Scottish High Court of Justiciary Decisons

NICHOLAS JOHN PAXTON v. HER MAJESTY'S ADVOCATE [1999] ScotHC 208 (13th August, 1999)

The appellant is Nicholas John Paxton who was convicted at the High Court at Edinburgh of a charge of culpable homicide in that he did on 25 September 1996

The appellant appealed against his conviction on the ground that there had been a miscarriage of justice because the jury had returned a verdict which no reasonable jury, properly directed, could have returned (Section 106(3)(b) of the Criminal Procedure (Scotland) Act 1995). In presenting the appeal, Miss Scott specifically conceded that the jury had been properly directed. On the indictment the charge of culpable homicide was an alternative to charges of supplying methadone and diazepam. The appellant admitted supplying both drugs to the deceased on the occasion in question. His appeal related solely to the jury's conclusion that the methadone supplied by the appellant had caused the deceased's death. Miss Scott therefore accepted that, if his appeal were successful, the court should quash the conviction of culpable homicide and substitute convictions of the two alternative charges of supplying methadone and diazepam.

The essential circumstances of the offence are not in dispute. On the evening of 25 September 1996 the deceased visited the appellant and, in the course of the visit, the deceased asked him for some methadone and diazepam. The deceased was a young man who was inclined to dabble indiscriminately in drugs. The appellant gave him two drinks of methadone, which on the evidence - as the Crown accept - could have amounted in total to 40 ml. but no more. The deceased drank the methadone. The appellant also gave the deceased some diazepam tablets which the deceased consumed. Thereafter he fell asleep - though it is not clear exactly how quickly this happened. The following morning the deceased was found lying dead in the house.

Professor Busuttil and Dr. Fineron carried out a post-mortem examination. They noticed two points of significance: first, both lungs were markedly engorged with blood and swollen but were otherwise unremarkable, and there was no evidence of inhalation of gastric contents; secondly, there was marked swelling of the brain. Although Professor Busuttil regarded the swelling of the brain as of some significance, both he and Dr. Fineron considered that it was really non-specific. The effects on the lungs and brain were clearly secondary. Having carried out their examination of the body of the deceased, however, Professor Busuttil and Dr. Fineron could not determine the cause of the death of this healthy young man. They accordingly took samples which were sent for analysis by toxicologists. The results showed that there was methadone in the deceased's blood in a concentration of 0.25 mg. per litre and there was also diazepam in the blood in a concentration of 0.15 mg. per litre. Methadone was found in an unquantified amount in his urine and in a concentration of 1.29 mg. per kilogram in his liver. The toxicologists' report contained a statement that "the concentration of methadone in the liver lies at the lower end of the range associated with fatal poisoning."

The submissions made in support of the appeal concentrated on the expert evidence as to the significance of the post-mortem findings of methadone. Although the exact way in which the various experts put their views varied, Miss Scott accepted that there was evidence from Professor Busuttil and Dr. Fineron to the effect that consumption of 40 ml. of methadone could be fatal in a "naïve" user - by which was meant a user who did not have a tolerance for methadone at the relevant time. Dr. Okely, an expert drugs analyst and toxicologist, said that, to develop a tolerance, a user would need to take methadone daily for up to 7 to 10 days, and that, unless a person had been taking the drug regularly for the previous seven days, he would be a naïve user for the purposes of toxicity leading to death. On the other hand, there might be a gap of two days in taking the drug and still be a tolerance. Dr. Sole also indicated that it would take anything up to 10 days of continuous use to establish a tolerance. Professor Busuttil said that a tolerance to methadone could be lost very quickly.

The basic evidence for the Crown therefore consisted in the evidence from Miss Deonne Gullan to the effect that the appellant had given the deceased 40 ml. of methadone which he had drunk; evidence that he had then fallen asleep and died in his sleep; evidence that methadone had been found in the deceased's blood in a concentration of 0.25 mg. per litre; expert evidence that drinking 40 ml. of methadone could be fatal for someone who did not have a tolerance for the drug; and finally, evidence that, despite investigation by the expert pathologists, no other cause for the deceased's death had been discovered. Miss Scott submitted that, although this evidence would have entitled a reasonable jury to conclude that the deceased had probably died as a result of taking the methadone, it did not justify the jury in concluding beyond reasonable doubt that the consumption of methadone had caused the deceased's death.

