchair might have lead to the production of rotary forces that accelerated the head and increased the force of contact with the floor. He noted that the three external injuries (bruises) found on the baby’s head were consistent with Faulder’s explanation but were difficult to explain if the injuries were due to shaking or a single impact injury. He also referred to the lack of retinal haemorrhages saying that in his opinion the cause of retinal haemorrhages was not fully understood. In his view subdural haemorrhages could be caused by shaking or impact but they might also be consistent with injury caused in the manner described by Faulder.

[53] The judge directed the jury in his summing-up that the first question for it to decide was:

‘Was this or may it have been accident or design? If you come to the conclusion that this is or may have been a tragic accident it follows that the defendant cannot be guilty of count 1 or count 2 and must be acquitted by you. That is the simple issue for you to decide.’

[54] After deliberating for just less than two hours the jury returned a verdict of guilty of count 2.

[55] On conviction Faulder applied for leave to appeal against conviction and sentence and for an extension of time. His applications were refused by the single judge.

The triad and the unified hypothesis

[56] At the heart of these appeals, as they were advanced in the notices of appeal and the appellants’ skeleton arguments, was a challenge to the accepted hypothesis concerning ‘shaken baby syndrome’ (SBS); or, as we

believe it should be more properly called, non-accidental head injury (NAHI). The accepted hypothesis depends on findings of a triad of intracranial injuries consisting of encephalopathy (defined as disease of the brain affecting the brain’s function); subdural haemorrhages (SDH); and retinal haemorrhages (RH). For many years the coincidence of these injuries in infants (babies aged between one month and two years) has been considered to be the hallmark of NAHI. Not all three of the triad of injuries are necessary for NAHI to be diagnosed, but most doctors who gave evidence to us in support of the triad stated that no diagnosis of pure SBS (as contrasted with impact injuries or impact and shaking) could be made without both encephalopathy and subdural haemmorhages. Professor Carol Jenny, a paediatrician and consultant neuro-trauma specialist called by the Crown, went further and said that she would be very cautious about diagnosing SBS in the absence of retinal haemmorhages. In addition, the Crown points to two further factors of circumstantial evidence, namely that the injuries are invariably inflicted by a sole carer in the absence of any witness; and that they are followed by an inadequate history, incompatible with the severity of the injuries.

[57] Between 2000 and 2004 a team of distinguished doctors led by Dr Jennian Geddes, a neuropathologist with a speciality in work with children, produced three papers setting out the results of their research into the triad. In the third paper ‘Geddes III’, the team put forward a new hypothesis, ‘the unified hypothesis’, which challenged the supposed infallibility of the triad. It was called the unified hypothesis because it relied on the proposal that there was one unified cause of the three intracranial injuries constituting the triad; that cause was not necessarily trauma. It is important to note that the new hypothesis did not seek to show that the triad was inconsistent with NAHI. It did, however, seek to show that it was not diagnostic.

[58] When Geddes III was published it was, and still is, very controversial. It is not overstating the position to say that this paper generated a fierce debate in the medical profession, both nationally and internationally. In the course of the hearing of these appeals we have heard evidence from a number of very distinguished medical experts with a range of different specialities most of whom had in witness statements expressed views on one side or other of the debate. However, early on in the hearing it became apparent that substantial parts of the basis of the unified hypothesis could no longer stand. Dr Geddes, at the beginning of her cross-examination, accepted that the unified hypothesis was never advanced with a view to being proved in court. She said that it was meant to stimulate debate. Further, she accepted that the hypothesis might not be quite correct; or as she put it:

‘I think we might not have the theory quite right. I think possibly the emphasis on hypoxia – no, I think possibly we are looking more at raised pressure being the critical event. ‘

And later in her evidence:

‘Q. Dr Geddes, cases up and down the country are taking place where Geddes III is cited by the defence time and time again as the reason why the established theory is wrong.

A. That I am very sorry about. It is not fact; it is hypothesis but, as I have already said, so is the traditional explanation. … I would be very unhappy to think that cases were being thrown out on the basis that my theory was fact. We asked the editor if we could have “Hypothesis Paper” put at the top and he did not, but we do use the word ‘hypothesis’ throughout.’

[59] Despite these frank admissions the triad and Geddes III have been a focus of much of the medical issues in these appeals. We propose to set out the salient features of each in a little more detail. We do so not only as a backdrop to these appeals but in an effort to inform those involved in future trials as to the current accepted state of medical science, as we understand it from the evidence before us, on some of the very difficult issues which are raised in criminal and civil trials involving allegations of NAHI.

The anatomy

[60] In order to explain the two hypotheses it is necessary to set out some of the anatomy involved in terms which can be understood by laymen and which from a medical viewpoint may seem somewhat simplistic. At the outset, in order to assist the reader, we attach as annexes to this judgment a glossary of medical terms (appendix A), and diagrams of the head (appendix B).

[61] The brain is encased in three membranes. The one immediately surrounding the brain is the pia mater. The next one is the arachnoid. Between the pia and the arachnoid is an area known as the subarachnoid space. The third membrane, which surrounds the brain and continues down the body surrounding and protecting the spinal cord, is the dura. Between the dura and the arachnoid is the subdural space. Between the dura and the arachnoid there are veins running between the two membranes which are called bridging veins.

[62] The brain is divided into two halves or cerebral hemispheres. The two hemispheres are separated by the falx which itself is part of the dura. Below the cerebral hemispheres the brain is joined to the spinal cord at the craniocervical junction, which, as its name implies, is situated in the neck. The spinal cord extends down from the brain, through the foramen magnum and into the spine.

The triad

[63] As already stated when the three elements of the triad coincide for some years conventional medical opinion has been that this is diagnostic of NAHI. Typically the brain is found to be encephalopathic; bleeding is found in the subdural space between the dura and the arachnoid subdural haemmorhages; and there are retinal haemorrhages. There may also be other pathological signs such as subarachnoid bleeding and injuries at the cranio-cervical junction. Further, there may be injuries to nerve tissue (axonal injuries) and external signs of broken bones, bruising and other obvious injuries such as extradural oedema (bruising). Determining these findings requires medical experts from a number of different disciplines interpreting often very small signs within the complex structures of an infant’s brain and surrounding tissue.

[64] The mechanism for these injuries is said to be the shaking of the infant, with or without impact on a solid surface, which moves the brain within the skull damaging the brain and shearing the bridging veins between the dura and the arachnoid. The shaking may also cause retinal haemorrhages. In the sense that the explanation for the triad is said to be caused by shaking and/or impact it also is a unified hypothesis, albeit that each element is said to be caused individually by trauma.

[65] The triad of injuries becomes central to a diagnosis of NAHI when there are no other signs or symptoms of trauma such as bruises or fractures.

The unified hypothesis (‘Geddes III’)

[66] Dr Geddes and her colleagues, following research into almost fifty paediatric cases without head injury, proposed that the same triad of injuries could be caused by severe hypoxia (lack of oxygen in the tissues) which in turn led to brain swelling. The hypothesis was that brain swelling combined with raised intracranial pressure (ICP) could cause both subdural haemorrhages and retinal haemmorhages. Thus, it was argued that any incidents of apnoea (cessation of breathing) could set in motion a cascade of events which could cause the same injuries as seen in the triad. It will be appreciated that there are many events which could accidentally cause an episode of apnoea.

[67] In Geddes III the unfied hypothesis was summarised as follows:

‘Our observations in the present series indicate that, in the immature brain, hypoxia both alone and in combination with infection is sufficient to activate the pathophysiological cascade which culminates in altered vascular permeability and extravasation of blood within and under the dura. In the presence of brain swelling and raised intracranial pressure, vascular fragility and bleeding would be exacerbated by additional hemodynamic forces such as venous hypertension, and the effects of both sustained systemic arterial hypertension and episodic surges in blood pressure.’

Thus, it was suggested that all the injuries constituting the triad could be attributed to a cause other than NAHI. We understand that this paper has been much cited in both criminal and civil trials since its publication.

[68] The criticism of Geddes III is that it is not hypoxia and/or brain swelling which causes subdural haemorrhages and retinal haemorrhages but trauma. As an example of why the hypothesis is not correct Dr Jaspan, giving evidence in the appeal of Rock, demonstrated that CT scans taken of Heidi’s brain showed that there was little or no brain swelling at a time when subdural haemorrhages and retinal haemorrhages were shown to be present. As a result of critical papers published in the medical journals, as we have already stated, Dr Geddes when cross-examined frankly admitted that the unified hypothesis could no longer credibly be put forward. In cross-examination she accepted that she could no longer support the hypothesis that brain swelling was the cause of subdural haemorrhages and retinal haemmorhages. She did, however, state that she believed that raised intracranial pressure (ICP) might prove to be an independent cause of both lesions. When asked by Mr Horwell if she had published a paper on this hypothesis she said that she had not and that her research was still

incomplete. It was clear from subsequent questions in cross-examination that this work was still in its early stages and that many questions remain, as yet, unresolved.

[69] In our judgment, it follows that the unified hypothesis can no longer be regarded as a credible or alternative cause of the triad of injuries. This conclusion, however, is not determinative of the four appeals before us. There are many other medical issues involved in cases of alleged NAHI. Further, there remains a body of medical opinion which does not accept that the triad is an infallible tool for diagnosis. This body of opinion, whilst recognising that the triad is consistent with NAHI, cautions against its use as a certain diagnosis in the absence of other evidence. These four appeals raise different medical issues and do not necessarily fail because the unified hypothesis has not been validated. But it does mean that the triad, itself a hypothesis, has not been undermined in the way envisaged by the authors of Geddes III.

[70] Mr Horwell, in his final submissions invited the Court to find that the triad was proved as a fact and not just a hypothesis. On the evidence before us we do not think it possible for us to do so. Whilst a strong pointer to NAHI on its own we do not think it possible to find that it must automatically and necessarily lead to a diagnosis of NAHI. All the circumstances, including the clinical picture, must be taken into account. In any event, on general issues of this nature, where there is a genuine difference between two reputable medical opinions, in our judgment, the Court of Criminal Appeal will not usually be the appropriate forum for these issues to be resolved. The focus of this Court will be (as ours has been) to decide the safety of the conviction bearing in mind the test in fresh evidence appeals which we set out below. That is not to say that such differences cannot be resolved at trial. At trial, when such issues arise, it will be for the jury (in a criminal trial) and the judge (in a civil trial) to resolve them as issues of fact on all the available evidence in the case (see R v Kai-Whitewind [2005] EWCA 1092).

[71] Before we leave Geddes III we must mention some evidence given by the first witness we heard, Dr Waney Squier, a consultant neuropathologist, which was the subject of some further investigation by the Crown’s witnesses and further oral evidence. Dr Squier produced a slide taken from the brain of a four week old baby which she said demonstrated blood oozing from the dura into the subdural space. In her opinion this showed that intradural haemorrhages could leak into the subdural space and could be mistaken for subdural haemorrhages caused by shearing of the bridging veins. In that respect it challenged the diagnostic value placed on subdural haemmorhages by the triad. Mr Horwell asked for the slide and other slides made in respect of the same brain to be released for examination by the Crown’s experts. We heard evidence in respect of this discrete issue on the last day of evidence.

[72] In summary, two paediatric neuropathologists, Dr Rorke-Adams and Dr Harding, said that the slide did not show intradural bleeding but was an example of the process of organisation of an earlier subdural haemorrhage.

[73] It is unnecessary for us to go into the detail of this dispute. It is sufficient to say that having heard both sides forcefully express their views we are unable to resolve this issue and find, as Mr Horwell invited us to, that Dr Squier’s evidence on it cannot be accepted. We content ourselves with the observation that even on the interpretation of objective evidence there can be two views expressed by highly experienced and distinguished medical experts.

Geddes I and II

[74] Although, for the reasons already explained, the unified hypothesis can no longer stand as a credible alternative to the triad, a number of issues of general importance in respect of the triad remain. So far we have made no mention of the first two papers produced by Dr Geddes and her co-authors, which we will refer to as Geddes I and Geddes II. These papers represent conclusions reached in respect of research into a cohort of infants all of whom died from inflicted head injuries. Using a technique pioneered by Dr Geddes, the authors sought to identify axonal damage (damage to the nerve tissues) in the brains of these infants. The technique involved detecting the presence of beta-amyloid precursor protein (B-APP) (a protein that builds up where axons have been damaged). The research showed that widespread axonal damage, interpreted as vascular rather than traumatic, was present in 13 of the 37 cases. Conversely, widespread traumatic axonal damage was found in only two cases and in both cases there were other very clear signs of trauma (for example bilateral skull fractures). The authors concluded that their findings strongly suggested that severe traumatic axonal damage is a rarity in infant NAHI unless there is considerable impact, and that the diffuse brain damage which was responsible for loss of consciousness in the majority of cases was caused by starvation of oxygen (hypoxic) rather than direct trauma to the brain.

[75] The principle conclusion of Geddes II was that shaking an infant might cause a stretching injury at the cranio-cervical junction to nerves which control the child’s cardio-respiratory system. In all the cases analysed the stretch injury itself was survivable, what was life-threatening was the consequent hypoxic injury and brain swelling that followed as a result of the damaged cardio-respiratory nerves failing to function. The minimum degree of shaking force required to produce such a stretch injury is unknown and a death may be caused in the manner suggested by much less force than hitherto supposed. Although the results of this research, as we understand it, are not challenged by those who criticise the unified hypothesis, Mr Horwell submitted that its effect was limited. For instance he submitted that it had no application to, and could not explain, cases involving subdural bleeding and/or retinal haemmorhages.

Degree of force

[76] This leads on to a very important issue which arises in these appeals and will no doubt arise in many cases where the triad of injuries are present. It is the question of how much force is necessary to cause those injuries. There is a measure of common ground between the doctors on this issue. Generally it is agreed that there is no scientific method of correlating the amount of force used and the severity of the damage caused. To state the obvious, it is not possible to carry out experiments on living children. Further, experience shows that the human frame reacts differently in different infants to the same degree of force. However the medical opinion on this issue appears to be divided into those who maintain that severe injuries can confidently be ascribed to a traumatic cause, for example (but not only) Dr Rorke-Adams, a very experienced paediatric neuropathologist, and those who maintain that very little force may cause very serious injuries, for example Dr John Plunkett, a distinguished anatomical, clinical and forensic pathologist.

[77] It is quite impossible for this court to make any finding on this issue beyond referring to some general propositions with which both counsel agreed. First, common sense suggests that the more severe the injuries the more probable they will have been caused by greater force than mere ‘rough handling’. We note that the most recent Update from the Ophthalmology Child Abuse Working Party; Royal College of Ophthalmologists (2004) concludes:

‘It is highly unlikely that the forces required to produce retinal haemorrhage in a child less than 2 years of age would be generated by a reasonable person during the course of (even rough) play or an attempt to arouse a sleeping or apparently unconscious child.’

[78] Secondly, as Mr Peter Richards, a very experienced neurosurgeon with a speciality in paediatrics, pointed out, if rough handling of an infant or something less than rough handling, commonly caused the sort of injuries which resulted in death, the hospitals would be full of such cases. In our view this points to the fact that cases of serious injuries caused by very minor force such as might occur in normal handling or rough handling of an infant, are likely to be rare or even extremely rare.

[79] But, thirdly, as Dr Plunkett demonstrated by his research and in particular by reference to an amateur video of a child falling from a 3 foot high railing, described as part of a play tree-house, which resulted in catastrophic injuries, there will be cases where a small degree of force or a minor fall will cause very severe injuries. We shall have more to say about Dr Plunkett’s research later in this judgment, but at this stage we repeat that the evidence suggests that cases where this occurs are likely to be very rare.

[80] Fourthly, although the younger the infant or child, the more vulnerable it is likely to be, it is not possible to conclude that age is necessarily a factor in deciding whether injuries are caused by strong force or a minimal degree of force or impact. The balance of the evidence is that, although an infant’s skull is more pliable than that of an older child, the internal organs and vessels are as robust as those of an older child. The vulnerability of an infant arises from the fact that its head is generally larger in proportion to its body than in an older child and its neck muscles are weaker and not as well developed as in older children, hence the significance of injuries at the site of the craniocervical junction.

Biomechanics

[81] In simple terms ‘biomechanics’ is the application of traditional engineering principles to living organisms.

[82] Many of the experts who gave evidence before us made reference to research in the field of biomechanics. The following extracts from the evidence demonstrate how the ‘biomechanics’ argument was deployed by both sides.

[83] Dr Squier referred to the ‘huge amount of evidence about the biomechanics’ of shaking which had caused her to revise her views on the diagnosis of shaking.

[84] Dr Geddes stated that belief that thin film subdural haemorrhages were caused by the rupture of bridging veins was ‘biomechanically exceptionally unlikely’. She relied upon biomechanical research to support the view that shaking on its own cannot cause subdural haemorrhages and retinal haemorrhages without also significant structural damage to the neck and probably also a degree of axonal injury.

[85] Dr Plunkett stressed the importance of understanding the mechanics of injury.

[86] Dr Adams, referring to biomechanical research by Ommaya, considered that shaking was an improbable direct cause of retinal haemorrhage.

[87] Mr Richards warned that, however good the biomechanical calculations may be, they do not always appear to give an answer that is common sense. He went on to stress that limits of current knowledge and understanding:

‘Nobody really knows whether, when you shake a child, it is just back and forth or there is rotation as well. What does the head do? Does it decelerate against the back? Does it decelerate against the chin? When you put the child down, there must be an element of deceleration. It is a complex problem.’

[88] Of course none of the witnesses who gave evidence in the appeal was themselves an expert in biomechanics. Such were the number of references to biomechanics during the early days of the hearing that it became inevitable that some direct expert evidence on the subject was required. To that end the appellants filed a report by Dr Thibault and the Crown filed a report by Dr Gina Bertocci (dealing specifically with the case of Cherry). Because of the logistics involved, not least the constraints of time, it was not possible for either of these witnesses to give oral evidence. Consequently we are left to evaluate this important area by comparing and contrasting the views expressed on paper by Dr Thibault and Dr Bertocci.

[89] Dr Thibault is a biomechanical engineer whose work has a particular emphasis on ‘Paediatric Head Injury Mechanics’. Dr Thibault is not a doctor of medicine and holds a PhD in mechanical engineering. He has apparently performed experiments that have sought to mirror the age-dependant mechanical behaviour of the infant skull, sutures and brain. Part of the work in this field is to determine the amount of physical force that a living system can tolerate and thereby identify the ‘injury threshold’ or ‘injury tolerance criteria’. When the relevant threshold or criteria is exceeded the system or tissue will fail; for example stress on a bone will cause the bone to fracture if the stress exceeds the injury threshold.

[90] Dr Thibault explained that whereas there is a substantial body of research into the mechanics of adult head injury, until recently there has been relatively little similar work in relation to paediatric head injury. He reported:

‘It has been demonstrated experimentally and validated through real-world accident analysis that various intracranial pathologies result

from excessive angular acceleration of the head. In general, angular acceleration of the head creates relative motion between the brain and the skull, causing potentially injurious strain within the intracranial neural and vascular tissues (bridging vessels, deep central white matter). The nature, distribution and severity of the resulting pathology depend not only on the angular acceleration magnitude, but also on its direction, onset rate and duration.’

[91] Like Dr Plunkett, Dr Thibault (relying on the research of Prange and others) drew attention to the ability of the skull of an infant to react to force by deforming itself and thereby causing internal injury to the brain substance and/or cranial vascular system.

[92] In general terms, Dr Thibault joined issue with the conventional view that short falls are a frequent occurrence for young children and serious or fatal injuries from such falls are rare. Recourse is also typically made to information about high speed traffic accidents or falls from two storey buildings. Dr Thibault considered such an approach to be simply ‘arbitrary, unscientific and meaningless’ in that there is no attempt to evaluate the actual loads and forces at play in each individual case, which would need to include data regarding the child’s orientation at impact, kinematics (motion) of the body, impact surface and anatomical impact locations. Dr Thibault is clear that impacts arising from falls can result in serious and fatal brain injuries.

[93] The appellants rely upon the report of Dr Thibault for the following submissions:

(a) Shaking only could not produce the documented pathologies seen in these children;

(b) If ‘violent shaking’ of the sort required to produce the documented injuries had taken place one would have expected cervico-medullary injury, cervical spine and spinal cord injury.

[94] The Crown’s expert, Dr Bertocci, is also a mechanical engineer by training and is Associate Professor of Biomechanics and Director of the Injury Risk Assessment and Prevention Laboratory in the University of Louisville, Kentucky, USA. Her primary area of research is injury biomechanics in cases of child abuse and paediatric falls. Dr Bertocci’s report is very largely focussed upon the Cherry case and is not intended to be a comprehensive analysis of the biomechanical factors in play in each of these cases.

[95] One general observation that Dr Bertocci, however, made is based upon her research into falls either from ground level or from 9 inches above ground. Her conclusion in this regard is that the forces involved in such falls are well below the threshold said to be required to produce diffuse axonal injury in an infant, suggesting that there is a very low risk of DAI in such falls.

[96] In this section of our judgment we have done no more than summarise this evidence. Where such evidence is called by one or other party or both in future litigation it will be for the jury (in a criminal trial) or the judge (in a civil trial) to evaluate it in the light of the cross-examination and all the other evidence.

Retinal haemorrhages

[97] Retinal haemorrhage is the third limb of the triad. It will be recalled that Professor Carol Jenny told us that in her view in a case of pure shaking extreme caution should be exercised before a diagnosis of NAHI is made in the absence of retinal haemmorhage. We see the force of this evidence. In cases of injuries alleged to have been caused by an impact or impacts, the evidence suggests that it is not a prerequisite for retinal haemorrhages to be found. Again, we understand the logic of this proposition.

