concomitant drugs of misuse and drug using behaviours associated with fatal opiate-related...

RESEARCH REPORT

© 2003 Society for the Study of Addiction to Alcohol and Other Drugs

Addiction,

98

, 191–197

Blackwell Science, Ltd

Oxford, UK

ADDAddiction

0965-2140© 2003 Society for the Study of Addiction to Alcohol and Other Drugs

98Original Article

Drugs of misuse, drug-using behaviours and opiate-related poi-

soningPhillip Oliver & Jenny Keen

Correspondence to:

Phillip OliverUniversity of SheffieldAddiction Research UnitInstitute of General Practice and Primary CareNorthern General HospitalSheffield, S5 7AUUKTel:

+

44 114 271 5925Fax:

+

44 114 242 2136E-mail: [email protected]

Submitted 29 October 2001; initial review completed 11 January 2002;

final version accepted 2 October 2002

Concomitant drugs of misuse and drug using behaviours associated with fatal opiate-related poisonings in Sheffield, UK, 1997–2000

Phillip Oliver

1

& Jenny Keen

1,2

Addiction Research Unit, Institute of General Practice and Primary Care, University of Sheffield, Northern General Hospital, Sheffield

1

and Primary Care Clinic

for Drug Dependence, North Sheffield Primary Care Trust, Sheffield, UK

2

ABSTRACT

Aims

To examine the degree of involvement of concomitant drugs of misuseand other previously identified behavioural risk factors in acute accidentalopiate-related poisoning fatalities in Sheffield, 1997–2000.

Design

Retrospective analysis of coroners’ records.

Setting

Sheffield, UK.

Participants

All those who died from an acute accidental opiate-related poison-ing in Sheffield between 1 January 1997 and 31 December 2000.

Measurements

Coronial data were collated under the headings: demographiccharacteristics, circumstances of death and toxicological findings.

Findings

Ninety-four deaths occurred over the study period. The majority ofcases were regular users of illicit drugs. Approximately 20% of deaths werepreceded by a period of abstinence from drug use, with imprisonment and hos-pitalization as the most common reasons. Sixty-one per cent of cases had con-comitant drugs of misuse detected from toxicology most commonlybenzodiazepines and/or alcohol. These were, however, found in relatively smallconcentrations and opiate blood concentrations were no lower in deaths wheremultiple substances were involved. Despite evidence to suggest that smoking isthe preferred route of heroin administration in this region, the vast majority ofcases involved injecting.

Conclusions

Administration of an opiate via intravenous injection was themost consistent factor associated with these deaths over the period of this study.Co-administration of other central nervous system depressants, at least in lowerquantities appear to be a feature rather than a risk factor

per se

in such fatalities.

KEYWORDS

Benodiazepines, fatal poisonings, heroin, methadone, opiate

overdose.

INTRODUCTION

Over the past few decades deaths from drugs of misusehave risen considerably in England and Wales. Dependingupon the definition used, between 1000 and 3000 deathsfrom drug-misuse occurred in 1998 (EMCDDA 1999;ONS 2000) and it has been estimated that the number ofyears of working life lost from drug-misuse deaths is nowapproaching that of road traffic fatalities (ACMD 2000).

Research indicates that in both the United Kingdom andother countries accidental poisonings involving opiatesand in particular heroin are responsible for the majorityof these deaths (Frischer

et al

. 1993; Cassidy

et al

. 1995;EMCDDA 1999).

It is known that the majority of those who die fromopiate-related poisonings have a long history of heroinmisuse and dependence (Zador, Sunjic & Darke 1996;Oliver

et al

. 2001), and there is good reason to suspect


Addiction,

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, 191–197

192

Phillip Oliver & Jenny Keen

that the number of heroin users in the Sheffield area hasincreased in the past decade. However, the pattern ofdeaths observed and previous research (Hall & Darke1998) suggest that no simple relationship exists betweenthe extent of heroin misuse and the number of occur-rences of fatal overdose.

