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Neonates less than 45 weeks corrected gestational age may

be more susceptible to paracetamol-induced liver toxicity,

therefore, treatment with acetylcysteine should be

considered in all paracetamol p. 444 overdoses, and advice

should be sought from the National Poisons Information

Service.

Acute overdose

Hepatotoxicity may occur after a single ingestion of more

than 150 mg/kg paracetamol taken in less than 1 hour.

Rarely, hepatotoxicity may develop with single ingestions as

low as 75 mg/kg of paracetamol taken in less than 1 hour.

Patients who have ingested 75 mg/kg or more of paracetamol

in less than 1 hour should be referred to hospital.

Administration of charcoal, activated p. 1366 should be

considered if paracetamol in excess of 150 mg/kg is thought

to have been ingested within the previous hour.

Patients at risk of liver damage and, therefore, requiring

acetylcysteine, can be identified from a single measurement

of the plasma-paracetamol concentration, related to the

time from ingestion, provided this time interval is not less

than 4 hours; earlier samples may be misleading. The

concentration is plotted on a paracetamol treatment graph,

with a reference line (‘treatment line’) joining plots of

100 mg/litre (0.66 mmol/litre) at 4 hours and 3.13 mg/litre

(0.02 mmol/litre) at 24 hours. Acetylcysteine treatment

should commence immediately in patients:

. whose plasma-paracetamol concentration falls on or above

the treatment line on the paracetamol treatment graph;

. who present 8–24 hours after taking an acute overdose of

more than 150 mg/kg of paracetamol, even if the plasmaparacetamol concentration is not yet available;

acetylcysteine can be discontinued if the plasmaparacetamol concentration is later reported to be below

the treatment line on the paracetamol treatment graph,

provided that the patient is asymptomatic and liver

function tests, serum creatinine and INR are normal.

The prognostic accuracy of a plasma-paracetamol

concentration taken after 15 hours is uncertain, but a

concentration on or above the treatment line on the

paracetamol treatment graph should be regarded as carrying

a serious risk of liver damage. If more than 15 hours have

elapsed since ingestion, or there is doubt about appropriate

management, advice should be sought from the National

Poisons Information Service.

‘Staggered’ overdose, uncertain time of overdose, or

therapeutic excess

A ‘staggered’ overdose involves ingestion of a potentially

toxic dose of paracetamol over more than one hour, with the

possible intention of causing self-harm. Therapeutic excess

is the inadvertent ingestion of a potentially toxic dose of

paracetamol during its clinical use. The paracetamol

treatment graph is unreliable if a ‘staggered’ overdose is

taken, if there is uncertainty about the time of the overdose,

or if there is therapeutic excess. In these cases, patients who

have taken more than 150 mg/kg of paracetamol in any

24-hour period are at risk of toxicity and should be

commenced on acetylcysteine immediately, unless it is more

than 24 hours since the last ingestion, the patient is

asymptomatic, the plasma-paracetamol concentration is

undetectable, and liver function tests, serum creatinine and

INR are normal.

Rarely, toxicity can occur with paracetamol doses between

75–150 mg/kg in any 24-hour period; clinical judgement of

the individual case is necessary to determine whether to

treat those who have ingested this amount of paracetamol.

For small adults, this may be within the licensed dose, but

ingestion of a licensed dose of paracetamol is not considered

an overdose.

Although there is some evidence suggesting that factors

such as the use of liver enzyme-inducing drugs (e.g.

carbamazepine p. 311, efavirenz p. 644, nevirapine p. 645,

phenobarbital p. 335, phenytoin p. 323, primidone p. 336,

rifabutin p. 575, rifampicin p. 582, St John’s wort), chronic

alcoholism, and starvation may increase the risk of

hepatotoxicity, the CHM has advised that these should no

longer be used in the assessment of paracetamol toxicity.

Significant toxicity is unlikely if, 24 hours or longer after

the last paracetamol ingestion, the patient is asymptomatic,

the plasma-paracetamol concentration is undetectable, and

liver function tests, serum creatinine and INR are normal.

Patients with clinical features of hepatic injury such as

jaundice or hepatic tenderness should be treated urgently

with acetylcysteine. If there is uncertainty about a patient’s

risk of toxicity after paracetamol overdose, treatment with

acetylcysteine should be commenced. Advice should be

sought from the National Poisons Information Service

whenever necessary.

