Poisoning
Comprehensive evaluation of the poisoned patient
Taking a history in poisoning
• What toxin(s) have been taken and how much?
• What time were they taken and by what route?
• Has alcohol or any drug of misuse been taken as well?
• Obtain details from witnesses of the circumstances of the overdose (e.g. family, friends ambulance personnel)
• Ask the general practitioner for background and details of prescribed medication
• Assess suicide risk (full psychiatric evaluation when patient has physically recovered)
• Assess capacity to make decisions about accepting or refusing treatment
• Establish past medical history, drug history and allergies, social and family history
Evaluation of the envenomed patient
Assessment of type and extent of envenomingTaking a history in envenoming
• When was the patient exposed to a bite/sting?
• Was the organism causing it seen and what did it look like (size, colour)?
• What were the circumstances (on land, in water etc.)?
• Was there more than one bite/sting?
• What first aid was used, when and for how long?
• What symptoms has the patient had (local and systemic)?
• Are there symptoms suggesting systemic envenoming (paralysis, myolysis, coagulopathy etc.)?
• Past medical history and medications?
Acute poisoning is common, accounting for about 1% of hospital admissions in the UK. Common or otherwise important substances involved are shown in Box 9.1. In developed countries, the most frequent cause is intentional drug overdose in the context of self-harm and usually involves prescribed or ‘over-the-counter’ medicines. Accidental poisoning is also common, especially in children and the elderly (Box 9.2). Toxicity also may occur as a result of alcohol or recreational substance use, or following occupational or environmental exposure. Poisoning is a major cause of death in young adults, but most deaths occur before patients reach medical attention, and mortality is much lower than 1% in those admitted to hospital.
9.1 Important substances involved in poisoning
• Analgesics: paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs)
• Antidepressants: tricyclic antidepressants (TCAs), selective serotonin re-uptake inhibitors (SSRIs) and lithium
• Cardiovascular agents: β-blockers, calcium channel blockers and cardiac glycosides
• Drugs of misuse: opiates, benzodiazepines, stimulants (e.g. amphetamines, MDMA, cocaine)
9.2 Poisoning in old age
• Aetiology: commonly results from accidental poisoning (e.g. due to confusion or dementia) or drug toxicity as a consequence of impaired renal or hepatic function or drug interaction. Toxic prescription medicines are more likely to be available.
• Psychiatric illness: self-harm is less common than in younger adults but more frequently associated with depression and other psychiatric illness, as well as chronic illness and pain. There is a higher risk of subsequent suicide.
• Severity of poisoning: increased morbidity and mortality result from reduced renal and hepatic function, reduced functional reserve, increased sensitivity to sedative agents and frequent comorbidity.
In developing countries, the frequency of self-harm is more difficult to estimate. Household and agricultural products, such as pesticides and herbicides, are more freely available, are common sources of poisoning and are associated with a much higher case fatality. In China and South-east Asia, pesticides account for about 300 000 suicides each year.
General approach to the poisoned patient
A general approach is shown on pages 206–207.
Triage and resuscitation
Patients who are seriously poisoned must be identified early so that appropriate management is not delayed. Triage involves:
• immediate assessment of vital signs
• identifying the poison(s) involved and obtaining adequate information about them
• identifying patients at risk of further attempts at self-harm and removing any remaining hazards.
Those with possible external contamination with chemical or environmental toxins should undergo appropriate decontamination (Fig. 9.1). Critically ill patients must be resuscitated (p. 180).
The Glasgow Coma Scale (GCS) is commonly employed to assess conscious level, although it has not been specifically validated in poisoned patients. The AVPU (alert/verbal/painful/unresponsive) scale is also a rapid and simple method. An electrocardiogram (ECG) should be performed and cardiac monitoring instituted in all patients with cardiovascular features or where exposure to potentially cardiotoxic substances is suspected. Patients who may need antidotes should be weighed when this is feasible, so that appropriate weight-related doses can be prescribed.
Substances that are unlikely to be toxic in humans should be identified so that inappropriate admission and intervention are avoided (Box 9.3).