A number of factors operating at both an individualand population level have been identified which mayaffect the risk of fatal opiate poisoning. At an individuallevel, important aspects of drug-using behaviour such asusing after periods of abstinence (Seaman, Brettle & Gore1998; Darke

et al

. 2000a), injecting (Donoghoe 1998;ACMD 2000) and combining other drugs of misuse(Monforte 1977; Ruttenber & Luke 1984; Zador

et al

.1996), have been shown to increase the risk of fatal over-dose. With respect to the latter factor, alcohol and benzo-diazepines are the most commonly reported concomitantdrugs detected in fatal opiate poisonings, both in theUnited Kingdom and other countries (Hammersley,Cassidy & Oliver 1995; Gerostamoulos, Staikos &Drummer 2001). Although blood alcohol concentra-tions from such cases have been reported previously andassociated with deaths from smaller amounts of heroin(Ruttenber, Katler & Santinga 1990; Zador

et al

. 1996),there is a paucity of similar data with respect to benzodi-azepines. The purpose of the present study is to examinein detail the characteristics of all deaths from acute acci-dental opiate poisonings in Sheffield between 1997 and2000; to describe the degree of involvement of behav-ioural factors, and report the toxicological findings fromthese deaths.

METHODS

Case selection criteria

This study presents data on all deaths investigated by theCity of Sheffield Coroner between 1 January 1997 and 31December 2000 who were adjudged by the forensicpathologist to have died from an accidental acute opiate-related poisoning. Deaths in which either a convincingacute toxicological cause of death could not be confi-dently demonstrated or where a verdict of suicide waspassed, were excluded from analysis.

Data sources

In accordance with the Coroners Act, 1988 and the Cor-oners Rules, 1984, all sudden, unexpected or suspiciousdeaths are investigated by the Coroner’s Office. If a deathis then considered to be from unnatural causes an inquestis held. In preparation for this inquest, a full and detailedinvestigation into the circumstances and cause of death

will be carried out. The records produced from this inves-tigation form the basis of the data presented in this paperand typically contain information such as emergencyservice reports, witness statements, prescription drugdetails, a full autopsy and toxicological findings.

All toxicological analyses were carried out by theDepartment of Clinical Chemistry of the Royal Hallam-shire Hospital, Sheffield. Blood concentrations reportedare from samples taken from the same cadaver location(leg) and were available in all but two cases, both of whichhad decompositional changes that prohibited blood anal-ysis. In these cases, stomach contents, muscle analysisand despositional evidence were used to determine causeof death. Classification of the primary drug responsible fordeath was made on the basis of the forensic pathologist’sreport. Where more than one substance was detectedfrom blood toxicology only those substances which weredetected at or above therapeutic levels (Stead & Moffat1983) are reported.

Data collection procedure

Following a search of the literature and discussions withthe Coroner’s Office a standardized database was pro-duced using SPSS (version 10) for Windows. Data werecollated under the following headings: demographiccharacteristics, previous drug use and treatment history,prescription medication, circumstances of death and fulltoxicological findings. Records were then read throughcarefully to extract all relevant information. A case wascategorized as having a history of drug misuse on thebasis of either general practitioner/treatment specialistreports or interviews with friends/family members. Ethi-cal approval for this study was granted by the SouthSheffield research ethics committee.

RESULTS

Number of deaths and case characteristics

A total of 94 cases were identified. The majority of caseswere male (89%) with a male to female ratio of 8.4 : 1 forthe 4 years. The mean age at the time of death was30 years (95% confidence interval (CI) 29–32 years).Eighty-nine per cent of the cases were single and 87%were unemployed (see Table 1). Over the 4-year period45% of the cases were recorded as living alone. Therewere no statistically significant differences between malesand females with respect to any of these characteristics.Similarly, the demographic profile of individuals who diedbetween 1997 and 2000 remained relatively stable ineach of the 4 years, with little variation in either meanage, gender, marital status or living arrangements.

Drugs of misuse, drug-using behaviours and opiate-related poisoning

193


Addiction,

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, 191–197

Drug-using profile

Where the information was available (

n

=

92), 94% of thecases were described by either friends, family or health-care professionals as being regular user’s of illicit drugs.The most commonly reported drug consumed was her-oin, which was described as being used regularly by 80%of these cases and with a mean length of involvement ofnearly 8 years (95% CI

=

6.3–9.2). Reliable informationon treatment for heroin dependence was available in 80cases. Of these 20 individuals (25%) were enrolled inmethadone maintenance treatment (MMT). No statisti-cally significant differences were observed for these vari-ables over the 4 years.

