Dr Joyce Cooper

Objectives: To identify factors influencing Australian consumer decision-making and attitudes towards non-prescription medicine (NPM) purchases, pharmacy's role in providing these medications and views around sources of evidence for effectiveness of these products. Methods: Cross-sectional survey of a general population sample of 1731 adults using an Australian online consumer panel stratified by gender, age and location (State/Territory). Beliefs about NPM purchases and evidence of their efficacy were assessed using a 5-point Likert scale (strongly disagree-strongly agree). Non-parametric measures (Ridit analysis and Mann¿Whitney U-test) were used to explore associations between responses and previous experience with medicines. Key findings: The most important factors when purchasing NPMs were effectiveness and safety. However, personal experience was the most common method of determining effectiveness. Most respondents believed buying NPMs in pharmacies gave access to advice, but were less likely to agree that pharmacies were associated with safe and effective treatments. Around half the respondents agreed that it is wrong to sell treatments lacking scientific evidence; many also agreed that it is up to consumers to decide what they want even without scientific evidence. Individuals experiencing an ineffective NPM were less likely to trust scientific evidence of efficacy as the sole source of effectiveness information; regular prescription medicine users often agreed that scientific evidence is needed to support effectiveness. Conclusions: Consumers have conflicting views regarding the need for scientific evidence and the desire for patient autonomy in NPM purchases. This presents a challenge for pharmacists wishing to maintain professional obligations to provide evidence-based treatments to consumers.

Context: Desvenlafaxine is used to treat major depression. Desvenlafaxine is also the active metabolite of venlafaxine. Venlafaxine overdose can cause serotonin toxicity, seizures and cardiovascular effects, but there is limited information on desvenlafaxine overdose. Objective: We aimed at investigating the clinical effects and complications from desvenlafaxine overdose. Materials and methods: This was a retrospective observational study of desvenlafaxine overdoses over a six-year period. Demographic details, dose and timing of the overdose, together with clinical effects, treatment and complications were extracted from a local hospital network database or the medical records of patients following hospital admission with a desvenlafaxine overdose. Results: There were 182 cases of desvenlafaxine overdose included in the study. From the 182 cases, 75 were desvenlafaxine (± alcohol) only ingestions and 107 included one or more co-ingested drugs. In single-agent desvenlafaxine ingestions, median age was 25 years (range: 13¿68 years) with a median ingested dose of 800 mg (range: 250¿3500 mg; interquartile range (IQR): 600¿1400 mg), and 54/75 (72%) were female. The Glasgow Coma Score (GCS) was 15 in 68/74 (92%) patients, 13¿14 in 5/74 (7%), and was seven in one patient following aspiration. Mild hypertension (systolic blood pressure [BP] > 140¿180 mmHg) occurred in 23/71 patients (32%), and tachycardia occurred in 29/74 (39%) patients. There were no abnormal QT intervals and no QRS >120 m s. Serotonin toxicity was diagnosed by the treating physician in 7/75 (9%) patients, but only one of these met the Hunter Serotonin Toxicity Criteria. None of the 75 patients who took desvenlafaxine only (± alcohol) had seizures, were admitted to intensive care or died. In comparison, the 107 patients taking desvenlafaxine in overdose with other medications developed more pronounced toxicity. Generalised seizures occurred in 5/107 (5%), but in three of these cases co-ingestants were possible proconvulsants. Fifteen patients had a GCS =9 and none had an abnormal QT or QRS. Severe effects appeared to be associated with coingestants. Conclusion: Desvenlafaxine overdose causes minor effects with mild hypertension and tachycardia. The risk of seizures or serotonin toxicity is low.

Aims To investigate the pharmacokinetics (PK) of sertraline in overdose and the effect of single dose activated charcoal (SDAC). Methods Patients presenting to a toxicology unit with sertraline overdoses had demographic and clinical information recorded, and serial serum collected for measurement of sertraline concentrations. Monolix® version 4.2 was used to develop a population PK model of sertraline overdose and the effect of SDAC. Uncertainty in dose time was accounted for by shifting dose time using lag time with between subject variability (BSV). BSV on relative fraction absorbed was used to model uncertainty in dose. Results There were 77 timed sertraline concentrations measured in 28 patients with sertraline overdoses with a median dose of 1550 mg (250-5000 mg). SDAC was given to seven patients between 1.5 and 4 h post-overdose. A one compartment model with lag time of 1 h and first order input and elimination adequately described the data. Including BSV on both lag time and relative fraction absorbed improved the model. The population PK parameter estimates for absorption rate constant, volume of distribution and clearance were 0.895 h-1, 5340 l and 130 l h-1, respectively. The calculated half-life of sertraline following overdose was 28 h (IQR 19.4-30.6h). When given up to 4 h post-overdose, SDAC significantly increased the clearance of sertraline by a factor of 1.9, decreased the area under the curve and decreased the maximum plasma concentration (Cmax). Conclusions Sertraline had linear kinetics in overdose with parameter values similar to those in therapeutic use. SDAC is effective in increasing clearance when given 1.5 to 4 h post-overdose.

Objective. To describe the clinical effects, pharmacokinetics, and pharmacodynamics of plasma and acetylcholinesterase in an aldicarb overdose. Case Report. A 57-year-old female was found unconscious and incontinent of urine after ingesting aldicarb. She was bradycardic, hypotensive, hypersalivating, clammy, had small pupils, and generalized weakness. She was intubated, ventilated, and treated with large atropine doses (50 mg and 20 mg/h infusion) and adrenaline. She improved hemodynamically over 24 h, but remained comatose for another 24 h, before recovering without sequela. Aldicarb concentration at admission was 2.18 µg/ml and concentration-time data best fitted a two compartmental model with first order absorption and a time of ingestion 4.5 h preadmission. The half-life of distribution was 0.4 h and half-life of elimination, 13 h. Plasma cholinesterase concentration at admission was 0.3 kU/L (Reference range[RR]:4.3-10.6 kU/L) and red cell cholinesterase was 10 U/gHb (RR:38-66 U/gHb). The IC50 was 0.15 µg/ml and 0.26 µg/ml for plasma and red cell cholinesterase, respectively. Discussion. Aldicarb poisoning causes rapid onset severe toxicity with muscarinic and nicotinic excess, seizures, and decreased consciousness. Cholinesterases rapidly recover once aldicarb concentrations decrease and precede clinical recovery.

A key motivator for the use of serious games has been the notion that ¿gamification¿ provides users with an additional level of engagement. This study examines a traditional model of usability in terms of engagement and efficacy, presenting the results obtained from a formative evaluation of a serious game prototype that has been developed to assist in pharmacy education.