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Biomedical subjects

R J Lokan

Publications and source records attributed to R J Lokan.

8 recordsLinked to original sources
PubMed2000

The prevalence of alcohol, cannabinoids, benzodiazepines and stimulants amongst injured drivers and their role in driver culpability: part ii: the relationship between drug prevalence and drug concentration, and driver culpability.

Blood samples from 2,500 injured drivers were analysed for alcohol, cannabinoids (measured by the presence of THC), benzodiazepines and stimulants. The relationship between the prevalence and concentration of drugs and the culpability of the driver was examined using an objective method for assessing culpability. There were no significant differences between males and females with respect to culpability. However, there was a relationship between age and culpability: drivers under 26 years and over 60 years were more likely to be culpable. Drivers who tested positive for alcohol only, benzodiazepines only and the combinations of alcohol and THC and alcohol and benzodiazepines were significantly more likely to be culpable for the crash compared with the drug-free group. Conversely, a lower percentage of drivers who only tested positive for THC were culpable for the crash compared with drug-free drivers. This difference was not statistically significant. For car drivers in single-vehicle crashes, the majority of drivers were judged culpable irrespective of drug use. In multiple-vehicle crashes, car drivers testing positive for alcohol only or benzodiazepines only were more likely to be culpable for the crash compared with drug-free drivers. For motorcycle riders in both single- and multiple-vehicle crashes, there were no significant differences between the drug-positive and drug-free groups. A higher percentage of drug-free riders in multiple-vehicle crashes were culpable compared with riders who only tested positive for THC, but this difference was not statistically significant. There was a significant concentration-dependent relationship between alcohol and culpability: as blood alcohol concentration increased, so did the percentage of culpable drivers. When THC was used alone, there was no significant increase in culpability. For those drivers with benzodiazepines at therapeutic concentrations and above, there was a significant increase in culpability. The relationship between stimulants and culpability was not significant, although a higher proportion of stimulant-positive drivers were culpable compared with drug-free drivers. The combinations of alcohol and THC, and alcohol and benzodiazepines also produced a significant increase in culpability, but this increase was not significantly greater than that produced by alcohol alone.

Accidents, Traffic↗
PubMed2000

The prevalence of alcohol, cannabinoids, benzodiazepines and stimulants amongst injured drivers and their role in driver culpability: part i: the prevalence of drug use in drive the drug-positive group.

Blood samples from 2,500 injured drivers were analysed for alcohol, cannabinnoids, benzodiazepines and stimulants. Overall, three-quarters of drivers tested negative for drugs. Alcohol was the most frequently detected drug. Cannabinoids were also detected at high rates, but the majority of drivers tested positive for THC-acid, the inactive metabolite of THC. Benzodiazepines and stimulants were detected at low rates, and detection rates for combinations of drugs were also low. Males were more likely to test positive for drugs, especially alcohol and THC, whereas females were more likely to test positive for benzodiazepines. A similar proportion of car drivers and motorcycle riders tested positive for drugs, although riders were more likely to test positive for THC. Single-vehicle crashes were particularly associated with alcohol for both car driver and riders, and for riders, multiple-vehicle crashes were particularly associated with THC.

Accidents, Traffic↗
PubMed1999

Putrefactive pleural effusions as an alternative sample for drug quantification.

In the investigation of drug-related deaths it is occasionally necessary to examine putrefied bodies. In such cases the availability of conventional body fluids for toxicologic analysis is usually limited, whereas blood-stained pleural effusion is often present in adequate quantity in the pleural cavity. Fifty-five cases involving numerous drugs are presented in which pleural effusion drug concentrations are compared with corresponding blood or liver concentrations. More than 90% of comparisons produced coincident interpretations of the role that drugs played in the deaths. In most instances pleural effusion analysis was shown to be a valid alternative to the analysis of blood or other conventional fluids or tissues in cases exhibiting advanced putrefaction.

Autopsy↗
PubMed1998

Amphetamine derivative fatalities in South Australia--is "Ecstasy" the culprit?

OBJECTIVE: To analyze features of a series of fatalities caused by amphetamine-derivative designer drugs marketed as "Ecstasy" in South Australia, and to identify reasons for the recent marked increase in number of these deaths. MATERIALS AND METHODS: Following the death of a 26-year-old woman after alleged ingestion of Ecstasy tablets, a retrospective search of files at State Forensic Science, Adelaide and the South Australian State Coroner's Department was undertaken from February 1992 to January 1997 to identify similar cases. RESULTS: Six fatalities were found, all of which have occurred since September 1995 (M:F ratio, 1:1; age range, 22 to 36 years; average age, 27.7 years). All individuals had histories of recent ingestion of illegal drugs thought to be Ecstasy (methylenedioxymethamphetamine, MDMA) at the time of purchase. Delay occurred in seeking medical attention, despite severe symptoms. Causes of death involved documented hyperthermia in 3 cases (temperatures of 41.5-46.1 degrees C), with features of hyperthermia in one other case, and intracranial hemorrhage in another. Drugs in toxic/lethal amounts identified at postmortem included paramethoxyamphetamine (PMA) in all cases, amphetamine/methamphetamine in 4 cases, and methylenedioxymethamphetamine (MDMA or Ecstasy) in only 2 cases. Interaction with a prescription medication (fluoxetine) may have occurred in 1 case. CONCLUSIONS: The number of deaths due to amphetamine derivatives apparently due to substitution of PMA for MDMA (Ecstasy) have recently increased markedly in Adelaide. Potential users should be warned that PMA has been associated with a much higher rate of lethal complications than other designer drugs, and that no guarantee can be made that tablets sold as Ecstasy are not PMA.

Adult↗
PubMed1980

Tuinal as a drug of abuse.

Six case reports are presented to illustrate the problems of abuse of Tuinal (equal parts of sodium quinalbarbitone and sodium amylobarbitone). Over a four-year period in South Australia, Tuinal has risen from causing no deaths to be second only to pentobarbitone as a cause of death. While deaths from pentobarbitone overdosage are largely suicidal, Tuinal deaths are largely accidental, the result of a lack of tolerance in combination with alcohol potentiation.

Adolescent↗
PubMedDate not supplied

Application of a simple extraction procedure using aqueous ammonia to the analysis of basic drugs in blood by gas chromatography.

A simple and reliable previously reported extraction procedure has been extended to the analysis of a wide range of basic and neutral drugs in postmortem blood and other tissues. The method employs 200 microliters of blood treated with water and ammonia and extracted with diethyl ether. The concentrated extract is generally sufficiently clean for direct analysis by gas chromatography and high pressure liquid chromatography. Recovery, precision and linearity data are presented for selected drugs.

Ammonia↗
PubMedDate not supplied

An apparent fatal valproic acid poisoning.

While extensive data on therapeutic concentrations of valproic acid in plasma exist, data on toxic or fatal levels are very limited and superficial, interpretation of isolated blood levels obtained post-mortem is therefore a difficult task. A case of sudden death is described here. The circumstances are known and strongly indicate a fatal, suicidal poisoning by valproic acid at a dose of 56.4 g. Valproic acid was quantified in tissues by gas chromatography, and its identity confirmed by gas chromatography/mass spectrometry. The tissue concentrations found post-mortem were as follows: blood 720 mg/L; liver 800 mg/kg; stomach contents 1700 mg. Phenobarbitone and propoxyphene were also present at therapeutic concentrations. This data should provide a useful reference for interpretive purposes.

Adult↗