Circumstances of death

Sixty-one per cent of deaths over the 4-year periodoccurred in the decedent’s own place of residence with afurther 29% taking place at either a friend’s or familymember’s home. Only three deaths occurred in a publicplace. Witness statements indicated that around 20% ofdeaths occurred with others present; however, these datashould be treated with caution because statements wereoften contradictory and it was not always clear whetherthis meant that the actual overdose event was observed orthat others were simply in the same house/location at thetime of overdose.

Coroners’ records indicated that a period of abstinenceimmediately preceded 19 deaths over the 4 years. Prisonwas the most common cause of abstinence (nine cases)followed by hospitalization (five cases). The mean numberof days between release from prison and death occurringwas 4.1 days.

Primary toxicological findings

Four different opioids were indicated by the pathologist’sreport to be the primary cause of death: heroin (70 cases,75%), methadone (22 cases, 23%), codeine (one case)and meptazinol (one case) (see Table 2). Heroin wasdetected alone in 28 cases and in combination with otherdrugs of abuse in 42 cases. Methadone was detectedalone in eight cases and with concomitants in 14 cases.For the remaining opioids, codeine was detected in com-

Table 1

Demographic characteristics and circumstances of deathof those who died from an acute opiate-related poisoning in Shef-field between 1997 and 2000.

Total(

n

=

94)

AgeMean 30.15(SD) (7.83)

Gender (%)Male 89

Marital status (%)Single 89Married/cohabiting 11

Employment status (%)Unemployed 87

Accommodation at time of death (

n

=

91)Lived alone (%) 45

Known user of illicit drugs? (

n

=

92)Yes

n

(%) 94Number of years using heroin (

n

=

74)Mean 7.77(SD) (6.3)

Receiving MMT? (

n

=

80)Yes (%) 25

Prescribed benzodiazepines? (

n

=

81)Yes (%) 43

Place of death (%)Own residence 61Friend or families residence 29Hospital 6Public place 3Hotel room 1

Was someone else present at overdose? (

n

=

91)Yes (%) 19

Cases in which a period of abstinenceimmediately preceded death

Prison (

n

) 9Hospitalization 5Undefined 4Detox 1Percentage of all deaths 20

MMT

=

Methadone Maintenance Treatment.

Table 2

Toxicological findings.

Total(

n

=

92

1

)

Heroin

n

(%) 28 (30)Median blood conc. (total morphine) (

m

g/l) 527Min–max 91–1687

Heroin plus other drugs

n

(%) 42 (45)Median blood conc. (total morphine) (

m

g/l) 519Min–max 93–2500

Methadone

n

(%) 8 (9)Median blood conc. (

m

g/l) 491Min–max 100–1370

Methadone plus other drugs

n

(%) 14 (15)Median blood conc. (

m

g/l) 1142Min–max 77–2240

Codeine plus other drugs

n

(%) 1 (1)Blood conc. (

m

g/l) [2600]

2

Meptazinol

n

(%) 1 (1)Blood conc. (

m

g/l) [2100]

2

1

Blood toxicology results for two cases were unavailable. These deaths wereclassified on the basis of other pathological indicators (e.g. muscle samples)and despositional evidence but are not included in blood concentration data.

2

Concentrations given in square parentheses are from single cases.


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, 191–197

194


bination with other substances and meptazinol wasdetected alone. For heroin deaths the median totalblood morphine concentration was 413.5

m

g/l (min–max

=

91–2500). Mean blood methadone concentrationwas 961

m

g/l (SD

=

629

m

g/l).

Concomitant drugs of abuse

A total of 61% of the cases over the 4-year period had con-comitant drugs of abuse at or above therapeutic levelsdetected in addition to the primary opiates described inthe preceding section. There were eight different concom-itants and a total of 13 different drug combinations. Ben-zodiazepines were detected most frequently (45% ofall cases) followed by alcohol (17%), methadone (4%),heroin (3%) and dihydrocodeine (3%). Cocaine,amphetamine and methylenedioxymethamphethamine(‘ecstasy’) were detected in one case each.

Benzodiazepines were detected in 37% of heroindeaths and 64% of methadone deaths. Three differentbenzodiazepine classes were detected. These were diaz-epam (29 cases), temazepam (13 cases) and nitrazepam(nine cases). Diazepam was detected in 33% of heroindeaths and 27% of methadone deaths, temazepam wasdetected in 7% of heroin deaths and 36% of methadonedeaths and nitrazepam was detected in 9% of heroindeaths and 5% of methadone-related deaths.