9.3 Substances of very low toxicity
• Writing/educational materials
• Cleaning/bathroom products (except dishwasher tablets, which are corrosive)
• Pharmaceuticals: oral contraceptives, most antibiotics (but not tetracyclines and antituberculous drugs), H2-blockers, proton pump inhibitors, emollients and other skin creams, baby lotion
• Miscellaneous: plasticine, silica gel, household plants, plant food
Clinical assessment and investigations
History and examination are described on page 206. Occasionally, patients may be unaware or confused about what they have taken, or may exaggerate (or less commonly underestimate) the size of the overdose, but rarely mislead medical staff deliberately. In regions of the world where self-poisoning is illegal, patients may be reticent about giving a history.
Toxic causes of abnormal physical signs are shown on page 207. The patient may have a cluster of clinical features (‘toxidrome’) suggestive of poisoning with a particular drug type, e.g. anticholinergic, serotoninergic (see Box 9.11, p. 213), stimulant, sedative, opioid (see Box 9.12, p. 217) or cholinergic (see Box 9.14, p. 221) feature clusters. Poisoning is a common cause of coma, especially in younger people, but it is important to exclude other potential causes (p. 1159), unless the aetiology is certain.
Urea, electrolytes and creatinine should be measured in all patients with suspected systemic poisoning. Arterial blood gases should be checked in those with significant respiratory or circulatory compromise, or when poisoning with substances likely to affect acid–base status is suspected (Box 9.4). Calculation of anion and osmolar gaps may help to inform diagnosis and management (Box 9.5).
9.4 Causes of acidosis in the poisoned patient
| Cause | Normal lactate* | High lactate |
| Toxic | Salicylates | Metformin |
| Methanol | Iron | |
| Ethylene glycol | Cyanide | |
| Paraldehyde | Sodium valproateCarbon monoxide | |
| Other | Renal failureKetoacidosisSevere diarrhoea | Shock |
*Unless circulatory shock is present, when it will be high in any case.
9.5 Anion and osmolal gaps in poisoning
| Anion gap | Osmolal gap | |
| Calculation | [Na+ + K+] − [Cl− + HCO3−] | [Osm (measured)] [2 × Na + Urea + Glucose (all mmol/L)]1 |
| Reference range | 12–16 mmol/L | < 10 mOsm/kg |
| Common toxic causes of elevation2 | EthanolEthylene glycolMethanolSalicylatesIronCyanide | EthanolEthylene glycolMethanol |
1Osm (measured) stands for measured osmolality. For non-SI units, the corresponding formula is [Osm (measured)] – [2 × Na (meq/L) + Urea/2.8 (mg/dL) + Glucose/18 (mg/dL)].
For a limited number of specific substances, management may be facilitated by measurement of the amount of toxin in the blood (Box 9.6). Qualitative urine screens for potential toxins, including near-patient testing kits, have a limited clinical role.
9.6Psychiatric assessment
All patients presenting with deliberate drug overdose should undergo psychiatric evaluation by a health professional with appropriate training prior to discharge (p. 238). This should take place once the patient has recovered from any features of poisoning, unless there is an urgent issue, such as uncertainty about their capacity to decline medical treatment.
General management
Patients presenting with eye/skin contamination should undergo local decontamination procedures (see Fig. 9.1).
Gastrointestinal decontamination
Patients who have ingested potentially life-threatening quantities of toxins may be considered for gastrointestinal decontamination if poisoning has been recent (Box 9.7). Induction of emesis using ipecacuanha is no longer recommended.
9.7 Use of gastric decontamination methods
‘Single-dose activated charcoal may be considered if a patient has ingested a potentially toxic amount of a poison (known to be adsorbed to charcoal) up to 1 hr previously.’1
‘Multiple-dose activated charcoal should be considered only if a patient has ingested a life-threatening amount of carbamazepine, dapsone, phenobarbital, quinine or theophylline.’2
‘Gastric lavage should not be employed routinely, if ever, in the management of poisoned patients.’3
‘Whole bowel irrigation should be considered for:
• poisoning with sustained-release or emetic-coated drugs
• patients who have ingested substantial amounts of iron (as morbidity is high and other options are limited)
• removal of ingested packets of illicit drugs.
Activated charcoal
Given orally as slurry, activated charcoal absorbs toxins in the bowel as a result of its large surface area. If given sufficiently early, it can prevent absorption of an important proportion of the ingested dose of toxin. Efficacy decreases with time and current guidelines do not advocate use more than 1 hour after overdose in most circumstances (see Box 9.7). However, use after a longer interval may be reasonable when a delayed-release preparation has been taken or when gastric emptying may be delayed. Some toxins do not bind to activated charcoal (Box 9.8) so it will not affect their absorption. In patients with impaired swallowing or a reduced level of consciousness, activated charcoal, even via a nasogastric tube, carries a risk of aspiration pneumonitis, which can be reduced (but not eliminated) by protecting the airway with a cuffed endotracheal tube.
