Drug Overdose

Introduction

Poisoning is a common emergency presentation, ranging from a small accidental paediatric ingestion to a life-threatening deliberate overdose in an adult. The overwhelming majority of poisoned patients are managed with supportive care and observation rather than a specific antidote, which is why the general approach - resuscitation, a careful history, risk assessment, and knowing when a specific treatment does exist - matters more than memorising every possible ingestion.

In the UK, deliberate self-poisoning with prescribed or over-the-counter medication accounts for the majority of adult presentations, most often paracetamol, other analgesics, and psychotropic medication such as antidepressants and benzodiazepines, frequently with alcohol co-ingested. Accidental poisoning is more common in young children, typically involving medication found in the home, and recreational drug toxicity forms a further distinct group with its own patterns of presentation and complication.

TOXBASE, the UK National Poisons Information Service database, is the standard reference for management advice on a specific agent, with a telephone service for complex or unusual cases.¹ This article covers the general framework and the handful of overdoses with well-defined specific treatment; paracetamol overdose, the commonest single-agent poisoning in the UK, is covered separately given how frequently it is tested.

General approach

1. ABCDE assessment and resuscitation - treat physiological derangement as it is found, before or alongside identifying the agent
2. History - what was taken, how much, when, by what route, whether anything else was co-ingested (including alcohol), and any collateral information from family, paramedics or packaging found at the scene
3. Examination for a toxidrome - pupil size, skin (dry versus sweaty), bowel sounds, temperature and tone can suggest a class of drug even before any history is available
4. Blood glucose in every patient with reduced consciousness
5. Check TOXBASE for agent-specific guidance, and call the National Poisons Information Service telephone line for complex or unusual presentations
6. Risk-assess and plan psychiatric review in every case of deliberate self-poisoning, in parallel with medical treatment rather than after it

Decontamination

Gastrointestinal decontamination has a narrow, well-defined role and is not appropriate for every ingestion - most patients gain nothing from it and it carries real risks of its own.

• Activated charcoal (50 g in adults) binds many drugs within the gut if given within 1 hour of ingestion, in a patient with a protected airway. It is ineffective for alcohols, metals (iron, lithium), corticosteroids and most electrolytes, and is contraindicated in a patient with reduced consciousness unless the airway is secured, given the risk of aspiration
• Multiple-dose activated charcoal enhances elimination of certain drugs already absorbed (for example carbamazepine, theophylline, dapsone) by interrupting enterohepatic or enteroenteric recirculation, given as repeated doses rather than as decontamination
• Whole bowel irrigation with polyethylene glycol solution is reserved for specific situations - iron overdose, lithium, or ingested packets of drugs (body packers) - since charcoal does not bind these effectively
• Gastric lavage is now rarely used, reserved for exceptional cases of very recent, large, life-threatening ingestion, given a poor evidence base and significant risk of aspiration and oesophageal injury

Specific antidotes

A specific antidote exists for only a minority of poisonings, but knowing which ones is high-yield, both clinically and for exams.

Tricyclic antidepressant overdose

Tricyclic overdose remains an important cause of death in deliberate self-poisoning because of its narrow therapeutic index and cardiotoxicity, working through sodium channel blockade in the myocardium (a quinidine-like effect) alongside anticholinergic and antihistaminergic effects.

• Anticholinergic features - dry mouth, dilated pupils, urinary retention, tachycardia, agitation progressing to drowsiness and coma
• Cardiotoxicity - widened QRS complex, prolonged QT, arrhythmia (including ventricular tachycardia), and hypotension
• Seizures in significant overdose

Beta-blocker and calcium channel blocker overdose

Both classes can cause profound bradycardia and hypotension that is often refractory to standard inotropes and vasopressors, and the two can look very similar - a helpful discriminator is that calcium channel blocker toxicity more often preserves consciousness relative to the degree of hypotension, since it does not directly impair cardiac conduction to the same extent as severe beta-blockade, though this is not absolute.

• Glucagon bypasses the blocked beta-receptor to raise intracellular cyclic AMP directly, improving heart rate and contractility - useful in beta-blocker overdose, less reliably effective in calcium channel blocker toxicity
• IV calcium (calcium chloride or gluconate) can improve contractility in calcium channel blocker overdose by overcoming the blockade with a mass-action effect
• High-dose insulin-euglycaemia therapy - high-dose IV insulin with concurrent dextrose to maintain normoglycaemia improves myocardial contractility in both, and is now considered first-line for significant toxicity refractory to initial measures, working by shifting the poisoned, carbohydrate-starved myocardium back towards glucose utilisation
• Extracorporeal life support for refractory cardiogenic shock in severe cases, where available

Salicylate (aspirin) overdose

Salicylates directly stimulate the respiratory centre (causing an early respiratory alkalosis) and uncouple oxidative phosphorylation (causing a later metabolic acidosis with a raised anion gap), producing a mixed acid-base picture that is itself a classic exam feature.

• Features - tinnitus, hyperventilation, sweating, nausea and vomiting, and in severe toxicity, confusion, seizures and coma
• Salicylate level guides severity and the need for treatment, interpreted alongside the clinical picture and time since ingestion
• Urinary alkalinisation with IV sodium bicarbonate increases renal elimination of salicylate by ion trapping in alkaline urine, and is first-line for moderate toxicity
• Haemodialysis for severe toxicity - very high levels, significant acidosis, renal failure, pulmonary oedema, or significant neurological features

Psychiatric assessment after deliberate self-poisoning

Medical stabilisation is only half of managing a deliberate overdose. Every patient needs a structured risk assessment covering intent, ongoing suicidal ideation, protective factors and immediate safety, ideally by a mental health professional, before discharge is considered.²

• Assess capacity if the patient wishes to leave before treatment (for example N-acetylcysteine) is complete - capacity can fluctuate with intoxication and needs reassessing rather than assuming a single assessment holds throughout the admission
• Involve liaison psychiatry for formal risk assessment once medically stable, and earlier if there is any immediate safety concern
• Consider the Mental Health Act where a patient with a treatable, life-threatening overdose lacks capacity and is trying to leave against medical advice, in line with local policy and legal advice
• Do not treat 'medical clearance' and psychiatric risk assessment as sequential - safety planning, removing means, and involving family or crisis services can and should start alongside medical treatment

Red flags

Prognosis

Most poisoned patients recover fully with supportive care, and outcome is generally determined by the specific agent, the dose, co-ingestants, and how quickly treatment (supportive or specific) is started. Beyond the acute admission, the more important determinant of long-term outcome is often the psychiatric and social response to a deliberate overdose - the medical episode is frequently the easier problem to solve.