There can be variation in the licensing of
different medicines containing the same drug.
Gel
EXCIPIENTS: May contain Hydroxybenzoates (parabens)
▶Ametop (Forum Health Products Ltd)
Tetracaine 40 mg per 1 gram Ametop 4% gel | 1.5 gram p £1.08
DT = £1.08
Anaesthesia
Chapter 16
Emergency treatment of poisoning
CONTENTS
Active elimination from the gastro-
page 1438
intestinal tract
Chemical toxicity
Cyanide toxicity
2.1
Organophosphorus toxicity
2.2
Drug toxicity
Benzodiazepine toxicity
3.1
Poisoning, emergency treatment
Emergency treatment of poisoning
Overview
These notes provide only an overview of the treatment of
poisoning, and it is strongly recommended that either
TOXBASE or the UK National Poisons Information
Service be consulted when there is doubt about the degree
of risk or about management.
Hospital admission
Patients who have features of poisoning should generally be
admitted to hospital. Patients who have taken poisons with
delayed action should also be admitted, even if they appear
well. Delayed-action poisons include aspirin p. 130, iron,
paracetamol p. 465, tricyclic antidepressants, and co-
phenotrope p. 71 (diphenoxylate with atropine, Lomotil ®);
the effects of modified-release preparations are also delayed.
A note of all relevant information, including what treatment
has been given, should accompany the patient to hospital.
Further information
TOXBASE, the primary clinical toxicology database of the
National Poisons Information Service, is available on the
internet to registered users at www.toxbase.org (a backup site
is available at www.toxbasebackup.org if the main site cannot
be accessed). It provides information about routine
diagnosis, treatment, and management of patients exposed
to drugs, household products, and industrial and agricultural
chemicals.
Specialist information and advice on the treatment of
poisoning is available day and night from the UK National
Poisons Information Service on the following number: Tel:
0344 892 0111.
Advice on laboratory analytical services can be obtained
from TOXBASE or from the National Poisons Information
Service. Help with identifying capsules or tablets may be
available from a regional medicines information centre or
from the National Poisons Information Service (out of
hours).
General care
It is often impossible to establish with certainty the identity
of the poison and the size of the dose. This is not usually
important because only a few poisons (such as opioids,
paracetamol, and iron) have specific antidotes; few patients
require active removal of the poison. In most patients,
treatment is directed at managing symptoms as they arise.
Nevertheless, knowledge of the type and timing of poisoning
can help in anticipating the course of events. All relevant
information should be sought from the poisoned individual
Digoxin toxicity
page 1440
3.2
Heparin toxicity
3.3
Opioid toxicity
3.4
Paracetamol toxicity
3.5
Methaemoglobinaemia
Snake bites
and from carers or parents. However, such information
should be interpreted with care because it may not be
complete or entirely reliable. Sometimes symptoms arise
from other illnesses and patients should be assessed
carefully. Accidents may involve domestic and industrial
products (the contents of which are not generally known).
The National Poisons Information Service should be
consulted when there is doubt about any aspect of suspected
poisoning.
Respiration
Respiration is often impaired in unconscious patients. An
obstructed airway requires immediate attention. In the
absence of trauma, the airway should be opened with simple
measures such as chin lift or jaw thrust. An oropharyngeal or
nasopharyngeal airway may be useful in patients with
reduced consciousness to prevent obstruction, provided
ventilation is adequate. Intubation and ventilation should be
considered in patients whose airway cannot be protected or
who have respiratory acidosis because of inadequate
ventilation; such patients should be monitored in a critical
care area.
Most poisons that impair consciousness also depress
respiration. Assisted ventilation (either mouth-to-mouth or
using a bag-valve-mask device) may be needed. Oxygen is
not a substitute for adequate ventilation, although it should
be given in the highest concentration possible in poisoning
with carbon monoxide and irritant gases.
Blood pressure
Hypotension is common in severe poisoning with central
nervous system depressants. A systolic blood pressure of less
than 70 mmHg may lead to irreversible brain damage or renal
tubular necrosis. Hypotension should be corrected initially
by raising the foot of the bed and administration of an
infusion of either sodium chloride p. 1101 or a colloid.
Vasoconstrictor sympathomimetics are rarely required and
their use may be discussed with the National Poisons
Information Service.
Fluid depletion without hypotension is common after
prolonged coma and after aspirin poisoning due to vomiting,
sweating, and hyperpnoea.