[98] It is agreed between the expert ophthalmologists and ophthalmic surgeons that a rapid rise in intracranial pressure can cause retinal haemorrhages although the amount and type of pressure required to cause such haemorrhages is a matter of debate. The appellants’ expert ophthalmic surgeon, Dr Gillian Adams, said that retinal haemorrhages could be caused by a spike or surge of venous pressure. Mr Peter Richards said that in his experience of carrying out brain surgery artificially induced very high venous pressure did not cause retinal haemorrhages.

[99] Some of the ophthalmic experts stated that retinal haemorrhages caused by shaking or impact demonstrate entirely different characteristics from retinal haemorrhages arising from other causes. Others said that no distinction can be made between retinal haemorrhages arising from different causes.

[100] Again, in the context of these appeals, we make no findings in respect of these differences of opinion. In future cases before a criminal or civil court, the type and extent of retinal haemorrhage and its place in the constellations of symptoms will be a matter for the court to evaluate in each individual case. We bear them in mind when reaching our conclusions in these four appeals. We also bear in mind Mr Horwell’s submission that the real question in these appeals is how much force is necessary to cause not just one element of the triad but all three.

The Law

[101] The principles on which this court should act in appeals involving fresh evidence are not in dispute. They were clearly set out in R v Pendleton [2001] UKHL 65, [2002] 1 All ER 524, [2002] 1 WLR 72 by Lord Bingham of Cornhill (see in particular [18] and [19]). They were repeated by Lord Brown of Heaton-under-Heywood in a recent case in the Privy Council: Dial v State of Trinidad and Tobago [2005] UKPC 4, [2005] 1 WLR 1660. Lord Brown said (see [31] and [32]):

‘[31] In the board’s view the law is now clearly established and can be simply stated as follows. Where fresh evidence is adduced on a criminal appeal it is for the Court of Appeal, assuming always that it accepts it, to evaluate its importance in the context of the remainder of the evidence in the case. If the court concludes that the fresh evidence raises no reasonable doubt as to the guilt of the accused it will dismiss the appeal. The primary question is for the court itself and is not what effect the fresh evidence would have had on the mind of the jury. That said, if the court regards the case as a difficult one, it may find it helpful to test its view ‘by asking whether the evidence, if given at the trial, might reasonably have affected the decision of the trial jury to convict’: R v

Pendleton [2002] 1 All ER 524 at [19]. The guiding principle nevertheless remains that stated by Viscount Dilhorne in Stafford v DPP [1973] 3 All ER 762, [1974] AC 878 at 906, and affirmed by the House in R v Pendleton:

“While … the Court of Appeal and this House may find it a convenient approach to consider what a jury might have done if they had heard the fresh evidence, the ultimate responsibility rest with them and them alone for deciding the question [ whether or not the verdict is unsafe]”

[32] That is the principle correctly and consistently applied nowadays by the criminal division of the Court of Appeal in England-see, for example, R v Hakala [2002] EWCA Crim 730, [2002] All ER (D) 277 (Mar), R v Hakala [2002] EWCA Crim 730, [2002] All ER (D) 277 (Mar) and R v Ishtiaq Ahmed [2002] EWCA Crim 2781, [2002] All ER (D) 80 (Dec). It was neatly expressed by Judge LJ in R v Hakala, at [11], thus:

“However the safety of the appellant’s conviction is examined, the essential question, and ultimately the only question for this court, is whether, in the light of the fresh evidence, the convictions are unsafe.” ‘

[102] Mr Mansfield QC also drew our attention to passages in the judgments of this court in R v Cannings and R v Kai-Whitewind [2005] EWCA Crim 1092, [2005] All ER (D) 14 (May). In particular in opening he referred to [22] of Cannings:

‘These observations serve to highlight the second problem which can arise in this case, and case like Sally Clark and Trupti Patel. We have read bundles of reports from numerous experts of great distinction in this field, together with transcripts of their evidence. If we have derived an overwhelming and abiding impression from studying this material, it is that a great deal about death in infancy, and its causes, remain as yet unknown and undiscovered. That impression is confirmed by counsel on both sides. Much work by dedicated men and women is devoted to this problem. No doubt one urgent objective is to reduce to an irreducible minimum the tragic waste of life and consequent life-scarring grief suffered by parents. In the process however much will also be learned about those deaths which are not natural, and are indeed the consequence of harmful parental activity. We cannot avoid the thought that some of the honest views expressed with reasonable confidence in the present case (on both sides of the argument) will have to be revised in years to come, when the fruits of continuing medical research, both hear and internationally, become available. What may be unexplained today may be perfectly well understood tomorrow. Until then, any tendency to dogmatise should be met with an answering challenge.’

But as the court was careful to point out later in the judgment at paragraph 178 this does not mean that fanciful doubts are a basis for rejecting expert evidence. With the general observations, referred to above and the legal principles in mind, we turn to the individual appeals. Furthermore, the limits of Cannings and its proper use were carefully explored in Kai-Whitewind, at [73]-[92], in observations with which we wholeheartedly agree.

Harris

[103] Mr Mansfield QC submits that there is a body of fresh evidence which is sufficient to cause this court on a review to quash the conviction. Mr Horwell submits that the fresh evidence has not in any way undermined the safety of the conviction.

[104] Before we outline and discuss the fresh evidence we must refer in a little more detail to the evidence given at trial. Although Harris said that Patrick had been showing signs of some infection before 4 December 1998, on that day he was seen by a health visitor, Margaret Savill, and a doctor, Dr Michael Tory, at Boulton Clinic in Alvaston both of whom pronounced him fit to be given his third immunisation against diphtheria, tetanus, whooping cough, polio and HIB. Statements of their evidence to that effect were read at trial. In his statement, Dr Tory said that a child would not be given this injection unless he was satisfied that it was not suffering from a raised temperature, vomiting or diarrhoea. A mild cold or snuffle would not have prevented the injection being given.

[105] On arrival at Harris’ home at 2.41am the paramedic crew noted that Patrick was unconscious, cold, not moving, pulseless and not breathing. At 2.55am the crew diagnosed that he was suffering from cardio-respiratory arrest. Dr Adams, an ophthalmic surgeon called on behalf of Harris, interpreted diagrams of the eyes made by the crew as showing that the pupils were fixed and dilated. In any event this finding was made by Dr Bertenshaw who examined Patrick at 03.15am at the Derby Children’ Hospital.

[106] After being transferred from Derby to the Queens Medical Centre in Nottingham a CT scan was carried out at 11.50am. The findings were recorded by the radiologist and his conclusion was:

‘Diffuse cerebral swelling and oedema secondary to hypoxia/ischaemia. Thin subdural haematoma in the para-falsine region. The appearances are suspicious of shaking or shaking – impact injury’

[107] Following Patrick’s death a post-mortem was carried out by Dr Bouch with Dr McKeever, a paediatric pathologist, in attendance. The findings relevant to this appeal are set out in Dr Bouch’s witness statement of 22 March 1999. Paragraph 5 reads:

‘The post-mortem examination confirmed a markedly swollen and softened brain and softened spinal cord with small amounts of subdural haemorrhage around the tentorium cerebelli at the foramen magnum and in the subdural space along the length of the spinal cord. Detailed examination by Professor Lowe confirmed widespread hypoxic (anoxic or ischaemic) changes within the brain resulting in marked swelling, necrosis of the cerebellum, haemorrhage into the left lateral ventricle and subarachnoid haemorrhage over the surface of the spinal chord and medulla. Professor Green confirmed extensive haemorrhages through the retina and the vitreous of both eyes with some retinal detachment’

Dr Bouch recorded the cause of death as cerebral hypoxia/ischaemia; intracranial haemorrhage; shaken baby syndrome. In his witness statement Dr Bouch said he had been advised that Patrick may have been shaken as part of an attempt to revive him. He said that he could not exclude such a shake as having caused the injuries but commented ‘accepted medical

opinion is that the force required to produce injuries from shaking is greater than that resulting from rough handling of an infant’. As already noted, Dr Punt said that the blood on the surface of the brain was not sufficient to cause Patrick’s death. In his opinion it was the injury to the brain, caused by shaking, which caused his death.

The new evidence on the appeal

[108] In this appeal we have heard evidence from the following witnesses called on behalf of Harris: Dr Waney Squier, a consultant neuropathologist, with a speciality in examining children’s brains; Dr Jennian Geddes, although her evidence was primarily confined to general matters; Professor Philip Luthert, a consultant ophthalmic pathologist and neuropathologist; Dr Gillian Adams, a consultant ophthalmic surgeon; Professor James Morris, a consultant pathologist; Dr Robert Sunderland, a consultant paediatrician; and Dr Philip Anslow, a consultant neuroradiologist.

[109] The Crown called the following witnesses: Dr Lucy Rorke-Adams, a consultant paediatric neuropathologist; Mr Peter Richards, a consultant neurosurgeon; Dr Richard Bonshek, a consultant ophthalmic pathologist; Mr R Gregson, a consultant ophthalmic surgeon; Dr William Lawler, a forensic pathologist; Dr Carole Jenny, a consultant paediatrician and consultant neuro trauma specialist; Professor Klein, a consultant physician; Dr Timothy Jaspan, a consultant radiologist; Dr Paul Giangrande, a consultant haematologist; and Dr Mark Peters, a consultant paediatric intensivist. We have also read statements submitted from the following experts on behalf of the Crown: Dr Harish Vyas, a consultant in paediatric intensive care and respiratory medicine; and Dr Angie Wade a senior lecturer in medical statistics.

[110] All these witnesses are clearly very experienced doctors in their own field. We shall summarise the evidence which they gave according to their respective specialities and only so far as is necessary to explain the important issues in this appeal.

The neuropathologists

[111] The reports provided by Dr Waney Squier and Dr Rorke-Adams disclosed a head-on collision between these two experts on the pathological findings and on the cause of death. In our judgment they are the two of the most important witnesses in this appeal. Much of the debate has been focussed on the pathological findings and their interpretation.

[112] Dr Waney Squier is a consultant and clinical lecturer at the Department of Neuropathology at the Radcliffe Infirmary, Oxford. Dr Rorke-Adams is the clinical professor of paediatrics at the University of Pennsylvania. She is clearly a very experienced and well respected member of her profession.

[113] Dr Waney Squier started with the forensic disadvantage of having provided a report dated 10 February 2000 for Harris’s trial solicitors in which she concluded that Patrick’s injuries were non-accidental and consistent with shaking. Unsurprisingly, she was not called at trial to give evidence on Harris’ behalf. She explained that, influenced by the research carried out by Dr Geddes since the trial, she had re-examined her own work in the light of the Geddes research. As a result in this case she had changed her mind and

now concluded that the brain findings were of severe swelling and hypoxic/ischaemic injury; and that there was no incontrovertible evidence of trauma. She relied upon the history given by Harris and the clinical evidence as support for her conclusions.

[114] Dr Rorke-Adams, having examined all the pathological evidence, the history and the clinical history concluded that the injuries to the brain, the subdural haemorrhages and retinal haemorrhages, were all clear evidence of traumatic injuries caused by strong force.

[115] In the course of their evidence each of these witnesses commented on brain slices and photographs taken at the post mortem. Their evidence in respect of the findings demonstrated by the photographs and slices was in sharp conflict in a number of instances.

[116] Photographs, G-H 1, 2 and 3, were said by Dr Rorke-Adams to show clear evidence of brain injury caused by trauma. She said that there could be no other cause. Dr Squier was of the opinion that the injuries shown in the photographs 1 and 3 and damage to nerve tissue at the cervicocranial junction were probably not caused by trauma and were consistent with herniation of the brain at the foramen magnum. She said herniation was caused by the pressure of the swelling brain when it impacted with the narrowing channel of the foramen magnum. As to the blood shown in photograph 2 Dr Squier said this was intrafalcine bleeding (bruising) within the membrane, seen at post mortem which was an extremely common finding in babies who have suffered from failure from blood or oxygen supply.

[117] There was no dispute that photographs G-H 4 and 5 showed subdural haemorrhages in the areas of the spinal cord. However, Dr Rorke-Adams gave as the explanation for these that the vertebral arteries must have been ruptured causing massive subarachnoid bleeding and subdural haemorrhages. She accepted that the post mortem revealed no soft tissue injuries to the neck but pointed out this explanation fitted with the combination of findings.

[118] Dr Squier described the subdural haemorrhages of the spine as probably caused by blood seeping down from the haemorrhage at the craniocervical junction. She said it was a common finding. Further, she did not accept that such subdural haemorrhages as were found at post mortem were caused by trauma. She said that it was local tissue necrosis causing bleeding exacerbated by a clotting disorder (DIC). In addition she said that she had seen cases where bleeding had seeped from the dura into the subdural space. As an example of this she provided her findings in the case to which we have referred in [71] to [73].

[119] In our judgment there are difficulties with the evidence of both these doctors in respect of their findings. The problem so far as Dr Squier is concerned is three-fold. First her explanation of herniation as the cause of haemorrhages in the area of the foramen magnum is, on the evidence we have heard, to say the least controversial. Dr Rorke-Adams dismissed this explanation as impossible. Mr Peter Richards said that in his 20 years experience as a surgeon he had never seen a case of herniation of the brain causing haemorrhaging at this site. He described Dr Squier’s evidence on this point as astonishing. Secondly, Dr Squier can provide no explanation for the mechanism that triggered these injuries. All she can say is that the primary source of the injuries was some form of brain swelling, but she was unable to

give any precise cause for the swelling. In her view the most likely explanation was sepsis or infection; and the least likely was trauma. Beyond that she frankly admitted she did not know. Thirdly, Dr Giangrande, whose evidence was not challenged, said that there was no question of DIC playing any part in any of these injuries.

[120] So far as Dr Rorke-Adams is concerned, in our judgment, there are also difficulties in respect of her evidence. First, the injury to the brain which she described by reference to photographs G-H 1, 2 and 3 are not referred to in the post mortem report of Dr Bouch. Secondly, her explanation of a rupture of the vertebral artery may not be entirely consistent with there being no evidence of a soft tissue injury to the neck. But, as she pointed out, at post mortem the vertebral arteries were not dissected. Thirdly, subdural haemorrhages of the spine would appear to be very rare. Fourthly, the subdural haemorrhages described by her are neither thin-film nor situated in the classic position for SBS namely at the top of the head.

[121] Before leaving the evidence of the two neuropathologists it is convenient to refer to the evidence given in this appeal by the neuroradiologists, Dr Anslow and Dr Jaspan. And we should also refer to the evidence of Mr Peter Richards. Dr Anslow and Dr Jaspan agreed that the CT scan taken at 11.50am on 5 December at the Queens Medical Centre showed a swollen brain. The sole issue between them was whether the scan showed subdural haemorrhages in the area of the posterior falx (photograph G-H 2). Dr Jaspan concluded that it was subdural; Dr Anslow that it was intradural. In the end this dispute was resolved by Dr Rorke-Adams stating that the photograph taken at post mortem, rather than the scan, showed interdural bleeding or interfalcine bleeding that is bleeding between the two dural layers in and either side of the falx.

[122] Mr Richards, an obviously very experienced neurosurgeon, had no doubt that a finding that the triad of injuries was present was correct. He was equally not in doubt that the force used to cause these injuries must have been more than rough handling. In cross-examination he agreed that he was unable to say what was the minimum force which could give rise to similar injuries.

The ophthalmic witnesses

[123] The measure of agreement between the witnesses in this area of expertise was a little greater than that between Dr Squier and Dr Rorke-Adams. There was no dispute that the retinal haemorrhages were quite severe injuries and that they could have been caused by shaking. Dr Rorke-Adams had described the retinal haemorrhages as severe and towards the top end of the scale. This description was similar to descriptions given by other witnesses. There was also no dispute that on their own retinal haemorrhages findings were not diagnostic of SBS. Next, it was agreed that a sharp surge in ICP could cause retinal haemorrhages although the degree of raised ICP necessary to cause such injuries was not agreed. We have already referred to Mr Richards’ experience of carrying out brain surgery procedures designed to increase venous pressure substantially, but which had not caused retinal haemorrhages (see paragraph 99).

[124] On the question of the force required to produce retinal haemorrhages by shaking we have referred to the 2004 paper produced by the working party of the Royal College of Ophthalmologists. No witness was able to provide a measure of the force required. Mr Mansfield QC asked each witness what was the minimum force required. For obvious reasons no witness was able to provide an answer to this question.

[125] Dr Adams expressed the opinion that the fact that the ambulance crew noted Patrick’s pupils to be fixed and dilated at 2.41am on 5 December was a sign that the brain was swollen at that stage. She said fixed and dilated pupils were a clinical sign of brain swelling. Brain swelling caused stretching of the third nerve which in turn affected the pupils of the eyes. In her opinion the retinal haemorrhages were caused by raised intercranial pressure, a more probable cause than shaking. However, she said that in the absence of evidence of brain swelling the cause of retinal haemorrhages may well be shaking. On the question of the force necessary to cause retinal haemorrhages she said that the fact that the injuries were at the top end of the scale did not provide any information as to their aetiology and ‘You have to look at the whole picture.’

[126] Dr Jaspan and Mr Richards did not accept that there could have been brain swelling at 2.41am. Dr Jaspan, in his report, said that if a CT scan had been carried out at the time when retinal haemorrhages was first seen at Derby Children’s Hospital little brain swelling would have been evident. In evidence, Dr Jaspan said one to two hours after an apnoeic incident one can start to see mild and subtle signs of swelling. The swelling may then progress swiftly in relatively few hours; or in other cases it could take twenty-four to forty-eight hours. Mr Richards said that ICP is normal for some hours after an apnoeic incident, possibly four to five hours before it starts to rise slowly. Mr Gregson also disagreed with Dr Adams on this point. He said that the more likely explanation was at that time, in a period of cardio-arrest, the part of the brain which controls the pupils had become hypoxic (Patrick was noted as pulseless). This would have caused the pupils to become fixed and dilated. This explanation was put to Dr Adams, she said her explanation was more probable and that the explanation given by Mr Gregson was one which only occurred when the infant was near death.

[127] The impact of this issue is that, if Dr Adams may be correct, brain swelling may have taken place sooner than supposed by the Crown’s witnesses making it possible that there was a cause for the retinal haemorrhage findings other than shaking.

[128] Professor Luthert described the critical issue of the retinal haemorrhage findings in this appeal as whether it was feasible that there had been a significant and rapid increase in intracranial pressure so as to cause them. When asked whether subdural haemorrhages and retinal haemorrhages were associated with cardiac arrest, he said it was not in the context of events in hospital but the possibility of low brainstem damage might be important and might well produce a pattern of cardio-respiratory arrest which is rather different from that seen in other contexts. Although he described the retinal haemorrhages findings in Patrick’s case as typical of those found in cases of alleged NAHI, Professor Luthert was one of those doctors who was concerned that the triad was a hypothesis and that the full aetiology of the injuries comprising the triad was not ‘necessarily known.’

[129] Mr Gregson described the retinal haemorrhages findings as very severe and was of the opinion that they could only have been caused by a

severe degree of trauma. Dr Bonshek agreed with this opinion. In his report he described the injuries as highly suggestive of non-accidental injury. Both Mr Gregson and Dr Bonshek agreed that the degree of injury was not necessarily commensurate with the degree of force used to create it.

Evidence of a possible infection

[130] One of the difficulties faced by Harris at trial and in this appeal is to suggest what was the cause of Patrick’s collapse, if it was not shaking. Of course, as Mr Mansfield QC properly pointed out, a defendant faced with an allegation of unlawfully shaking an infant so as to cause injury or death, does not have to provide evidence of, let alone prove, an alternative cause. Nevertheless in cases such as this both prosecution and defence will seek to prove respectively either that there was no alternative cause or that there was one. Not surprisingly we have heard a good deal of evidence on the issue of whether or not Patrick’s condition might have been caused by some form of infection. We have already noted Dr Squier’s opinion that the primary cause of brain swelling in this case was or may have been infection. To deal with this issue we heard evidence principally, but not exclusively, from Professor Morris and Dr Sunderland called on behalf of Harris; and Dr Carole Jenny, Professor Klein and Dr Mark Peters called on behalf of the Crown.

[131] We shall deal with this issue comparatively shortly for the reason that in his final submissions Mr Mansfield QC accepted that every possible infection suggested by Professor Morris and Dr Sunderland as a possible cause of Patrick’s collapse was effectively disproved by the evidence called on behalf of the Crown.

[132] Apart from the fact that there is some evidence that Patrick had, at worst, an upper respiratory chest infection, probably a cold, for a day or two before 4 December 1998 there was no evidence at all to suggest that he had any other infection, let alone one which might have been sufficiently severe as to cause his death. In the end Professor Morris was driven to suggest that there was a possibility that the ambulance crew arrived at the precise moment when Patrick was suffering an unexplained episode from which he would not have recovered. Professor Morris suggested that it was the resuscitative procedures which had kept him alive thereby giving his brain time to swell. We regard this suggestion as speculative and fanciful.

[133] Dr Sunderland suggested that the history given by Harris of Patrick grunting and having difficulty breathing might have been bronchilitis caused by respiratory syncital virus (RSV). In our judgment this suggestion was effectively demolished by the evidence of Dr Mark Peters.

[134] There is however one matter which cannot be disposed of so summarily. Professor Morris advanced the theory that although Patrick’s death could not be categorised as a SIDS (sudden infant death syndrome), it could be akin to SUDI: that is a sudden unexplained death from a natural cause or natural disease. His report prepared for this appeal sets out statistics relating to SIDS and SUDIs. These statistics have been comprehensively criticised in a statement made by Dr Angie Wade. Further, she points out that Professor Morris is a pathologist not a statistician.