Acetylcysteine dose and administration

For paracetamol overdosage, acetylcysteine is given in a

total dose that is divided into 3 consecutive intravenous

infusions over a total of 21 hours. The tables below include

the dose of acetylcysteine, for adults and children of bodyweight 40 kg and over, in terms of the volume of

acetylcysteine Concentrate for Intravenous Infusion

required for each of the 3 infusions. The requisite dose of

acetylcysteine is added to glucose Intravenous Infusion 5%

p. 1041.

First infusion

Body-weight Volume of Acetylcysteine Concentrate for

Intravenous Infusion 200 mg/mL required

to prepare first infusion

40–49 kg 34 mL

50–59 kg 42 mL

60–69 kg 49 mL

70–79 kg 57 mL

80–89 kg 64 mL

90–99 kg 72 mL

100–109 kg 79 mL

110 kg 83 mL (max. dose)

First infusion (based on an acetylcysteine dose of approx.

150 mg/kg)—add requisite volume of Acetylcysteine

Concentrate for Intravenous Infusion to 200 mL Glucose

Intravenous Infusion 5%; infuse over 1 hour.

Second infusion

Body-weight Volume of Acetylcysteine Concentrate for

Intravenous Infusion 200 mg/mL required

to prepare second infusion

40–49 kg 12 mL

50–59 kg 14 mL

60–69 kg 17 mL

70–79 kg 19 mL

80–89 kg 22 mL

90–99 kg 24 mL

100–109 kg 27 mL

110 kg 28 mL (max. dose)

Second infusion (based on an acetylcysteine dose of approx.

50 mg/kg; start immediately after completion of first

infusion)—add requisite volume of Acetylcysteine

Concentrate for Intravenous Infusion to 500 mL Glucose

Intravenous Infusion 5%; infuse over 4 hours.

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Third infusion

Body-weight Volume of Acetylcysteine Concentrate for

Intravenous Infusion 200 mg/mL required

to prepare third infusion

40–49 kg 23 mL

50–59 kg 28 mL

60–69 kg 33 mL

70–79 kg 38 mL

80–89 kg 43 mL

90–99 kg 48 mL

100–109 kg 53 mL

110 kg 55 mL (max. dose)

Third infusion (based on an acetylcysteine dose of approx.

100 mg/kg; start immediately after completion of second

infusion)—add requisite volume of Acetylcysteine

Concentrate for Intravenous Infusion to 1 litre Glucose

Intravenous Infusion 5%; infuse over 16 hours.

Antidepressant poisoning

Tricyclic and related antidepressants

Tricyclic and related antidepressants cause dry mouth, coma

of varying degree, hypotension, hypothermia, hyperreflexia,

extensor plantar responses, convulsions, respiratory failure,

cardiac conduction defects, and arrhythmias. Dilated pupils

and urinary retention also occur. Metabolic acidosis may

complicate severe poisoning; delirium with confusion,

agitation, and visual and auditory hallucinations are

common during recovery.

Assessment in hospital is strongly advised in case of

poisoning by tricyclic and related antidepressants but

symptomatic treatment can be given before transfer.

Supportive measures to ensure a clear airway and adequate

ventilation during transfer are mandatory. Intravenous

lorazepam or intravenous diazepam (preferably in emulsion

form) may be required to treat convulsions. Activated

charcoal given within 1 hour of the overdose reduces

absorption of the drug. Although arrhythmias are worrying,

some will respond to correction of hypoxia and acidosis. The

use of anti-arrhythmic drugs is best avoided, but intravenous

infusion of sodium bicarbonate can arrest arrhythmias or

prevent them in those with an extended QRS duration.

Diazepam given by mouth is usually adequate to sedate

delirious patients but large doses may be required.

Selective serotonin re-uptake inhibitors (SSRIs)

Symptoms of poisoning by selective serotonin re-uptake

inhibitors include nausea, vomiting, agitation, tremor,

nystagmus, drowsiness, and sinus tachycardia; convulsions

may occur. Rarely, severe poisoning results in the serotonin

syndrome, with marked neuropsychiatric effects,

neuromuscular hyperactivity, and autonomic instability;

hyperthermia, rhabdomyolysis, renal failure, and

coagulopathies may develop.