Hypertension, often transient, occurs less frequently than
hypotension in poisoning; it may be associated with
sympathomimetic drugs such as amfetamines,
phencyclidine, and cocaine.
Heart
Cardiac conduction defects and arrhythmias can occur in
acute poisoning, notably with tricyclic antidepressants,
some antipsychotics, and some antihistamines. Arrhythmias
often respond to correction of underlying hypoxia, acidosis,
or other biochemical abnormalities, but ventricular
arrhythmias that cause serious hypotension require
treatment. If the QT interval is prolonged, specialist advice
should be sought because the use of some anti-arrhythmic
drugs may be inappropriate. Supraventricular arrhythmias
are seldom life-threatening and drug treatment is best
withheld until the patient reaches hospital.
Body temperature
Hypothermia may develop in patients of any age who have
been deeply unconscious for some hours, particularly
following overdose with barbiturates or phenothiazines. It
may be missed unless core temperature is measured using a
low-reading rectal thermometer or by some other means.
Hypothermia should be managed by prevention of further
heat loss and appropriate re-warming as clinically indicated.
Hyperthermia can develop in patients taking CNS
stimulants; children and the elderly are also at risk when
taking therapeutic doses of drugs with antimuscarinic
properties. Hyperthermia is initially managed by removing
all unnecessary clothing and using a fan. Sponging with
tepid water will promote evaporation. Advice should be
sought from the National Poisons Information Service on the
management of severe hyperthermia resulting from
conditions such as the serotonin syndrome.
Both hypothermia and hyperthermia require urgent
hospitalisation for assessment and supportive treatment.
Convulsions during poisoning
Single short-lived convulsions (lasting less than 5 minutes)
do not require treatment. If convulsions are protracted or
recur frequently, lorazepam p. 355 or diazepam p. 360
(preferably as emulsion) should be given by slow intravenous
injection into a large vein. Benzodiazepines should not be
given by the intramuscular route for convulsions. If the
intravenous route is not readily available, midazolam
oromucosal solution p. 356 [unlicensed use in adults and
children under 3 months] can be given by the buccal route or
diazepam can be administered as a rectal solution.
Methaemoglobinaemia
Drug- or chemical-induced methaemoglobinaemia should be
treated with methylthioninium chloride p. 1442 if the
methaemoglobin concentration is 30% or higher, or if
symptoms of tissue hypoxia are present despite oxygen
therapy. Methylthioninium chloride reduces the ferric iron
of methaemoglobin back to the ferrous iron of haemoglobin;
in high doses, methylthioninium chloride can itself cause
methaemoglobinaemia.
Poison removal and elimination
Prevention of absorption
Given by mouth, charcoal, activated p. 1438 can bind many
poisons in the gastro-intestinal system, thereby reducing
their absorption. The sooner it is given the more effective it
is, but it may still be effective up to 1 hour after ingestion of
the poison—longer in the case of modified-release
preparations or of drugs with antimuscarinic
(anticholinergic) properties. It is particularly useful for the
prevention of absorption of poisons that are toxic in small
amounts, such as antidepressants.
Active elimination techniques
Repeated doses of charcoal, activated by mouth enhance the
elimination of some drugs after they have been absorbed;
repeated doses are given after overdosage with:
. Carbamazepine
. Dapsone
. Phenobarbital
. Quinine
. Theophylline
If vomiting occurs after dosing it should be treated (e.g. with
an antiemetic drug) since it may reduce the efficacy of
charcoal treatment. In cases of intolerance, the dose may be
reduced and the frequency increased but this may
compromise efficacy.
Charcoal, activated should not be used for poisoning with
petroleum distillates, corrosive substances, alcohols,
malathion, cyanides and metal salts including iron and
lithium salts.
Other techniques intended to enhance the elimination of
poisons after absorption are only practicable in hospital and
are only suitable for a small number of severely poisoned
patients. Moreover, they only apply to a limited number of
poisons. Examples include:
. haemodialysis for ethylene glycol, lithium, methanol,
phenobarbital, salicylates, and sodium valproate;
. alkalinisation of the urine for salicylates.
Removal from the gastro-intestinal tract
Gastric lavage is rarely required; for substances that cannot
be removed effectively by other means (e.g. iron), it should
be considered only if a life-threatening amount has been
ingested within the previous hour. It should be carried out
only if the airway can be protected adequately. Gastric lavage
Emergency treatment of poisoning
is contra-indicated if a corrosive substance or a petroleum
distillate has been ingested, but it may occasionally be
considered in patients who have ingested drugs that are not
adsorbed by charcoal, such as iron or lithium. Induction of
emesis (e.g. with ipecacuanha) is not recommended because
there is no evidence that it affects absorption and it may
increase the risk of aspiration.
