18 Poisoning
Care of the unconscious patient
• All self-ventilated patients should be nursed in the left lateral position with the lower leg straight and the upper leg flexed; in this position the risk of aspiration is reduced. A clear passage for air should be ensured.
• Nursing care of the mouth and pressure areas should be instituted. Immediate catheterization of the bladder in unconscious patients is usually unnecessary, as it can be emptied by gentle suprapubic pressure.
• Insertion of a venous cannula is usual, but administration of IV fluids is unnecessary unless the patient has been unconscious for more than 12 hours or is hypotensive.
Ventilatory support
• If respiratory depression is present, as determined by pulse oximetry or preferably by arterial blood gas (ABG) analysis, an oro-pharyngeal airway should be inserted and oxygen should be administered.
• The gag reflex can be assessed by positioning the patient on one side and making him or her gag using a suction tube.
• In many severely poisoned patients the reflexes are depressed sufficiently to allow intubation without the use of sedatives or relaxants. The complications of endotracheal tubes are discussed on p. 544.
Cardiovascular support
• Although hypotension (systolic BP < 80 mmHg) is a recognized feature of acute poisoning, the classic features of shock — tachycardia and pale cold skin — are observed only rarely.
• In patients with marked hypotension, volume expansion with crystalloids should be used, guided by monitoring of central venous pressure (CVP).
• Urine output (aiming for 35–50 mL/hour) is also a useful guide to the adequacy of the circulation.
Other problems
• Hypothermia: rectal temperature below 35°C. The patient should be covered with a ‘space blanket’ and, if necessary, given IV and fluids at normal body temperature. The administration of heated (37°C), humidified oxygen delivered by face mask is also useful.
• Skin blisters: may be found in poisoned patients who are, or have been, unconscious. Such lesions are not diagnostic of specific poisons, but are sufficiently common in poisoned patients (and sufficiently uncommon in patients unconscious from other causes) to be of diagnostic value.
• Rhabdomyolysis: can occur from pressure necrosis in drug-induced coma, or it may complicate, for example, ecstasy (MDMA) use in the absence of coma. Patients with rhabdomyolysis are at risk of developing:
• Convulsions: occur, for example, in poisoning due to tricyclic antidepressants, mefenamic acid or opioids. Usually the seizures are short-lived, but if they are prolonged, diazepam 10–20 mg IV or lorazepam 4 mg IV should be administered.
• Stress ulceration and bleeding: measures to prevent stress ulceration of the stomach should be started on admission in all patients who are unconscious and require intensive care. A proton pump inhibitor, e.g. omeprazole 40 mg, should be administered intravenously over 5 mins or as an infusion over 20–30 mins.
Reduction of poison absorption
• Poison absorption through the lungs is reduced by moving the person from the toxic atmosphere, without the rescuers themselves being put at risk.
• Contaminated clothing should be removed to reduce dermal absorption. In addition, contaminated skin should be washed thoroughly with soap and water.
• The efficacy of current methods for the removal of unabsorbed drugs from the gastrointestinal tract remains unproven. Efforts to remove small amounts of non-toxic drugs are not worthwhile or appropriate.
Gastric lavage
• Gastric lavage should not be used routinely. It is used if a patient has ingested a potentially life-threatening amount of a poison and the procedure is undertaken within 60 mins of ingestion. Even then, clinical benefit has not been confirmed in controlled studies.
• Gastric lavage is contraindicated if airway protective reflexes are lost, unless the patient is intubated.
Single-dose activated charcoal
• The effectiveness of activated charcoal decreases with time. (In volunteers the mean reduction in absorption was 40%, 16% and 21% at 1 hour, 2 hours and 3 hours.) Activated charcoal should therefore only be used in those who have ingested a potentially toxic amount of a poison (known to be adsorbed by charcoal) up to 1 hour previously. There are insufficient data to support or exclude its use after 1 hour.
Increasing poison elimination
Urine alkalinization
• Before commencing urine alkalinization, correct plasma volume depletion and hypokalaemia, as administration of sodium bicarbonate will exacerbate pre-existing hypokalaemia.
• Sodium bicarbonate, most conveniently administered as an 8.4% solution (1 mmol bicarbonate/mL), is infused intravenously to ensure that the pH of the urine, which is measured by narrow-range indicator paper or a pH meter, is > 7.5 and preferably close to 8.5. In most cases the administration of 225 mmol bicarbonate will be required to produce urine alkalinization initially.