Median blood concentrations for diazepam,temazepam and nitrazepam were 253

m

g/l, 1028

m

g/land 256

m

g/l, respectively. To provide some context tothese values,

The Disposition of Toxic Drugs and Chemicalsin Man

, 5th edition (Baselt 2000) gives an average 1-hourpeak blood concentration of 148

m

g/l for a single orallyadministered 10 mg dose of diazepam; an average peakplasma level of 305

m

g/l for a 10-mg oral dose oftemazepam and 84

m

g/l for the same dose of nitrazepam.Inspection of the blood concentration distributions in Fig.1 one suggest that whereas cases involving diazepamappear to involve levels of diazepam predominately at thelower end of the spectrum, those involving temazepamand nitrazepam are distributed more randomly with ahigher proportion of cases appearing to involve largerrelative dosages.

Alcohol was detected in 16 cases, with a medianblood–alcohol concentration (BAC) of 0.07 g/100 ml(min–max

=

0.01–0.28). However, only six of these caseswere above 0.08 g/100 ml (the legal limit in the UnitedKingdom set by the Road Traffic Act, 1972). Alcoholdetections were all heroin-related, comprising 23% of allheroin deaths.

There were no significant differences between thetotal morphine concentrations when concomitant drugsof misuse were present or absent (519

m

g/l versus527

m

g/l). Blood methadone concentrations, however,

were significantly higher in cases in which a concomitantdrug of misuse was detected (median

=

1142

m

g/l versus491

m

g/l,

Z

=

2.535,

P

=

0.011). Further detailed analysisincluding correlations between BAC or blood benzodiaz-epine concentrations and total morphine levels were notcalculated, as there were inadequate numbers of cases inwhich either of these concomitants was detected along-side morphine alone, thus limiting the usefulness of thesemeasures.

Mode of administration

Heroin was considered to have been injected in 84% of allheroin deaths (plus two cases in which heroin was a con-comitant) and injection could not be ruled out in a fur-ther three cases. This figure ranged from 80% in 2000 to100% in 1998. The route of methadone administrationwas by injection in 11 cases (50%) and possible injectionin a further four cases. Administration of benzodiaz-epines by injection was identified in 11 cases: five heroin-related and six methadone-related.

Cases with low blood morphine concentrations

Ten cases of heroin poisoning (14%) were identified withwhat were considered low total blood heroin concentra-tions for a non-opiate-naive individual (

<

200

m

g/l). Twoof these cases were believed to be novice users and twowere recorded in the coroner’s notes as having a period ofabstinence prior to death. In the remaining six cases threeinvolved concomitant use of alcohol and two concomi-tant use of benzodiazepines (one of which also involvedalcohol). In all these cases heroin was believed to havebeen injected.

DISCUSSION

The demographic and drug-using profiles of those whodied in this study are in broad agreement with previousresearch. Consistent with the existing literature both inthe United Kingdom (Ghodse

et al

. 1978; Cassidy

et al

.1995; Bentley & Busuttil 1996) and in other countries(Darke & Zador 1996), the vast majority of casesdescribed in this report were male. The average age of thedecedents was 30 years, with most having a history ofheroin misuse. This result is unsurprising, given theremarkably consistent mean age of death in similarstudies (Darke & Zador 1996) and the increased risk ofmortality from opiate overdose faced by opiate users(Oppenheimer

et al

. 1994).Approximately one in five of the cases described in this

report died following a period of abstinence from theirregular drug use. Slightly higher proportions of cases

Drugs of misuse, drug-using behaviours and opiate-related poisoning

195


Addiction,

98

, 191–197

involving such interruptions have been reported in her-oin (Ingold 1986) and methadone (Cooper

et al

. 1999)mortality studies, as well as non-fatal (Gossop

et al

. 1996)literature. This suggests that this factor is less of a featurein Sheffield opiate-related deaths than elsewhere,although it remains possible that methodological hetero-geneity could explain these differences.

The most commonly reported forms of abstinencewere imprisonment and hospital admission. Elevated riskof fatal overdose following release from prison has beenfound previously by Seaman

et al

. (1998) and also byShewan

et al

. 2000). The latter authors found thataround 28% of the female fatal drug overdoses in Strath-clyde, Scotland between October 1993 and September1995 were recently released ex-prisoners. Similar studieswould be useful to assess fully the risk of fatal overdosefaced by opiate misusers discharged from hospital.