Whole bowel irrigation (by means of a bowel cleansing
preparation) has been used in poisoning with certain
modified-release or enteric-coated formulations, in severe
poisoning with iron and lithium salts, and if illicit drugs are
carried in the gastro-intestinal tract (‘body-packing’).
However, it is not clear that the procedure improves
outcome and advice should be sought from the National
Poisons Information Service.
Alcohol, acute intoxication
Acute intoxication with alcohol (ethanol) is common in
adults but also occurs in children. The features include
ataxia, dysarthria, nystagmus, and drowsiness, which may
progress to coma, with hypotension and acidosis. Aspiration
of vomit is a special hazard and hypoglycaemia may occur in
children and some adults. Patients are managed
supportively, with particular attention to maintaining a clear
airway and measures to reduce the risk of aspiration of
gastric contents. The blood glucose is measured and glucose
given if indicated.
Aspirin poisoning
The main features of salicylate poisoning are
hyperventilation, tinnitus, deafness, vasodilatation, and
sweating. Coma is uncommon but indicates very severe
poisoning. The associated acid-base disturbances are
complex.
Treatment must be in hospital, where plasma salicylate,
pH, and electrolytes can be measured; absorption of aspirin
may be slow and the plasma-salicylate concentration may
continue to rise for several hours, requiring repeated
measurement. Plasma-salicylate concentration may not
correlate with clinical severity in the young and the elderly,
and clinical and biochemical assessment is necessary.
Generally, the clinical severity of poisoning is less below a
plasma-salicylate concentration of 500 mg/litre
(3.6 mmol/litre), unless there is evidence of metabolic
acidosis. Activated charcoal can be given within 1 hour of
ingesting more than 125 mg/kg of aspirin. Fluid losses should
be replaced and intravenous sodium bicarbonate may be
given (ensuring plasma-potassium concentration is within
Paracetamol overdose treatment graph
Emergency treatment of poisoning
the reference range) to enhance urinary salicylate excretion
(optimum urinary pH 7.5–8.5).
Plasma-potassium concentration should be corrected
before giving sodium bicarbonate as hypokalaemia may
complicate alkalinisation of the urine.
Haemodialysis is the treatment of choice for severe
salicylate poisoning and should be considered when the
plasma-salicylate concentration exceeds 700 mg/litre
(5.1 mmol/litre) or in the presence of severe metabolic
acidosis.
Opioid poisoning
Opioids (narcotic analgesics) cause coma, respiratory
depression, and pinpoint pupils. The specific antidote
naloxone hydrochloride p. 1440 is indicated if there is coma
or bradypnoea. Since naloxone has a shorter duration of
action than many opioids, close monitoring and repeated
injections are necessary according to the respiratory rate and
depth of coma. When repeated administration of naloxone is
required, it can be given by continuous intravenous infusion
instead and the rate of infusion adjusted according to vital
signs. The effects of some opioids, such as buprenorphine,
are only partially reversed by naloxone.
Dextropropoxyphene and methadone have very long
durations of action; patients may need to be monitored for
long periods following large overdoses.
Naloxone reverses the opioid effects of
dextropropoxyphene. The long duration of action of
dextropropoxyphene calls for prolonged monitoring and
further doses of naloxone may be required.
Norpropoxyphene, a metabolite of dextropropoxyphene,
also has cardiotoxic effects which may require treatment
with sodium bicarbonate p. 1099 or magnesium sulfate
p. 1112, or both. Arrhythmias may occur for up to 12 hours.
Paracetamol poisoning
In all cases of intravenous paracetamol poisoning
clinicians are encouraged to contact the National Poisons
Information Service for advice on risk assessment and
management.
Toxic doses of paracetamol p. 465 may cause severe
hepatocellular necrosis and, much less frequently, renal
tubular necrosis. Nausea and vomiting, the only early
features of poisoning, usually settle within 24 hours.
Persistence beyond this time, often associated with the
onset of right subcostal pain and tenderness, usually
indicates development of hepatic necrosis. Liver damage is
maximal 3–4 days after paracetamol overdose and may lead
to hepatic failure, encephalopathy, coma, and death.
The following guidance provides only an overview of the
management of paracetamol overdosage from the National
Poisons Information Service TOXBASE database.
