Biomedical subjects

John R M Caplehorn

Publications and source records attributed to John R M Caplehorn.

4 recordsLinked to original sources

PubMed2003

The incidence of drugs in drivers killed in Australian road traffic crashes.

The incidence of alcohol and drugs in fatally injured drivers were determined in three Australian states; Victoria (VIC), New South Wales (NSW) and Western Australia (WA) for the period of 1990-1999. A total of 3398 driver fatalities were investigated which included 2609 car drivers, 650 motorcyclists and 139 truck drivers. Alcohol at or over 0.05 g/100ml (%) was present in 29.1% of all drivers. The highest prevalence was in car drivers (30.3%) and the lowest in truckers (8.6%). WA had the highest rate of alcohol presence of the three states (35.8%). Almost 10% of the cases involved both alcohol and drugs. Drugs (other than alcohol) were present in 26.7% of cases and psychotropic drugs in 23.5%. These drugs comprised cannabis (13.5%), opioids (4.9%), stimulants (4.1%), benzodiazepines (4.1%) and other psychotropic drugs (2.7%). 8.5% of all drivers tested positive for Delta(9)-tetrahydrocannabinol (THC) and the balance of cannabis positive drivers were positive to only the 11-nor-Delta(9)-tetrahydrocannabinol-9-carboxylic acid (carboxy-THC) metabolite. The range of THC blood concentrations in drivers was 0.1-228 ng/ml, with a median of 9 ng/ml. Opioids consisted mainly of morphine (n=84), codeine (n=89) and methadone (n=33), while stimulants consisted mainly of methamphetamine (n=51), MDMA (n=6), cocaine (n=5), and the ephedrines (n=61). The prevalence of drugs increased over the decade, particularly cannabis and opioids, while alcohol decreased. Cannabis had a larger prevalence in motorcyclists (22.2%), whereas stimulants had a much larger presence in truckers (23%).

Accidents, Traffic↗

PubMed2003

A comparison of buprenorphine treatment in clinic and primary care settings: a randomised trial.

OBJECTIVE: To compare outcomes, costs and incremental cost-effectiveness of heroin detoxification performed in a specialist clinic and in general practice. DESIGN AND SETTING: Randomised controlled trial set in a specialist outpatient drug treatment centre and six office-based general practices in inner city Sydney, Australia. PARTICIPANTS: 115 people seeking treatment for heroin dependence, of whom 97 (84%) were reinterviewed at Day 8, and 78 (68%) at Day 91. INTERVENTIONS: Participants were randomly allocated to primary care or a specialist clinic, and received buprenorphine for 5 days for detoxification, then were offered either maintenance therapy with methadone or buprenorphine, relapse prevention with naltrexone, or counselling alone. MAIN OUTCOME MEASURES: Completion of detoxification, engagement in post-detoxification treatment, and heroin use assessed at Days 8 and 91. Costs relevant to providing treatment, including staff time, medication use and diagnostic procedures, with abstinence from heroin use on Day 8 as the primary outcome measure. RESULTS: There were no significant differences in the proportions completing detoxification (40/56 [71%] primary care v 46/59 [78%] clinic), participating in postwithdrawal treatment (28/56 [50%] primary care v 36/59 [61%] clinic), reporting no opiate use during the withdrawal period (13/56 [23%] primary care v 13/59 [22%] clinic), and in duration of postwithdrawal treatment by survival analysis. Most participants in both groups entered postwithdrawal buprenorphine maintenance. On an intention-to-treat basis, self-reported heroin use in the month before the Day 91 interview was significantly lower than at baseline (27 days/month at baseline, 14 days/month at Day 91; P < 0.001) and did not differ between groups. Buprenorphine detoxification in primary care was estimated to be $24 more expensive per patient than treatment at the clinic. The incremental cost-effectiveness ratio reveals that, in this context, it costs $20 to achieve a 1% improvement in outcome in primary care. CONCLUSIONS: Buprenorphine-assisted detoxification from heroin in specialist clinic and primary care settings had similar efficacy and cost-effectiveness. Buprenorphine treatment can be initiated safely in primary care settings by trained GPs.

Adolescent↗

PubMed2002

Methadone dose and post-mortem blood concentration.

The relationship of methadone dose with post-mortem blood concentration was investigated using data collected from 1994 coronial cases in the Australian state of New South Wales. Data on 31 subjects were summarized using linear regression. The weight-adjusted methadone dose, gender, methadone maintenance treatment status and its interaction with adjusted-dose were all significant predictors of post-mortem blood methadone concentration. Data on the death of a young man from the toxic effects of three daily doses of 30 mg methadone are used to give an example of a pair of observed (0.74 mg/l) and predicted (0.48 mg/l) post-mortem blood concentrations. The estimated post-mortem blood concentration for male maintenance patients is at least twice the trough plasma levels estimated from previously published studies of living maintenance patients. The estimated post-mortem blood concentration for female maintenance patients is at least three times the estimated trough level of living subjects. We conclude that post-mortem methadone redistribution is probably the principal cause of the observed differences between males and females in post-mortem blood concentrations and the differences between estimated concentrations for living and deceased subjects.

Drug Overdose↗

PubMed2002

Fatal methadone toxicity: signs and circumstances, and the role of benzodiazepines.

OBJECTIVE: To describe the signs and symptoms and circumstances of fatal methadone toxicity and investigate the role of benzodiazepines in these deaths. METHODS: Data were extracted from 1994 New South Wales (NSW) coronial files and cause of death established independently. Cases were grouped according to the likely source of methadone. Data describing the clinical history and circumstances of death were extracted from witnesses' and police statements. RESULTS: Methadone contributed to the deaths of 57 of the 87 adult coronial cases in which it was detected in NSW in 1994. The most commonly reported early signs of severe methadone toxicity were ataxia, slurred speech and evident euphoria. The late signs were unconsciousness, loud snoring and brown pulmonary oedema fluid coming from the mouth or nose. Death occurred an average 5.1 and 6.0 hours after oral ingestion and intravenous injection of methadone, respectively. Benzodiazepines were significantly more likely to have contributed to deaths from methadone toxicity among maintenance patients and people taking methadone tablets for pain relief than deaths involving diverted methadone syrup and deaths to which methadone did not contribute (OR 4.8, 95% 1.7 to 14.4). CONCLUSIONS AND IMPLICATIONS: Benzodiazepines may contribute to deaths from methadone toxicity by increasing upper airways obstruction. Victims would have had a greater chance of survival if they had either been placed in the coma position or given mouth-to-mouth ventilation and an ambulance had been called. Benzodiazepines are more likely to contribute to fatal methadone toxicity in newly admitted maintenance patients and those taking methadone tablets for pain relief.

Adult↗