Heroin-related deaths in New South Wales, 1992: toxicological findings and circumstances
Deborah Zador, Sandra Sunjic and Shane Darke
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Objective: To describe the circumstances of death
and toxicological findings in all heroin-related deaths in New South
Wales in 1992.|
Design: Coronial files of all cases of heroin-related deaths were reviewed. A standardised form was used to collect information on sociodemographics, history of drug use, circumstances of death, and results of toxicological analysis for each case.
Results: 152 heroin-related deaths were identified. Subjects had a mean age of 29.7 years, 82% were male, and 98% were not enrolled in a methadone treatment program at the time of their deaths. Deaths occurred in the home environment in 68% of cases and in the company of at least one other person in 58%. There was intervention before the subject's death in only 21% of cases. Two or more drug classes were detected in 71% of subjects; alcohol was detected in 45%, with a mean blood alcohol concentration of 0.14 g/100mL.
Conclusions: Fatal heroin overdose is potentially preventable. Educating users about the risks of co-administering alcohol and other depressant drugs with heroin, the comparative safety of injecting heroin in the company of others and the need to call for intervention sooner may reduce the frequency of heroin-related deaths.
Over the decade to 1990, mortality from opiate drugs increased by 170%
while that from other drugs declined by 8%.1 There is little information
available on the circumstances or characteristics of Australian
heroin-related deaths. Swensen reviewed 108 opioid drug-caused
deaths in Western Australia from 1974 to 1984 and found that
propoxyphene was the most common cause, accounting for 36 deaths
(33%), followed by methadone in 19 cases (18%), heroin in 12 cases
(11%), and morphine in another 12 cases (which may include deaths from
heroin).2 Walsh analysed 23
accidental opioid drug deaths in the Newcastle area of New South Wales
from 1970 to 1987 and found that most (83%) were caused by
reports of cases in this study indicated that in 61% help or
intervention by observers was delayed. Both studies found a higher
proportion of deaths at weekends, leading both authors to suggest
that these deaths involved recreational users rather than
The findings of these two studies cannot be generalised to heroin deaths in Australia because of their relatively small numbers of subjects studied over prolonged periods, the inclusion of all opioid (not just heroin) drug deaths, and the absence of data for Sydney (where most heroin deaths in this country occur). If interventions to reduce the rising mortality rate from opioid drug use are to be developed, then more needs to be known about the circumstances of fatal heroin overdose.
Hence, the major aims of this study were to describe the sociodemographic characteristics, circumstances of death and the toxicological findings at autopsy of all cases of fatal heroin overdose in NSW for the year for which the most recent data on drug-caused mortality were available.
The approval of the South Western Sydney Area Health Service's
Research Ethics Committee was obtained. Permission of the NSW
Registry of Births, Deaths and Marriages was obtained to enable the
Australian Bureau of Statistics (ABS) to release a list of all
heroin-caused deaths in NSW from 1 January to 31 December 1992.
ABS records were searched according to the following International Classification of Diseases version 9 (ICD-9) codes: 304.0/304.7 (opiate dependence), E850.0 (accidental opiate poisoning) and E950.0 (opiate-caused suicide).4 Permission was obtained from the Department of Courts Administration to inspect coronial files. A case was identified as a heroin-related death based on the coroner's conclusion alone or in conjunction with results of toxicological analysis. Deaths due to other opiates were excluded from the study.
Coronial files contained police reports, ambulance officers' statements, other witnesses' statements, autopsy reports, and results of toxicological analysis. A standardised data collection form was developed to record information on sociodemographic characteristics, history of drug use, circumstances of death, and toxicological findings.
Subjects were designated "believed to be a frequent user" if their coronial files provided evidence of two or more criteria indicative of regular heroin use (e.g., known history of heroin use, partner or friends known to be heroin users, history of heroin overdose or treatment for dependence, criminal record and/or unemployment). Subjects were designated "believed to be an infrequent user" if they were known to be primarily dependent on another drug (such as alcohol), were not known to be regular heroin users, and were employed full-time. A "novice" was a person who died from using heroin for the first time.
Information on history of admission to methadone maintenance treatment was obtained from data at the Pharmaceutical Services Section, NSW Department of Health. Information on history of admission to other treatment programs for opioid dependence (e.g., detoxification units or residential re habilitation programs) could not be obtained for this study.
Data for circumstances of death included the day and date, suburb or town, type of location (e.g., hotel room), time of death, time between injection of heroin and death, presence of other persons, and intervention. A death was considered "instant" if photographs showed a needle and syringe still in situ, if the posture of the body was consistent with a sudden collapse (e.g., slumped against toilet cubicle wall), or if witnesses provided evidence of instant death.
"Intervention" was treatment received by the subject while still alive, and did not include treatment by ambulance officers or after admission to hospital if the subject was clinically dead.