Miss Scott said that the position might have been different if the evidence had shown that the deceased was someone who had never taken methadone. Then the jury would have been entitled to proceed on the basis that he was a naïve user and they could therefore have properly formed the view, beyond a reasonable doubt, that the consumption of 40 ml. of methadone had caused his death. Here, however, as we have narrated, the evidence showed not only that the deceased had a history of taking drugs, but more particularly that he had previously taken methadone. Indeed the appellant was convicted of Charge 1 on the indictment which included an averment that between 1 January 1993 and 31 October 1996 he was concerned in supplying methadone to the deceased. Miss Gullan had given evidence that the appellant would supply methadone to the deceased once a fortnight. There was also an indication from the deceased's medical records that he had admitted to using methadone in about September 1996. In that situation it was not open to the jury, said Miss Scott, to proceed on the basis that on the evening in question the deceased was a naïve user, even though Ruth Hubbard and John Paul Balfour had given evidence that they had been with him during the day and had not seen him taking any methadone. In the light of Dr. Okely's evidence in particular, if the deceased had used methadone sufficiently regularly to develop a tolerance, it could have persisted even though he had not taken any for one or two days before 25 September. At best for the Crown the position about the deceased's consumption of methadone in the days running up to the incident in question was unknown. That was not sufficient: it would only have been if the Crown had proved that, despite his known consumption of the drug, the deceased did not have a tolerance for methadone on 25 September that the expert evidence would have entitled the jury to conclude beyond a reasonable doubt that the methadone supplied by the appellant caused the deceased's death.

The well-known authority of Hendry v. H. M. Advocate 1987 J.C. 63, explaining the earlier case of H. M. Advocate v. McGinlay 1983 S.L.T. 562, shows that it is for the jury rather than for the expert witnesses themselves to determine whether they are satisfied that a cause of death has been established beyond reasonable doubt. Since that is the precise question which the jury must answer, it is regarded as improper to try to elicit an answer to it from the expert witnesses. Any indication to the contrary in McGinlay had been inappropriate. Miss Scott pointed out that in Hendry a Court of Five Judges had explicitly stated, however, that the actual decision in McGinlay had been correct. When that decision was read in the light of the explanation in Hendry, it was authority for the proposition that a jury was not entitled to find a causal link established where the expert witnesses were not prepared to go further than to say that "there was a possible connection" between the assault and the death or that "on a balance of probabilities" such a connection existed. Similarly, in this case it would not be enough if the expert witnesses were not able to express a confident view that the deceased had died as a result of taking the methadone supplied by the appellant. And they could not do so, except on the hypothesis that the deceased did not have a tolerance for methadone on 25 September. Since that hypothesis had not been proved, the Crown's case must fail.

We accept that the evidence led on behalf of the Crown did not positively establish that the deceased did not have a tolerance for methadone on the evening in question. We also accept that the background history was relevant to the confidence with which Professor Busuttil would be able to affirm that the methadone caused the deceased's death. As he said "the level of probability and possibilities will change according to the background history". If the deceased used methadone "regularly in terms of a day", Professor Busuttil considered that it was "only a probable" that the methadone caused his death and the more he used it or was habituated, the lower the probability would be, though it would still be there as a possibility. Information about the deceased's background would therefore help the interpretation of the traces of methadone in the deceased's body. Dr. Fineron agreed with the proposition that in the case of a naïve user the findings of the level of methadone in the deceased's body suggested a high probability that it had been the cause of death. Depending on how regularly the person concerned had used the drug, then, if he had built up a tolerance, Dr. Fineron agreed that that level of methadone was a probable cause of death. He put the matter in much the same way by agreeing that, with information that the deceased did not use methadone, there was a higher probability; with information that he was a regular user, a probability and that without the exact information he was unable to say in terms of probability. Having regard to this evidence and to the fact that there was no evidence as to the exact nature of the deceased's prior consumption, we accept that there was no evidential basis upon which either Professor Busuttil or Dr. Fineron could be understood as saying more than that it was probable that the deceased died as a result of consuming the 40 ml. of methadone supplied by the appellant.