[135] In our judgment, leaving aside Professor Morris’ statistics, the general point being made by him is the obvious point that the science relating to infant deaths remains incomplete. As Mr Richards said when asked a

question in the context of the amount of force necessary to cause injuries, he agreed that the assessment of injuries is open to a great deal of further experimentation and information. He assented to the proposition ‘We don’t know all we should’. Similarly, Professor Luthert in his evidence said:

‘My reason for making that statement is simply that there are many cases where questions are raised as to how the child died and, because there is a big question mark over the circumstances, it is rather tempting to assume that ways of causing death in this fashion that we do know about are the only reasonable explanations. But in fact I think we have had examples of this-I have heard already. There are areas of ignorance. It is very easy to try and fill those areas of ignorance with what we know, but I think it is very important to accept that we do not necessarily have a sufficient understanding to explain every case.’

As noted by the court in Cannings and Kai-Whitewind these observations apply generally to infant deaths.

Professor Whitwell

[136] We have left Professor Whitwell’s evidence until last when dealing with the evidence in this appeal. She was one of the team of doctors who co-authored Geddes III with Dr Geddes. In our judgment her view must necessarily be considered in the light of Dr Geddes’ concessions in respect of Geddes III.

[137] In this case having examined all the material, Professor Whitwell produced a report in which she referred to the fact that the major pathology was of hypoxic-ischaemic trauma damage which she said might be secondary to trauma or other cause of cardio-respiratory arrest. She went on to raise the question of the degree of force necessary to produce localised neck injuries. Her opinion expressed in the final paragraph of her report was that the injuries to the brain may have arisen in the background of a ‘shaking’ incident but there was a possibility of an underlying natural cause of the collapse. She said the neuropathological findings may be open to several interpretations.

[138] In evidence she gave some support to Dr Squier’s opinion that bleeding and injuries to the nerve roots could have been caused by herniation. But she agreed in cross-examination that the most significant factor in her opinion was a stretching injury to the nerve roots.

The submissions

[139] Mr Horwell submitted that the new evidence did not undermine the conviction. He asked the Court to accept that the triad had survived intact. He pointed to the fact that at 1.00am on 5 December 1998 Dr Barber examined Patrick and found him to be well. At 2.30am Patrick was found to be suffering cardio-respiratory arrest. Mr Horwell submitted that the only credible explanation for this sudden collapse was shaking by Harris. The triad of injuries was established and there was no credible alternative cause of these injuries. In addition, Dr Rorke-Adams’ evidence of injuries to the brain should be accepted. He submitted that her evidence together with the evidence of the doctors dealing with the ocular injuries demonstrated that unlawful force had been used. He argued that Harris was asking the court to accept that the cause of death was a series of coincidences involving two unlikely syndromes. He invited the Court to find that all suggested causes of Patrick’s collapse and death other than the triad had been disproved. The conviction was therefore safe.

[140] Mr Mansfield QC submitted that there were disagreements between the experts as to the cause of death. He rightly pointed out that it was not for Harris to prove an alternative cause of Patrick’s death. He submitted that this Court could not decide matters which a jury should decide such as the differences of opinion expressed by Dr Squier and Dr Rorke-Adams. Finally, he submitted that in a case such as this, where the clinical evidence and the history given by the mother, ran completely contrary to a finding of unlawful force, the Court was entitled to accept that this was one of those cases where the explanation for Patrick’s injuries and his death was just not known; and/or that the amount of force used by her was no more than any mother might use to revive her baby and therefore not unlawful.

Conclusion in this appeal

[141] In considering all the evidence in this appeal we have kept well in mind that our task is to decide whether the conviction is safe. We also bear in mind Lord Bingham’s test in Pendleton in a case of any difficulty (which in our view this is) of ‘asking whether the evidence, if given at the trial might reasonably have affected the decision of the trial jury to convict.’ This approach, in our judgment, merits careful consideration in this appeal.

[142] We have already stated that so far as the evidence relating to an alternative cause of death based on a possible infection is concerned, in our judgment, this evidence does not form any basis for holding that the conviction is unsafe.

[143] So far as the other issues are concerned, the evidence at trial and the evidence adduced by the Crown in this appeal, provide a strong case against Harris. Mr Horwell’s submission that the triad is established and that any attempt to undermine it is based on speculation is a powerful one. Nevertheless strong as is the case against Harris we have concerns about the safety of the conviction.

[144] First, in order to dismiss the appeal, we would have to accede to Mr Horwell’s submission that we should reject Dr Squier’s evidence in its entirety. If Dr Squier may be right, such evidence of subdural bleeding as she accepts was present was small; untypical of the usual thin-film subdural haemorrhages found in triad cases; in the sense that it was not found at the top of the head and probably not caused by trauma. Secondly, if Dr Squier is, or may be, right there is no pathological evidence of trauma. At one stage Mr Horwell in cross-examination, suggested to Dr Squier that she had lost objectivity in her evidence in this appeal. This was a bold assertion and one which we find difficult to accept. It was put at the end of her evidence when Dr Squier was describing subdural haemorrhages in another case which she said represented bleeding seeping from the dura into the subdural space (see [71] to [73] above). As we have said already we find it impossible to conclude that on this issue Dr Squier’s evidence is plainly wrong and that Dr Rorke-Adams must be correct.

[145] The importance of Dr Squier’s evidence is that it throws doubt on the significance of such subdural haemorrhages as there are; and it throws doubt on the evidence of injuries to the brain described by Dr Rorke-Adams. We are far from saying that we accept Dr Squier’s evidence in preference to that of Dr Rorke-Adams. Indeed, in view of the weight of evidence disputing her opinions we have reservations about whether Dr Squier can be right. But equally, in all the circumstances of this case, the differences between them are ones which the jury would have had to have assessed in the light of all the evidence in the case.

[146] Secondly, although the evidence of the findings of retinal haemorrhages is powerful supporting evidence of shaking, on its own it is not diagnostic of shaking. If the subdural haemorrhages are undermined, the retinal haemorrhages findings will not fill the gap although we recognise that both can be considered together. There is also the issue of whether Dr Adams may be correct in her view that fixed and dilated pupils seen by the ambulance crew was a sign of brain swelling at that time.

[147] Thirdly, although as we have already stated the amount of force required to cause the triad of injuries will in most case be more than just rough handling, the evidence suggests that there will be rare cases when injuries will not correspond to the amount of force used. It is at least possible that in such rare cases (maybe very rare cases) very little force will cause catastrophic injuries.

[148] In this connection the evidence shows that in recent years the medical profession has become more aware of the degree of force necessary to cause injuries by the growing science of biomechanics. This knowledge, and to an extent Geddes I and II, in our judgment, have had the effect of moderating to some extent the conventional view that strong force is required to cause the triad of injuries. In this case Dr Bouch rejected as an explanation for the injuries he found, shaking by Harris to revive Patrick. Today he might have taken a less firm stance. This knowledge might also have acted as a counter-balance to the evidence given at trial by Professor Green on the amount of force necessary to cause the retinal haemorrhages.

[149] The above factors, which have all arisen out of post-trial material have to be assessed against the background of the clinical evidence which in our judgment is significant and important. As Dr Anslow said in his report of 3 June 2005:

‘The clinical history is perhaps the most important clinical tool available to the clinician and to reject the carer’s version of events in favour of another requires the highest possible level of medical evidence. After all, the Doctor is effectively accusing the carer of lying.’

Dr Anslow is not a clinician but in our judgment his words of caution are apt in cases of this sort.

[150] At the outset of this judgment we have set out the clinical history. In summary, Harris was described as a careful and caring mother. She called out Dr Barber late at night because of her concerns for Patrick. Dr Barber described her as being calm and controlled at that time. The prosecution’s case at trial was that in the interval between Dr Barber leaving the house and 2.30am when Harris telephoned the emergency services she must have violently and unlawfully shaken Patrick. In our judgment this history combined with the absence of findings of bruises to any part of the head, face or body; and the absence of fractures or any other sign apart from the triad of injuries, does not fit easily with the Crown’s case of an unlawful assault based on the triad of injuries, itself a hypothesis.

[151] The Crown relies upon the fact that Patrick was in the sole care of Harris throughout the evening of 4/5 December. It is also correct that Harris admitted shaking Patrick in an effort to revive him; and bouncing him on her knee when she was telephoning the emergency services. But, those actions are not suggestive of unlawful force being used by her although it is possible that a jury might now find them to be sufficient to cause the injuries seen by Dr Bouch albeit not unlawful.

[152] As we have said the Crown’s evidence and arguments are powerful. We are conscious that the witnesses called on behalf of Harris have not identified to our satisfaction a specific alternative cause of Patrick’s injuries. But, in this appeal the triad stands alone and in our judgment the clinical evidence points away from NAHI. Here the triad itself may be uncertain for the reasons already expressed. In any event, on our view of the evidence in these appeals, the mere presence of the triad on its own cannot automatically or necessarily lead to a diagnosis of NAHI.

[153] The central issue at trial was whether Harris caused the death of her son, Patrick by the use of unlawful force. We ask ourselves whether the fresh evidence, which we have heard as to the cause of death and the amount force necessary to cause the triad, might reasonably have affected the jury’s decision to convict. For all the reasons referred to we have concluded that it might. Accordingly the conviction is unsafe and this appeal must be allowed. The conviction will be quashed.

Rock

The focus of the appeal

[154] The history of this matter has already been set out; we turn directly to the appeal. Certain matters are common ground. First, there is no dispute that Rock did shake Heidi; there is likewise no dispute (given the full thickness bruise to the back of the head) that she suffered an impact. Secondly, there is no realistic suggestion that disease or infection could possibly have played a role in Heidi’s death. The thrust of the appeal was instead that the conviction was unsafe in the light of research subsequent to the trial, calling into question the minimum degree of force necessary to cause the pathology in this case. Rock, it was submitted, was not safely convicted of any offence; at the very least, his conviction of murder was unsafe and a conviction of manslaughter should be substituted.

[155] For its part, the Crown vigorously resisted the notion that there was any real alternative to unlawful killing. Here, as elsewhere, it was to be borne in mind that the minimum degree of force in question was the degree of force necessary to cause all the injuries suffered; Geddes I and II did not address the minimum degree of force necessary to tear bridging veins and cause retinal haemorrhages; the ‘unified hypothesis’ (i.e., Geddes III) which might have done so, has of course gone. The surrounding circumstances and the injuries suffered amply supported the safety of the conviction. While conceding in terms that if there had been the ‘triad’ and no more, ‘that was unlikely ever in itself to be sufficient’ to support a charge of murder (as distinct from manslaughter), here it was contended that there were additional features which justified the jury’s verdict-bearing in mind that the intention to cause grievous bodily harm could be both rapidly formed and almost instantly regretted.

The new evidence on the appeal

[156] In the view which we take of this appeal, it is unnecessary to review the new evidence at length; it suffices to summarise the position reached on the totality of the new material.

[157] As to radiology, save for one area (to be mentioned shortly) there was no or no real dispute between Dr Anslow (called by Rock) and Dr Jaspan (called by the Crown). The first CT scan, taken on the 2 June 1998 at about 10.21 pm, some 21/2 hours after Heidi’s admission into hospital, showed a minimally swollen brain but the presence of subdural blood. On the 4 June, some 39 hours later, the second CT scan revealed a very different picture. This showed, apart from cerebellar tonsillar herniation and established hypoxic ischaemic brain damage, a grossly swollen brain but the same small amount of subdural bleeding-notwithstanding a ‘huge’ (Dr Jaspan’s word) increase in pressure. Dr Anslow accepted that subdural bleeding at a time when there was no evidence of raised intra-cranial pressure (‘ICP’), was a ‘very strong indicator’ of trauma. On the assumption that Geddes III did not apply, he could think of no cause other than trauma to account for the subdural bleeding.

[158] The only area of dispute between Dr Anslow and Dr Jaspan was whether a lesion in the corpus callosum revealed by MRI scans was caused by trauma; Dr Jaspan was firmly of the opinion that it was; Dr Anslow said that it might be an artefact. As we have already indicated such disputes between reputable experts potentially give rise to difficult issues on an appeal of this nature. In the event, notwithstanding the powerful nature of Dr Jaspan’s evidence in this regard, it is unnecessary for us to resolve this dispute. We proceed on the assumption that Dr Anslow might be correct.

[159] In cross-examination, Mr. Mansfield QC put to Dr Jaspan one of the ‘scenarios’ developed by Dr Geddes (see below), involving a departure from the evidence given by Rock at trial. This set of facts assumed that Heidi had struck her head when falling and was subsequently the subject of two well-intentioned shakes by Rock. Asked whether this was a possible scenario capable of explaining the injuries sustained by Heidi, Dr Jaspan’s initial (and firm) answer was ‘no’. He based this answer on his views as to the cause of the corpus callosum lesion. If wrong about that, he accepted that the scenario ‘might just be feasible’. Immediately thereafter, Dr Jaspan was re-examined by Mr Horwell as follows:

‘Q. If you leave the corpus callosum out of the equation, when you say it just might be feasible, what do you mean?

A. Because in medicine there is never a hundred per cent certainty. So, if I was asked is there a hundred per cent certainty that it could happen, I would have to be honest and say no, there must be almost the freak situation where that could happen.

Q. What are the chances from your clinical experience?

A. By inference, 99 per cent unlikely.’

In his final submissions, Mr Mansfield QC sought to suggest that these answers disclosed a major concession on Dr Jaspan’s part. Having seen and heard Dr Jaspan give evidence and having reviewed the transcript of his answers, we respectfully disagree. The essence of Dr Jaspan’s views remained plain and unaltered, albeit couched in rather more moderate and less graphic language than apparently deployed at trial.

[160] Turning to the neuropathologists, in her report dated 14 April 1999, prepared for the trial (but which remained understandably unused by the defence), Dr Geddes said this:

‘I believe that both the intracranial and the intraocular bleeding are likely to have been the result of vigorous to-and-fro movements of the brain inside the skull, of the type that occurs in a shaking injury.’

Subsequently, Dr Geddes has (as is well-known) revised her thinking. That said, in her evidence at trial, Dr Geddes accepted the presence of subdural haemorrhages but was unable to provide an explanation for them. She remained of the view that for violent shaking to have produced the subdural and retinal haemorrhages here, she would have expected some form of widespread diffuse axonal injury and damage to the muscles in the neck and spinal column. She accepted, however, in answer to questions from the Court, that, on any view, Heidi must have had some insult to the brain, not explained by Rock’s account of events. She could not rule out impact plus shaking.

[161] In her report of 24 May 2005, Dr Geddes posited three ‘scenarios’ (to which reference has already been made) which might have caused the pathological findings in this case. She could not be certain which of the three actually happened. The first scenario involved a low-level fall in which Heidi, among other things, knocked the back of her head, resulting in hyperflexion of the neck which damaged her brain stem. The second, also involved a fall, followed by a resuscitative (i.e., well-intentioned) shake by Rock, causing damage to her brain stem. In both these scenarios, damage to the brain stem resulted in Heidi’s breathing stopping, her brain swelling rapidly and consequential subdural and retinal bleeding. The third scenario involved an assault on Heidi. We are bound to observe that the suggested sequence of the first two scenarios is troubling, given the apparent conflict with the radiology evidence (see above). Moreover, Dr Geddes was closely cross-examined as to the factual basis for the first scenario, involving a departure from Rock’s own account of events-in which he was adamant that Heidi had not struck her head. Pressed on this point, Dr Geddes said that she was duty bound to point out that there was impact (given the bruise at the back of Heidi’s head); she thought that Rock must have been wrong in his account but had not given the matter attention when writing her 1999 report; she was (notwithstanding the factual evidence) prepared to speculate to this degree in now giving her evidence to the Court.

[162] Dr Rorke-Adams and Dr Geddes disagreed as to (i) the extent of subarachnoid bleeding in this case; and (ii) the cause of a ‘hole’ or ‘tear’ in the corpus callosum (in a location different from that which formed the subject of the disagreement between the radiologists, already referred to). Once again, it is not necessary to resolve this dispute and, we proceed on the assumption that Dr Geddes might be correct. For our part, we find the

agreement between Dr Rorke-Adams and Dr Geddes that there were here subdural haemorrhages considerably more significant than the areas in which they disagreed. As Dr Rorke-Adams put it: ‘Subdural haemorrhage is essentially always traumatic in origin except under very unusual circumstances …’ In itself, of course, that answer cannot resolve the source of the trauma nor, insofar as it was inflicted by another, the intention with which it was inflicted.

[163] On the appeals, evidence was given by Dr Plunkett, who has undertaken research into ‘low-level’ infant falls-ie, falls of less than 10′. The conclusions which Dr Plunkett drew from his study were that (i) low-level falls were capable of causing serious injury or death; but (ii) that there was no inevitability about it; as he expressed it:

‘I do not know either an upper limit or a lower limit of impact velocity below which there is no injury and above which there is always injury.’

Dr Plunkett’s evidence related to the cases of Rock, Cherry and Faulder. We shall have more to say of his evidence, in particular with regard to the Cherry case.

[164] For the moment, we confine ourselves to Dr Plunkett’s evidence with regard to the appeal of Rock. Here, basing himself on the bruise on the back of Heidi’s scalp, Dr Plunkett expressed the opinion that her death was the result of an impact injury; this was an instance of a ‘low-velocity impact event with a bad outcome’. Plainly therefore, Dr Plunkett’s evidence entailed a departure from the evidence, as given by Rock; on no view, could a fall onto her bottom (as described by Rock) have explained this fatality. In Dr Plunkett’s view, Heidi’s head must have struck something, a matter unexplained on Rock’s account.

[165] We come next to the evidence of the ophthalmic experts, Professor Luthert and Dr Adams, called by Rock and Dr Gregson, called by the Crown. It is convenient to take Dr Gregson’s evidence first. He put the matter starkly; the significance of the eye injuries was crucial to this case. The retinal injuries were at the very top of the range or not far from it. There were in addition para-macular retinal folds, a type of detached retina. In his evidence-in-chief, Dr Gregson explained this matter as follows:

‘Q. The retina is completely detached from the eye?

A. The retina is folded up very much like a rug would be if you pushed it together. It is not detached in the same way as boxers get retinal detachments, but the fact that it is folded means it is not in the place that it should be.’

A little earlier, Dr Gregson had observed that in children of Heidi’s age, he knew of no other cause for para-macular folds other than trauma; this was so, regardless of when the para-macular folds had first appeared. Moreover, the presence of para-macular folds was indicative of severe injury-‘a lot of trauma’ was required. His reason for this view was as follows ‘the retina wants to stay attached; it does not want to fold. It requires an effort to detach it’.

[166] Turning to Professor Luthert, we begin with his written material. In his report of 14 April 1999, he was of the opinion that, absent any alternative explanation, severe trauma, such as shaking combined with impact, was the most likely explanation for the pathological findings in Heidi’s eyes. In his letter dated 12 January 2005, he maintained the view that such trauma (i.e., shaking, impact or both) was the most likely cause of Heidi’s death and the condition of her brain and eyes. He added this:

‘I do not believe that the presence of retinal haemorrhages necessarily implies a specific level of force although I think the level of force is likely to be more than would be seen in even rough normal play.’

[167] In his oral evidence, Professor Luthert stated that it was difficult in an individual case to extrapolate from the severity of a retinal haemorrhage to any assumed degree of applied force. By contrast, in the generality of cases, it was to be expected that there would be a (broad) correlation between the degree of trauma and the seriousness of the injury suffered. That said, there was ‘not necessarily a tight correspondence between level of trauma and severity of outcome’.

[168] Initially in his evidence, Professor Luthert said that it was difficult to ‘exclude with total confidence’ the possibility that the fall described by Rock had caused the retinal injuries. Pressed, unsurprisingly, on this point, he ultimately accepted that a fall onto her bottom would not be expected to cause injuries of this nature. Although he said that he had seen ‘more severe’ retinal injuries, he further accepted that these were ‘highly significant’, a description which he later amplified as meaning ‘extremely significant and abnormal pathology’. While he did not view the presence of para-macular folds as diagnostic of shaking, he agreed that they could not ‘in their entirety’ have been artefactual-a necessary concession, as they had been noted during Heidi’s lifetime. He agreed in cross-examination that the ‘most likely explanation’ for Heidi’s retinal injuries was shaking. In re-examination, Professor Luthert said that a version of the facts, in effect based on Dr Geddes’ first two scenarios, was not fanciful.

[169] Returning to his written report of the 2 June 2005, Professor Luthert explained that since the original trial and following publications by Dr Geddes and Dr Plunkett, he had reconsidered the minimum degree of force required to generate the ‘triad’. He went on to say this:

‘The minimum level of force required to produce this syndrome can not be defined, but the recent Royal College of Ophthalmologists Working Party concluded ‘It is highly unlikely that the forces required to produce retinal haemorrhage in a child less than 2 years of age would be generated by a reasonable person during the course of (even rough) play or an attempt to arouse a sleeping or apparently unconscious child.’ In my opinion, it is now not possible to exclude the possibility that a well-intentioned but ill-advised shake might cause the pattern of pathology seen in Heidi. The same Working Party commented ‘It seems clear that minor falls can, only exceptionally, give rise to subdural and retinal bleeding. In these cases, it may well be that the biomechanics of the impact induce the rotational forces necessary to produce the picture considered typical of SBS.’ So it is difficult to exclude with total confidence the possibility that the fall caused the injuries seen. Finally, it is also feasible that Heidi was assaulted.’

In answer to questions from the Court as to this passage, Professor Luthert asserted that he had relied on Geddes I and II but not Geddes III. Professor Luthert said that he had been a member of the Working Party and agreed with its conclusions. While he was (in effect) contemplating the infliction of some force going beyond rough play, by itself that did not determine the intention of the person inflicting the force.

[170] In a nutshell, the evidence given by Dr Adams was to the following effect:

(i) The fall as described by Rock was not the cause of Heidi’s retinal haemorrhages;

(ii) The injuries to Heidi’s eyes were at the very top end of the scale;

(iii) The cause of those injuries was shaking or shaking and an impact;

(iv) Simply by looking at the retinal haemorrhages, it could not be said ‘definitively’ what level of force had been applied.

