These redefined criteria for serotonin toxicity should be more sensitive to serotonin toxicity and less likely to yield false positives.

Excess serotonin in the central nervous system leads to a condition commonly referred to as the serotonin syndrome, but better described as a spectrum of toxicity — serotonin toxicity. Serotonin toxicity is characterised by neuromuscular excitation (clonus, hyperreflexia, myoclonus, rigidity), autonomic stimulation (hyperthermia, tachycardia, diaphoresis, tremor, flushing) and changed mental state (anxiety, agitation, confusion). Serotonin toxicity can be: mild (serotonergic features that may or may not concern the patient); moderate (toxicity which causes significant distress and deserves treatment, but is not life‐threatening); or severe (a medical emergency characterised by rapid onset of severe hyperthermia, muscle rigidity and multiple organ failure). Diagnosis of serotonin toxicity is often made on the basis of the presence of at least three of Sternbach's 10 clinical features. However, these features have very low specificity. The Hunter Serotonin Toxicity Criteria use a smaller, more specific set of clinical features for diagnosis, including clonus, which has been found to be more specific to serotonin toxicity. There are several drug mechanisms that cause excess serotonin, but severe serotonin toxicity only occurs with combinations of drugs acting at different sites, most commonly including a monoamine oxidase inhibitor and a serotonin reuptake inhibitor. Less severe toxicity occurs with other combinations, overdoses and even single‐drug therapy in susceptible individuals. Treatment should focus on cessation of the serotonergic medication and supportive care. Some antiserotonergic agents have been used in clinical practice, but the preferred agent, dose and indications are not well defined.

Venlafaxine and dothiepin are pro-convulsant in overdose. Venlafaxine is more likely to cause serotonin toxicity, but less likely to cause coma than TCAs. SSRIs are less likely to cause coma, require ICU admission, or prolong the QRS, but are more likely to cause serotonin toxicity. Antidepressants other than TCAs or venlafaxine should be considered in patients at risk of seizure or suicide.

E stimates of admissions for deliberate self-poisoning vary from 1%1 up to 5%2 of public hospital admissions. More than 50% of these admissions occur between 6 pm and 2 am. 3 Deliberate self-poisoning (including carbon monoxide) is the cause of death in 42% of suicides.'With a few exceptions, deliberate self-poisoning is managed on an ad-hoc basis in Australian hospitals. Commonly, the patient is managed in the emergency department and, if required, admission occurs under the general physician of the day or under the specialty which best corresponds to the patient's toxicological problem. Other models include medical management for most patients occurring entirely within the emergency department/intensive care axis. In one centre, 30% of patients with deliberate self-poisoning were not formally admitted." In many centres, expertise in toxicology comes from outside the service providing the patient care (e.g., from Poisons Information Centres).In these models of management, not every patient with deliberate self-poisoning receives formal psychiatric assessment. Despite evidence that psychiatric intervention after parasuicide is worthwhile," psychiatric resources are commonly concentrated on those patients who require admission and those who have the most medically severe poisoning." However, significant suicidal risk is present for many patients with toxicologically "trivial" poisonings. Service structureIn 1986 the Department of Clinical Pharmacology, then located at the Royal Newcastle Hospital, was requested to manage deliberate self-poisoning and other toxicology patients. The Hunter Area Toxicology Service (HATS) was established jointly by the Department of Clinical Toxicology and Pharmacology and the Department of Liaison Psychiatry in January 1987. The only increase in staff was one registrar position in clinical pharmacology.All deliberate self-poisoning patients are formally admitted under the HATS clinical toxicologist, who retains primary responsibility for care during the whole admission.

Severe lithium neurotoxicity occurs almost exclusively in the context of chronic therapeutic administration of lithium, and rarely results from acute ingestion of lithium, even in patients currently taking lithium. As such it is an iatrogenic illness, occurring in patients who have identifiable clinical risk factors: nephrogenic diabetes insipidus, older age, abnormal thyroid function and impaired renal function. Although administration of drugs which impair lithium clearance appeared to contribute minimally to chronic lithium poisoning in the absence of other factors, these drugs may well 'uncover' the predisposing risk factors and certainly should not be considered safe to use as a consequence of this study. The serious morbidity suffered by lithium toxic patients, and the cost to society due to long hospital stays, might be reduced by careful prescribing, vigilant monitoring and awareness of these factors, as they develop in otherwise stable patients. Review of existing therapeutic guidelines may be warranted.

A postcard intervention halved self-poisoning events and reduced psychiatric admissions by a third after 5 years. Substantial savings occurred in general hospital and psychiatric hospital bed days.

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The differences claimed between oral and intravenous N-acetylcysteine regimes are probably artifactual and relate to inappropriate subgroup analysis. A shorter hospital stay, patient and doctor convenience, and the concerns over the reduction in bioavailability of oral N-acetylcysteine by charcoal and vomiting make intravenous N-acetylcysteine preferable for most patients with acetaminophen poisoning.