Heroin-related deaths in Victoria: a review of cases for 1997 and 1998.

The objectives of this paper were to determine the number of heroin-related deaths in Victoria for the years 1997-1998 and to detail the demography and toxicology findings, and also compare heroin death rates for this decade. The number of deaths attributed to the intravenous use of heroin has increased dramatically in Victoria since 1990. The increases were 5-fold. There were 166 deaths in 1997 and 268 in 1998. The heroin death is typified by a median age of 30 for males and 29 for females, although the age range is from children as young as 15 to adults in their sixth decade of life. Over 85% of cases were using other central nervous system depressants, with benzodiazepines (45%) and alcohol (36%) being the most common. Approximately 60% occurred indoors at a private residence, the remainder occurred in public places and other locations. A similar number (60%) died alone. A wide distribution of deaths occurred throughout the metropolitan and regional areas showing a growing spread in the heroin problem in the community.

Flecainide toxicity: cause and contribution to death.

In this report, we describe in detail one fatality in which flecainide toxicity was considered to be the primary cause of death and discuss the possible contribution of flecainide in another case. The concentration of flecainide in postmortem specimens is discussed in relation to other drugs as well as some of the difficulties associated with the interpretation of postmortem drug levels.

Postmortem redistribution of morphine and its metabolites.

The postmortem redistribution of morphine, morphine-3-glucuronide, morphine-6-glucuronide and total morphine was assessed in 40 heroin-related deaths. In blood taken from subclavian, heart, and femoral regions, concentrations of morphine and its metabolites were similar. While there was a trend for higher concentrations in heart blood, when compared with femoral or subclavian blood, this was not significant. There was also no significant difference in concentrations between admission and autopsy blood in which the postmortem interval was on average 59 h. From our observations, significant postmortem redistribution of morphine and its metabolites seems unlikely.

Involvement of codeine in drug-related deaths.

The incidence and role of codeine in drug-related deaths in Victoria was investigated over a 5-year period. There were a total of 107 cases involving codeine, representing 8.8% of all drug-related deaths in this period in Victoria. There were only six fatalities in which codeine was considered the major poison. The mean (+/- SD) concentration of codeine in femoral blood was 4.0 +/- 2.3 mg/L (range, 2.1-8.0 mg/L). The mean concentration of free codeine was 1.3 +/- 0.9 mg/L (range, 0.4-2.8 mg/L). The remaining 101 cases involved a combination of codeine and other drugs. The mean total codeine blood concentration was 1.8 +/- 3.3 mg/L (range, 0.04-26 mg/L), which was significantly lower than in those cases where codeine was the major poison (p < 0.002). The mean concentration of free codeine was 0.82 +/- 4.9 mg/L (range, 0.02-9.0 mg/L), which was not significantly different (p > 0.05) from the six codeine-only cases. The most common drugs found in this group, other than codeine, were acetaminophen (62%), diazepam (46%), salicylate (20%), and ethanol (25%). The association of other psychoactive drugs in these deaths made the contribution of codeine difficult to assess. Free codeine concentrations > 0.4 mg/L and total codeine concentrations > 2.0 mg/L may be sufficient to cause death in the absence of any other contributing factors.

Solid phase extraction of morphine and its metabolites from postmortem blood.

A simple and rapid high-performance liquid chromatographic method is described for the determination of morphine-3-glucuronide, morphine-6-glucuronide, normorphine and morphine in postmortem blood. A solid phase extraction technique employing C18 Sep-Pak cartridges was used to recover morphine and its metabolites from 0.5 ml of blood. Reverse phase ion-pair chromatography was used to achieve separation with a C18 bonded column. The mobile phase consisted of acetonitrile, lauryl sulphate and sodium dihydrogen orthophosphate buffer at low pH. Electrochemical detection (ECD) in series with ultraviolet (UV) spectrophotometric detection (210 nm) was used for quantitation. The lower limit of detection using ECD was 10 ng/ml for all analytes and a linear response was observed to 5000 ng/ml. Coefficients of variation for all analytes ranged between 3-13% for both intra- and inter-assay. This method is reproducible, quick and easy to perform and allows morphine conjugates and morphine to be measured simultaneously in postmortem blood.

Simultaneous determination of 6-monoacetylmorphine, morphine and codeine in urine using high-performance liquid chromatography with combined ultraviolet and electrochemical detection.

A method is described for the simultaneous determination of 6-monoacetylmorphine (6-MAM), morphine and codeine in post-mortem urine specimens using reversed-phase high-performance liquid chromatography with dual ultraviolet spectrophotometric and electrochemical detection. The limits of detection for a 1-ml urine sample were 0.04 mg/l for 6-MAM and 0.05 mg/l for both morphine and codeine. The presence of 6-MAM in urine indicates prior use of heroin and enables differentiation between morphine- and heroin-related deaths.

Incidence of psychoactive cannabinoids in drivers killed in motor vehicle accidents.

A high performance liquid chromatography (HPLC) assay was developed for the psychoactive cannabinoids Delta-9-Tetrahydrocannabinol (THC) and 11-Hydroxy-THC (11-OH-THC) using electrochemical detection (ECD). A C8 bonded column was used and the mobile phase consisted of acetonitrile, methanol and 0.01 M sulphuric acid at a flow rate of 1.5 mL/min. The detection limits for both THC and 11-OH-THC were 1.0 ng/mL. Preliminary screening of 193 drivers using an enzyme-multiplied immunoassay technique (EMIT) showed 21 tested positive on either blood, urine or both. Of these subjects 13 were confirmed as positive by the HPLC/ECD method in blood. Blood concentration for THC ranged from 1.4 ng/mL up to 20 ng/mL and for 11-OH-THC 2.5 ng/mL up to 85 ng/mL.