[171] For completeness, we note that in her reports Dr Adams had raised the question of whether a lumbar puncture might have been the cause of the retinal damage. Suffice to say that no evidence emerged to support this line of inquiry and Mr. Richards gave cogent evidence, which we accept, as to its irrelevance; we say no more of this point.

Conclusions

[172] At the outset, we should underline that this is not a case where the expert medical evidence and the presence of the ‘triad’ stand alone. We accept of course that Rock was a man of good character and that in general, he had been very good with Heidi. But there was also evidence of some hostility towards her, prior to the events of the 2 June 1998. Perhaps more tellingly, there was the evidence from the neighbour, Ms Banham, that, on the night, she heard Heidi screaming for a significant period of time and Rock shouting at her to ‘fucking shut up’; then it all went quiet. For completeness, we do not think that the reliability of Ms Banham’s evidence is called into question by the mere fact of there being some unused and untested material from police officers, apparently saying that they could not hear shouting between the two houses.

[173] Against that background, we come to the evidence in this case of the presence of the ‘triad’; namely, encephalopathy, subdural haemorrhages and retinal haemorrhages. There is, moreover, the bruise found at the back of Heidi’s head.

[174] How were these injuries caused? Having regard to the evidence we have summarised, it is plain that Rock’s explanation-a fall in which Heidi did not strike her head-cannot account for them. We are, moreover, unable to accept that Rock’s version of events was innocently mistaken, along the lines that he had simply not seen her strike her head. As set out above, he was adamant that he had prevented her hitting her head. We naturally have regard to the burden of proof resting on the Crown throughout. That burden may however be satisfied by reliance on such inferences which it is proper to draw from Heidi’s injuries, taken together with Ms. Banham’s evidence and the absence of an explanation from Rock, with whom Heidi was alone at the relevant time.

[175] We turn then to the inferences which it is proper to draw. We do so with great caution, mindful both of the gravity of the matter and that (as already underlined) the mere presence of the ‘triad’ does not automatically or necessarily lead to a diagnosis of NAHI and/or a conclusion of unlawful killing. All the facts of the individual case must be taken into account.

[176] Given the assumptions that we have thought it right to make with regard to the disputes between Dr Anslow and Dr Jaspan and between Dr Geddes and Dr Rorke-Adams, encephalopathy does not take the matter further-save for the fact of its presence. The position is, however, very different with regard to subdural haemorrhages and retinal haemorrhages.

[177] As has been seen, the presence of subdural haemorrhages was common ground between the relevant experts. It was also indisputable that the subdural haemorrhages preceded the development of brain swelling and that there was no evidence of any increase in subdural bleeding notwithstanding the rise in intracranial pressure following the swelling of the brain. Pausing there, these features would themselves have gone a very long way to undermine the credibility of Geddes III, had that hypothesis not in any event been withdrawn in the manner already described. Matters do not end there. Without Geddes III, Geddes I and II cannot suggest a mechanism to explain the subdural haemorrhages; strikingly, as we have seen, Dr Geddes in her evidence could not explain them. There is accordingly no realistic challenge here to the ‘traditional’ mechanism of the tearing of bridging veins. If so, it necessarily follows that Heidi was subject to a degree of force sufficient to tear those veins.

[178] We return to the retinal injuries. On the totality of the evidence, we are sure that these were at the top end of the scale (Dr Gregson and Dr Adams) and we are not deterred from that conclusion by anything said by Professor Luthert, if indeed he ultimately disagreed. We cannot necessarily infer from the severity of those injuries, including the presence of the para-macular folds, that any precise or specific degree of force was used; we are acutely conscious both of ‘thin skull’ cases on the one hand and of ‘lucky’ victims on the other. We have, however, no realistic doubt that the force used must have been-as even Professor Luthert was minded to agree-in excess of anything generated by a reasonable person in the course of rough play. We further have no real doubt that the cause of those injuries was shaking or shaking plus an impact; if anything, we favour the latter given the presence of the bruise at the back of the head. In all the circumstances, we regard as fanciful the notion that Heidi’s retinal injuries can be explained by a fall in which she struck her head and was then the subject of a well-intentioned resuscitative shake (Geddes, first and second scenarios).

[179] We have not overlooked the evidence of Dr Plunkett but we are unable to regard it as of assistance in this case. First, there is no proper factual foundation for Dr Plunkett’s evidence; his opinion rests on a version of events relying on Rock’s account of an accidental fall but departing from it so as to account for Heidi striking her head when falling. Secondly, Dr Plunkett’s suggestion that the bruise at the back of Heidi’s head caused her death, lacks credibility. Quite apart from more general considerations as to the relevance of Dr Plunkett’s study to cases such as these (see below, when dealing with Cherry), his thesis here does not begin to address the subdural haemorrhages and retinal injuries.

[180] We are accordingly left with a powerful Crown case for unlawful killing, based on the surrounding circumstances (Rock’s shouting on the night), and the nature and severity of Heidi’s injuries (the subdural haemorrhages and retinal damage). All that there is to set against that case is the suggestion of accident, based on a manifestly flawed account from Rock, the one person who could have explained what happened, supplemented by a variety of speculative suggestions from the experts-necessarily lacking a sound factual base. We remind ourselves that our task is not to retry Rock; our inquiry is as to the safety of his conviction. On all the evidence, we are amply satisfied as to the safety of his conviction for unlawful killing.

[181] For completeness, we are not deterred from that conclusion by the following matters:

(i) On behalf of Rock, some play was made with the moderation in language employed by Crown experts between the trial and the appeal; in this regard, as we have seen, considerable emphasis was placed on the alleged ‘concession’ made by Dr Jaspan, an emphasis we have already indicated we regard as misplaced. We think that the submission as to moderation of language is correct as far as it goes; but we do not think it goes very far. Doubtless, as expert thinking has evolved, so, rightly, the language has moderated and become less graphic or emotive. Those are welcome developments. But when the totality of the evidence is considered, there is nothing in any of this to suggest that the safety of Rock’s conviction is undermined.

(ii) Dr Geddes, as we have seen, was puzzled as to the absence of other injuries, if indeed Heidi had been the subject of violent shaking. We have given this matter anxious consideration but ultimately regard it as decisively outweighed by the overwhelming evidence pointing to a degree of force (or violence) at least going beyond even rough play. There is, as has frequently been urged on us, no precise correlation between force inflicted and the gravity of the injuries suffered.

(iii) As seen in the passages set out earlier, the Judge summed up in robust terms. On the evidence before him, no proper criticism could be made of those passages. Given the totality of the evidence now before the Court, even though an alteration in expression might have been warranted, we do not think that any change to the substance of the summing-up would have been such so as to undermine the safety of a conviction for unlawful killing on this ground.

[182] What remains is whether Rock’s conviction for murder as distinct from manslaughter is safe. In R v Stacey [2001] EWCA Crim 2031, (2001) 64 BMLR 115 a ‘shaking’ case, the Court said this:

‘[48] Other grounds of appeal having been examined, and in the end abandoned, that leaves only the question of whether the jury was entitled to find that she intended to do really serious harm. We are troubled about that. One brief period of violent shaking by a frustrated mother and child-minder was all that was required to explain this death. Apart from the bruises to the neck, no other injuries were found. As the judge said, an intent to do serious bodily harm may be quickly formed and soon regretted; but so may a less serious intent, simply to stop a child

crying by handling him in a way any responsible adult would realise would cause serious damage or certainly might do so. That would only provide the mental element necessary for manslaughter.

[49] Even allowing for the jury’s obvious advantage in seeing the appellant give evidence, we have been unable to discern anything which, in our judgment, would have made it safe for the jury to convict this appellant of the more serious charge. In our judgment, the less serious charge was the only safe verdict. If the jury had had the additional benefit of hearing the fresh medical evidence we have heard, they might well have come to the same conclusion.’

[183] Stacey was of course a case on its own facts but the reasoning of the Court has, with respect, an undoubted resonance. As already foreshadowed, the Crown’s stance, very fairly, was to accept that a verdict of murder was unlikely ever to be justified on the basis of the ‘triad’ standing alone; it follows that the verdict of murder could be justified here, only, if at all, on the basis of (i) the bruise at the back of the head and (ii) Ms. Banham’s evidence.

[184] Elaboration is unnecessary. Those two additional features go in this case to underpin the safety of the conviction as to unlawful killing; but they do not assist on the question of murder or manslaughter. Necessarily therefore the conviction of murder cannot be sustained. We are fortified in reaching this conclusion by a consideration of the additional medical evidence we have heard. A brief period of violence (going beyond even rough play) was all that was required to cause Heidi’s fatal injuries; such violence undoubtedly furnishes the mental element necessary for a conviction of manslaughter; but it does not necessarily demonstrate an intention to cause grievous bodily harm, the relevant intention if the conviction of murder was to be upheld.

[185] Accordingly, we set aside Rock’s conviction for murder and substitute a conviction for manslaughter. To this extent only, this appeal is allowed. We shall hear submissions on sentence for the offence of manslaughter.

Cherry

[186] We again do not repeat the facts of this matter, which have already been set out. It will be recollected that on Cherry’s account, he left the child alone for a matter of minutes downstairs while he went upstairs; when he returned minutes later, she was, as the Judge put it in the summing-up, in a ‘poor state’ on the floor. Essentially the decision for the jury was whether they could be sure that Sarah’s death was caused by an unlawful act on the part of Cherry (a formulation to which we shall return, later) or whether her death was or might have been attributable to an accidental fall from a chair some 6-8 inches high (‘the chair’).

[187] On this appeal, Mr Mansfield QC’s submissions proceeded as follows:

(i) The Crown’s position had shifted between trial and appeal; at trial, this was a case of impact; now it was a case of both shaking and impact; but that was not how the matter had been placed before the jury.

(ii) There was new evidence to the effect that death or serious injury from low level falls could not be ruled out. In addition, there was a possibility that Sarah had aspirated vomit. Death could have resulted from a combination of the two. In any event, if this was a case of both shaking and impact, the innocent combination of an accidental fall followed by a resuscitative shake could not be ruled out.

(iii) Great care had to be taken in approaching the bruising on Sarah’s head and body, both in the light of the new evidence and the course which the trial had taken.

(iv) In all the circumstances, the conviction was unsafe.

[188] The Crown resists the appeal and contends that nothing has emerged to undermine the safety of the conviction. In a nutshell, the evidence as to low-level falls is inapplicable to a fall of the nature postulated here. Upon analysis, there was no evidence capable of suggesting that aspiration of vomit was a relevant consideration. As to the new evidence, it had all to be taken into account; Cherry could not pick and choose; the introduction of a shaking component did nothing to undermine the safety of the conviction. Evidence of Sarah’s other injuries, properly and fairly considered, lent support to the Crown’s case and suggested that the notion of an accidental fall was fanciful.

The new evidence on the appeal

[189] We begin with the pathologists. As already observed, Professor Whitwell conducted the post-mortem and was a prosecution witness at the trial; on the appeal, she now gave evidence for Cherry.

[190] In her witness statement for the trial, Professor Whitwell attributed Sarah’s injuries and brain damage, taken in conjunction with the scalp bruising (already described), to ‘direct blunt trauma’. She went on to say this:

‘The degree of trauma necessary to produce such damage is considerable and the findings are not consistent with a simple fall onto a carpeted surface. They are consistent with the head being forcibly propelled against a hard surface or a blunt object contacting the head.

Apart from the brain injuries there are a number of bruises on the body. The sighting of a number of these is highly suggestive of non-accidental injury rather than being caused accidentally-in particular the bruises to the buttock, face, thigh and arm.’

[191] Her report of 2 June 2005, prepared for the appeal, evidences her revised views. She said that the possibility of Sarah suffering a fatal injury as a result of falling from the chair had to be considered afresh in the light of Dr Plunkett’s research. The ‘primary brain pathology’ was due to lack of oxygen; this hypoxic-ischaemic injury could have been caused as a result of primary injury to the brain, causing Sarah to stop breathing and/or as a result of ‘vomiting with inhalation of vomit into the lungs’. She would ‘still to some extent be unhappy as regards the scalp bruises arising in a fall but it has to be a considered possibility that Sarah’s head impacted against some other surface as well as the ground’.

[192] In her oral evidence at the appeal, she explained that her change of view was based on Dr Plunkett’s work and her own experience. She had not found diffuse axonal injury; such trauma as she found was associated with impact. The need to explain Sarah’s scalp bruising (in two separate locations) led to Professor Whitwell contemplating that Sarah might have struck her

head both on the window and then on the ground in the course of her fall; indeed, she later underlined that two impacts were needed to explain this bruising.

[193] Professor Whitwell agreed that at post-mortem, there was no evidence of vomit or aspiration. She agreed that Sarah had up to a maximum of 22 bruises; she was ‘concerned’ about that number of bruises. They were probably ‘more than’ fair wear and tear for a 21 month old. In the absence of proper explanation, they were highly suggestive of abuse. There had been no developments in science between the trial and the appeal to alter her view as to the relevance of the two sites of scalp bruising. Her view at the trial (and she was the person who had conducted the post-mortem) was that those two areas of bruising had been caused at about the same time. She had herself identified traumatic injury to the brain. She accepted that the subdural bleeding occurred because of the tearing of bridging veins.

[194] Dr Rorke-Adams was firmly of the view that Sarah’s injuries were inconsistent with a fall from the chair; she placed emphasis on the multiple areas of injury and the extent of those injuries. Sarah’s injuries were caused by ‘trauma’; the ‘pattern of injury’ was characteristic of both shaking and impact; it was a combination of both. Although the degree of injury could not be correlated with the degree of force, considering the injuries as a whole, they must have been caused by ‘strong force’.

[195] Pausing here, it will be apparent that there was agreement between Professor Whitwell and Dr Rorke-Adams: (i) that there had been traumatic injury to the brain; (ii) that there were subdural haemorrhages; (iii) that those haemorrhages had been caused by the tearing of bridging veins. There was some dispute between these two witnesses as to whether further injury to the brain, which it is unnecessary to detail, was also attributable to trauma or was artefactual in origin. Impressed as we were by Dr Rorke-Adams’ evidence in this regard (the coincidence relied upon by Professor Whitwell seemed unlikely), this is another of those areas where we do not think it would be right simply to discount a reputable expert’s contrary views. We therefore proceed with this appeal on the assumption (in favour of Cherry) that the brain damage suffered by Sarah did not extend beyond the areas of agreement between Professor Whitwell and Dr Rorke-Adams, summarised above.

[196] We move next to the evidence of Dr Plunkett, which it is helpful to consider here in a little greater detail than in the preceding appeal of Rock. Dr Plunkett said that there was nothing inevitable about a serious injury resulting from a fall from the chair but ‘the potential for serious injury or even death exists’. The floor surface did not matter; it was immaterial whether it was carpet over concrete or just concrete.

[197] Questioned as to his research, Dr Plunkett explained that he had worked from a database for head and neck injuries involving playground equipment, recorded by the United States Consumer Product Safety Commission (‘CPSC’). Over 11 1/2 years, he had identified 18 fatalities from head and neck injuries involving falls. None of the children (or infants) in his study had formal retinal examinations. These cases included falls from swings, which, he agreed were complex or complicated falls. He further

agreed that none of these cases were similar to a shaken baby case. The distance of a fall is said to be measured with reference to the closest part of the body to the ground at the beginning of a fall.

[198] Case no. 5 in Dr Plunkett’s study was said to be closest to a fall from a 6-8 inch chair; this was suggested on the basis that the child in question had suffered the equivalent of a 12 inch fall. Dr Plunkett’s paper described this fall as follows:

‘A 23 month-old was playing on a plastic gym set in the garage at her home …She had climbed the attached ladder to the top rail above the platform and was straddling the rail, with her feet 0.70 metres (28 inches) above the floor. She lost her balance and fell headfirst onto a 1-cm (3/8 inch) thick piece of plush carpet remnant covering the concrete floor. She struck the carpet first with her outstretched hands, then with the right front side of her forehead, followed by her right shoulder. Her grandmother had been watching … And videotaped the fall. She cried after the fall but was alert and talking … However, approximately 5 minutes later she vomited and became stuporous … A CT scan indicated a large right-sided subdural haematoma … The haematoma was immediately evacuated. She remained comatose postoperatively, developed cerebral oedema with herniation, and was removed from life support 36 hours after the fall …’

Dr Plunkett suggested that, as her head had been some 42 inches above the ground when the fall began and as her body length was some 30 inches, it was equivalent to her falling from a chair 12 inches high. We confess some difficulty with this reasoning but we nonetheless continue with our consideration of Dr Plunkett’s evidence. We do acknowledge that we felt, as indeed Dr Anslow later expressed it, ‘shocked’ that a fall, as captured on the video (which was shown to the Court), could have resulted in a fatality; this, indeed, may be the strength of Dr Plunkett’s evidence, so far as it goes. None the less, it is pertinent to record the following: (i) It transpired, as explained by Dr Plunkett in his oral evidence following the playing of the video, that the rail from which the child fell was in fact 39 inches above the floor, not 28 inches; (ii) she fell a sufficient distance for her to rotate and so as to fall onto her head with some 2/3 of her body weight contributing to the impact; (iii) there was a lucid interval after the fall (unlike the cases before us); (iv) the haematoma was large and lop-sided (again unlike the thin film haematomas encountered in cases such as the present); Dr Plunkett agreed that the mass effect of this haematoma caused the child’s death. Notwithstanding all these factors, Dr Plunkett continued to maintain that the Case 5 fall was ‘exactly comparable’ to a 12 inch fall. The velocity was relevant and what was not known was the ‘minimal impact velocity’ required to cause these types of injuries.

[199] Closely cross-examined, Dr Plunkett agreed this:

‘Q. … your paper does not establish the proposition that any impact, no matter how minor, can lead to fatal consequences, does it?

A. That is correct.’

After some questioning from the Court, Dr Plunkett acknowledged the common sense proposition that the lesser the distance of the fall, the less

likely it was to cause an injury to a vulnerable part of the body. In any event though for a time it seemed that Dr Plunkett was resistant to the suggestion, the distance of a fall is a necessarily relevant consideration. Dr Plunkett’s own formula for impact velocity was as follows: Velocity (V) squared = 2 x Acceleration (A) x Distance (D). From this it must follow that, all other things being equal, a reduction in D will result in a reduced V.

[200] Reverting to the individual case of Cherry, Dr Plunkett asserted that the bruising on Sarah’s body amounted to ‘normal wear and tear’. We observe at once that this answer was manifestly unconvincing.

[201] Standing back from Dr Plunkett’s evidence, we do not say that his work does not have utility. As recorded, we were ourselves very surprised by the outcome in case no. 5, as shown on the video. However, we think that it is important to look closely at both the limits of his study and its relevance to any individual case; the true comparability of the falls he studied to the cases before the Court merits careful scrutiny. We return to this theme when indicating our conclusions on the Cherry appeal.

[202] Mr Richards gave evidence for the Crown in this case as well. In his opinion, Sarah died as a result of a severe inflicted non-accidental head injury. His oral evidence included the following passage:

‘Q. You have used the word ‘severe’. Degree of force required in this particular case?

A. Far in excess of anything we see in normal life with children of this age. Children are toddling around at this age. They fall over all the time. It they suffered severe head injury from little falls, the casualty departments would be inundated with them, the intensive cares would be full of them, my operating theatres would be operating or dealing with them on a daily basis. I have not seen a child of this age suffer a severe head injury in my 24-year neurosurgical career from a minor injury as described or …as considered. This very short 6-inch fall.’

Other than being prepared to accept never to say never, try as Mr Mansfield QC might, Mr Richards did not shift in substance from this answer.

[203] We turn next to the issue of aspiration of vomit. Given that, for very good reason to which we shall come, it played an ever diminishing role on the appeal, we shall take it very shortly indeed.

[204] Mr Wrightson, a neurosurgeon, whose evidence on behalf of Cherry we heard by way of video-link from New Zealand, said this, in his report for the appeal:

‘… there is no doubt that Sarah vomited and aspirated material into her lungs. The vomiting was described by Mr. Cherry and was confirmed by those who arrived to help. A chest X-ray later in the day of injury showed “widespread airspace shadowing throughout both lungs”. The hypoxia which this would have caused is likely to have resulted in or at least contributed to the gross cerebral swelling that was present.’

In his oral evidence, Mr Wrightson said, early on, that this was ‘the key to the whole situation’. There was no reason for Cherry to have invented the evidence he gave. As to aspiration, the ambulance personnel described a

‘bubbly’ chest. At the hospital, copious bloodstained fluid came out from the lungs; the chest x-ray and the findings on post-mortem were likewise said to support these conclusions.

[205] Under cross-examination, Mr Wrightson agreed that there was no sign of vomit at the scene; that the neighbours who attended (one of whom was a nurse) did not suggest that Sarah had vomited; that one of the paramedics had said that he did not see any signs of vomiting; that, at the post-mortem, no sign of aspiration pneumonia was found.

[206] Dr Peters, a consultant paediatric intensivist, was called by the Crown. His impressively clear evidence may be summarised as follows:

(i) Neurogenic pulmonary oedema (‘NPO’) was a condition involving fluid in the lungs as a result of something catastrophic happening to the brain. It is characteristically immediate. The description given by the para-medics was ‘almost a text-book’ description of NPO:

‘A combination of the noisy chest, with obvious fluid, with pink frothy secretions coming out of the mouth and the child making respiratory effort to overcome this fluid in the chest are all typical. It could read like a text-book description.’