Management of SSRI poisoning is supportive. Activated

charcoal given within 1 hour of the overdose reduces

absorption of the drug. Convulsions can be treated with

lorazepam, diazepam, or midazolam oromucosal solution

[unlicensed use in adults and children under 3 months] (see

Convulsions). Contact the National Poisons Information

Service for the management of hyperthermia or the

serotonin syndrome.

Antimalarial poisoning

Overdosage with quinine, chloroquine, or

hydroxychloroquine is extremely hazardous and difficult to

treat. Urgent advice from the National Poisons Information

Service is essential. Life-threatening features include

arrhythmias (which can have a very rapid onset) and

convulsions (which can be intractable).

Antipsychotic poisoning

Phenothiazines and related drugs

Phenothiazines cause less depression of consciousness and

respiration than other sedatives. Hypotension, hypothermia,

sinus tachycardia, and arrhythmias may complicate

poisoning. Dystonic reactions can occur with therapeutic

doses (particularly with prochlorperazine and

trifluoperazine), and convulsions may occur in severe cases.

Arrhythmias may respond to correction of hypoxia, acidosis,

and other biochemical abnormalities, but specialist advice

should be sought if arrhythmias result from a prolonged QT

interval; the use of some anti-arrhythmic drugs can worsen

such arrhythmias. Dystonic reactions are rapidly abolished

by injection of drugs such as procyclidine hydrochloride

p. 411 or diazepam p. 343 (emulsion preferred).

Second-generation antipsychotic drugs

Features of poisoning by second-generation antipsychotic

drugs include drowsiness, convulsions, extrapyramidal

symptoms, hypotension, and ECG abnormalities (including

prolongation of the QT interval). Management is supportive.

Charcoal, activated p. 1366 can be given within 1 hour of

ingesting a significant quantity of a second-generation

antipsychotic drug.

Benzodiazepine poisoning

Benzodiazepines taken alone cause drowsiness, ataxia,

dysarthria, nystagmus, and occasionally respiratory

depression, and coma. Charcoal, activated can be given

within 1 hour of ingesting a significant quantity of

benzodiazepine, provided the patient is awake and the

airway is protected. Benzodiazepines potentiate the effects

of other central nervous system depressants taken

concomitantly. Use of the benzodiazepine antagonist

flumazenil p. 1368 [unlicensed indication] can be hazardous,

particularly in mixed overdoses involving tricyclic

antidepressants or in benzodiazepine-dependent patients.

Flumazenil may prevent the need for ventilation,

particularly in patients with severe respiratory disorders; it

should be used on expert advice only and not as a diagnostic

test in patients with a reduced level of consciousness.

Beta blockers poisoning

Therapeutic overdosages with beta-blockers may cause

lightheadedness, dizziness, and possibly syncope as a result

of bradycardia and hypotension; heart failure may be

precipitated or exacerbated. These complications are most

likely in patients with conduction system disorders or

impaired myocardial function. Bradycardia is the most

common arrhythmia caused by beta-blockers, but sotalol

may induce ventricular tachyarrhythmias (sometimes of the

torsade de pointes type). The effects of massive overdosage

can vary from one beta-blocker to another; propranolol

overdosage in particular may cause coma and convulsions.

Acute massive overdosage must be managed in hospital and

expert advice should be obtained. Maintenance of a clear

airway and adequate ventilation is mandatory. An

intravenous injection of atropine sulfate p. 1334 is required

to treat bradycardia. Cardiogenic shock unresponsive to

atropine sulfate is probably best treated with an intravenous

injection of glucagon p. 724 [unlicensed] in glucose 5% (with

precautions to protect the airway in case of vomiting)

followed by an intravenous infusion. If glucagon is not

available, intravenous isoprenaline (available from ‘specialorder’ manufacturers or specialist importing companies) is

an alternative. A cardiac pacemaker can be used to increase

the heart rate.

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Calcium-channel blockers poisoning

Features of calcium-channel blocker poisoning include

nausea, vomiting, dizziness, agitation, confusion, and coma

in severe poisoning. Metabolic acidosis and hyperglycaemia

may occur. Verapamil and diltiazem have a profound cardiac

depressant effect causing hypotension and arrhythmias,

including complete heart block and asystole. The

dihydropyridine calcium-channel blockers cause severe

hypotension secondary to profound peripheral

vasodilatation.