9.8
Multiple doses of oral activated charcoal (50 g 6 times daily in an adult) may enhance the elimination of some drugs at any time after poisoning and are recommended for serious poisoning with some substances (see Box 9.7). This interrupts enterohepatic circulation or reduces the concentration of free drug in the gut lumen, to the extent that drug diffuses from the blood back into the bowel to be absorbed on to the charcoal: so-called ‘gastrointestinal dialysis’. A laxative is generally given with the charcoal to reduce the risk of constipation or intestinal obstruction by charcoal ‘briquette’ formation in the gut lumen.
Gastric aspiration and lavage
Gastric aspiration and/or lavage is very infrequently indicated in acute poisoning, as it is no more effective than activated charcoal and complications are common, especially aspiration. Use may be justified for life-threatening overdoses of some substances that are not absorbed by activated charcoal (see Box 9.8).
Whole bowel irrigation
This is occasionally indicated to enhance the elimination of ingested packets of illicit drugs or slow-release tablets such as iron and lithium that are not absorbed by activated charcoal. It involves the administration of large quantities of osmotically balanced polyethylene glycol and electrolyte solution (1–2 L/hr for an adult), usually by a nasogastric tube, until the rectal effluent is clear. Contraindications include inadequate airway protection, haemodynamic instability, gastrointestinal haemorrhage, obstruction or ileus. Whole bowel irrigation may precipitate nausea and vomiting, abdominal pain and electrolyte disturbances.
Urinary alkalinisation
Urinary excretion of weak acids and bases is affected by urinary pH, which changes the extent to which they are ionised. Highly ionised molecules pass poorly through lipid membranes and therefore little tubular reabsorption occurs and urinary excretion is increased. If the urine is alkalinised (pH > 7.5) by the administration of sodium bicarbonate (e.g. 1.5 L of 1.26% sodium bicarbonate over 2 hrs), weak acids (e.g. salicylates, methotrexate and the herbicides 2,4-dichlorophenoxyacetic acid and mecoprop) are highly ionised, resulting in enhanced urinary excretion.
Urinary alkalinisation is currently recommended for patients with clinically significant salicylate poisoning when the criteria for haemodialysis are not met (see below). It is also sometimes used for poisoning with methotrexate. Complications include alkalaemia, hypokalaemia and occasionally alkalotic tetany (p. 447). Hypocalcaemia may occur but is rare.
Haemodialysis and haemoperfusion
These techniques can enhance the elimination of poisons that have a small volume of distribution and a long half-life after overdose, and are appropriate when poisoning is sufficiently severe to justify invasive elimination methods. The toxin must be small enough to cross the dialysis membrane (haemodialysis) or must bind to activated charcoal (haemoperfusion) (Box 9.9). Haemodialysis may also correct acid–base and metabolic disturbances associated with poisoning (p. 209).
9.9
Lipid emulsion therapy
Lipid emulsion therapy, or ‘lipid rescue’, is being used increasingly for the management of poisoning with lipid-soluble agents, such as local anaesthetics, tricyclic antidepressants, calcium channel blockers and lipid-soluble β-blockers such as propranolol. It involves intravenous infusion of 20% lipid emulsion (e.g. Intralipid®) at an initial dose of 1.5 mL/kg, followed by a continued infusion of 0.25 mL/kg/min until there is clinical improvement. It is thought that lipid-soluble toxins partition into the intravenous lipid, reducing target tissue concentrations. The elevated myocardial concentration of free fatty acid induced by Intralipid administration may also have beneficial effects on myocardial metabolism and performance by counteracting the inhibition of myocardial fatty acid oxidation produced by local anaesthetics and some other cardiotoxins. This reverses cardiac depression by enabling increased ATP synthesis and energy production. Animal studies have suggested efficacy and case reports of use in human poisoning have also been encouraging, with recovery of circulatory collapse reported in cases where other treatment modalities have been unsuccessful. No controlled trials of this technique have been performed, however, and as a result, its efficacy remains uncertain.
Supportive care
For most poisons, antidotes and methods to accelerate elimination are inappropriate, unavailable or incompletely effective. Outcome is dependent on appropriate nursing and supportive care, and on treatment of complications (Box 9.10). Patients should be monitored carefully until the effects of any toxins have dissipated.