(ii) At no stage was there any evidence of aspirated vomit. The most relevant evidence was that of Sarah’s appearance at intubation. Had aspiration been a major cause of respiratory failure then, typically, when the tube was placed into the lungs there would be a ‘welling up’ from the chest of whatever was aspirated. No suggestion of aspirated vomit was made by the intensive care staff; to the contrary the fluid seen remained pink and frothy and became more blood-stained as time passed. This was a typical pattern of NPO. Had the fluid been erythromycin (a very common child’s antibiotic which Sarah had been given), Dr Peters would have expected the paediatric staff to recognise the difference between it and blood-staining.

(iii) To cause respiratory distress suddenly, massive aspiration was necessary. If so, however, it would have been apparent on intubation and subsequent care. Conversely, unless it was massive, it would not be a ‘credible cause’ of this respiratory distress of this severity.

[207] The ophthalmic evidence can be disposed of summarily. Dr Gregson, called by the Crown, fairly conceded that the retinal haemorrhages in this case were superficial only and were not typical of those discussed in the other appeals before the Court. They were not typical of shaking. In the circumstances, we do not think that the Crown case derives any support from the retinal haemorrhages. Conversely, however, we were not in any way persuaded that the absence of ‘typical’ retinal haemorrhages somehow assisted Cherry’s case on the appeal.

[208] For our part, this being a case where impact as well as shaking is alleged we regard the absence of ‘typical’ retinal haemorrhages as neutral. We say no more of this point. In the event, it is unnecessary to consider the otherwise interesting (sub-) issue as to when the retinal haemorrhages in truth first appeared.

[209] Finally in this case we have considered detailed written reports from two experts in biomechanics: Dr Thibault and Dr Bertocci for Cherry and for the Crown respectively. Dr Thibault, whose approach to ‘injury thresholds’ we have described earlier, considered that the forces applied to the head in a 3 foot impact fall onto carpet represented approximately 50,000 radians per second squared, whereas the injury threshold associated with subdural haemorrhage and diffuse axonal haemorrhage were between 8,000 and 12,000 radians per second squared. A 3 foot fall therefore, in Dr Thibault’s view, is well within the physical context in which subdural bleeding and DAI may occur. Dr Thibault identified the primary point of impact to be the occipital region. The cause of subdural bleeding is accepted to be rupture of bridging veins, but such a rupture could occur, in Dr Thibault’s opinion, as a result of the substantial internal rotational forces that arise when a child falls and impacts her head. He concluded that whilst deliberate inflicted injury cannot be ruled out, the injuries were entirely consistent with the mechanics of the speculated accidental fall.

[210] Dr Bertocci explained that her habitual starting point when asked to determine whether a given account fits the resulting injuries is to begin with an assessment of any bruising found on the child: ‘bruising represents points of force application and a roadmap to the child’s exposure’ to force. Dr Thibault considered that the two apparently separate sites of impact could be explained by a fall inducing a well-distributed contact load across the occipital region resulting in dynamic in-bending of the skull and contusion to the outer left and right margins of the total contact area. The presence of bruising on two opposite sides of the head indicated to Dr Bertocci two very different lines of force applied from differing directions, and is not consistent with a fall from a chair. Further, Dr Bertocci observed that the size of the scalp bruises at 2.5cm and 3.5cm are much larger than bruises found in children injured through accidents. Finally, Dr Bertocci summarised published research and her own unit’s experiments with an automotive ’12 month old’ crash test dummy. Her conclusion, which is again in total contrast to that of Dr Thibault, was that a 12 month old falling from a 9 inch vertical position impacting their head on a padded carpet surface would produce head accelerations that are well below published biomechanical injury thresholds. She concluded that Sarah’s injuries are not attributable to a fall from a 9 inch chair.

Conclusions

[211] As is apparent, encephalopathy and subdural haemorrhages are present in this case. With regard to the latter, there is no dispute here that they were caused by the tearing of bridging veins. Two elements of the ‘triad’ are thus present. For reasons already set out, although there were retinal haemorrhages (the third element of the triad), these are neutral and do not advance the argument of either party on the appeal.

[212] Next it is convenient to mention the issue of aspiration of vomit, essentially to dispose of it. We found Dr Peters’ analysis of the evidence on this issue compelling. Mr Wrightson’s views to the contrary do not survive this analysis. We accept Dr Peters’ evidence and dismiss aspiration of vomit as a credible cause or contributory cause of Sarah’s death.

[213] We turn to the topic of low-level falls. We have already indicated our general views with regard to Dr Plunkett’s evidence. Having given the matter anxious consideration, we are not persuaded that the postulated fall from the 6-8 inch chair was a credible cause or contributory cause of Sarah’s death. Our reasons are these:

(i) On any realistic view, the fall here (if fall there was or might have been) was of a very different type and nature from those forming the subject of Dr Plunkett’s study. The factual differences between any fall here and Dr Plunkett’s Case 5 (said to be the closest comparable) are marked indeed, not least with regard to the nature of the subdural bleeding found.

(ii) Even if the reservations in i) above are put to one side, notwithstanding the extent of Dr Plunkett’s research, there is no example of a 6-8 inch fall, from a static object, causing death or serious injury to a 21 month old child. As he himself agreed in cross-examination (see above), it does not follow from Dr. Plunkett’s study that any impact, no matter how minor, can lead to fatal consequences.

(iii) Even if (contrary to the above) it was thought that Dr Plunkett’s study did mean that a fall from the chair here was capable of furnishing a realistically possible innocent explanation for Sarah’s death, it remains necessary to address the two separate sites of scalp bruising. Professor Whitwell conducted the post-mortem; as she agreed in her oral evidence, her impression (at least at the time of the trial) was that the two separate areas of scalp bruising had been caused at about the same time. Inevitably and as Professor Whitwell further agreed, no scientific developments since the trial could alter the relevance of these two separate sites of bruising. Accordingly, for the fall to be capable of providing an innocent explanation of these injuries, it was necessary to postulate two impacts (window and floor) in the course of the same fall. As it seems to us, this is pure speculation and stretches credibility altogether too far.

(iv) We have set out earlier Mr Richards’ observations (i) that if such falls did generate severe injuries, casualty departments and the like would be inundated; but (ii) that in more than 20 years of practice he had never encountered a severe head injury in a child of this age arising from a 6 inch fall. Some caution is necessary in approaching these observations; first, there is no claim that serious injury is the inevitable result of falls of this nature; secondly, ‘never’ is an unfortunate word. None the less, when this evidence based on practical experience is considered cumulatively with reasons (i)-(iii) above, it furnishes powerful support for the conclusion that the notion of an accidental fall in this case, causing or contributing to Sarah’s death, is simply fanciful.

(v) We are not swayed from our view by the evidence of biomechanics summarised earlier. This is a complex, developing and (as yet) necessarily uncertain area of scince, as illustrated by the stark divergence of opinion between Dr Bertocci and Dr Thibault. Be that as it may, Dr Thibault’s views are altogether too difficult to reconcile with evidence of primary fact in this case, for the conviction to be regarded as unsafe by reason of the biomechanical evidence.

[214] Pulling the threads together, this is a case of a sudden collapse of a 21 month old child. Cherry was alone at home with her. His factual account cannot explain her injuries and death. Upon analysis, the possible explanations advanced on his behalf on the appeal do not carry credibility. The case cannot be one of SIDS, given, as is undisputed, her traumatically caused subdural haemorrhaging. As it seems to us, in the light of those subdural haemorrhages and the separate sites of scalp bruising, the inference can properly be made that her injuries and death were attributable to a combination of shaking and impact. On any realistic view (and in this case we are of course only concerned with a count of manslaughter), the force involved must have been such that the risk of some harm to Sarah would have been foreseeable to all sober and reasonable people. In the circumstances, unless there is anything in the argument as to the shift in the Crown’s case between trial and appeal rendering the conviction unsafe (see below), we are amply satisfied of the safety of Cherry’s conviction for manslaughter.

[215] We are fortified in this conclusion by the evidence as to up to 22 bruises on Sarah’s body. As Professor Whitwell was driven to agree, these were highly suggestive of abuse, in the absence of proper explanation of which there was and has been none. In approaching this evidence, we have thought it right to proceed with caution; as the summing-up suggests, at the trial, Cherry was treated as a good stepfather and there had been no suggestion of any improper behaviour towards Sarah or any of the other children. But on the state of the evidence at the trial, there may have been no need for the Crown to explore this wider area. Cherry, having introduced new lines of inquiry on the appeal, cannot, we think, complain at all the evidence being revisited. While even then we would have hesitated long and hard before treating this question of bruising as determinative of the appeal, in this appeal we see no unfairness in taking it into account as an additional reason pointing towards the safety of the conviction.

[216] Finally, we turn to Mr Mansfield’s submission that the conviction was unsafe because of the shift in the Crown’s position between trial and appeal; at trial, this had been a case of impact; now it was one of both shaking and impact. Cherry did not have a fair opportunity to deal with the ‘new’ case; nor did the jury consider it. With respect, we cannot agree.

[217] First, as a matter of principle and as already foreshadowed in dealing with the evidence of bruising to Sarah’s body, once an appellant has introduced new evidence on the appeal, he can hardly complain if such evidence is answered or rebutted by the Crown. Unavoidably, in such a process, the nature of the case may take on a different hue and there may be some change in the manner in which the Crown puts its case. But it cannot be, that on this ground alone, a conviction must be regarded as unsafe; fresh evidence, once admitted, may serve to confirm, not only to undermine, the safety of a conviction. Accordingly, if on all the evidence before this Court, the only reasonable conclusion is that, considered in the round, the conviction is safe, the Court should give effect to that conclusion: R v Hanratty [2002] EWCA Crim 1141 at [101]-[104], [2002] 3 All ER 534 at [101]-[104].

[218] Secondly, however, this principle is qualified by consideration of fact and degree. In an individual case where an issue of this kind arises, it may be that the Crown’s change of position between trial and appeal is such that the conviction cannot be considered safe. Whether it does or not will necessarily depend on the facts of the particular case. Here, we see nothing in the development of the Crown’s case on the appeal that renders Cherry’s conviction unsafe. The essential question for the jury was whether Sarah’s death was accidental or the result of some unlawful act on the part of Cherry. That was the fundamental divide; in this case, given the nature of Cherry’s evidence, the mechanism was necessarily of secondary importance.

It is true that the mechanism favoured by the Crown at trial was one of impact. It is further true that on appeal the Crown’s case as to mechanism has evolved to one of a combination of shaking and impact. That evolution, however, cannot have caused Cherry any prejudice. Moreover, any suggestion here that a well-intentioned shake was capable of giving rise to a possible defence depended on the credibility of the explanations we have already dismissed, namely those relating to the low-level fall and/or the aspiration of vomit.

[219] In all the circumstances, we are fully satisfied as to the safety of the conviction. This appeal must be dismissed.

Faulder

Appeal

[220] Faulder’s notice of appeal relies upon two post-trial developments. Firstly the publication of Geddes I and II which, it is said, provides a basis for questioning the explanations previously advanced for N’s injuries, and, secondly, a judgment given by Eady J in a libel case, Reed and Lillie v Newcastle City Council [2002] EWHC 1600 (QBD), [2002] All ER (D) 140 (Jan) in which Dr San Lazaro, a key prosecution expert witness in the Faulder case, had been severely criticised. In addition the notice of appeal relies upon a new explanation, the MORO reflex, which might explain N’s sudden movement and subsequent fall from Faulder’s outstretched arm. Finally, the notice relies upon fresh expert evidence from Professor Whitwell, which calls into question the Crown’s view at trial that this was primarily a shaking injury, her opinion being that there was evidence of a number [of] impacts (which might fit Faulder’s account) and that the primary cause of collapse was likely to be cessation of breathing and consequent brain damage, rather than primary brain damage due to direct trauma.

[221] The ‘Statement of Reasons’ supporting the Criminal Cases Review Commission decision in Faulder’s case refers to the trial evidence given by Dr San Lazaro and Dr Alexander to the effect that N’s primary injury was as a result of direct impact between the brain and the skull, which would require massive and violent force comparable to a child being hit by a car travelling at 40 mph. As the Commission’s statement observes, ‘within this paradigm, Mr Faulder’s explanation is inadequate.’ The Commission refers to Geddes I and II and postulates that Faulder’s explanation becomes more plausible if the cause of N’s collapse is cessation of breathing. The Commission concludes that:

(a) had the jury been aware of the new evidence they might not have been certain that Faulder’s account was untrue; and

(b) the medical evidence now available provides a possible alternative explanation for N’s injuries and challenges the prosecution case that the injuries must have been caused by shaking.

The Injuries

[222] In Faulder’s case the injuries and symptoms relating to N that require consideration are:

Bruises

(i) Area of erythema (ill defined flushing of the skin) that was ‘grazed/bruised’ located directly on top of the head;

(ii) A triangular fresh bruise 2cm by 2cm above the forehead;

(iii) A 2cm linear bruise on the left side of the head above the ear;

(iv) A small deep blue bruise over the right forehead;

(v) A second small deep blue bruise over the right forehead but more centrally sited;

(vi) Marked swelling over the top of the occipital bone in the midline.

Subdural haemorrhage

(vii) Thin fresh subdural haemorrhage along the falx with a thin layer of subdural blood over the surface of the brain (seen on the first CT scan at 7.44 am on the morning after admission, it remained largely unchanged in subsequent scans);

Brain swelling and HII

(viii) In the first scan (12 hours after the 999 call) there is no significant brain swelling or injury. Subsequent scans over the following three days show developing brain swelling and hypoxic-ischaemic injury in both cerebral hemispheres.

[223] It is of note that in Faulder’s case there is no evidence of retinal haemorrhaging or primary brain injury.

[224] In the course of Faulder’s appeal we have considered evidence from the following experts on behalf of the appellant: Professor Whitwell, Dr Plunkett and Dr Sunderland. In response the Crown have particularly relied upon evidence from Dr Jaspan, Mr Richards, Professor Jenny, Dr Lawler and Dr Rorke-Adams.

Appellant’s experts

[225] For the appellant Professor Whitwell, relying upon the Geddes I and II research, considered that the hypoxic-ischaemic injury to the brain could arise as a result of oxygen starvation caused by a sudden bending and stretching of the nerve tracts in the cranio-cervical region. As N survived, there was obviously no opportunity to use the BAPP test for axonal damage to confirm this opinion. In N’s case the damage may have been ischaemic and localised, but the mechanism was the same as in the case of hypoxia. The Professor, who is a pathologist, rightly conceded that in this case, which did not result in death, her expertise did not permit her to comment upon the interpretation of the radiological evidence.

[226] Professor Whitwell considered that the findings were all consistent with some form of impact. The injuries to the head indicated a number of impacts, the multiplicity of which gave rise to concern, but in cross examination she also questioned whether all of the external injuries were clearly present at the time of admission, or, in relation to two, arose as a result of therapeutic intervention. She advised that the forces required to produce subdural haemorrhages in a child of this young age are unknown.

[227] Dr John Plunkett’s evidence was based upon his own research into young children and low level falls. He drew attention to the fact that the skull of a 7 week old infant differs fundamentally from that of an older infant or adult. A scalp impact to a 7 week old would cause the skull to bend inwards or deform, with a consequent deformation or movement within the brain itself. This movement, Dr Plunkett advised, could cause subdural haemorrhages and functional brain damage, for example breathing difficulties. Both Dr Plunkett and Professor Whitwell accepted that the subdural haemorrhages were assumed to have been caused by tearing of bridging veins. The minimal impact velocity needed to cause these injuries is not known, but as N did not have any skull fracture or brain contusion, Dr Plunkett postulated that the impact velocity was extremely low. In this manner, Dr Plunkett considered that all of N’s injuries could be explained by the account of the fall given by Faulder. Dr Plunkett did not however accept that N had as many as 6 external head injuries believing that there were only three. In particular Dr Plunkett considered that marked swelling seen on the scans was a manifestation of the triangular shaped bruise seen earlier over the top of the occipital bone which, he explained, had migrated to the back of the head by reason of gravity. This explanation and the further explanation proffered by Professor Whitwell that the two forehead bruises were caused during treatment, were rejected by each of the relevant experts for the Crown. In so far as may be necessary we were not persuaded by Dr Plunkett or Professor Whitwell on these issues and, having seen the relevant photographs, scans and medical notes, have no difficulty in finding that there were indeed six separate sites of external head injury as listed above at paragraph 219.

[228] Dr Sunderland’s written report to the CCRC introduced the ‘MORO Reflex’ (a recognised automatic response seen in babies under 8 weeks old) as an explanation for N arching his back or throwing his arms out. It was therefore surprising that it was only after a substantial number of questions in cross examination that Dr Sunderland responded to junior counsel for the Crown by saying ‘I am allowing you to develop your proposition. At some point I must help you. I do not think the MORO reflex is relevant to Faulder. But I am cutting in, you develop your proposition.’ We found Dr Sunderland’s contribution in this regard fell short of that which is required by the court from an expert witness.

[229] Dr Sunderland, having had Faulder’s detailed account put to him, stated that a baby of N’s age could have behaved in the manner described.

[230] Dr Thibault, an expert in biomechanics who was, as we have said, not available to give oral evidence, produced an analysis of the evidence which concluded that Faulder’s account accorded with a biomechanical analysis of the injuries. Dr Thibault’s opinion is however upon the basis that there were only two impacts: one being the linear bruise above the left ear (number (iii) in our list) and the other which caused both of the marks above the right eye (numbers (iv) and (v)). Dr Thibault discounted the swelling on the back of the head (number (vi)) which is only visible on the scan on the basis that if this had been traumatic one would have expected the treating clinicians to have noted it and, further, there is no note of any surface marking at the same location indicating an impact. The report does not consider the area of erythema located directly on top of the head ((i)) or the triangular fresh bruise 2cm by 2cm above the forehead ((ii)), these marks are shown in the photographs, however the photographs were not made available to Dr Thibault.

[231] Dr Thibault considered that the linear bruise was consistent with contact with part of the high chair, whereas the two marks on the forehead were consistent with impact on a flat surface, for example the floor. The fall as described by Faulder would, according to Dr Thibault, have been sufficient in magnitude to deform the skull and cause shifting and deformation of the underlying bridging veins and neural tissue thereby producing acute SDH. He also postulated the temporary deformation causing a temporary herniation at the cranio-cervical junction leading to consequent interference with the respiratory system and thereby hypoxic-ischaemic injury.

Crown’s Experts

[232] For the prosecution Dr Jaspan described the existence of the subdural haemorrhages and the development of what became extensive hypoxic-ischaemic injury in both cerebral hemispheres. He considered that the most substantial impact was that which caused swelling to the right parietal region, with the other bruises resulting from injuries of lesser magnitude. Dr Jaspan, in a balanced report, drew attention to the fact that only four of the eight elements that would normally constitute a diagnostic ‘full house’ for inflicted injury were present in this case, namely: unexplained encephalopathy, scalp bruising, subdural haemorrhages and secondary hypoxic-ischaemic injury. He therefore considered that accidental trauma could not be entirely excluded, but some form of inflicted injury was the most likely cause.

[233] Mr Richards, who in his written evidence questioned whether a 7 week old baby would have come to fall in the manner described by Faulder, in oral evidence came to accept that N may have fallen from Faulder’s arm in an ordinary ‘gravity roll’, which did not depend upon any overt momentum from the child himself other than throwing his arms up because he felt unstable. If such a fall took place, Mr Richards would have anticipated a hairline skull fracture or a fractured clavicle. On the other hand, such a fall was unlikely to cause such severe brain substance injury and subdural haemorrhages. He concluded that it was highly likely that N suffered inflicted NAHI.

[234] Professor Jenny clearly identified the six external head injuries found on N. Her evidence on this point, which we accept, was confirmed by Dr Lawlor. Professor Jenny’s opinion was that N had sustained multiple blunt injuries to the head which were not accounted for by the history of a fall given by his father. Professor Jenny disagreed with the prosecution experts at trial, who had concentrated upon shaking rather than some form of impact causing the injuries.

[235] When considering the triad as a diagnostic tool Professor Jenny regarded the presence of characteristic retinal haemorrhaging as being particularly important in identifying shaking as the mechanism of trauma. She explained that ‘you really have difficulty diagnosing Shaken Baby Syndrome, as opposed to abusive head trauma, if you do not have those retinal haemorrhages, because they seem to be very characteristic of that particular biomechanical event’.

[236] Dr Rorke-Adams’ conclusion was to the same effect, namely that N was subjected to blunt force trauma to the head. She too expressly disagreed with the crown’s experts at trial. Dr Rorke-Adams considered that there was discordance between Faulder’s account and the severity of the injuries to N.

[237] Dr Rorke-Adams, relying firstly upon her interpretation of the CT scans and secondly upon the fact that N experienced a left-sided paralysis after the incident, considered that the primary injury was to the right side of the brain, and therefore was focussed on a particular location rather than being diffuse and evenly distributed throughout the brain. Dr Rorke-Adams was the only witness to put forward this interpretation of the evidence. As a pathologist Dr Rorke-Adams was at a similar disadvantage to Professor Whitwell in this case. Equally, Dr Rorke-Adams is not a radiologist. Dr Jaspan in a very thorough report on the series of scans does not identify any particular difference in presentation between the two sides of the brain. We are therefore cautious about placing undue weight about Dr Rorke-Adams’s conclusion that there was a focal (as opposed to a diffuse) brain injury.

[238] Dr Rorke-Adams conclusion in favour of a focal injury to one part of the brain is the main reason for her dismissing Professor Whitwell’s proposition that the brain injury may be secondary to a stretching injury at the cranio-cervical junction. Given our caution about Dr Rorke-Adams’ view on this point, it follows that we do not feel able to dismiss Professor Whitwell’s opinion on that basis as being untenable.

[239] The prosecution expert on biomechanics, Dr Bertocci, due to the short notice available to her, did not make observations about this case.

Changes in the Crown’s Case

[240] The appellant asserts that the Crown’s case against him at trial has now been changed in three significant respects relating to (1) his account of the fall, (2) whether there was a primary injury to the brain itself and (3) whether the injury was caused by shaking or impact.