Charcoal, activated should be considered if the patient

presents within 1 hour of overdosage with a calcium-channel

blocker; repeated doses of activated charcoal are considered

if a modified-release preparation is involved. In patients with

significant features of poisoning, calcium chloride p. 1045 or

calcium gluconate p. 1045 is given by injection; atropine

sulfate is given to correct symptomatic bradycardia. In

severe cases, an insulin and glucose infusion may be

required in the management of hypotension and myocardial

failure. For the management of hypotension, the choice of

inotropic sympathomimetic depends on whether

hypotension is secondary to vasodilatation or to myocardial

depression—advice should be sought from the National

Poisons Information Service.

Iron salts poisoning

Iron poisoning in childhood is usually accidental. The

symptoms are nausea, vomiting, abdominal pain, diarrhoea,

haematemesis, and rectal bleeding. Hypotension and

hepatocellular necrosis can occur later. Coma, shock, and

metabolic acidosis indicate severe poisoning.

Advice should be sought from the National Poisons

Information Service if a significant quantity of iron has been

ingested within the previous hour.

Mortality is reduced by intensive and specific therapy with

desferrioxamine mesilate p. 1028, which chelates iron. The

serum-iron concentration is measured as an emergency and

intravenous desferrioxamine mesilate given to chelate

absorbed iron in excess of the expected iron binding

capacity. In severe toxicity intravenous desferrioxamine

mesilate should be given immediately without waiting for

the result of the serum-iron measurement.

Lithium poisoning

Most cases of lithium intoxication occur as a complication of

long-term therapy and are caused by reduced excretion of

the drug because of a variety of factors including

dehydration, deterioration of renal function, infections, and

co-administration of diuretics or NSAIDs (or other drugs that

interact). Acute deliberate overdoses may also occur with

delayed onset of symptoms (12 hours or more) owing to slow

entry of lithium into the tissues and continuing absorption

from modified-release formulations.

The early clinical features are non-specific and may

include apathy and restlessness which could be confused

with mental changes arising from the patient’s depressive

illness. Vomiting, diarrhoea, ataxia, weakness, dysarthria,

muscle twitching, and tremor may follow. Severe poisoning

is associated with convulsions, coma, renal failure,

electrolyte imbalance, dehydration, and hypotension.

Therapeutic serum-lithium concentrations are within the

range of 0.4–1 mmol/litre; concentrations in excess of

2 mmol/litre are usually associated with serious toxicity and

such cases may need treatment with haemodialysis if

neurological symptoms or renal failure are present. In acute

overdosage much higher serum-lithium concentrations may

be present without features of toxicity and all that is usually

necessary is to take measures to increase urine output (e.g.

by increasing fluid intake but avoiding diuretics). Otherwise,

treatment is supportive with special regard to electrolyte

balance, renal function, and control of convulsions. Gastric

lavage may be considered if it can be performed within

1 hour of ingesting significant quantities of lithium. Wholebowel irrigation should be considered for significant

ingestion, but advice should be sought from the National

Poisons Information Service.

Stimulant-drug poisoning

Amfetamines cause wakefulness, excessive activity,

paranoia, hallucinations, and hypertension followed by

exhaustion, convulsions, hyperthermia, and coma. The early

stages can be controlled by diazepam p. 343 or lorazepam

p. 339; advice should be sought from the National Poisons

Information Service on the management of hypertension.

Later, tepid sponging, anticonvulsants, and artificial

respiration may be needed.

Cocaine

Cocaine stimulates the central nervous system, causing

agitation, dilated pupils, tachycardia, hypertension,

hallucinations, hyperthermia, hypertonia, and hyperreflexia;

cardiac effects include chest pain, myocardial infarction, and

arrhythmias.

Initial treatment of cocaine poisoning involves

intravenous administration of diazepam to control agitation

and cooling measures for hyperthermia (see Body

temperature); hypertension and cardiac effects require

specific treatment and expert advice should be sought.