Multiple-dose activated charcoal (MDAC)
• Multiple doses of activated charcoal aid the elimination of some drugs from the circulation by interrupting their entero-hepatic and enter-enteric circulations.
• MDAC should be used only if a patient has ingested a life-threatening amount of carbamazepine, dapsone, phenobarbital, quinine or theophylline.
• Current recommendations are that adults should receive 50–100 g initially, followed by 50 g 4-hourly or 25 g 2-hourly until charcoal appears in the faeces or recovery occurs.
Haemodialysis, haemodiafiltration and haemofiltration (p. 358)
• Haemodialysis is of little value in patients who ingest poisons with large volumes of distribution, e.g. tricyclic antidepressants, because the plasma contains only a small proportion of the total amount of drug in the body.
• Haemodialysis is indicated in patients with severe features and high plasma concentrations of ethanol, ethylene glycol, isopropanol, lithium, methanol or salicylate.
• Although haemofiltration and haemodiafiltration are widely available and increase elimination of poisons such as ethylene glycol and methanol, haemofiltration is much less efficient than haemodialysis and therefore should not be used unless haemodialysis is unavailable. Haemodiafiltration is preferable to haemofiltration.
Specific poisons
Specific management for each poison is set out below alphabetically. Antidotes are available for only a small number of poisons (Table 18.1) and dosage recommendations are given under each poison.
Table 18.1 Antidotes of value in poisoning
| Poison | Antidote |
|---|---|
| Anticoagulants (oral) | Vitamin K1 |
| Arsenic | DMSA* Dimercaprol (BAL) |
| Benzodiazepines | Flumazenil |
| β-adrenoceptor-blocking drugs | Atropine Glucagon |
| Carbon monoxide | Oxygen |
| Copper | DMPS† |
| Cyanide | Oxygen Dicobalt edetate Hydroxocobalamin Sodium nitrite Sodium thiosulphate |
| Diethylene glycol | Fomepizole, ethanol |
| Digoxin | Digoxin-specific antibody fragments |
| Ethylene glycol | Fomepizole, ethanol |
| Iron salts | Desferrioxamine (deferoxamine) |
| Lead (inorganic) | Sodium calcium edetate DMSA* |
| Methaemoglobinaemia | Methylthioninium chloride (methylene blue) |
| Methanol | Fomepizole, ethanol |
| Mercury (inorganic) | DMPS† |
| Nerve agents | Atropine Pralidoxime, obidoxime |
| Opioids | Naloxone |
| Organophosphorus insecticides | Atropine Pralidoxime, obidoxime |
| Paracetamol | Acetylcysteine |
| Thallium | Berlin (Prussian) blue |
* Dimercaptosuccinic acid (succimer).
† 2,3-dimercaptopropanesulfonate (unithiol).
Acetone
Clinical features
• Acetone has an irritating effect on the mucous membranes of the eyes, nose and throat, causing burning and erythema. It also causes reversible corneal injury.
• Nausea, vomiting, light-headedness, headache, excitement, restlessness, chest tightness and incoherent speech are characteristic of intoxication. Coma, convulsions and respiratory failure supervene in severe cases. Kidney and liver damage can also occur.
Treatment
• Give 50–100 g of activated charcoal in an adult who presents within 1 hour of a substantial ingestion, providing the airway is secure. In vitro studies suggest that acetone is adsorbed to activated charcoal.
• Monitor blood glucose 1–2-hourly in symptomatic patients and correct hyperglycaemia with insulin. Take blood for renal and liver function assessment and measurement of creatine kinase activity.
• Give IV crystalloids, e.g. 0.9% saline, if vomiting is severe. Treat agitation and convulsions with IV diazepam 10–20 mg.
Amfetamines
The N-methylated derivative, metamfetamine, is now used widely; the crystalline form of this salt is known as ‘crystal meth’ or ‘ice’. Ecstasy (MDMA) is discussed on page 675.
Clinical features
• Euphoria, extrovert behaviour, a lack of desire to eat or sleep, tremor, dilated pupils, tachycardia and hypertension are seen.
• More severe intoxication is associated with agitation, paranoid delusions, hallucinations and violent behaviour.
• Convulsions, rhabdomyolysis, hyperthermia and cardiac arrhythmias may develop in severe intoxication.
Treatment
• Monitor electrolytes, renal function, liver function and creatine kinase (because of rhabdomyolysis) activity.
• Agitation may be controlled by diazepam 10–20 mg IV or haloperidol 2.5–5.0 mg IV or IM in an adult.