(1) The appellant’s account of the fall

[241] The appellant has consistently given an account of N’s fall from his outstretched arm to the effect that N’s head was cupped in his hand and N’s body ran along his forearm. At some stage N arched his back, slipped off the arm and fell, catching his back on a push-chair and his head on the bar of a high-chair before hitting the floor headfirst. At trial, Dr San Lazaro did not accept that a 7 week old child could make sufficient jerking, arching or rolling movement to propel itself from a carer’s arm. That was also the position of a number of the Crown’s experts on paper at the start of this appeal. During oral evidence, as we have already noted, Mr Richards came to accept that N may have fallen in the manner described by Faulder simply as a result of a gravity roll from his insecure position lying along Faulder’s arm. It follows that the prosecution expert testimony is no longer entirely at odds with Faulder’s account on this point.

(2) Causation of brain injury

[242] At trial, Dr Alexander considered that the fall described by Faulder bore no relationship to the severity of the brain injury. His opinion was that the subdural haemorrhages and brain injury were the result of shaking and were the sort of injuries seen ‘in older children who have been hit by a car at 40 mph, spun round and eventually hit the floor’. He described the mechanism for the brain injury by imagining that the brain was similar in substance to porridge, with the shaking causing the brain to accelerate and decelerate many times causing a spinning effect which was ‘just like putting a food mixer inside the brain.’ He further postulated that the trauma to the brain may have interfered with breathing, thereby causing further brain damage. Dr San Lazaro, at trial, explained that only ‘very severe forces’ or ‘severe massive deceleration forces’ would account for the brain injuries which were caused by ‘violent shaking and slamming down’. In the CCRC report for this appeal, Dr Lazaro and Dr Alexander are quoted as stating in letters written to the CCRC in 2001 that N’s injuries included ‘brain contusions’.

[243] At trial, Dr Gholkal, a consultant radiologist, did not positively identify any primary brain injury.

[244] Before us, with the exception of Dr Rorke-Adams, whose opinion relating to a localised focal brain injury we have already described, none of the Crown’s experts suggested that there was evidence of direct trauma to the brain. Dr Jaspan identifies secondary hypoxic-ischaemic injury and asserts that there is no evidence of primary brain injury or brain contusions.

[245] N survived these events and thus the only direct evidence of the condition of his brain is radiological. Given the careful and clear evidence of the prosecution radiologist, Dr Jaspan, on this point we consider that the opinion of both Dr San Lazaro and Dr Alexander that there was primary brain injury is not tenable.

Shaking or Impact

[246] At trial both Dr Alexander and Dr San Lazaro advised that these injuries were caused by very severe shaking. We have already observed that a number of the Crown’s experts on appeal have expressly disagreed with this conclusion. They regard this as a case of N being the victim of a number of blunt impact blows to the head.

[247] This significant change in the case being put against Faulder is of consequence in at least two respects. Firstly, he has never been required to consider, and neither was the jury required to consider, the allegation that he hit N at least five or six times around the head. Secondly, the degree and type of force now relied upon must differ from the ‘hit by a car at 40 mph’ description put forward at trial.

[248] Whilst we note that the judge in describing the central issue in the case to the jury focused upon the defendant’s intention (‘did the defendant deliberately injure the child?’) rather than upon any particular mechanism for injury. The expert evidence presented to the jury was that the severity of primary brain injury could not be explained by Faulder’s account. Before us the position is different in that the injury to the brain substance is broadly accepted to be secondary hypoxic-ischaemic injury. The primary injuries being the external bruising and swelling, the subdural haemorrhages and unexplained encephalopathy (brain failure). Whilst Faulder’s account is not accepted by the Crown, it is nevertheless an account of a series of impacts and is therefore significantly closer to the case now put by the Crown than was the position at the trial.

[249] An essential question raised in Faulder’s appeal is therefore what effect, if any, this change of mechanism and force has upon the central issue of the defendant’s intention.

[250] In summary the prosecution’s position at the conclusion of the appeal differed from the Crown case at trial in the following material respects:

(a) Faulder’s account of N falling from his outstretched arm is now accepted as a possible event;

(b) The brain injury is now seen to be a secondary hypoxic-ischaemia rather than as a result of primary intra-cranial trauma;

(c) The mechanism for injury is now stated to be a number of blunt force impacts to the head, rather than the massive violent shaking mechanism put forward at trial.

Dr San Lazaro

[251] The Amended Grounds of Appeal rely in part upon the fact that Dr San Lazaro’s credibility and impartiality have subsequently been seriously challenged in the case of Lillie v Newcastle City Council (above). It is indeed the case that Eady J considered Dr San Lazaro’s role in a substantial child sexual abuse investigation and, having heard her give evidence, found that, in order to meet what she perceived to be the needs of the children she examined, she was prepared to throw ‘objectivity and scientific rigour to the winds in a highly emotional misrepresentation of the facts’. She was, according to Eady J’s findings, ‘unbalanced, obsessive and lacking in judgment’.

[252] In the event this point was not raised in the appellant’s Skeleton Argument filed at the start of the appeal hearing and did not feature in the written closing submissions. Mr Mansfield QC told us that he was effectively not relying upon this ground in support of Faulder’s appeal. We consider that this was a realistic concession. There is no challenge to the primary evidence of fact given by Dr San Lazaro. If Dr San Lazaro had remained the leading Crown expert in the case, there might well have been some concern arising from Eady J’s findings, however the wealth of medical evidence that has now been acquired indicates that even were her evidence to be totally ignored there is a substantial body of expert opinion that supports the Crown’s case as it is now cast.

Overview of Faulder’s case

[253] We now seek to draw together the various central issues in Faulder’s appeal. Before doing so, it is helpful to highlight the fact that there are now no less than five different explanations for N’s injuries that have been put forward by experts either at trial or on appeal, they are:

(a) Shaking and slamming down involving very severe force (Dr San Lazaro and Dr Alexander at trial);

(b) Non-specific inflicted head injury (Dr Jaspan and Mr Richards) involving secondary, but not primary, brain injury (Dr Jaspan);

(c) Multiple (at least six) blows to the head (Professor Jenny and Dr Rorke-Adams) causing primary localised brain injury (Dr Rorke-Adams);

(d) A bending and stretching injury to the respiratory nerves in the cranio-cervical junction causing a secondary brain damage. On the basis that the minimum degree of force required to cause subdural haemorrhages is unknown, all the symptoms could have been caused in the fall described by Faulder (Professor Whitwell);

(e) A blow to the skull during the fall from Faulder’s arm, causing the baby’s skull temporarily to deform and directly injure the underlying brain substance, which may then hinder respiration and cause secondary brain damage (Dr Plunkett).

[254] On the evidence that is now before the court, there is unanimity that what occurred was primarily an impact injury. The central questions remaining are:

(i) What is the minimum degree of force required to cause these injuries? and

(ii) Might the injuries have been incurred by a fall as described by Faulder?

[255] For the reasons that we have already given, we conclude that there were six separate sites of injury found on N’s head when he was examined at hospital. This is an important finding as whilst three or possibly four impacts could conceivable fit with Mr Faulder’s account, it is not possible to stretch the sequence of events he describes to explain all six injuries.

[256] Coming to a conclusion about the external head injuries is, however, a very much more straightforward task compared to consideration of the internal injuries. Having heard all of the evidence we are not in a position to reject Professor Whitwell’s opinion that the key event was a nerve injury at the cranio-cervical junction. That opinion is based on the Geddes I and II research, which has been largely accepted by the scientific community. If that opinion is correct, then the severity of the brain injury does not arise from the degree of force used, but from the extent to which the brain is starved of oxygen and/or blood. Questions of degree of force, on the Whitwell basis, are confined to the minimum force needed (a) to cause the cranio cervical junction nerve damage and (b) the subdural haemorrhage.

[257] We have already expressed our overall conclusions upon the necessary degree of force in triad cases by stating four general propositions (paras 72-80). Applying those propositions to Faulder’s case we are therefore mindful that there will be rare cases where comparatively minor falls may generate serious injuries and that an infant may be particularly vulnerable to injury at the site of the craniocervical junction as postulated by Professor Whitwell in this case.

[258] In not rejecting Professor Whitwell’s opinion, we have particularly borne in mind Dr Jaspan’s cautious analysis (‘an unequivocal stance cannot be taken’). Dr Jaspan considered that only four of a possible eight signs for NAHI were present. We would add that of those four, only two are direct evidence of a primary event involving force (scalp bruising and subdural haemmorhage) whereas the other two are, or could be, secondary consequences of the primary event (unexplained encephalopathy and secondary hypoixic-ischaemic injury).

[259] There are no retinal haemorrhages in this case. On Professor Jenny’s evidence, that would be a cause for concern were the Crown’s case to have remained one of pure shaking, but is a lesser matter of note in the context of an impact injury.

[260] We have already considered Dr Plunkett’s evidence in relation to the appeals of Rock and Cherry (in particular we summarise our view at [201] above). It is, as we have said, important to look closely at the relevance of Dr Plunkett’s research to each individual case. In relation to Faulder’s appeal we are troubled by Dr Plunkett declining to accept that N had more than

three sites of injury. Our approach has been to evaluate each case by considering all of the symptoms as a whole, as well as individually. Dr Plunkett’s inability to include and account for the six sites of injury must devalue, but not eliminate, the importance of his evidence in this particular case.

[261] The jury were directed to treat Faulder as a man of good character and that is a factor that we too bear in mind. We also have particular regard to the fact that, unlike the Crown case, his account of the key event has been consistent throughout.

[262] If the number of external marks of impact had been four or less we would have little hesitation in holding that there is sufficient within the evidence of Professor Whitwell, when set against the conflicting and contradictory evidence that has, when looked at as a whole, been presented by the Crown, to render this conviction unsafe.

[263] We have approached each of these cases by attempting to look at the evidence as a whole. Do the two or three external marks that fall outside Mr Faulder’s account tip the balance in favour of dismissing the appeal?

[264] In considering this question we are conscious of the fact that this was not a matter that the jury were ever asked to contemplate in this case. In the same regard we consider it is relevant to question how fair it is for the Crown to change its case so radically from ‘very severe shaking’ to ‘at least six blows to the head’ in an attempt to uphold the conviction.

[265] In conclusion we are struck in this appeal by the very radical change in the Crown case; the jury considered one case, shaking, yet that case is now rejected and we have been asked to consider a totally different allegation of multiple blows to the head. During the summing up at trial the jury were told that Dr San Lazaro was ‘very, very experienced’ and ‘specialises in child protection and abuse’ cases. They were also reminded that Dr San Lazaro had said ‘I am as certain as you can be in medicine’ in her opinion that this was a shaking injury. This ‘certain’ opinion from the Crown’s principal witness is now rejected by Crown experts who are equally firm in their own opinion. We have to consider the evidence in its totality, both at trial and before us. There are, as we have observed, now five different explanations put forward by experts for N’s injuries.

[266] In relation to Cherry’s appeal we have stressed that the mere fact that there has been some change in the manner in which the Crown puts its case will not automatically lead to a conclusion that the conviction is unsafe. It will be a matter of fact and degree to be considered in each individual case. In contrast to Cherry’s case, the turnaround in the Crown’s case in Faulder could hardly be more substantial. This factor, coupled with the introduction of potentially credible alternative explanations presented by the defence experts, drives us to the conclusion that, despite the number of bruises found, this conviction must now be considered unsafe. We therefore allow the appeal and quash the conviction.

Final Comments

[267] In earlier sections of this judgment we have made comments on the triad of injuries, the ‘unified hypothesis’-Geddes I, II, III, and some general issues. We do not think it possible or desirable to add anything further to

those observations. In our judgment, these appeals demonstrate that cases of alleged NAHI are fact-specific and will be determined on their individual facts.

[268] We have been asked by Mr Horwell to give some guidance in respect of expert witnesses in cases such as these. In his final submissions Mr Horwell submitted that these appeals demonstrated that there had been a significant failure within the criminal justice system to control and manage expert evidence. He argued that there must be a change in approach and invited the court to consider giving guidance.

[269] Whether or not there has been a failure by the criminal justice system to control and manage expert evidence we are reluctant to give any new guidance on expert evidence arising from the facts of these cases. It may, however, be helpful to re-iterate current guidance.

[270] As to expert evidence generally, the evidential rules as to admissibility are clear (see for example R v Bonython (1984) 38 SASR 45 and R v Clarke (RL) [1995] 2 Cr App R 425 (facial mapping)). We see no reason for special rules where medical experts are involved. There is no single test which can provide a threshold for admissibility in all cases. As R v Clarke demonstrates developments in scientific thinking and techniques should not be kept from the court. Further, in our judgment, developments in scientific thinking should not be kept from the court, simply because they remain at the stage of a hypothesis. Obviously, it is of the first importance that the true status of the expert’s evidence is frankly indicated to the court.

[271] It may be helpful for judges, practitioners and experts to be reminded of the obligations of an expert witness summarised by Cresswell J in National Justice Cia Naviera SA v Prudential Assurance Co Ltd, The Ikarian Reefer [1993] 2 Lloyd’s Rep 68 at 81. Cresswell J pointed out amongst other factors the following, which we summarise as follows:

(1) Expert evidence presented to the court should be and seen to be the independent product of the expert uninfluenced as to form or content by the exigencies of litigation.

(2) An expert witness should provide independent assistance to the court by way of objective unbiased opinion in relation to matters within his expertise. An expert witness in the High Court should never assume the role of advocate.

(3) An expert witness should state the facts or assumptions on which his opinion is based. He should not omit to consider material facts which detract from his concluded opinions.

(4) An expert should make it clear when a particular question or issue falls outside his expertise.

(5) If an expert’s opinion is not properly researched because he considers that insufficient data is available then this must be stated with an indication that the opinion is no more than a provisional one.

(6) If after exchange of reports, an expert witness changes his view on material matters, such change of view should be communicated to the other side without delay and when appropriate to the court.

[272] Wall J, as he then was, sitting in the Family Division also gave helpful guidance for experts giving evidence involving children (see Re AB (child abuse: expert witnesses) [1995] 1 FCR 280). Wall J pointed out that there will be cases in which there is a genuine disagreement on a scientific or medical issue, or where it is necessary for a party to advance a particular hypothesis to explain a given set of facts. He added:

‘Where that occurs, the jury will have to resolve the issue which is raised. Two points must be made. In my view, the expert who advances such a hypothesis owes a very heavy duty to explain to the court that what he is advancing is a hypothesis, that it is controversial (if it is) and placed before the court all material which contradicts the hypothesis. Secondly, he must make all his material available to the other experts in the case. It is the common experience of the courts that the better the experts the more limited their areas of disagreement, and in the forensic context of a contested case relating to children, the objective of the lawyers and the experts should always be to limit the ambit of disagreement on medical issues to the minimum.’

We have substituted the word jury for judge in the above passage.

[273] In our judgment the guidance given by both Cresswell J and Wall J are very relevant to criminal proceedings and should be kept well in mind by both prosecution and defence. The new Criminal Procedure Rules provide wide powers of case management to the court. Rule 24 and para 15 of the plea and case management form make provision for experts to consult together and, if possible, agree points of agreement or disagreement with a summary of reasons. In cases involving allegations of child abuse the judge should be prepared to give directions in respect of expert evidence taking into account the guidance to which we have just referred. If this guidance is borne in mind and the directions made are clear and adhered to, it ought to be possible to narrow the areas of dispute before trial and limit the volume of expert evidence which the jury will have to consider.

[274] We see nothing new in the above observations.

[275] Lastly, we wish to express our gratitude to all counsel, solicitors and the many expert witnesses for the prodigious amount of work and time which they have given to these appeals. Cases of this sort raise difficult and complex medical issues. The court is very dependent upon the skill of the advocates and the ability of the witnesses to elucidate the evidence and inform the court on the issues involved. We have received enormous assistance from all concerned and pay tribute to their efforts.

DISPOSITION:
Appeal allowed.

Public Prosecutor v. Lin Lian Chen [1992] 2 MLJ 561:

Tarmizi bin Yacob & Anor v Public Prosecutor and another appeal FEDERAL COURT (PUTRAJAYA) ARIFIN ZAKARIA CJ (MALAYA), RICHARD MALANJUM CJ (SABAH AND SARAWAK) AND JAMES FOONG FCJ CRIMINAL APPEAL NOS 05–37 OF 2004 (W) AND 05–38 OF 2004 (W) Federal Court:

[2011] 4 MLJ 1
Tarmizi bin Yacob & Anor v Public Prosecutor and another appeal
FEDERAL COURT (PUTRAJAYA)

ARIFIN ZAKARIA CJ (MALAYA), RICHARD MALANJUM CJ (SABAH AND SARAWAK) AND JAMES FOONG FCJ

CRIMINAL APPEAL NOS 05–37 OF 2004 (W) AND 05–38 OF 2004 (W)

27 July 2010
Criminal Procedure — Prosecution — Consent of public prosecutor — Charge amended from s 39B(1)(a) to s 39B(1)(c) of the Dangerous Drugs Act 1952 — Amendment made by deputy public prosecutor at trial — Whether trial a nullity — Whether informer should have been called to testify — Whether appellants acted together with common intention in preparing sale of cannabis

The appellants in both the appeals herein were convicted under s 39B(1)(c) of the Dangerous Drugs Act 1952 (‘DDA’) and sentenced to death. Their appeal to the Federal Court was against the dismissal of their respective appeals to the Court of Appeal against conviction and sentence. Initially both appellants were charged under s 39B(1)(a) of the DDA but at the end of the prosecution’s case the deputy public prosecutor amended the charge to one under s 39B(1)(c), to wit, that they, in furtherance of a common intention, carried out an act preparatory to or for the purpose of trafficking in 2,996.4g cannabis.

The prosecution’s narration of the events was that a chief inspector of police (PW10), posing as a drug buyer, was introduced by his informer (‘Mud’) to the second appellant to discuss the purchase of cannabis. At the appointed time and place for the sale and purchase to take place PW10 met with both appellants. While PW10 and the second appellant waited, the first appellant went to get the drugs and returned in about 20 minutes carrying a bag from which the first appellant took out and showed the cannabis to PW10. PW10 signalled the police party that lay in ambush observing the proceedings. The appellants fled on seeing the police approaching; the first appellant throwing away the bag he was carrying as he fled. Both appellants were apprehended by the police after a brief struggle. In calling for their defence the trial court found as a fact that both appellants had a common intention in acting together to ensure the sale of the cannabis and that they had knowledge of the drugs as inferred from their attempts to resist arrest and escape the police party and the act of the first appellant in throwing away the bag containing the drugs. Their defence failed to cast any reasonable doubt on the prosecution’s case. In the Federal Court the appellants submitted that (i) the trial was a nullity because the public prosecutor had not consented to the charge being amended (ii) the prosecution ought to have called the informer ‘Mud’ to testify and/or offered him to the defence (iii) as the second appellant only negotiated the sale of the

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cannabis with PW10 and was never in possession of the drugs he was not involved in trafficking and (iv) as the first appellant did not participate in the negotiations or in the preparatory act but only had custody and control of the cannabis he should be found guilty of only possession and not trafficking.The prosecution replied that (i) consent to the amended charge was superfluous as the prosecution was conducted by a deputy public prosecutor (ii) Mud was not an agent provocateur but only an informer whose identity was protected by s 40 of the DDA. Mud merely introduced the second appellant to PW10 and did nothing else and (iii) the appellants acted together, with a common intention, to sell the cannabis to PW10.

Held, dismissing the appeals and affirming the appellants’ conviction and sentence:

  • (1)
    Consent of the public prosecutor to the amended charge was superfluous as the prosecution was conducted by the deputy public prosecutor in which case the consent of the public prosecutor was implicit in his actions and no further written consent of the public prosecutor was required:Garmaz s/o Pakhar & Anor v Public Prosecutor [1995] 3 SLR 701 followed. Public Prosecutor v Lee Chwee Kiok [1979] 1 MLJ 45 not followed (see paras 35 & 33).
  • (2)
    There was no necessity for the evidence of Mud in the narrative of the prosecution’s case. It was not disputed that the only role Mud played was to introduce PW10 to the second appellant. Just because Mud was known to the second appellant did not make him an agent provocateur (see para 43).
  • (3)
    In this case the trafficking was the sale of cannabis or the purchase of it by PW10. What transpired on the night of 5 April 1996 was the final chapter in the preparation of the trafficking of the drugs which constituted the supply and delivery of 3kg of the cannabis by the first appellant for the purpose of both the appellants jointly handing it over to PW10 in exchange for payment as earlier agreed. There was common intention to ensure the sale of the cannabis to PW10 (see paras 48 & 49).
  • (4)
    To constitute actual delivery it was not necessary that the agreed price had to be paid upon or before the physical delivery of the drugs. Here, the transaction was completed when the appellants produced the cannabis to PW10 and were only waiting for payment (see para 50).
  • (5)
    There was no misdirection in the evaluation of the evidence adduced or in the standard of proof applied by the trial judge in coming to his decision. Overwhelming evidence was adduced showing the roles played by the appellants to make the cannabis available to PW10 for purchase. The very act of each of them attempting to flee from the scene to avoid

    4 MLJ 1 at 3

    arrest by the police was a clear indication both of them knew what they were dealing in with PW10 (see paras 51 & 52).