Ecstasy

Ecstasy (methylenedioxymethamfetamine, MDMA) may

cause severe reactions, even at doses that were previously

tolerated. The most serious effects are delirium, coma,

convulsions, ventricular arrhythmias, hyperthermia,

rhabdomyolysis, acute renal failure, acute hepatitis,

disseminated intravascular coagulation, adult respiratory

distress syndrome, hyperreflexia, hypotension and

intracerebral haemorrhage; hyponatraemia has also been

associated with ecstasy use.

Treatment of methylenedioxymethamfetamine poisoning

is supportive, with diazepam to control severe agitation or

persistent convulsions and close monitoring including ECG.

Self-induced water intoxication should be considered in

patients with ecstasy poisoning.

‘Liquid ecstasy’ is a term used for sodium oxybate

(gamma-hydroxybutyrate, GHB), which is a sedative.

Theophylline poisoning

Theophylline and related drugs are often prescribed as

modified-release formulations and toxicity can therefore be

delayed. They cause vomiting (which may be severe and

intractable), agitation, restlessness, dilated pupils, sinus

tachycardia, and hyperglycaemia. More serious effects are

haematemesis, convulsions, and supraventricular and

ventricular arrhythmias. Severe hypokalaemia may develop

rapidly.

Repeated doses of activated charcoal can be used to

eliminate theophylline even if more than 1 hour has elapsed

after ingestion and especially if a modified-release

preparation has been taken (see also under Active

Elimination Techniques). Ondansetron p. 436 may be

effective for severe vomiting that is resistant to other

antiemetics [unlicensed indication]. Hypokalaemia is

corrected by intravenous infusion of potassium chloride

p. 1057 and may be so severe as to require 60 mmol/hour

(high doses require ECG monitoring). Convulsions should be

controlled by intravenous administration of lorazepam or

diazepam (see Convulsions). Sedation with diazepam may be

necessary in agitated patients.

Provided the patient does not suffer from asthma, a shortacting beta-blocker can be administered intravenously to

reverse severe tachycardia, hypokalaemia, and

hyperglycaemia.

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Cyanide poisoning

Oxygen should be administered to patients with cyanide

poisoning. The choice of antidote depends on the severity of

poisoning, certainty of diagnosis, and the cause. Dicobalt

edetate p. 1367 is the antidote of choice when there is a

strong clinical suspicion of severe cyanide poisoning, but it

should not be used as a precautionary measure. Dicobalt

edetate itself is toxic, associated with anaphylactoid

reactions, and is potentially fatal if administered in the

absence of cyanide poisoning. A regimen of sodium nitrite

p. 1367 followed by sodium thiosulfate p. 1367 is an

alternative if dicobalt edetate is not available.

Hydroxocobalamin p. 1026 (Cyanokit ®—no other

preparation of hydroxocobalamin is suitable) can be

considered for use in victims of smoke inhalation who show

signs of significant cyanide poisoning.

Ethylene glycol and methanol poisoning

Fomepizole (available from ‘special-order’ manufacturers or

specialist importing companies) is the treatment of choice

for ethylene glycol and methanol (methyl alcohol)

poisoning. If necessary, ethanol (by mouth or by

intravenous infusion) can be used, but with caution. Advice

on the treatment of ethylene glycol and methanol poisoning

should be obtained from the National Poisons Information

Service. It is important to start antidote treatment promptly

in cases of suspected poisoning with these agents.

Heavy metal poisoning

Heavy metal antidotes include succimer (DMSA)

[unlicensed], unithiol (DMPS) [unlicensed], sodium calcium

edetate [unlicensed], and dimercaprol. Dimercaprol in the

management of heavy metal poisoning has been superseded

by other chelating agents. In all cases of heavy metal

poisoning, the advice of the National Poisons Information

Service should be sought.

Noxious gases poisoning

Carbon monoxide

Carbon monoxide poisoning is usually due to inhalation of

smoke, car exhaust, or fumes caused by blocked flues or

incomplete combustion of fuel gases in confined spaces.

Immediate treatment of carbon monoxide poisoning is

essential. The person should be moved to fresh air, the

airway cleared, and high-flow oxygen 100% administered

through a tight-fitting mask with an inflated face seal.