To avoid underestimating the potentially toxic
paracetamol dose ingested by obese patients who weigh
more than 110 kg, use a body-weight of 110 kg (rather than
their actual body-weight) when calculating the total dose of
paracetamol ingested (in mg/kg).
Acetylcysteine p. 1442 prevents or reduces the severity of
liver damage if given up to, and possibly beyond (in patients
at risk of severe liver disease) 24 hours of ingesting
paracetamol p. 465. It is most effective if given within
8 hours of paracetamol ingestion, after which effectiveness
declines. Very rarely, giving acetylcysteine p. 1442 by mouth
[unlicensed route] is an alternative if intravenous access is
not possible.
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 overdoses, and if uncertain
advice should be sought from the National Poisons
Information Service.
Acute overdose
Acute overdose involves ingestion of a potentially toxic dose
of paracetamol in 1 hour or less. Serious toxicity is unlikely
to occur from a single ingestion of less than 75 mg/kg of
paracetamol taken in less than 1 hour. Patients should be
referred to hospital for medical assessment if they have
ingested paracetamol in the context of self-harm, are
symptomatic, have ingested 75 mg/kg or more of
paracetamol in 1 hour or less, or where the time of ingestion
is uncertain but the dose ingested is 75 mg/kg or more.
Although the benefit of gastric decontamination is
uncertain, charcoal, activated p. 1438 should be considered if
the patient presents within 1 hour of ingesting paracetamol
in excess of 150 mg/kg.
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 cannot be interpreted. 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, see Paracetamol overdose
treatment graph.
Acetylcysteine treatment should commence in patients:
. whose plasma-paracetamol concentration falls on or above
the treatment line on the paracetamol treatment graph;
. who present within 8 hours of ingestion of more than
150 mg/kg of paracetamol, if there is going to be a delay of
8 hours or more in obtaining the paracetamol
concentration after the overdose;
. who present 8–24 hours after ingestion of an acute
overdose of more than 150 mg/kg of paracetamol, even if
the plasma-paracetamol concentration is not yet available;
. who present more than 24 hours after ingestion of an
overdose, if they are clearly jaundiced or have hepatic
tenderness, their ALT is above the upper limit of normal
(patients with chronically elevated ALT should be
discussed with the National Poisons Information Service),
their INR is greater than 1.3 (in the absence of another
cause), or the paracetamol concentration is detectable.
Consider acetylcysteine treatment in patients who present
within 24 hours of an overdose if biochemical tests suggest
acute liver injury, even if the plasma paracetamol
concentration is below the treatment line on the
paracetamol treatment graph.
If the patient is not at risk of liver toxicity (i.e. the
paracetamol concentration is below the treatment line or
undetectable; the INR and ALT are normal; and the patient
is asymptomatic) no treatment with an antidote is indicated;
acetylcysteine may be discontinued if it has been started.
Where the time of ingestion is unknown, patients should
be managed as a staggered overdose.
Staggered overdose or therapeutic excess
Patients who have ingested more than 150 mg/kg of
paracetamol in any 24-hour period are at risk of serious
toxicity. Toxicity rarely occurs with paracetamol doses
between 75–150 mg/kg in any 24-hour period. Doses
consistently less than 75 mg/kg in any 24-hour period are
very unlikely to be toxic; however risk may be increased if
this dose is repeatedly ingested over 2 or more days.
Ingestion of a licensed dose of paracetamol is not considered
an overdose.
A staggered overdose involves ingestion of a potentially
toxic dose of paracetamol over more than 1 hour, with the
possible intention of causing self-harm. All patients who
have taken a staggered overdose should be referred to
hospital for medical assessment. The MHRA advises that all
patients who have ingested a staggered overdose should be
treated with acetylcysteine without delay.
Therapeutic excess is the ingestion of a potentially toxic
dose of paracetamol with intent to treat pain or fever and
without self-harm intent during its clinical use. All patients
should be referred to hospital for medical assessment if they
are symptomatic, have ingested more than a licensed dose
and more than or equal to 75 mg/kg in any 24-hour period, or
have ingested more than the licensed dose but less than
75 mg/kg/24 hours on each of the preceding 2 or more days.
Patients with clinical features of hepatic injury such as
jaundice or hepatic tenderness should be treated urgently
with acetylcysteine. For other patients, management is
determined by the maximum dose of paracetamol ingested
in any 24-hour period.