Perayu-perayu di dalam kedua-dua rayuan telah disabitkan di bawah s 39B(1)(c) Akta Dadah Berbahaya 1952 (‘ADB’) dan telah dihukum mati. Rayuan mereka kepada Mahkamah Persekutuan adalah terhadap penolakan rayuan mereka masing-masing kepada Mahkamah Rayuan terhadap sabitan dan hukuman. Pada awalnya, kedua-dua perayu telah dituduh di bawah s 39B(1)(a) ADB tetapi pada akhir kes pihak pendakwaan timbalan pendakwa raya telah meminda tuduhan kepada satu yang tertakluk di bawah s 39B(1)(c), iaitu, bahawa mereka, sebagai lanjutan niat bersama, telah melakukan tindakan persediaan kepada atau bagi tujuan pengedaran 2,996.4g kanabis. Penceritaan kejadian pihak pendakwaan adalah bahawa ketua penyiasat polis (‘PW10’), menyamar sebagai pembeli dadah, telah diperkenalkan oleh pemberi maklumat (‘Mud’) kepada perayu kedua untuk berbincang tentang pembelian kanabis. Pada masa dan tempat yang ditetapkan bagi jual beli tersebut, PW10 bertemu dengan kedua-dua perayu. Sementara PW10 dan perayu kedua sedang menunggu, perayu pertama pergi mendapatkan dadah dan pulang selepas 20 minit membawa beg di mana perayu mengeluarkan dan menunjukkan kanabis kepada PW10. PW10 memberi isyarat kepada pihak polis yang sedang berselindung di dalam belukar dan memerhatikan prosiding tersebut. Perayu-perayu terus melarikan diri apabila melihat kedatangan polis; perayu pertama membuang beg yang dibawanya semasa dia melarikan diri. Kedua-dua perayu telah ditangkap oleh polis selepas pergelutan singkat. Dalam memanggil pembelaan mereka, mahkamah perbicaraan mendapati adalah fakta bahawa kedua-kedua perayu mempunyai niat bersama untuk bertindak bersesama untuk memastikan jualan kanabis dan bahawa mereka mempunyai pengetahuan tentang dadah tersebut melihatkan kepada percubaan mereka untuk mengelakkan diri daripada ditahan dan melarikan diri daripada pihak polis dan tindakan perayu pertama membuang beg yang mengandungi dadah tersebut. Pembelaan mereka gagal untuk meletakkan sebarang keraguan berpatutan ke atas kes pendakwaan.

Dalam Mahkamah Persekutuan, perayu-perayu berhujah bahawa (i) perbicaraan adalah terbatal oleh kerana pendakwa raya tidak memberi kebenaran terhadap tuduhan yang dipinda; (ii) pihak pendakwaan sepatutnya memanggil pemberi maklumat ‘Mud’ untuk memberi keterangan dan/atau menawarkannya kepada pembelaan; (iii) memandangkan perayu kedua hanya berunding tentang penjualan kanabis dengan PW10 dan tidak pernah dalam milikan dadah tersebut, dia tidak terbabit dalam pengedaran; dan (iv) memandangkan perayu pertama tidak terlibat dalam perundingan atau tindakan persediaan tetapi hanya mempunyai jagaan dan kawalan kanabis tersebut, dia patut didapati bersalah hanya untuk milikan dan bukan untuk pengedaran. Pihak pendakwaan membalas bahawa (i) kebenaran kepada tuduhan yang dipinda tidak diperlukan memandangkan pendakwaan telah

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dilakukan oleh timbalan pendakwa raya (ii) Mud bukanlah ejen perangkap tetapi hanya pemberi maklumat yang mana identitinya dilindungi oleh s 40ADB. Mud sekadar memperkenalkan perayu kedua kepada PW10 dan tidak lebih dari itu; dan (iii) perayu-perayu bertindak bersama-sama, dengan niat bersama untuk menjual kanabis kepada PW10.

Diputuskan, menolak rayuan dan mengesahkan sabitan dan hukuman perayu-perayu:

  • (1)
    Kebenaran pendakwa raya untuk tuduhan yang dipinda adalah tidak perlu memandangkan pendakwaan telah dilakukan oleh timbalan pendakwa raya di mana kebenaran pendakwa raya adalah tersirat daripada tindakannya dan kebenaran bertulis selanjutnya oleh pendakwa raya adalah tidak perlu: Garmaz s/o Pakhar & Anor v Public Prosecutor [1995] 3 SLR 701 diikut; Public Prosecutor v Lee Chwee Kiok [1979] 1 MLJ 45 tidak diikut (lihat perenggan 35 & 33).
  • (2)
    Keterangan Mud adalah tidak perlu di dalam penceritaan kes pihak pendakwaan. Tidak dapat dipertikaikan bahawa peranan yang dimainkan oleh Mud hanyalah untuk memperkenalkan PW10 kepada perayu kedua. Hanya kerana Mud dikenali oleh perayu kedua tidak bermakna dia adalah ejen perangkap (lihat perenggan 43).
  • (3)
    Dalam kes ini pengedaran tersebut adalah penjualan kanabis atau pembeliannya oleh PW10. Apa yang berlaku pada malam 5 April 1996 adalah bab terakhir dalam persediaan untuk pengedaran dadah yang mana membawa kepada bekalan dan penyerahan 3kg kanabis oleh perayu pertama bagi tujuan untuk diberikan kepada PW10 oleh kedua-dua perayu sebagai ganti untuk pembayaran yang dipersetujui sebelum itu. Terdapat niat bersama untuk memastikan penjualan kanabis kepada PW10(lihat perenggan 48 & 49).
  • (4)
    Untuk membentuk penyerahan sebenar, adalah tidak perlu bahawa harga yang dipersetujui hendaklah dibayar apabila atau sebelum penyerahan fizikal dadah tersebut. Di sini, transaksi telah disempurnakan apabila perayu-perayu menyediakan kanabis kepada PW10 dan hanya menunggu untuk bayaran (lihat perenggan 50).
  • (5)
    Tidak terdapat salah arah dalam penilaian keterangan yang dikemukakan atau standard pembuktian yang digunakan oleh hakim bicara dalam membuat keputusannya. Keterangan kukuh yang dikemukakan menunjukkan peranan yang dimainkan oleh perayu-perayu untuk menyediakan kanabis untuk pembelian oleh PW10. Tindakan setiap daripada mereka yang cuba untuk melarikan diri daripada tempat kejadian untuk mengelakkan diri daripada ditahan oleh polis adalah petunjuk yang jelas bahawa kedua-duanya tahu akan urusniaga mereka dengan PW10 (lihat perenggan 51 & 52).
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Notes

For cases on consent of Public Prosecutor to prosecute, see 5(2) Mallal’s Digest (4th Ed, 2010 Reissue) paras 3093–3095.

Cases referred to

Garmaz s/o Pakhar & Anor v PP [1995] 3 SLR 701, HC (refd)

Gnanasegaran a/l Pararajasingam v PP [1997] 3 MLJ 1, CA (refd)

Lee Lee Chong v PP [1998] 4 MLJ 697, CA (refd)

Pendakwa Raya v Mansor bin Mohd Rashid & Anor [1996] 3 MLJ 560, FC (refd)

PP v Lee Chwee Kiok [1979] 1 MLJ 45 (refd)

PP v Sa’ari Jusoh [2007] 2 CLJ 197, FC (refd)

Ti Chuee Hiang v PP [1995] 2 MLJ 433, SC (refd)

Legislation referred to

Dangerous Drugs Act 1952 ss 2, 39B(1)(a), (1)(c), 39B(2), 40A

Penal Code s 34

Appeal From: Criminal Appeal Nos W–05–53 of 1997 and W–05–54 of 1997 (Court of Appeal, Putrajaya).
Gurbachan Singh (Ratnam with him) (Bachan & Kartar) for the appellants.
Ahmad Bache (Deputy Public Prosecutor, Attorney General’s Chambers) for the respondent.
Jaya Prakash watching brief for the Indonesian Consulate.

Richard Malanjum FCJ (delivering judgment of the court)
INTRODUCTION

[1] There are two appeals before us heard together. In both the appeals the respective appellants were convicted and sentenced to death on the amended charge under s 39B(1)(c) of the Dangerous Drugs Act 1952 (‘the Act’) read with s 34 of the Penal Code and punishable under s 39B(2) of the Act by the High Court Kuala Lumpur on 5 August 1997. Their respective appeals to the Court of Appeal were dismissed on 2 December 2004. They now appeal to this court on 15 grounds of appeal.

[2] Initially both the appellants were charged under s 39B(1)(a) of the Act read with s 34 of the same Code and punishable under s 39B(2) of the Act. However, at the end of the case for the prosecution the learned deputy public prosecutor amended the charge to one of s 39B(1)(c) of the Act.

[3] In this judgment the appellant in the first appeal is described as the first appellant and the appellant in the second appeal as the second appellant and

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together as the appellants.

FACTUAL BACKGROUNDS

[4] The amended charge preferred against the appellants in the High Court reads:

Bahawa kamu bersama-sama pada 5 April 1996, lebih kurang 9.45 malam, di Jalan Raja Alang, Kampung Baru, Kuala Lumpur, Wilayah Persekutuan, dalam mencapai niat bersama, kamu telah di pihak kamu melakukan satu perbuatan persediaan untuk mengedar dadah berbahaya, iaitu 2996.4 gram cannabis, suatu kesalahan di bawah seksyen 39B(1)(c)Akta Dadah Berbahaya 1952 (Disemak 1980) dibaca bersama dengan seksyen 34 Kanun Keseksaan dan boleh dihukum di bawah seksyen 39B(2)Akta Dadah Berbahaya 1952.

[5] It is the case for the prosecution that on 4 April 1996 at around 5pm. Chief Inspector Amir Hamzah bin Hanudin (‘PW10’) from the Unit Risikan Jenayah Ibu Pejabat Bukit Aman, acting as a drug buyer, was introduced by his source a person known as Mud to Agam, the second appellant, an Indonesian, at the Restoran Hashimah Paya Jaras, Sungai Buluh.

[6] After Mud had introduced PW10 to the second appellant he asked Mud to leave. PW10 then began discussion with the second appellant. PW10 informed the second appellant that he wished to buy 10 kilo of drugs ‘ganja’ (‘cannabis’). The second appellant agreed to supply at the price of RM1,700 per kilo. PW10 did not agree on the price. Further negotiation took place on the price and it was finally agreed at RM1,600 per kilo. The second appellant then told PW10 that the cannabis was at Kampung Baru, Kuala Lumpur in the area of Jalan Raja Alang and could only be collected in the evening or at night.

[7] At about 7pm on the same evening the second appellant invited PW10 to come with him to Kampung Baru to collect the cannabis. PW10 drove his car, a red GTO Mitsubishi with registration No WDX 983. The second appellant sat on the passenger seat.

[8] On arrival at the place the second appellant went out for 15–20 minutes but only to come back to say that the cannabis was not yet available. The second appellant then told PW10 they were to return to Paya Jaras and on the way back the second appellant informed PW10 that the cannabis could not be obtained that evening as it was not safe to do so. The second appellant then said to PW10 that he could get someone to deliver the cannabis at Paya Jaras with an additional payment of RM300. PW10 disagreed and advised the second appellant that if there was any further development he was to call him on his

4 MLJ 1 at 7

mobile phone. In reply the second appellant asked PW10 to come to Kampung Baru at the same location around 3pm the next day.[9] At around 11.30am the next day PW10 went to the Operation Room of the Narcotics Department Task Force of the Bukit Aman Police Headquarters at Cheras to brief the members of the task force (‘the police’) on the pending transaction at Jalan Raja Alang Kampung Baru in which he would pose as a buyer of the cannabis.

[10] It was therefore agreed during the briefing:

  • (a)
    that the police would focus on the agreed location;
  • (b)
    that PW10 would used the same car; and
  • (c)
    that the police would move to ambush only after PW10 had given the signal by opening the boot of his car.

[11] At around 7.50pm on 5 April 1996 the second appellant called PW10 on his mobile phone. The first four calls of the same number PW10 did not answer. It was only the fifth call that he answered and it was the second appellant.

[12] Over the phone the second appellant told PW10 that the cannabis was available and that PW10 was to come to Jalan Raja Alang in front of Yuli Clinic at around 9pm. PW10 agreed.

[13] PW10 then informed the police who were with him at the Golf Club PDRM of the agreed location and emphasised to them that the seller would be entering his car.

[14] PW10 arrived at the designated location at about 9.10pm and knew that the police had also arrived due to the presence of one member in short pants near the public telephone booth. PW10 parked his car under a street light in order to have clear sight of what might happen.

[15] At about 9.20pm the second appellant arrived with another person introduced to PW10 as Tarmizi, the first appellant. PW10 asked both of them to enter his car. The first appellant was seated on the front passenger seat while the second appellant was at the back seat. The first appellant proceeded to inform PW10 that he only had 3kg of the cannabis. PW10 agreed to buy and the first appellant asked for payment.

[16] When the first appellant asked for the money PW10 showed him and said that he would only pay upon seeing the cannabis. The first appellant

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therefore went out of the car walking to the rear of the car towards a corner not far from it. PW10 then asked the second appellant to come to the front seat.[17] While waiting for the first appellant PW10 was informed by the second appellant that only 3kg could be obtained for the transaction but he would arrange again next time.

[18] After about 15–20 minutes the first appellant came back. PW10 asked the second appellant to come out with him and moved to the rear of the car. The three met at the rear of the car. The first appellant told PW10 he had the cannabis inside the bag he was carrying. The first appellant brought it in front of PW10 and the second appellant. From inside the bag the first appellant proceeded to take out a compact bundle wrapped with transparent plastics. PW10 smelt it, looked at it and pressed it before suspecting it was cannabis.

[19] The first appellant and second appellant asked PW10 to be quick. PW10 went to get the money inside the car but at the same time pulling the lever to open the boot to signal the police to act. At that time the cannabis was still with the first appellant. When PW10 was about to return to the rear of the car he saw the police heading for the first appellant and second appellant. PW10 went back into his car, turned on the engine and sped off.

[20] The transaction between PW10 and the appellants were witnessed by Chief Inspector Fisol (‘PW5’) who led the police that night and Det Cpl Rosdi (‘PW8’). They were about 10–15 meters away from the car of PW10. They identified the first appellant as a tall, well-built man wearing a red short–sleeve T–shirt and dark jeans while the second appellant was wearing a white T–shirt and dark pants.

[21] When the signal to act came on PW5 and PW8 ran to apprehend the first appellant and second appellant respectively. However after a struggle with PW5 the first appellant managed to free himself and threw away the bag he was carrying before running away. PW5 did not pursue him but stayed back to watch over the bag thrown by the first appellant. It was Inspector Zambri who made another attempt to apprehend the first appellant. He too failed. He was injured when he was pushed and fell down. The first appellant was then pursued by Det Cpl Khalid (‘PW7’) who managed to arrest him after firing two shots at him and injuring his right leg. Several members of the police also came to assist PW7. The second appellant also tried to escape but was caught by PW8 with the help of Det Sjn Abdullah.

[22] The first appellant and second appellant were both identified by PW7 and PW8 as the two persons with PW10 that night based on their clothing.

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[23] After the arrest of the first appellant and second appellant PW5 examined the content of the bag in their presence. PW5 found three compressed slabs suspected to be cannabis. PW6, the chemist, (Cheong Meow Kioon) did the analysis of the three slabs seized by the police. In his evidence PW6 said that he was given three compressed slabs of plant material wrapped with plastic sheet and secured with adhesive tape. He found the nett weight of each slab to be 1,018.4g, 991.4g and 986.6g respectively and giving the total weight of 2,996.4g. And after he had carried out the essential analysis on the three slabs by way of several established and accepted tests he found all the plant material of the three slabs to be cannabis as defined in s 2 of the Act.

[24] At the end of the case for the prosecution and after giving the maximum evaluation of the evidence adduced by the prosecution the learned High Court judge called for the defence of both the first appellant and second appellant. In doing so he made several findings of fact related to the issues raised by learned counsel for the first appellant and second appellant, inter alia:

  • (a)
    that the first appellant and second appellant were identified by PW10 and corroborated by PW5, PW7 and PW8. In addition both the first appellant and second appellant were arrested at the scene of the event;
  • (b)
    that the identification of the first appellant and second appellant was possible that night since the views of the prosecution’s witnesses who observed the event were not hampered. There were street lights and building lights in the vicinity;
  • (c)
    that PW6 concluded that the three slabs he analysed were cannabis as defined in s 2 of the Act;
  • (d)
    that the first appellant and second appellant had the common intention since they acted together in the preparation for the sale of the cannabis; and
  • (e)
    that the first appellant and second appellant had knowledge of the cannabis. The acts of the first appellant in struggling with the police to resist arrest, throwing the bag containing the cannabis and running away indicated such knowledge. And so was the second appellant who also struggled with the police in an attempt to escape.

[25] The learned trial High Court judge did not think that the failure by the Prosecution to tender as evidence the Police Report Dang Wangi No 7049/96 had jeopardised the prosecution’s case as he opined it was not a first information report. And neither did the learned trial High Court judge find any break in the chain of evidence adduced by the prosecution. The evidence of PW10 was also held to be admissible under s 40A of the Act.

4 MLJ 1 at 10

[26] In his unsworn statement the first appellant said that he happened to be at the scene of the event when he heard shouts of ‘Polis, polis, polis’. As he was an illegal immigrant and feared of being apprehended he ran off. In the process he dropped his watch and while looking for it he heard a gun shot and felt pain on his right thigh. He fainted.

[27] The learned trial High Court judge did not find the version of the first appellant as having cast any reasonable doubt in the prosecution’s case. His reasons were as follows:

  • (a)
    that the first appellant did not deny that he was at the scene of the event that night;
  • (b)
    that there was no reason why the police would go for the first appellant if indeed there were other people in the vicinity at that time. Further it was illogical for the first appellant to say that he ran away as he was an illegal immigrant yet gave his watch a priority when he stopped to look for it at the risk of being arrested; and
  • (c)
    that there was nothing in the statement of the first appellant to contradict the evidence of the prosecution that at that time he was carrying a bag containing the cannabis and which he threw away when the police wanted to arrest him.

[28] The second appellant also made an unsworn statement from the dock. He said that on 4 April 1996 he did meet Mud with another person introduced to him as Abang Jo at the restaurant in Paya Jaras. While at the restaurant Mud and Abang Jo agreed to meet at Jalan Raja Alang the next day. The second appellant went on to say that he met Mud on 5 April 1996 at Jalan Raja Alang. Mud told him that there was a man in a car who asked him to go in. The second appellant said that he followed but did not enter the car. Then suddenly he heard gun shots and the shouts of ‘Polis, polis’. He was subsequently arrested.

[29] Having heard the version of the second appellant the learned trial High Court judge did not find it having cast any reasonable doubt on the prosecution’s case for the following reasons:

  • (a)
    the second appellant did not deny that he was at the scene of the event that night;
  • (b)
    the second appellant did not say who was the man inside the car;
  • (c)
    the second appellant did not deny that he struggled with the police; and
  • (d)
    there was no reason or even suggested reason why the police would arrest the second appellant.
4 MLJ 1 at 11

[30] The learned trial High Court judge thus found both the first appellant and second appellant guilty of the charge preferred against them. He convicted and sentenced them accordingly.

[31] The Court of Appeal dismissed the respective appeals of the appellants. Briefly, the Court of Appeal held:

  • (a)
    that preparatory act for the purpose of trafficking drugs consists of several continuing acts;
  • (b)
    that the evidence of the chemist (‘PW6’) was credible. There was no necessity for him to show in detail what he did in his laboratory; and
  • (c)
    that the consent of the public prosecutor was implied in this case since the prosecution was conducted by a deputy public prosecutor.

[32] Before us learned counsel for the appellants only pursued grounds of Appeal Nos 13, 14 and 15. But he raised the issue of absence of consent of the public prosecutor for the amended charge.

ISSUE OF CONSENT ON THE AMENDED CHARGE

[33] Learned counsel for the appellants submitted that the trial of his clients was a nullity in view of the absence of consent to the amended charge preferred against them at the close of the case for the prosecution. He cited the case of Public Prosecutor v Lee Chwee Kiok [1979] 1 MLJ 45. In that case the original charge was under s 39B(1)(a) of the Act but on the day of trial the learned deputy public prosecutor amended it to s 39A(1)(c) of the same Act. Harun J (as he then was) said this at p 1:

It will be observed that although the original and amended charges are two distinct offences, they are both created by the same section of the law viz s 39B(1) and both carry the same penalty. Both require the consent of the public prosecutor under s 39B(3). The learned deputy public prosecutor argued that the amendment was technical and as the public prosecutor had given his consent on the original charge he was at liberty to amend the charges in the manner he did. I do not think so. It was held in Abdul Hamid v Public Prosecutor [1956] MLJ 231 that a consent to prosecute ‘is an act of reason, accompanied with deliberation, the mind weighing, as in a balance, the good and evil on each side’. The public prosecutor has clearly exercised his mind in respect of the original charge when he gave his consent to prosecute some four months after the alleged offence. It was incumbent on him however to exercise the same degree of deliberation in respect of the amended charge. He has not done so … The facts of the case were fully before the public prosecutor at the time of giving his consent and he could have elected to proceed on the amended charge then. He did not do so. It would appear therefore that the public prosecutor

4 MLJ 1 at 12

has not given his consent to prosecute under the amended charge. That being so, the trial is a nullity on the authority of Lyn Hong Yap v Public Prosecutor [1956] MLJ 226.

[34] In his response the learned deputy submitted to us that consent would be superfluous in this case as the prosecution was conducted by a deputy public prosecutor. In its judgment the Court of Appeal held the same view.