• The peripheral sympathomimetic actions of amfetamines (e.g. hypertension and arrhythmias) are antagonized by β-adrenoceptor blocking drugs (e.g. propranolol 40–80 mg orally or 1–5 mg IV slowly).
• Treat rhabdomyolysis conventionally with aggressive IV fluids to maintain high urine flow. There are theoretical reasons why urine alkalinization (p. 663) may be helpful in preventing or reducing the severity of rhabdomyolysis-induced kidney injury.
Anticonvulsants
See carbamazepine (p. 671), gabapentin (p. 677), lamotrigine (p. 679), phenytoin (p. 688) and sodium valproate (p. 691).
Antidepressants
See selective serotonin reuptake inhibitors (p. 690), mirtazapine (p. 681), monoamine oxidase inhibitors (p. 682), tricyclic antidepressants (p. 692) and venlafaxine (p. 693).
Batteries
Treatment
• Endoscopic removal is used for batteries lodged in the oesophagus or batteries that remain in the stomach more than 48 hours after ingestion, as they are at greater risk of leaking.
• If a small battery lies within the stomach on the first X-ray and patients are asymptomatic, they can be observed at home and return if any gastrointestinal symptoms develop. The stools should be inspected to confirm successful passage.
• If larger or multiple batteries have been ingested and are seen on the initial X-ray, confirm successful passage through the pylorus by repeating the X-ray 48 hours after ingestion.
Beta2-adrenoceptor agonists
Clinical features
• Patients who are poisoned with a β2-agonist, e.g. salbutamol, have a feeling of excitement, often accompanied by tremor, sinus tachycardia, agitation, convulsions, and supraventricular and ventricular arrhythmias.
Treatment
• Severe hypokalaemia should be corrected as soon as possible, by administration of potassium 40–60 mmol/hour, diluted with 0.9% saline. As patients given potassium may develop significant hyperkalaemia during recovery, potassium concentrations should be monitored closely.
• A non-selective β-blocker, e.g. propranolol 1–5 mg, can be administered by slow IV injection to reverse hypokalaemia and sinus tachycardia but may exacerbate pre-existing obstructive pulmonary disease. Propranolol is more effective than atenolol in reversing the metabolic effects of salbutamol.
• Supraventricular tachycardia has been treated successfully with adenosine 6 mg IV over 2 secs followed by 12 mg after 1–2 mins if no response. If myocardial ischaemia occurs as a result of a tachyarrhythmia, propranolol 1–5 mg IV should be administered.
Beta-adrenoceptor-blocking drugs
Clinical features
• Widened QRS and ventricular dysrhythmias, first-degree heart block, intraventricular conduction defects, right and left bundle branch block, ST segment elevation, the Brugada syndrome, ventricular extrasystoles and absent P waves may also be seen on ECG.
• Bronchospasm and respiratory depression can occur. Cardiorespiratory arrest caused by asystole or ventricular fibrillation occurs.
Treatment
• IV glucagon 10 mg (150 mc/kg) in an adult is the treatment of choice for significant hypotension that persists despite volume replacement. This dose can be repeated every 3–5 mins but if there is no response it is unlikely that further boluses will be helpful. IV glucagon at this dose causes vomiting and should be given slowly. It can be diluted in 5% glucose and infused over 15 mins if necessary.
• Standard inotropes e.g. dobutamine may be added. Insulin and glucose therapy (hyperinsulinaemic euglycaemic therapy) is used experimentally in severe poisoning.
• If bradycardia is refractory to atropine 0.6–1.2 mg IV, repeated as necessary, and IV glucagon, transcutaneous or transvenous pacing may be necessary.
• If there is a favourable response in BP and/or pulse rate to glucagon, commence a glucagon infusion 5–10 mg/hour depending on response. Monitor blood glucose during glucagon therapy.
• Convulsions are usually short-lived and treatment is seldom necessary, though IV diazepam 10–20 mg in an adult is very effective if seizures persist.
Benzodiazepines
Treatment
• If respiratory depression is present, flumazenil 0.5–1 mg IV should be administered in an adult and this dose may be repeated, if necessary.
• If the patient does not respond to flumazenil 1 mg it is likely that another respiratory depressant has been co-ingested.
• Flumazenil should not be administered if the patient is benzodiazepine-dependent, has epilepsy or has ingested pro-convulsants concurrently. Hypoventilation in these circumstances should be treated by mechanical ventilation (p. 544).