Artificial respiration should be given as necessary and

continued until adequate spontaneous breathing starts, or

stopped only after persistent and efficient treatment of

cardiac arrest has failed. The patient should be admitted to

hospital because complications may arise after a delay of

hours or days. Cerebral oedema may occur in severe

poisoning and is treated with an intravenous infusion of

mannitol p. 229. Referral for hyperbaric oxygen treatment

should be discussed with the National Poisons Information

Service if the patient is pregnant or in cases of severe

poisoning, such as if the patient is or has been unconscious,

or has psychiatric or neurological features other than a

headache, or has myocardial ischaemia or an arrhythmia, or

has a blood carboxyhaemoglobin concentration of more than

20%.

Sulfur dioxide, chlorine, phosgene, and ammonia

All of these gases can cause upper respiratory tract and

conjunctival irritation. Pulmonary oedema, with severe

breathlessness and cyanosis may develop suddenly up to

36 hours after exposure. Death may occur. Patients are kept

under observation and those who develop pulmonary

oedema are given oxygen. Assisted ventilation may be

necessary in the most serious cases.

CS Spray poisoning

CS spray, which is used for riot control, irritates the eyes

(hence ‘tear gas’) and the respiratory tract; symptoms

normally settle spontaneously within 15 minutes. If

symptoms persist, the patient should be removed to a wellventilated area, and the exposed skin washed with soap and

water after removal of contaminated clothing. Contact

lenses should be removed and rigid ones washed (soft ones

should be discarded). Eye symptoms should be treated by

irrigating the eyes with physiological saline (or water if

saline is not available) and advice sought from an

ophthalmologist. Patients with features of severe poisoning,

particularly respiratory complications, should be admitted to

hospital for symptomatic treatment.

Nerve agent poisoning

Treatment of nerve agent poisoning is similar to

organophosphorus insecticide poisoning, but advice must be

sought from the National Poisons Information Service. The

risk of cross-contamination is significant; adequate

decontamination and protective clothing for healthcare

personnel are essential. In emergencies involving the release

of nerve agents, kits (‘NAAS pods’) containing pralidoxime

chloride p. 1367 can be obtained through the Ambulance

Service from the National Blood Service (or the Welsh Blood

Service in South Wales or designated hospital pharmacies in

Northern Ireland and Scotland—see TOXBASE for list of

designated centres).

Pesticide poisoning

Organophosphorus insecticides

Organophosphorus insecticides are usually supplied as

powders or dissolved in organic solvents. All are absorbed

through the bronchi and intact skin as well as through the

gut and inhibit cholinesterase activity, thereby prolonging

and intensifying the effects of acetylcholine. Toxicity

between different compounds varies considerably, and onset

may be delayed after skin exposure.

Anxiety, restlessness, dizziness, headache, miosis, nausea,

hypersalivation, vomiting, abdominal colic, diarrhoea,

bradycardia, and sweating are common features of

organophosphorus poisoning. Muscle weakness and

fasciculation may develop and progress to generalised flaccid

paralysis, including the ocular and respiratory muscles.

Convulsions, coma, pulmonary oedema with copious

bronchial secretions, hypoxia, and arrhythmias occur in

severe cases. Hyperglycaemia and glycosuria without

ketonuria may also be present.

Further absorption of the organophosphorus insecticide

should be prevented by moving the patient to fresh air,

removing soiled clothing, and washing contaminated skin. In

severe poisoning it is vital to ensure a clear airway, frequent

removal of bronchial secretions, and adequate ventilation

and oxygenation; gastric lavage may be considered provided

that the airway is protected. Atropine sulfate p. 1334 will

reverse the muscarinic effects of acetylcholine and is given

by intravenous injection until the skin becomes flushed and

dry, the pupils dilate, and bradycardia is abolished.

Pralidoxime chloride, a cholinesterase reactivator, is used

as an adjunct to atropine sulfate in moderate or severe

poisoning. It improves muscle tone within 30 minutes of

administration. Pralidoxime chloride is continued until the

patient has not required atropine sulfate for 12 hours.

Pralidoxime chloride can be obtained from designated

centres, the names of which are held by the National Poisons

Information Service.

Snake bites and animal stings

Snake bites

Envenoming from snake bite is uncommon in the UK. Many

exotic snakes are kept, some illegally, but the only

indigenous venomous snake is the adder (Vipera berus). The

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