[35] We agree with the view of the Court of Appeal and the submission of the learned deputy. The law was concisely and correctly summarised by Yong Pung How CJ (Singapore) in Garmaz s/o Pakhar & Anor v Public Prosecutor [1995] 3 SLR 701 when he said this at p 720:

The settled Malaysian position has been to consider a deputy public prosecutor as being capable of exercising all the rights and powers of the public prosecutor … It follows from this proposition that where prosecution is conducted by a DPP, the consent of the public prosecutor is implicit in his actions and no further written consent of the public prosecutor is required. Indeed, this was the holding of the Privy Council inPublic Prosecutor v Oie Hee Koi [1968] 1 MLJ 148. The ruling in Public Prosecutor v Oie Hee Koi [1968] 1 MLJ 148 was followed inPerumal v Public Prosecutor [1970] 2 MLJ 265, Public Prosecutor v Mohamed Halipah [1982] 1 MLJ 155, Public Prosecutor v Datuk Haji Dzulkifli [1982] 1 MLJ 340 and Public Prosecutor v Lim Boon Hock [1985] 2 MLJ 219.

[36] The learned Chief Justice also noted that in Public Prosecutor v Lee Chwee Kiok Harun J (as he then was) had not been referred to the Privy Council decision in Public Prosecutor v Oie Hee Koi.

[37] And in fact Yusof Abdul Rashid J in Public Prosecutor v Mohamed Halipah declined to follow the judgment of Harun J. He preferred to follow Public Prosecutor v Oie Hee Koi and said this at p 159:

It is to be noted that in the above case the prosecution was conducted before the High Court by a deputy public prosecutor who under the Criminal Procedure Code is vested with all the powers of the public prosecutor. On the authority of this case, it is clear that where the prosecution is conducted by a deputy public prosecutor the consent of the public prosecutor is implicit in his action and no written consent of the public prosecutor is required.

[38] In another case of Gnanasegaran a/l Pararajasingam v Public Prosecutor [1997] 3 MLJ 1 Mahadev Shankar JCA said this at pp 13–14:

If a deputy public prosecutor is present and goes on record when the accused is called upon to plead to an offence under this Act, no separate consent should be required (see Lyn Hong Yap v Public Prosecutor [1956] MLJ 226 and Perumal v Public Prosecutor [1970] 2 MLJ 265).

4 MLJ 1 at 13

[39] As such we find no merit in the contention of learned counsel for the appellants on the issue of absence of consent of the public prosecutor in respect of the amended charge.

GROUND 13 — THE FAILURE TO CALL AS A WITNESS THE INFORMER, MUD

[40] Next, learned counsel for the appellants argued that the learned judges of the Court of Appeal ‘erred and misdirected themselves in law and in fact in not holding that the informer (Mud) ought to have been called by the prosecution to unfold the narrative of the Prosecution’s case and/or offered him to the defence’. Learned counsel contended that PW10 was introduced by Mud to the second appellant and thus Mud must have been known to the second appellant. He cited the case of Ti Chuee Hiang v Public Prosecutor [1995] 2 MLJ 433 to support his contention.

[41] Learned deputy replied that Mud was only an informer hence his identity was protected by s 40 of the Act. He pointed out that Mud merely introduced the second appellant to PW10 and did nothing else. As such he was an Informer and not an agent provocateur. The learned deputy went on to say that Mud did less than the informer in Pendakwa Raya v Mansor bin Mohd Rashid & Anor [1996] 3 MLJ 560 yet the Federal Court in that case ruled that the informer was not an agent provocateur when it said this at p 578:

In Munusamy v Public Prosecutor [1987] 1 MLJ 492 (SC), Mohd Azmi SCJ (now FCJ) in delivering the judgment of the court, opined (at p 494) that ‘whether a person is an informer or has become an active agent provocateur would depend on the facts of each particular case’. In our instant case under appeal though Cholar introduced PW9 to the second respondent and was present when both transactions involving cannabis were struck, there was no evidence that he had done anything apart from being present. It appears obvious that his presence during the negotiation process and the transactions was merely to lend credence to PW9’s intention to purchase the cannabis in the minds of the respondents.

On the particular facts and circumstances of the instant case under appeal, we are of the view that Cholar was not an agent provocateur. But even if he was, there is more than sufficient credible evidence of the respondents’ involvement in the negotiation and agreement to sell to PW9 the 902g of cannabis subsequently brought out by the second respondent from room ‘K’ in the said house.

[42] In its judgment the Court of Appeal held that the role of Mud in this case was merely to introduce the second appellant to PW10 unlike the informer in Ti Chuee Hiang v Public Prosecutor who played an active role as an agent provocateur to arrange for the accused to meet the police and subsequently for his arrest.

4 MLJ 1 at 14

[43] We have perused the whole evidence adduced. We are of the view that there was no necessity for the evidence of Mud in the narrative of the prosecution’s case. In fact it was not disputed that the only role of Mud was to introduce PW10 to the second appellant. Just because Mud was known to the second appellant did not make him an agent provocateur. We therefore agree with the view of the Court of Appeal that the role of Mud could not be compared to that of the informer in Ti Chuee Hiang v Public Prosecutor ‘who had enticed the appellant to walk into a deliberate trap, which had been planned and organised by PPP Noorhashim and executed by a team of six police officers led by K/Inspector Mohd Amin bin Abd Raof (‘PW3′) who was then attached to Cawangan Anti Dadah, Bukit Aman, Kuala Lumpur, on the date and at the time and place referred to in the charge’.

[44] Accordingly, we also find no merit in this issue as raised by learned counsel for the appellants.

GROUNDS 14 AND 15 — CUSTODY, CONTROL AND POSSESSION OF THE CANNABIS

[45] Learned counsel for the appellants contended that the second appellant only did the negotiation with PW10 and he was not in possession of the cannabis. As such there was no question of him involved in the trafficking of the cannabis.

[46] In respect of the first appellant’s learned counsel argued that he did not participate in the negotiation or in the preparatory act. He only had the custody and control of the cannabis. As such the presumption of possession applied and thus he should only be guilty of possession and not for trafficking. The case of Public Prosecutor v Sa’ari Jusoh [2007] 2 CLJ 197 was cited in support.

[47] In response the learned deputy submitted that the appellants were charged with common intention for the offence. And that the evidence adduced must be considered as a whole including the overwhelming evidence that the appellants acted together to effect the sale of the cannabis to PW10.

[48] On this issue the Court of Appeal held that the preparatory act for the purpose of trafficking drugs covers a number of continuing acts. It begins from an agreement until the successful handing over of the drugs to another party. The acts in between carried out to achieve the purpose included such acts as getting the supply, wrapping, sending and meeting between the parties. In this case the trafficking was the sale of cannabis or the purchase of it by PW10. And what transpired on the night of 5 April 1996 along Jalan Raja Alang was the final chapter in the preparation of the trafficking of the drugs which

4 MLJ 1 at 15

constituted the supply and delivery of 3kg of the cannabis by the first appellant for the purpose of the first appellant and second appellant jointly handing it over to PW10 in exchange for the payment as earlier agreed.[49] The appellants were charged with common intention to ensure the sale of the cannabis to PW10. And such sale was proved by direct evidence without relying on any of the statutory presumptions in the Act. We are therefore in entire agreement with the view of the Court of Appeal in finding that the contention of learned counsel for the appellants has no merit.

[50] On the issue of delivery it is now a settled law that to constitute actual delivery it is not necessary that the agreed price must be paid upon or before the physical delivery of the drugs (see Wan Mazuki bin Wan Abdullah v Public Prosecutor Criminal Appeal No 05–56 of 2008 (T). As such the decision in Public Prosecutor v Sa’ari Jusoh should not be narrowly construed. And in this case the transaction was in fact completed since the appellants had produced the cannabis to PW10 and were only waiting for the payment when the police moved in to apprehend them.

[51] In respect of the complaint that there was misdirection in the evaluation of the evidence adduced and the standard of proof applied by the learned trial High Court judge before coming to his decision, we agree with the Court of Appeal that there was no such misdirection shown or apparent.

[52] While in essence the basic defence of the appellants was one of mere denial, there were overwhelming evidence adduced indicating the roles played by the first appellant and second appellant in order to make the cannabis available for PW10 to purchase. Indeed the very act of each of them in attempting to flee from the scene and avoiding arrest by the police was one clear indication that both knew what they were dealing in with PW10 (see Lee Lee Chong v Public Prosecutor [1998] 4 MLJ 697).

[53] As learned counsel for the appellants did not pursue the other grounds of appeal we need not have to deal with them. At any rate we are not persuaded that any of them could have made the difference to our conclusion.

[54] The respective appeals of the first appellant and second appellant are therefore dismissed. We affirmed their respective convictions and sentences imposed by the High Court and upheld by the Court of Appeal.

Appeals dismissed and appellant’s conviction and sentence affirmed.

LYN HONG YAP v PUBLIC PROSECUTOR CA KL MATHEW CJ, BROWN AG CJ (S) AND WILSON J FM CRIMINAL REFERENCE NO 2 OF 1953 2 December 1953 [1956] 1 MLJ 226

[1956] 1 MLJ 226
LYN HONG YAP v PUBLIC PROSECUTOR
CA KL

MATHEW CJ, BROWN AG CJ (S) AND WILSON J

FM CRIMINAL REFERENCE NO 2 OF 1953

2 December 1953
Prevention of Corruption Ordinance, 1950, s 12 — Criminal Procedure Code (Cap 6), s 422 — Consent of Public Prosecutor — Validity of consent — Whether want of consent curable — Practice where a consent or sanction is required

In this case the facts proved at the time relating to the question of consent were as follows: On June 13, 1952 the Police applied to the Magistrate at Kuala Kangsar for a summons to issue against the appellant in respect of an offence committed “on a day between 17th and 19th April 1952”. On June 19 the Magistrate made an order for the Summons to issue and it was issued on June 21. On July 1, the Dy. Public Prosecutor signed a document of consent under section 12 of the Prevention of Corruption Ordinance. The charge to which the appellant was called on to plead on July 3 and on which he was tried was that he had committed an offence under section 3(b) of the said Ordinance and punishable under section 3(c). Throughout the trial in the Sessions Court not a word was said by either of the two counsel who at different times represented the appellant as to the validity of the consent of the Public Prosecutor or as to any want of consent. The point was raised for the first time at the hearing of the second appeal and then in answer to a question of Thomson J. the Dy. Public Prosecutor informed the Court after going through his papers that his colleague in office who had signed the consent of July 1, 1952 had in fact given his consent to the institution of the proceedings and indeed had instructed them to be instituted on June 2, 1952, that was some eleven days before the application for process by the Police.

Thomson J. accepted this assurance and dismissed the appeal. The learned Judge held that the want of consent under section 12 of the Prevention of Corruption Ordinance is not an omission that can be cured by reason of section 422 of the Criminal Procedure Code.

The Court of Appeal agreed with the decision of Thomson J. and held that the consent of the Public Prosecutor in this case was not defective, and that the trial of the appellant was not a nullity.

The Court of Appeal further suggested that difficulties which might arise in cases where a consent or sanction is required, could be avoided if the practice were adopted on accompanying every application for a summons or a warrant of arrest with the consent or sanction in writing.

Cases referred to

R v Bates 6 Cr App R 153

R v Metz 11 Cr App R 164

Hori Ram Singh v R AIR 1939 PC 43 50

Gill v R AIR 1948 PC 128 133

Morarka v R AIR 1948 PC 82

Chong Tuck Loong v Public Prosecutor Perak Cr App No 73/1952 — Unreported

THOMSON J

The judgment of the Court below was as follows:

The appellant in this case appeared before the Sessions Court at Kuala Kangsar on 3rd July, 1952, charged with an offence in contravention of section 3 (b) of the Prevention of Corruption Ordinance, 1950. He claimed trial and was represented by Counsel. At the close of the case for the prosecution the learned President decided that there was no case to answer and acquitted and discharged him.

Against that order of acquittal and discharge the Public Prosecutor appealed and on 18th December, 1952, the appeal was allowed, the order of acquittal was set aside and the case was remitted to the Sessions Court to be further dealt with according to law. I am not concerned here with the matters that were at issue in that appeal.

On 22nd January, 1953, the case again came before the Sessions Court when the appellant was represented by a different Counsel. In the event, the appellant was convicted and fined $750 or nine months rigorous imprisonment in default of payment.

Against that conviction appellant appealed on a number of grounds the only ones of which I am concerned with here being certain grounds relating to the question of whether the consent of the Public Prosecutor given under section 12 of the Prevention of Corruption Ordinance was defective and whether therefore the Sessions Court was without jurisdiction and the trial was therefore a nullity.

The facts proved at the time relating to this question of consent are as follows.

On 13th June, 1952, the Police applied to the Magistrate at Kuala Kangsar for a summons to issue against the appellant in respect of an offence committed “on a day between 17th and 19th April, 1952”. On 19th June the Magistrate made an order for the summons to issue and it was issued on 21st June. On 1st July, the Deputy Public Prosecutor signed a document in the following terms:—

Consent under Section 12.

“Under the provisions of section 12 of the Prevention of Corruption Ordinance, 1950, I, Matthew Gilbert Neal, Deputy Public Prosecutor, Perak, hereby consent to the

1956 1 MLJ 226 at 227

prosecution of one LYN HONG YAP for an offence punishable under section 3(b) of the aforesaid Ordinance, alleged to have been committed at Liman, Kati, Kuala Kangsar, between 19th-20th April, 1952.Dated at Ipoh this 1st day of July, 1952.

(Sd.) M. G. Neal,
Deputy Public Prosecutor,
Perak.”

and the charge to which the appellant was called on to plead on 3rd July and on which he was tried was as follows:—

“That you on a day between 17th and 20th April, 1952 at 1.30 p.m. at No. 5 New Village, Liman Kati, in the district of Kuala Kangsar did corruptly agree to give a sum of $50 to an agent, namely, K. Retnasingam, Health Inspector, as an inducement to him to show favour to one Lee Kow in a matter in relation to the said K. Retnasingam’s principal affairs, namely, to grant the said Lee Kow a licence for Coffee and eating shop and that you have thereby committed an offence under Section 3(b) of Prevention of Corruption Ordinance No. 5 of 1950 and punishable under Section 3(c) of the same Ordinance.”

Throughout the trial in the Sessions Court not a word was said by either of the two Counsel who at different times represented the appellant as to the validity of the consent of the Public Prosecutor or as to any want of consent. The point was raised for the first time at the hearing of the second appeal and then in answer to a question by myself the Deputy Public Prosecutor who was appearing for the respondent informed me after going through his papers that his colleague in office who had signed the paper bearing the date 1st July, 1952, had in fact given his consent to the institution of the present proceedings and indeed had instructed them to be instituted on 2nd June, 1952, that is some 11 days before the application for process by the Police.

I accepted that assurance given from the Bar and having considered the other Grounds of Appeal and being of the opinion that it was abundantly clear on the evidence that the appellant had in fact committed the offence charged against him, I dismissed the appeal. I intimated, however, that if I were asked to do so I would give my certificate to allow the matter to be taken further.

The real question which arose on the appeal was not any question of what constitutes or does not constitute a valid consent by the Public Prosecutor but what course this Court should take when such a question is raised for the first time on appeal.

In my opinion the answer is to be found in an examination of the two English cases of Rex v Bates 6 Cr App R 153 and Rex v Metz 11 Cr App R 164.

In Bate’s case the appellant was convicted of an offence under the Explosives Substances Act, 1883, for the prosecution of which the consent of the Attorney-General was required. Although the point was not raised at the trial, and was indeed not raised by the appellant himself in the appeal, Counsel for the Crown stated from the Bar that he had ascertained that the consent of the Attorney-General was in fact not obtained. On that, the Court quashed the conviction on the ground that the absence of the consent of the Attorney-General took away the jurisdiction of the trial Court.

In Metz’s case the appellant had been convicted of an offence against the Trading with the Enemy Act, 1914, for the institution of a prosecution for which the consent of the Attorney-General was necessary. No evidence was given at the trial that such consent had been obtained but at the trial the point of want of consent was not taken. At the hearing of the appeal, Counsel for the Crown informed the Court from the Bar that the fiat of the Attorney-General, which apparently was in writing, had been produced at the Police Court and so came to the Court of trial (the Central Criminal Court) attached to the depositions. The appeal was dismissed. In dismissing it Lord Reading, observed that two points had been taken on behalf of the appellant and went on to say:—

“The first is that it is necessary that the consent of the Attorney-General should be given before a prosecution is instituted; under s. 1(4) of the Trading with the Enemy Act. It is not suggested that the prosecution was in fact instituted without the necessary consent, but it is said that there was no evidence of it at the trial. The point was not taken at the trial. As we now know, the consent was in fact proved at the police court. The document was in Court at the trial, but it was not formally proved. If the point had been taken at the trial the defect would have been immediately cured, so the point is a pure technicality. We do not think it possible for the point now to succeed in this Court when there was an opportunity for counsel to take it in the Court below if he desired.”

He went on to distinguish the case from that of Bates supra as follows:—

“Our attention has been called to the case of Bates, where the objection was taken that consent had not in fact been obtained, which is a totally different matter; it was there pointed out by Lord Alverstone that although the point had not been taken below it was necessary that there should be consent before the prosecution was instituted. No consent had been obtained, so the conviction was quashed.”

I was unable to find any distinction in principle between Metz’s case and the present case. In Metz’s case the Court accepted the assurance of counsel that the consent of the Attorney-General was in fact in existence and in the present case I accepted the assurance of Counsel that the consent of the Deputy Public Prosecutor (which, it is to be remembered, is not required to be in writing) was in fact in existence before the institution of the prosecution. In the circumstances, I did not feel it was necessary to examine the actual evidence on the point that was given at the trial. If Counsel for the appellant had wished to take the point he should have done so at the trial. If he had done so, it would have been open to the prosecution to ask for an adjournment to enable the Deputy Public

1956 1 MLJ 226 at 228

Prosecutor to appear in person when I have no doubt he would have made the same statement as he made at the hearing of the appeal. If an adjournment had not been granted and the point had succeeded the result would have been not an order of acquittal but an order dismissing the complaint and thus it would have been left open to the prosecution to institute further proceedings after a valid consent had been obtained. (See Hori Ram Singh v R AIR 1939 PC 43 50).I was fortified in this view by certain observations made by Lord Simonds in the case of Gill v R AIR 1948 PC 128 133. In that case their Lordships were concerned inter alia with the question of whether a sanction to a prosecution given under section 197 of the Indian Criminal Procedure Code was invalid by reason of the necessary facts not having been laid before the sanctioning authority. An inference had been drawn from certain circumstances that the necessary facts had been laid before the sanctioning authority and Lord Simonds observed:—

“It is an inference, which at this late stage of the proceedings cannot properly be challenged, that the same facts were before the sanctioning authority when the sanction was given. If it was desired to raise such a question, that should have been done at the earliest moment when the prosecution could have supported by evidence the inference which even without it can fairly be drawn.”

I would add that I do not think that what I have said is in any way inconsistent with the judgment of the Privy Council in the case of Morarka v R AIR 1948 PC 82. In that case the appellant had been convicted under an Indian statute relating to the control of cotton clothing which provided that no prosecution under it should be instituted without the previous sanction of the Provincial Government concerned, and the Court held that the sanction which had in fact been given was defective. The only material before the Court apparently consisted of the evidence given at the original trial and I fail to see that the decision has any bearing on the question at issue in the case of Rex v Metz 11 Cr App R 164 supra or in the present case.

In this connection, I have had occasion to consider my own judgment in the case of Chong Tuck Loong v Public Prosecutor Perak Cr App No 73/1952 — Unreported, in which I discussed this question of consent under the Prevention of Corruption Ordinance at some length. In that judgment I made the following observations:—

“… if that section (Section 12) is not complied with the Court has no jurisdiction to try offences under the Ordinance, and I do not think it can be said to be complied with unless it is clear either on the face of the proceedings or as a matter of reasonable inference that the Public Prosecutor (or, by reason of section 376 of the Criminal Procedure Code, the Solicitor-General or a duly appointed Deputy Public Prosecutor) has either taken an active part in the prosecution or has consented to the charges brought against the accused after applying his mind at the lowest to the facta probanda forming the material of these charges.”

In making these observations I was concerned with the particular facts of the case under appeal and my attention had not been invited to Metz’s case. On further consideration I have come to the conclusion that in making these observations I went too far and that they would more accurately state the law if the words, “either on the face of the proceedings or as a matter of reasonable inference” were omitted.

To avoid misunderstanding and to ensure a full examination of the question, I should say that in my opinion want of consent under section 12 of the Prevention of Corruption Ordinance is not an omission that can be cured by reason of section 422 of the Criminal Procedure Code. On that point to my mind the judgment of the Privy Council in the case of Morarka v R AIR 1948 PC 82, supra, is conclusive. It is true that in that case their Lordships were concerned with section 537 Of the Indian Code which does not contain the specific reference to sanctions which occurs in section 422 of our Code. It is to be noted, however, that until 1923 section 537 of the Indian Code did contain a reference to sanctions required under section 195 of that Code (our section 129) which was repealed in that year. An examination of the Indian decisions prior to 1923 (see the cases set out in the A.I.R. Commentary of the Indian Criminal Procedure Code at Vol. III pp. 2984-5) shows that the Indian Courts consistently held that the reference was only to sanctions required under the Indian section 195 and did not include sanctions under any other statutory provision.

MATHEW CJ

COURT OF APPEAL (Criminal Reference).

S. P. Seenivasagam for the appellant.

L. Talog Davies (Federal Counsel) for the respondent.

This is a Reference under section 34 of the Courts Ordinance. The point for our determination is:—

“Whether the consent of the Public Prosecutor in this case was defective and whether the trial of the appellant was thereby a nullity.”

We are in complete agreement with the very full and clear grounds of judgment delivered by Thomson J., and there is nothing that we can profitably add to what has been said therein. In consequence, we hold that the consent of the Public Prosecutor this case is not defective, and that the trial of the appellant was not a nullity.

We would suggest that difficulties of this kind, which might arise in cases where a consent or sanction is required, could be avoided if the practice were adopted of accompanying every application for a summons or a warrant of arrest with the consent or sanction in writing.

Order accordingly.
Solicitors: S Seenivasagam & Sons.