Calcium channel blockers
Clinical features
• The ECG may progress from sinus bradycardia through first, then higher, degrees of block, to asystole.
• When a sustained-release preparation has been ingested, the onset of severe features may be delayed for more than 12 hours.
Treatment
• Observe with cardiac and BP monitoring for at least 12 hours following overdose of a non-sustained-release preparation and at least 24 hours following overdose of a sustained-release preparation.
• Treat hypotension initially with IV crystalloid, 0.9% saline at a rate and volume appropriate to the age and co-morbidity of the patient. Expanding the intravascular volume in this way may be the only measure required in patients with hypotension secondary to peripheral vasodilatation who do not have evidence of impaired cardiac conduction.
• Correct metabolic acidosis that persists despite fluid resuscitation and adequate ventilation with 50–100 mmol of 8.4% sodium bicarbonate IV.
• Treat bradycardia with IV atropine 0.6–1.2 mg in an adult. This dose can be repeated as required. The response to atropine may be improved following parenteral calcium administration (see below).
• If there is evidence of cardiac conduction block, give 10% calcium chloride 5–10 mL IV (at 1–2 mL/min), or calcium gluconate solution, 10–20 mL to an adult. The initial dose can be repeated every 3–5 mins but if there is no response in BP or pulse rate after three such doses it is unlikely that further boluses will be helpful.
• If there is an initial response to calcium, give a continuous infusion; this may be given as 10% calcium chloride, 1–10 mL/hour. Serum calcium should be measured but note that modest hypercalcaemia is the aim of treatment.
• If significant hypotension persists despite volume replacement, give IV glucagon (see p. 668 for details).
• If there is a favourable response in BP to glucagon, commence a glucagon infusion 5–10 mg/hour depending on response. Monitor blood glucose during glucagon therapy.
• If hypotension persists despite the above measures administer a sympathomimetic amine intravenously. If hypotension is thought to be mainly due to reduced systemic vascular resistance, high-dose dopamine 10–30 mcg/kg/min is a reasonable choice. Alternatively, administer adrenaline (epinephrine) 0.1–1 mcg/kg/min.
• Insulin/glucose euglycaemia improves myocardial contractility and systemic perfusion and is used as an adjuvant to sympathomimetic amine therapy. Check serum potassium before commencing insulin/glucose and if it is < 3.0 mmol/L give 20 mmol K+ over 30 mins. If there is severe hypotension, give a loading bolus of IV 50 mL 50% glucose plus insulin 1.0 U/kg. An infusion of 10% glucose should be given, along with an infusion of insulin 0.5–1.0 U/kg/hour. Check blood sugar every 20 mins to determine the patient’s insulin and glucose requirements, then check hourly. Check serum potassium hourly and replace as necessary.
• Cardiac pacing is used if there is evidence of atrio-ventricular conduction delay but there may be failure to capture.
Cannabis (marijuana)
Clinical features
• Euphoria, distorted and heightened images, colours and sounds, altered tactile sensations, sinus tachycardia, hypotension and ataxia occur.
• Visual and auditory hallucinations, depersonalization and acute psychosis are particularly likely to occur after substantial ingestion in naïve cannabis users.
Carbamazepine
Clinical features
• Dry mouth, coma, convulsions, nystagmus, ataxia and incoordination occur. The pupils are often dilated, a divergent strabismus may be present, and complete external ophthalmoplegia has been reported.
Carbon monoxide
• Carbon monoxide combines with haemoglobin to form carboxyhaemoglobin (COHb), thereby reducing the total oxygen-carrying capacity of the blood and increasing the affinity of the remaining haem groups for oxygen. This shifts the oxyhaemoglobin dissociation curve to the left, impairing liberation of oxygen to the cells. Tissue hypoxia results.
Clinical features
• Symptoms of mild to moderate exposure to carbon monoxide may be mistaken for a viral illness with headache, dizziness, nausea and vomiting.
• A peak COHb concentration of ≤ 10% is not normally associated with symptoms. Peak COHb concentrations of 10–30% may result only in headache and mild exertional dyspnoea.
• Myocardial ischaemia, hypertonia and extensor plantar responses are relatively common in severe cases.
Treatment
• In addition to removing the patient from carbon monoxide exposure, administer high-flow oxygen using a tight-fitting face mask.
• Measure ABGs. Metabolic acidosis (p. 382) with normal oxygen tension but reduced oxygen saturation is characteristic.
• The use of hyperbaric oxygen remains controversial, as the results of clinical trials are conflicting.
