10 Poisoning, overdose, antidotes
Initial assessment
• The identity of the substance(s) taken.
• The time that has elapsed since ingestion.
• Whether alcohol was also taken.
Adults may be sufficiently conscious to give some indication of the poison or may have referred to it in a suicide note, or there may be other circumstantial evidence e.g. knowledge of the prescribed drugs that the patient had access to, empty drug containers in pocket or at the scene. The ambulance crew attending to the patient at home may have very valuable information and should be questioned for any clues to the ingested drug. Any family or friends attending with the patient should be similarly questioned.
Many substances used in accidental or self-poisoning produce recognisable symptoms and signs. Some arise from dysfunction of the central or autonomic nervous systems; other agents produce individual effects. They can be useful diagnostically and provide characteristic toxic syndromes or ‘toxidromes’ (Table 10.1).
Table 10.1 Characteristic drug ‘toxidromes’
| Toxidrome | Clinical features | Causative agents |
|---|---|---|
| Antimuscarinic | Tachycardia Dilated pupils Dry, flushed skin Urinary retention Decreased bowel sounds Mild increase in body temperature Confusion Cardiac arrhythmias Seizures | Antipsychotics Tricyclic antidepressants Antihistamines Antispasmodics Many plant toxins |
| Muscarinic | Salivation Lachrymation Abdominal cramps Urinary and faecal incontinence Vomiting Sweating Miosis Muscle fasciculation and weakness Bradycardia Pulmonary oedema Confusion CNS depression Seizures | Anticholinesterases Organophosphorus insecticides Carbamate insecticides Galantamine Donepezil |
| Sympathomimetic | Tachycardia Hypertension Hyperthermia Sweating Mydriasis Hyperreflexia Agitation Delusions Paranoia Seizures Cardiac arrhythmias |
Resuscitation
Rapid biochemical ‘screens’ of urine are widely available in hospital emergency departments and will detect a range of drugs (Table 10.2).
Table 10.2 Drugs that can be readily tested for and detected in urine in the emergency department
| Drugs detectable on rapid urine testing |
Supportive treatment
TOXBASE, the primary clinical toxicology database of the UK National Poisons Information Service, is available on the internet to registered users at: http://www.toxbase.org
Special problems introduced by poisoning are as follows:
• Airway maintenance is essential; some patients require a cuffed endotracheal tube but seldom for more than 24 h.
• Ventilation: a mixed respiratory and metabolic acidosis is common; the inspired air is supplemented with oxygen to correct the hypoxia. Mechanical ventilation is necessary if adequate oxygenation cannot be obtained or hypercapnia ensues.
• Hypotension: this is common in poisoning and, in addition to the resuscitative measures indicated above, conventional inotropic support may be required.
• In addition: there is recent interest in the use of high dose insulin infusions with euglycaemic clamping as a positive inotrope in the context of overdose with myocardial depressant agents. The very high insulin doses given (0.5–2 units/kg/h) have so far deterred physicians from the routine use of such therapy. There are, however, a number of case reports that support such an approach. Many of these are in the context of overdosage with non-dihydropyridine calcium channel blockers that are often resistant to conventional inotropic agents.
• Convulsions should be treated if they are persistent or protracted. Intravenous benzodiazepine (diazepam or lorazepam) is the first choice.
• Cardiac arrhythmia frequently accompanies poisoning, e.g. with tricyclic antidepressants, theophylline, β-adrenoceptor blockers.
• Acidosis, hypoxia and electrolyte disturbance are often important contributory factors and it is preferable to observe the effect of correcting these before considering resort to an antiarrhythmic drug. If arrhythmia does lead to persistent peripheral circulatory failure, an appropriate drug may be cautiously justified, e.g. a β-adrenoceptor blocker for poisoning with a sympathomimetic drug.
• Hypothermia may occur if CNS depression impairs temperature regulation. A low-reading rectal thermometer is used to monitor core temperature and the patient is nursed in a heat-retaining ‘space blanket’.
• Immobility may lead to pressure lesions of peripheral nerves, cutaneous blisters, necrosis over bony prominences, and increased risk of thromboembolism warrants prophylaxis.
• Rhabdomyolysis may result from prolonged pressure on muscles from agents that cause muscle spasm or convulsions (phencyclidine, theophylline); may be aggravated by hyperthermia due to muscle contraction, e.g. with MDMA (‘ecstasy’). Aggressive volume repletion and correction of acid–base abnormality are needed; urine alkalinisation and/or diuretic therapy may be helpful in preventing acute tubular necrosis but evidence is not conclusive.
Preventing further absorption of the poison
From the alimentary tract (‘gut decontamination’)1
Oral adsorbents
Activated charcoal (Carbomix) consists of a very fine black powder prepared from vegetable matter, e.g. wood pulp, coconut shell, which is ‘activated’ by an oxidising gas flow at high temperature to create a network of small (10–20 nm) pores with an enormous surface area in relation to weight (1000 m2/g). This binds to, and thus inactivates, a wide variety of compounds in the gut. Indeed, activated charcoal comes nearest to fulfilling the long-sought notion of a ‘universal antidote’.2 Thus it is simpler to list the exceptions, i.e. substances that are poorly adsorbed by charcoal:
• Metal salts (iron, lithium).
• Alcohols (ethanol, methanol, ethylene glycol).
• Clofenotane (dicophane, DDT).
To be most effective, five to ten times as much charcoal as poison, weight for weight, is needed. In the adult an initial dose of 50 g is usual, repeated if necessary. If the patient is vomiting, give the charcoal through a nasogastric tube. Unless a patient has an intact or protected airway its administration is contraindicated.
Accelerating elimination of the poison
• The poison should be present in high concentration in the plasma relative to that in the rest of the body, i.e. it should have a small volume of distribution.
• The poison should dissociate readily from any plasma protein binding sites.
• The effects of the poison should relate to its plasma concentration.
Methods used are:
Alteration of urine pH and diuresis
It is useful to alter the pH of the glomerular filtrate such that a drug that is a weak electrolyte will ionise, become less lipid soluble, remain in the renal tubular fluid, and leave the body in the urine (see p. 80).
Alkalinisation4 may be used for: salicylate (> 500 mg/L + metabolic acidosis, or in any case > 750 mg/L) phenobarbital (75–150 mg/L); phenoxy herbicides, e.g. 2,4-D, mecoprop, dichlorprop; moderately severe salicylate poisoning that does not meet the criteria for haemodialysis.
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