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Self-poisoning is a manifestation of an underlying psychiatric, drug and alcohol, or social disorder.
A wide range of clinical manifestations of toxicity may be observed following drug overdose.
An accurate risk assessment predicts the likely clinical course and informs planning for subsequent investigation, management and disposition.
The mainstay of management is timely institution of an appropriate level of supportive care.
Gastrointestinal decontamination should be considered in all cases based on risk versus benefit. In select cases, these procedures may have a significant impact on clinical outcome, even when delayed.
Specific antidotes and enhanced elimination techniques are rarely indicated, but their timely use may be life-saving in specific circumstances.
Drug overdose in adults usually occurs in the context of self-poisoning, which may be either recreational or deliberate.
Deliberate self-poisoning accounts for 1% to 5% of all public hospital admissions in Australia. The bulk of the medical management is carried out in the emergency department (ED), and emergency physicians are expected to be experts. Although management varies considerably depending on the nature and severity of the poisoning, some general principles apply.
Above all, it must be remembered that the acute overdose presentation is only a discrete time-limited event in the course of the underlying condition, which is usually psychosocial in origin.
The effects of ingestion of pharmaceuticals or illicit drugs range from the non-toxic to the life threatening and may involve any system. Poisoning is a dynamic presentation, and the patient may present at varying points in its time course. Consequently, rapid clinical deterioration or improvement may be observed after the initial presentation and assessment.
Acute morbidity and mortality are usually a consequence of the cardiovascular, respiratory or central nervous system (CNS) complications of the poisoning. Less commonly, hepatic, renal or metabolic effects can be potentially life threatening.
The most frequent life-threatening respiratory manifestation of poisoning is ventilatory failure, which is usually a consequence of CNS depression causing apnoea or bradypnoea. Less commonly, it is secondary to muscle paralysis, direct pulmonary toxicity or non-cardiogenic pulmonary oedema ( Box 25.1.1 ).
Alcohols
Antidepressants
Antihistamines
Barbiturates
Baclofen
Clonidine
Phenothiazines
Sedative-hypnotics
Opioids
Organophosphorous pesticides and warfare agents
Carbamate pesticides
Snakebite
Strychnine
Muscle relaxants
Pulmonary aspiration and pneumonitis
Hydrocarbons
Gastric contents
Activated charcoal
Non-cardiogenic pulmonary oedema
Cardiogenic pulmonary oedema
Adult respiratory distress syndrome
Paraquat
Cardiovascular manifestations of poisoning include tachycardia, bradycardia, hypertension, hypotension, conduction defects and arrhythmias ( Box 25.1.2 ). Bradycardia is relatively rare and is associated with a number of potentially life-threatening ingestions, whereas tachycardia is commonly observed and is usually benign. It may be due to intrinsic sympathomimetic or anticholinergic effects of a drug or a reflex response to hypotension or hypoxia. Hypotension is also common and may be due to a number of different mechanisms (see Box 25.1.2 ). Hypertension is usually associated with illicit drug use and is important because it may produce complications such as intracerebral haemorrhage if severe and uncontrolled.
Anticholinergics
Pure anticholinergics, e.g. Benztropine
Antihistamines
Phenothiazines
Atypical antipsychotics
Tricyclic antidepressants
Monoamine oxidase inhibitors
Sympathomimetics
Amphetamines
Cocaine
Caffeine
Theophylline
Synthetic cannabinoid receptor agonists
Venlafaxine
Tramadol
Digoxin
Drug withdrawal syndromes
β-Blockers
Calcium channel blockers
Clonidine
Digoxin
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