Over 60% of the cases over the 4 years had concomi-tant drugs of abuse detected in addition to opiates fromblood toxicology. Benzodiazepines and alcohol occurredas the most frequent concomitants in proportions similarto those reported elsewhere (Gerostamoulos

et al

. 2001).Such findings are so universal in the literature that com-bining central nervous system depressants is well docu-mented as a significant risk factor for opiate overdose(Warner-Smith

et al

. 2001). In the present study,however, it was difficult to tease out the degree ofinvolvement of such concomitants. Median blood con-centrations of heroin only and heroin in combinationwith other drugs did not differ greatly and indeed meth-adone levels were substantially higher in cases involvingboth methadone and other drugs of abuse. Using bloodlevels of the co-administered drugs as a guide to theirpotential contribution it can be seen that both alcoholand benzodiazepines (in particular diazepam) weredetected in largely ‘therapeutic’ quantities. This couldexplain why there were no significant differences in theaverage total blood morphine levels when concomitantswere present or absent. This notion is supported byGuitiérrez-Cebollada

et al

. (1994), who suggest that onlybenzodiazepine concentrations above 900 ng/ml are rel-evant in heroin overdose.

However, it is also worth pointing out that assessingthe relative contribution that a concomitant makes tofatal opiate overdose is difficult, especially given thepotency of the respiratory depressant effects of opiatesand the difficulty in determining an individuals ante-mortem opioid drug tolerance (Karch 1996). Althoughwe would stop short of suggesting that the involvement ofbenzodiazepines in opiate-related deaths has been over-stated, our current data suggest that, at least in lowerquantities, benzodiazepines are a feature rather than arisk factor

per se

in such fatalities. This distinction isimportant because, unlike alcohol, benzodiazepines may

Figure 1

Distribution of blood concentrations for benzodiazepinesdetected as concomitants in fatal opiate-related poisonings

0

2

4

6

8

10

12

50–150

150–250

250–350

350–450

450–550

550–650

650–750

750–850

850–950

950+

0

1

2

3

50–100

100–150

150–200

200–250

250–300

300–350

350–400

400–450

450–500

Fre

qu

ency

0

1

2

3

4

5

250–500

500–750

750–1000

1000–1250

1250–1500

1500–1750

1750–2000

2000–2250

2250–2500

2500+500+

Fre

qu

ency

Blood temazepam concentration

Blood nitrazepam concentration(mg/l)

Blood diazepam concentration (mg/l)

Fre

qu

ency

Temazepam

Diazepam

Nitrazepam

n = 13:5 heroin-related, 8 methadone-relatedMedian = 1028 mg/l,Min–Max = 366–3200

n = 9:6 heroin-related, 3 methadone-relatedMedian = 256 mg/l,Min–Max = 83–528

n = 29:21 heroin-related, 7 methadone-related, 1 codeine-relatedMedian = 253 mg/l,Min–Max = 53–1727


Addiction,

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196


have a role to play in the treatment of drug misuse(Seivewright & Iqbal 2002).

The results of this study again highlight the significantrole that injecting plays in acute fatal opiate poisonings.Around 80% of heroin deaths and 50% of methadonedeaths involved probable injecting and when deathsinvolving lower levels of morphine were analysed sepa-rately injecting was the only consistent factor. Researchboth in the United Kingdom and other countries hasrevealed this continually to be a major behavioural riskfactor (Donoghoe 1998). For example, between 1992and 1996 in New South Wales Australia, 99% of heroin-related deaths followed injection (Darke

et al

. 2000b).This is not particularly surprising, given that the pre-ferred route of administration by Australian heroin mis-users is almost exclusively injection (Maher

et al

. 1998).However, in a recent paper Gossop and colleagues foundthat more than 60% of treatment-seeking drug misusersfrom the North of England used ‘chasing the dragon’ astheir preferred route of heroin administration (Gossop

et al

. 2000). In spite of this figure, for Sheffield at least,heroin that has been injected remains the most commoncause of death.

ACKNOWLEDGEMENTS

This work was funded by Sheffield Health. Ethicsapproval was granted on 23/9/1999 by the South Shef-field Research Ethics Committee (SS99).

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