When there is uncertainty about whether the presentation
was due to therapeutic excess, the patient should be
Emergency treatment of poisoning
managed as a staggered overdose.
Clinically significant toxicity is unlikely and the patient is
not considered to be at risk if, there has been at least 4 hours
or more since the last paracetamol ingestion, the patient has
no symptoms suggesting liver damage, the paracetamol
concentration is less than 10 mg/L, their ALT is within the
normal range, and INR is 1.3 or less. Acetylcysteine can be
discontinued in patients not considered to be at risk of
clinically significant liver damage. If there is uncertainty
about a patient’s risk of toxicity after paracetamol overdose,
advice should be sought from the National Poisons
Information Service.
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 body-
weight 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 5% p. 1102 or sodium
chloride 0.9% Intravenous Infusion p. 1101. For information
on dosing/administration for adults and children who weigh
less than 40 kg, see Acetylcysteine Doses—Children,
available from TOXBASE.
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 5%
or sodium chloride 0.9% Intravenous Infusion p. 1101; 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 5%
or sodium chloride 0.9% Intravenous Infusion; infuse over
4 hours.
Emergency treatment of poisoning
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 5% or
sodium chloride 0.9% Intravenous Infusion; 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. 431 or diazepam p. 360 (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. 1438 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. 1439 [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
Overdosages with beta-blockers may cause cardiac effects
such as bradycardia, hypotension, syncope, conduction
abnormalities, and heart failure. Bradycardia is the most
common arrhythmia, but some beta-blockers may induce
ventricular tachyarrhythmias secondary to prolongation of
QT interval (e.g. sotalol) or QRS duration (e.g. propranolol).
Although the predominant effects of beta-blocker overdose
are on the heart, other features may also occur, such as
central nervous system effects (including drowsiness,
confusion, convulsions, hallucinations, and in severe cases
coma), respiratory depression, and bronchospasm. The
effects of overdosage can vary from one beta-blocker to
another; propranolol overdosage in particular may cause
coma and convulsions.
The following guidance provides only an overview of the
management of beta-blocker overdosage from the National
Poisons Information Service TOXBASE database.
All patients who have been exposed to beta-blockers as a
result of self-harm should be referred for assessment.
Medical assessment is recommended for all patients who are
symptomatic or have ingested more than a toxic dose; and in
those who are treatment naive or have taken more than their
therapeutic dose, and have a significant cardiac history,
asthma, chronic obstructive pulmonary disease, or are
elderly. All patients who have exceeded their prescribed
daily dose of 2 or more cardiotoxic agents should also be
referred for medical assessment irrespective of the dose
ingested. Hospital clinicians are encouraged to discuss all
serious cases with the UK National Poisons Information
Service.
For patients presenting with overdose, maintain a clear
airway and adequate ventilation. Although the benefit of
gastric decontamination is uncertain, charcoal, activated can
be considered if the patient presents within 1 hour of
ingestion of more than a potentially toxic dose.
For the management of hypotension, ensure adequate
fluid resuscitation; in an emergency, vasopressors and
inotropes can be initiated under the advice of an experienced
physician. Intravenous glucagon p. 763 [unlicensed] is a
treatment option for severe hypotension, heart failure, or
cardiogenic shock. In severe cases, an insulin and glucose
infusion can improve myocardial contractility and systemic
perfusion, especially in the presence of acidosis. Consider
intravenous sodium bicarbonate p. 1099 for correction of
metabolic acidosis that persists despite correction of hypoxia
and adequate fluid resuscitation—rapid correction is
particularly important if QRS duration is prolonged. For
symptomatic bradycardia, give intravenous atropine sulfate
p. 1404; dobutamine p. 235 [unlicensed] or isoprenaline
[unlicensed] (available from ‘special-order’ manufacturers or
specialist importing companies) may be considered if
bradycardia is associated with hypotension. A temporary
cardiac pacemaker can be used to increase the heart rate.
Treat bronchospasm with nebulised bronchodilators and
corticosteroids.
If convulsions occur give oxygen, and correct acid-base
and metabolic disturbances as required. Prolonged or
frequent convulsions should be controlled with intravenous
diazepam p. 360, lorazepam p. 355, or midazolam p. 356. If
convulsions are unresponsive to treatment, the patient
should be referred urgently to critical care.