9.10 Complications of poisoning and their management
| Examples of causative agents | Management | |
| Coma | Sedative agents | Appropriate airway protection and ventilatory supportPressure area and bladder careIdentification and treatment of aspiration pneumonia |
| Seizures | NSAIDsAnticonvulsantsTCAsTheophylline | Appropriate airway and ventilatory supportIV benzodiazepine (e.g. diazepam 10–20 mg, lorazepam 2–4 mg)Correction of hypoxia, acid–base and metabolic abnormalities |
| Acute dystonias | Typical antipsychoticsMetoclopramide | Procyclidine, benzatropine or diazepam |
| Hypotension | ||
| Due to vasodilatation | Vasodilator antihypertensivesAnticholinergic agentsTCAs | IV fluidsVasopressors (rarely indicated; p. 191) |
| Due to myocardial suppression | β-blockersCalcium channel blockersTCAs | Optimisation of volume statusInotropic agents (p. 191) |
| Ventricular tachycardia | ||
| Monomorphic, associated with QRS prolongation | Sodium channel blockers | Correction of electrolyte and acid–base abnormalities and hypoxiaSodium bicarbonate |
| Torsades de pointes, associated with QTc prolongation | Anti-arrhythmic drugs (quinidine, amiodarone, sotalol)AntimalarialsOrganophosphate insecticidesAntipsychotic agentsAntidepressantsAntibiotics (erythromycin) | Magnesium sulphate, 2 g IV over 1–2 mins, repeated if necessary |
Antidotes
Antidotes are available for some poisons and work by a variety of mechanisms: for example, by specific antagonism (isoprenaline for β-blockers), chelation (desferrioxamine for iron) or reduction (methylene blue for dapsone). The use of some antidotes is described in the management of specific poisons below.
Poisoning by specific pharmaceutical agents
Analgesics
Paracetamol
Paracetamol (acetaminophen) is the drug most commonly used in overdose in the UK. Toxicity results from formation of an intermediate reactive metabolite that binds covalently to cellular proteins, causing cell death. This results in hepatic and occasionally renal failure. In therapeutic doses, the toxic intermediate metabolite is detoxified in reactions requiring glutathione, but in overdose, glutathione reserves become exhausted.
Management
Management is summarised in Figure 9.2. Activated charcoal may be used in patients presenting within 1 hour. Antidotes for paracetamol act by replenishing hepatic glutathione and should be administered to all patients with paracetamol concentrations above the ‘treatment line’ provided on paracetamol poisoning nomograms. Acetylcysteine given intravenously (or orally in some countries) is highly efficacious if administered within 8 hours of the overdose. However, since efficacy declines thereafter, administration should not be delayed in patients presenting after 8 hours to await a paracetamol blood concentration result. The antidote can be stopped if the paracetamol concentration is shown to be below the nomogram treatment line.
The most important adverse effect of acetylcysteine is related to dose-related histamine release, the ‘anaphylactoid’ reaction, which causes itching and urticaria, and in occasional severe cases, bronchospasm and hypotension. Most cases can be managed by temporary discontinuation of acetylcysteine and administration of an antihistamine.
An alternative antidote is methionine 2.5 g orally (adult dose) every 4 hours to a total of 4 doses, but this is less effective, especially after delayed presentation. If a patient presents more than 15 hours after ingestion, liver function tests, prothrombin time (or international normalised ratio – INR), renal function tests and a venous bicarbonate should be measured, the antidote started, and a poisons information centre or local liver unit contacted for advice if results are abnormal. An arterial blood gas sample should be taken in patients with severe liver function abnormalities; metabolic acidosis indicates severe poisoning. Liver transplantation should be considered in individuals who develop life-threatening liver failure due to paracetamol poisoning (p. 932).
Salicylates (aspirin)
Clinical features
Salicylate overdose commonly causes nausea, vomiting, sweating, tinnitus and deafness. Direct stimulation of the respiratory centre produces hyperventilation and respiratory alkalosis. Peripheral vasodilatation with bounding pulses and profuse sweating occurs in moderately severe poisoning. Serious salicylate poisoning is associated with metabolic acidosis, hypoprothrombinaemia, hyperglycaemia, hyperpyrexia, renal failure, pulmonary oedema, shock and cerebral oedema. Agitation, confusion, coma and fits may occur, especially in children. Toxicity is enhanced by acidosis, which increases salicylate transfer across the blood–brain barrier.
