S.H.L. Thomas

J. White

Comprehensive evaluation of the poisoned patient

Insets (Self-cutting) From Douglas, et al. 2005; (Burn) www.firewiki.net; (Needle tracks) www.deep6inc.com; (Pupil) drugrecognition.com; (Conjunctiva) knol.google.com – see p. 230.

Evaluation of the envenomed patient

Taking a history in envenoming



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.

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:

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).

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).

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.

image 9.6   Laboratory analysis in poisoning

Psychiatric 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.

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.

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.

Evidence suggests that single or multiple doses of activated charcoal do not improve clinical outcomes after poisoning with pesticides or oleander.

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).

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.

Poisoning by specific pharmaceutical agents



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 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).

If multiple ingestions of paracetamol have taken place over several hours or days (i.e. a staggered overdose), acetylcysteine may be indicated. Recommended thresholds for treatment vary between countries.

Salicylates (aspirin)


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.


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.


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.


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).


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.

In patients with features suggesting severe toxicity associated with high lithium concentrations (e.g. > 4.0 mmol/L after chronic or ‘acute on chronic’ poisoning, or > 7.5 mmol/L after acute poisoning), haemodialysis should be considered. Lithium concentrations are reduced substantially during dialysis but rebound increases occur after discontinuation, and multiple sessions may be required.

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.

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.


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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Apr 9, 2017 | Posted by in GENERAL SURGERY | Comments Off on Poisoning

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