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 p. 1438 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. 1107 or calcium gluconate p. 1108 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. 1088, which chelates iron. The
serum-iron concentration is measured as an emergency and
intravenous desferrioxamine mesilate given to chelate
Emergency treatment of poisoning
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. Whole-
bowel 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 or lorazepam; 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
Emergency treatment of poisoning
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. 455 may be
effective for severe vomiting that is resistant to other
antiemetics [unlicensed indication]. Hypokalaemia is
corrected by intravenous infusion of potassium chloride
p. 1119 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
p. 355 or diazepam p. 360 (see Convulsions). Sedation with
diazepam may be necessary in agitated patients.
Provided the patient does not suffer from asthma, a short-
acting beta-blocker can be administered intravenously to
reverse severe tachycardia, hypokalaemia, and
hyperglycaemia.
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. 1438 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. 1438 followed by sodium thiosulfate p. 1438 is an
alternative if dicobalt edetate is not available.
Hydroxocobalamin p. 1085 (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. 243. 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 well-
ventilated 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. 1439 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. 1404 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
bite may cause local and systemic effects. Local effects
include pain, swelling, bruising, and tender enlargement of
regional lymph nodes. Systemic effects include early
anaphylactic symptoms (transient hypotension with
syncope, angioedema, urticaria, abdominal colic, diarrhoea,
and vomiting), with later persistent or recurrent
hypotension, ECG abnormalities, spontaneous systemic
bleeding, coagulopathy, adult respiratory distress syndrome,
and acute renal failure. Fatal envenoming is rare but the
potential for severe envenoming must not be
underestimated.
Early anaphylactic symptoms should be treated with
adrenaline/epinephrine p. 236. Indications for european
viper snake venom antiserum p. 1443 treatment include
systemic envenoming, especially hypotension, ECG
abnormalities, vomiting, haemostatic abnormalities, and
marked local envenoming such that after bites on the hand
or foot, swelling extends beyond the wrist or ankle within
4 hours of the bite. For those patients who present with
clinical features of severe envenoming (e.g. shock, ECG
abnormalities, or local swelling that has advanced from the
foot to above the knee or from the hand to above the elbow
within 2 hours of the bite), a higher initial dose of the
european viper snake venom antiserum is recommended; if
symptoms of systemic envenoming persist contact the
National Poisons Information Service.
Adrenaline/epinephrine injection must be immediately to
hand for treatment of anaphylactic reactions to the european
viper snake venom antiserum.
Antivenom is available for bites by certain foreign snakes
and spiders, stings by scorpions and fish. For information on
identification, management, and for supply in an emergency,
telephone the National Poisons Information Service.
Whenever possible the TOXBASE entry should be read, and
relevant information collected, before telephoning the
National Poisons Information Service.
Insect stings
Stings from ants, wasps, hornets, and bees cause local pain
and swelling but seldom cause severe direct toxicity unless
many stings are inflicted at the same time. If the sting is in
the mouth or on the tongue local swelling may threaten the
Emergency treatment of poisoning
upper airway. The stings from these insects are usually
treated by cleaning the area with a topical antiseptic. Bee
stings should be removed as quickly as possible.
Anaphylactic reactions require immediate treatment with
intramuscular adrenaline/epinephrine; self-administered
intramuscular adrenaline/epinephrine (e.g. EpiPen ®) is the
best first-aid treatment for patients with severe
hypersensitivity. An inhaled bronchodilator should be used
for asthmatic reactions, see also the management of
anaphylaxis. A short course of an oral antihistamine or a
topical corticosteroid may help to reduce inflammation and
relieve itching. A vaccine containing extracts of bee and
wasp venom can be used to reduce the risk of anaphylaxis
and systemic reactions in patients with systemic
hypersensitivity to bee or wasp stings.
Marine stings
The severe pain of weeverfish (Trachinus vipera) and
Portuguese man-o’-war stings can be relieved by immersing
the stung area immediately in uncomfortably hot, but not
scalding, water (not more than 45° C). People stung by
jellyfish and Portuguese man-o’-war around the UK coast
should be removed from the sea as soon as possible.
Adherent tentacles should be lifted off carefully (wearing
gloves or using tweezers) or washed off with seawater.
Alcoholic solutions, including suntan lotions, should not be
applied because they can cause further discharge of stinging
hairs. Ice packs can be used to reduce pain.
Other poisons
Consult either the National Poisons Information Service day
and night or TOXBASE.
The National Poisons Information Service (Tel: 0344
892 0111) will provide specialist advice on all aspects of
poisoning day and night.
Active elimination from the
gastro-intestinal tract
ANTIDOTES AND CHELATORS › INTESTINAL
ADSORBENTS
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