Management
Activated charcoal should be administered if the patient presents within 1 hour. Multiple doses of activated charcoal may enhance salicylate elimination but currently are not routinely recommended.
The plasma salicylate concentration should be measured at least 2 (in symptomatic patients) or 4 hours (asymptomatic patients) after overdose and repeated in suspected serious poisoning, since concentrations may continue to rise some hours after overdose. In adults, concentrations above 500 mg/L and 700 mg/L suggest serious and life-threatening poisoning respectively, although clinical status is more important than the salicylate concentration in assessing severity.
Dehydration should be corrected carefully, as there is a risk of pulmonary oedema, and metabolic acidosis should be identified and treated with intravenous sodium bicarbonate (8.4%), once plasma potassium has been corrected. Urinary alkalinisation is indicated for adults with salicylate concentrations above 500 mg/L.
Haemodialysis is very effective at removing salicylate and correcting acid–base and fluid balance abnormalities, and should be considered when serum concentrations are above 700 mg/L in adults with severe toxic features, or when there is renal failure, pulmonary oedema, coma, convulsions or refractory acidosis.
Non-steroidal anti-inflammatory drugs
Clinical features
Overdose of most non-steroidal anti-inflammatory drugs (NSAIDs) usually causes little more than minor abdominal discomfort, vomiting and/or diarrhoea, but convulsions can occur occasionally, especially with mefenamic acid. Coma, prolonged seizures, apnoea, liver dysfunction and renal failure can occur after substantial overdose but are rare. Features of toxicity are unlikely to develop in patients who are asymptomatic more than 6 hours after overdose.
Antidepressants
Tricyclic antidepressants
Tricyclic antidepressants (TCAs) are used frequently in overdose and carry a high morbidity and mortality relating to their sodium channel-blocking, anticholinergic and α-adrenoceptor-blocking effects.
Clinical features
Anticholinergic effects are common (Box 9.11). Life-threatening complications are frequent, including convulsions, coma, arrhythmias (ventricular tachycardia, ventricular fibrillation and, less commonly, heart block) and hypotension, which results from inappropriate vasodilatation or impaired myocardial contractility. Serious complications appear to be more common with dosulepin and amitriptyline.
9.11
Management
Activated charcoal should be administered if the patient presents within 1 hour. All patients with possible TCA overdose should have a 12-lead ECG and ongoing cardiac monitoring for at least 6 hours. Prolongation of the QRS interval (especially if > 0.16 s) indicates severe sodium channel blockade and is associated with an increased risk of arrhythmia (Fig. 9.3). QT interval prolongation may also occur. Arterial blood gases should be measured in suspected severe poisoning.
In patients with arrhythmias, significant QRS or QT prolongation or acidosis, intravenous sodium bicarbonate (50 mL of 8.4% solution) should be administered and repeated to correct pH. The correction of the acidosis and the sodium loading that result is often associated with rapid improvement in ECG features and arrhythmias. Hypoxia and electrolyte abnormalities should also be corrected. Anti-arrhythmic drugs should only be given on specialist advice. Prolonged convulsions should be treated with intravenous benzodiazepines (see Box 9.10). There is anecdotal evidence of benefit from lipid emulsion therapy in severe intractable poisoning.
Selective serotonin and noradrenaline re-uptake inhibitors
Selective serotonin re-uptake inhibitors (SSRIs) are a group of antidepressants that include fluoxetine, paroxetine, fluvoxamine, sertraline, citalopram and escitalopram. They are increasingly used to treat depression, partly because they are less toxic in overdose than TCAs. A related group of compounds termed serotonin–noradrenaline reuptake inhibitors (SNRIs), such as venlafaxine and duloxetine, are also in common use and are sometimes taken in overdose.
Clinical features and management
Overdose of SSRIs may produce nausea and vomiting, tremor, insomnia and sinus tachycardia. Agitation, drowsiness and convulsions occur infrequently and may be delayed for several hours after ingestion. Occasionally, features of serotonin syndrome may develop (see Box 9.11), especially if SSRIs are taken in combination or with other serotonergic agents. Cardiac arrhythmias occur infrequently and most patients require supportive care only. The toxic effects of SNRIs are similar but tachycardia, hypertension or hypotension and ECG changes (QRS and QT prolongation) may be more prominent and hypoglycaemia can also occur.