Information on results of toxicological analysis was obtained from reports of laboratory analyses (by the Division of Analytical Laboratories, NSW Department of Health, Lidcombe) of blood, urine and other tissue specimens taken at autopsy.
|For continuous variables, t tests were used, except for highly skewed variables, for which the Mann-Whitney U test (a non-parametric analogue of the t test) was used. Categorical variables were analysed with the chi-squared test and corresponding odds ratios (OR) and 95% confidence intervals (CI) were calculated. To determine which factors were independently associated with blood morphine concentration, we performed multiple linear regressions. SYSTAT was used for all analyses.5|
|For the 200 opiate-caused deaths identified by ABS in 1992, one file was unable to be located, one subject was noted to have died on 31 December 1991, one case was found not to be a coroner's case, and seven were found to be misclassifications (i.e., death due to drugs other than opiates). These 10 cases were excluded from the study. The study population thus comprised 190 cases. Of these, 152 (80%) were classified as heroin-related deaths, and the demographic characteristics of the people involved are shown in the Table. They were predominantly male (82%), with a mean age of 29.7 years (SD, 6.7; range, 18-59), and most were unemployed (76%).|
History of drug use
Most (90%) were well known to be heroin users. Eighty per cent were
judged to have been frequent heroin users, 17% were considered
infrequent heroin users, and two were novice users (1%). Both cases
involving novice users were classified as suicides by the coroner. In
three cases (2%) it was not possible to estimate the frequency of
heroin use from the coronial files.
Only 2% were enrolled in a methadone maintenance program at the time of their deaths, with 72% never having been enrolled in methadone treatment in NSW. Some subjects may have been previously enrolled in an interstate program, but this information was not available.
Circumstances of death
Twenty-six per cent of deaths occurred on Saturdays and Sundays,
compared with an expected 29%, assuming a uniform distribution ofdeaths over the seven days of the week. There was also no significant
variation between seasons -- summer (18%), autumn (25%), winter
(31%) and spring (26%). The times of deaths were distributed as
follows: midnight-6am, 23%; 6am- midday, 14%; midday-6pm, 28%; and
Eighty-five per cent of deaths occurred in the Sydney metropolitan region. Fatal heroin overdoses occurred throughout the Sydney area, with the highest frequency (19%) in the East Sydney region (including Kings Cross and Darlinghurst), and the second-highest (16%) in South-Western Sydney (including Cabramatta and Liverpool).
Fifty-three per cent of deaths occurred in the subject's usual place of residence or home, and a further 16% in the home of a friend or family member. Thus most (69%) occurred in a home environment.
Only 14% of deaths appeared to be "instant" events. The presence of other persons at some time during the interval between the injection of heroin and death was noted in 58% of cases, while 41% of subjects died alone. The presence of others was unable to be determined in 1% of cases.
In 79% of cases there was no intervention while the subject was still alive. An ambulance was called while the subject was alive in only 10% of cases and cardiopulmonary resuscitation was attempted by an onlooker in 11%.
Two subjects were deleted from toxicological analyses as they had
been maintained on life support systems for two or three days in
hospital intensive care units. Morphine was detected in 95% of
subjects at autopsy. The second most frequently detected drug was
alcohol (45%), with benzodiazepines in 26%. Methadone and
amphetamines were each detected in 6% of subjects, and cocaine,
antidepressant drugs and barbiturates were detected in 5%, 4% and
A single drug was found in only 27% of subjects -- morphine in 39 of 41, ethanol in one and oxazepam in one. In 71%, two or more different drugs were found at autopsy, and in 18% three or more drugs were detected. Men were more likely to have alcohol detected at autopsy than women (OR, 4.07; 95% CI, 1.44-11.47), while women were more likely to have benzodiazepines detected (OR, 2.82; 95% CI, 1.15-6.93).
The distribution of blood morphine concentrations is shown in Figure 1. Twelve subjects were deleted from this analysis because no morphine was found in their blood (although in seven morphine was detected elsewhere, e.g., bile, liver or urine). The median blood morphine level was 0.24 mg/L.
Alcohol was detected in 68 subjects (45%); Figure 2 shows the distribution of their blood alcohol concentrations (BACs). The mean BAC was 0.14 g/100 mL (SD, 0.08; range, 0.01-0.35 g/100 mL). Eighty-seven per cent had BACs of 0.05 or higher and 22% had BACs of 0.2 or higher. There were no statistically significant differences between men and women in either median blood morphine concentration (0.25 v. 0.19 mg/L; P < 0.4) or BAC (0.14 v. 0.1 g/100mL; P < 0.25).
The median blood morphine concentration in the subjects in whom alcohol was detected was significantly lower than in the group without alcohol detected (0.17 v. 0.34 mg/L; U = 3152; P < 0.001). There was also a statistically significant negative correlation between blood morphine and alcohol concentrations (rs = - 0.28; P < 0.01) The presence of benzo diazepines at autopsy did not significantly affect blood morphine concentrations (0.25 v. 0.24 mg/L; U = 1871; P < 0.7).