We do not accept, however, that in this case the jury would not, for that reason, have been entitled to find it established beyond a reasonable doubt that the deceased died from the effects of the methadone. In McGinlay, on which Miss Scott relied, the deceased had died of a heart attack. The cause of his death was therefore not in dispute. The issue was whether the force used in the assault and the stress of the assault on the deceased had caused the heart attack or whether the heart attack had been caused by something else entirely. Since it is well known that heart attacks occur frequently in situations where people are not assaulted, it is understandable that the court should have held that it was not sufficient for the Crown to lead expert evidence that it was probable that the assault had caused the onset of the heart attack. Here, by contrast, after a full investigation the experts have not been able to identify any possible cause, except the effects of the methadone, for the deceased's death. For that reason, the decision in McGinlay is distinguishable. Indeed, Hendry:

Applying that approach and looking at the whole of the evidence, we are satisfied that it was indeed open to the jury to hold it established beyond a reasonable doubt that the deceased died from taking the methadone.

Before gathering together the various strands of evidence, we should add a word about the evidence as to the level of methadone which could be fatal. As counsel pointed out, the evidence is not particularly easy to follow since it tends to run together two distinct matters, the level of dose which may be fatal and the level of methadone which may be found in the blood of someone who has died from methadone poisoning. It appears, however, that until recently both Professor Busuttil and Dr. Fineron would have regarded a level of 0.25 mg. of methadone per litre of blood in a deceased person as falling outside the normal range associated with a fatality. But in a scientific paper (K. Worm, A. Steentoft, B. Kringsholm, "Methadone and drug addicts" 106 International Journal of Legal Medicine 119-123 (1993)). Danish researchers found a median value of 0.28 mg. per litre in 59 dead addicts. In the light of this article Professor Busuttil no longer regarded the figure of 0.25 mg. per litre as falling outside the normal range and Dr. Fineron did not accept that 0.4 mg. should be generally accepted as the normal median value. Dr. Fineron was also influenced by a book by Stephen Karch, The Pathology of Drug Abuse, which also appears to have pointed to lower figures than had previously been accepted as the norm.

Moreover, Dr. Fineron gave evidence based on his own experience and research. Doubtless, as counsel submitted, this evidence was essentially anecdotal and the figures do not appear as yet to have been subjected to statistical analysis. None the less, anecdotal information has a role to play in medical diagnosis and there is no reason why a jury should not have regard to it. Basing his evidence on a review of cases in the Edinburgh area, Dr. Fineron said that "half our cases are below the 0.4 and probably about 25% to 30% fall into this 0.25 or less category where we've attributed death." The jury would be entitled to consider this evidence from an experienced pathologist which would suggest that, so far from being exceptional, a finding of 0.25 mg. of methadone per litre of blood in the case of the deceased would put this case into the same category as 25% to 30% of the cases in the Edinburgh area where a person had died from the effects of methadone.

We summarise the main elements of the evidence in this way. There was evidence of the appellant consuming 40 ml. of methadone supplied by the appellant and then falling asleep and dying in his sleep. There was evidence that 40 ml. could be a fatal dose for someone who did not have a tolerance for methadone. There was evidence that the deceased took methadone but there was no evidence that he had been taking it regularly on a daily basis before 25 September. There was evidence which would have justified the inference that he had not taken methadone earlier that day. There was evidence that 0.25 mg. of methadone per litre of blood had been found in the deceased's body and that this was not outside the normal median range identified in published research and was consistent with the position in 25% to 30% of the deaths in the Edinburgh area which Dr. Fineron and his colleagues attributed to the effects of methadone. There was evidence from two expert witnesses, Professor Busuttil and Dr. Fineron, to the effect that in their view there was no other explanation for the deceased's death and that, in the absence of any other explanation, it was probable that the deceased had died from the effects of methadone.

In our view these various adminicles combined to make up a body of evidence on which a reasonable jury would be fully entitled to hold beyond a reasonable doubt that the deceased died as a result of the effects of consuming the methadone supplied by the appellant. Moreover, having regard to the nature of the evidence when viewed as a whole, we cannot say that no reasonable jury could have been satisfied beyond a reasonable doubt that the appellant was guilty of culpable homicide (King v. H.M. Advocate 1999 S.C.C.R. 330). The appeal must accordingly be refused.