Lithium
Severe lithium toxicity is uncommon after intentional overdose and is more often encountered in patients taking therapeutic doses as the result of interactions with drugs such as diuretics or NSAIDs that can cause dehydration or renal impairment, or because an excessive dose has been prescribed. Severe toxicity is more common with acute overdose in patients taking chronic therapy (‘acute on chronic’ poisoning).
Clinical features
Nausea, diarrhoea, polyuria, dizziness and tremor may progress to muscular weakness, drowsiness, confusion, myoclonus, fasciculations, choreoathetosis and renal failure. Coma, convulsions, ataxia, cardiac dysrhythmias such as heart block, blood pressure disturbances and renal failure may all occur in severe poisoning.
Management
Activated charcoal is ineffective. Gastric lavage is of theoretical benefit if used early after overdose, but lithium tablets are likely to remain intact in the stomach and may be too large for aspiration via a lavage tube. Some advocate whole bowel irrigation after substantial overdose but efficacy is unknown.
Lithium concentrations should be measured immediately in symptomatic patients or after at least 6 hours in asymptomatic patients following acute overdose. Adequate hydration should be maintained with intravenous fluids. Convulsions should be treated as in Box 9.10.
Cardiovascular medications
Beta-adrenoceptor blockers
These have negative inotropic and chronotropic effects. Some have additional properties that may increase toxicity, such as blockade of sodium channels with propranolol, acebutolol and carvedilol, and blockade of potassium channels with sotalol.
Clinical features
The major features of toxicity are bradycardia and hypotension. Heart block, pulmonary oedema and cardiogenic shock occur in severe poisoning. Beta-blockers with sodium channel-blocking effects may cause seizures, confusion and coma, while sotalol may be associated with repolarisation abnormalities (including QTc prolongation) and torsades de pointes (p. 570).
Management
Intravenous fluids may reverse hypotension but care is required to avoid pulmonary oedema. Bradycardia and hypotension may respond to high doses of atropine (up to 3 mg in an adult). The adrenoceptor agonist isoprenaline may also be effective but high doses are often needed. Glucagon (5–10 mg over 10 mins, then 1–5 mg/hr by infusion), which counteracts the effect of β-blockers by stimulating intracellular production of cyclic adenosine monophosphate (cAMP), is now more commonly used. In severe cases, ‘hyperinsulinaemia euglycaemic therapy’ has been used, as described under calcium channel blockers. Lipid emulsion therapy may have a role in severe poisoning with lipid-soluble agents such as propranolol, carvedilol and oxprenolol.
Calcium channel blockers
Calcium channel blockers are highly toxic in overdose because of their inhibitory effects on L-type calcium channels. Dihydropyridines, such as nifedipine or amlodipine, affect vascular smooth muscle in particular, resulting in vasodilatation, whereas diltiazem and verapamil, which are used in the treatment of arrhythmias, have predominantly cardiac effects, including bradycardia and reduced myocardial contractility.
Clinical features
The usual presentation is with hypotension due to vasodilatation or myocardial depression. Bradycardias and heart block may also occur, especially with verapamil and diltiazem. Gastrointestinal disturbances, confusion, metabolic acidosis, hyperglycaemia and hyperkalaemia may also be present.
Management
Hypotension should be corrected with intravenous fluids, taking care to avoid pulmonary oedema. Persistent hypotension may respond to intravenous calcium gluconate (10 mg IV over 5 mins, repeated as required). Isoprenaline and glucagon may also be useful. Successful use of intravenous insulin with glucose (10–20% dextrose with insulin initially at 0.5–2.0 U/kg/hr, increasing to 5–10 U/kg/hr according to clinical response), so-called ‘hyperinsulinaemia euglycaemic therapy’, has been reported in patients unresponsive to other strategies. The mechanism of action remains to be fully elucidated, but in states of shock myocardial metabolism switches from use of free fatty acids to glucose. Calcium channel blocker poisoning is also associated with hypoinsulinaemia and insulin resistance, impeding glucose uptake by myocytes. High doses of insulin inhibit lipolysis and increase glucose uptake and the efficiency of glucose utilisation. Cardiac pacing may be needed for severe unresponsive bradycardias or heart block. Lipid emulsion therapy has been used in severe poisoning with apparent benefit, although evidence is largely anecdotal.
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