To determine which individual variables were related to blood morphine concentration, a simultaneous multiple linear regression was performed on log morphine level (because of the skewed distribution of blood morphine levels). Variables used were age, sex, the presence of alcohol and the presence of benzodiazepines. The presence of alcohol at autopsy was the only variable independently associated with lower blood morphine levels (b = - 0.28; P < 0.001); age (P < 0.96), sex (P < 0.2) and the presence of benzodiazepines (P < 0.7) did not significantly predict log blood morphine level. Diagnostic tests of the residuals indicated that the assumptions of the model were met.
Classification of deaths
|Fifty-seven per cent of all death certificates completed by the forensic pathologists reported the cause of death as either "narcotism", "acute narcotism" or "acute intravenous narcotism". Although alcohol was detected in 45% of subjects at time of death, it was noted on the death certificate in only 7% of cases. Most deaths (80%) were classified according to ICD-94 coding as cases of "dependence" (code 304.0), 10% as cases of accidental poisoning (E850.0), 9% as suicides (E950.0) and 1% as opiate drug dependence with contributions from other drugs (304.7).|
We found that heroin-related deaths occurred overwhelmingly in
people who were male, of an average age of 30 years, and frequent users.
Few occurred in those considered to be infrequent users. A recent
survey has shown that two-thirds of a large sample of heroin users have
had at least one non-fatal overdose and that 86% have been present at
another person's overdose.6
This suggests that campaigns designed to reduce the rising mortality
rate caused by heroin need to target regular users.
The finding that only a minority of cases had ever been in methadone treatment is consistent with other evidence that methadone treatment reduces mortality among the heroin-dependent.7,8 Some of our subjects might be alive today if they had entered and remained in methadone treatment.
A striking finding from the toxicological data was the relatively small number of subjects in whom morphine only was detected. Most died with more drugs than heroin alone "on board", with alcohol detected in 45% of subjects and benzodiazepines in just over a quarter. Both of these drugs act as central nervous system depressants and can enhance and prolong the depressant effects of heroin.
Our finding (and that of other studies9,10 ) of a significantly lower blood morphine level in subjects who tested positive for alcohol suggests that in the presence of alcohol less heroin is required to exert a fatal effect. Alternatively, alcohol-induced liver enzymes may increase the metabolism of heroin. The very low blood levels of morphine we found may also support these hypotheses. Some pathologists have been reluctant to attribute a heroin-caused death to true overdose because of the frequent finding of a low blood morphine concentration, and prefer to report the death as a case of "narcotism" (Johan Duflou, Deputy Director, Insti tute of Forensic Medicine, Sydney, personal communication, 1993). Further, Monforte showed that in 75% of a group of people who had died from fatal heroin "overdoses" blood morphine concentrations were not higher than in a group of heroin addicts who were victims of homicide.11
Bammer and Sengoz have also challenged the assumption that heroin deaths occur as a result of increased purity of heroin. In a recent paper they identified concomitant consumption of other drugs and reduced tolerance as alternative mechanisms for the cause of death in heroin fatalities.12
The disadvantage of continuing to describe heroin-related fatalities as "overdoses" is that it attributes the cause of death solely to heroin and detracts attention from the contribution of other drugs to the cause of death. Heroin users need to be educated about the potentially dangerous practice of concurrent polydrug and heroin use.
Our findings that an ambulance was called while the subject was still alive in only 10% of cases, and that a substantial minority of heroin users died alone, strongly suggest that education campaigns should also emphasise that it is safer to inject heroin in the company of others, and important to call for an ambulance early in the event of an overdose. Consideration should also be given to trialling the distribution of the opioid antagonist naloxone to users to reduce mortality from heroin use.
In conclusion, fatal heroin overdose is potentially preventable and research should now focus on reducing its occurrence. The introduction or intensification of education campaigns explaining the risk of polydrug use to heroin users may help to reverse the national trend in heroin-related deaths.
|This research was funded by South Western Sydney Area Health Service and the National Drug and Alcohol Research Centre. We would like to thank the following organisations for their assistance: Department of Courts Administration, in particular Glebe Coroners Court and Westmead Coroners Court, and the NSW Registry of Births, Deaths and Marriages. We would also like to thank Mr Stephen Bull of the Australian Bureau of Statistics (NSW office), Dr Johan Duflou, Professor Wayne Hall and Dr Alex Wodak.|
(Received 13 Jun, accepted 19 Oct 1995)
Authors' detailsDrug and Alcohol Services, Division of Public Health, South Western Sydney Area Health Service, Sydney, NSW.
Deborah Zador, MB BS, FAFPHM, Staff Specialist. Currently, Staff Specialist, Drug and Alcohol Services, Central Sydney Area Health Service, NSW.
Sandra Sunjic, BAppSc, MA, Clinical Nurse Specialist.
National Drug and Alcohol Research Centre, University of New South
Wales, Sydney, NSW.
Shane Darke, PhD, Lecturer.
No reprints will be available. Correspondence: Dr D Zador, Gladstone Hall Health Services, 114 Ewart Street, Dulwich Hill, NSW 2203.
© 1997 Medical Journal of Australia.
Received 6 June 2020, accepted 6 June 2020
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