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Oral poisoning: an update

Catherine Ward MBBS BSc Hons FRCA


Mark Sair PhD MRCP FRCA

Key points Oral poisoning: an update and cyanide poisoning, where the antidote for
cyanide is immediately required. All cases
The mainstay treatment of Acute poisoning accounts for .100 000 hospital
poisoning is resuscitation require:

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admissions per year in the UK with in excess of
and supportive care. 4000 deaths reported in England and Wales per † resuscitation;
Poisoning should be annum. Although the majority of poison-related † risk assessment;
considered in any patient deaths occur in the community, reduction of † substance identification;
exhibiting bizarre behaviour, in-hospital morbidity and mortality remains an † specific treatment (if available);
a reduced conscious level, important challenge. The largest proportion of † a period of observation.
or unexplained physiological enquiries to the National Poisons Information
instability. A focused and detailed poisoning history and
Service (NPIS) and Guy’s and St Thomas’
Ipecac is no longer examination are required to identify specific
Poisons Unit (GTPU) are concerning pre-school
recommended in the physical signs of poisoning followed by the
children.1 A recent report indicated that 85% of
treatment of acute selective use of antidotes and laboratory tests
poisonings occur in the home. Drugs accounted
poisoning. (Table 1). Most poisoned patients require sup-
for the majority, but industrial chemicals and
Activated charcoal should portive treatment only.
household products were involved in a signifi-
be given within 60 min of A risk assessment should be performed by
cant number. Only one-third of cases were
ingestion of poison but may obtaining specific information from ambulance
deliberate. The medications most commonly
have an effect for up to 2 h personnel or witnesses regarding the nature,
taken were acetaminophen, non-steroidal analge-
or longer post-ingestion. timing, and amount of drug or poison.
sics, and antidepressants.2
Acetaminophen levels are One-third of cases involve more than one toxin
The NPIS was commissioned by the Health
mandatory in all cases of and alcohol is a common contributing factor.
Protection Agency and consists of five regional
adult overdose. The patient’s clothing should be checked for
centres that operate a 24 h information service
notes or blister packets, which may give a clue
to health-care staff on the diagnosis, treatment,
to quantity and type of drug ingested. In cases
and management of poisoning. GTPU ceased
of deliberate self-harm, there may be previous
to be a provider to NPIS in November 2005
hospital admissions to aid diagnosis. The
Catherine Ward MBBS BSc Hons FRCA and operates independently with support from
patient’s general practitioner should be con-
Specialist Registrar Guy’s and St Thomas’ Foundation Trust.
Derriford Hospital
tacted for previous history as family or witness
Toxbase, the UK online toxicology database,
Plymouth sources are often unreliable.
UK
was established in 1998 and NPIS recommends
The Anaesthetic Department it as the first point of contact for registered
Level 5, Torbay District General Hospital health-care professionals. The website provides Supportive care and
Lawes Bridge
easily accessible information on acute poison- monitoring
Torquay TQ2 7AA
UK ing and its management.3 Patients suspected of being exposed to a poison
Tel: þ44 1803 654311
Fax: þ44 1803 654 312
or drug should be monitored in an appropriate
E-mail: caf.ward@btinternet.com clinical environment. Where coma is inevitable,
(for correspondence)
Initial approach to the
patients should be intubated pre-emptively or at
poisoned patient
Mark Sair PhD MRCP FRCA the first sign of deterioration in level of con-
Consultant in Intensive Care Medicine Poisoning should be considered in any patient sciousness. Tracheal intubation will protect the
and Anaesthesia exhibiting bizarre behaviour, a reduced con- airway and allow early administration of acti-
Derriford Hospital
scious level, or unexplained metabolic, cardio- vated charcoal (AC) via a nasogastric tube if
Plymouth
UK vascular, or respiratory instability. All cases are required. Patients who are at risk of cardiac
Department of Anaesthesia managed as acute medical emergencies using instability and acidosis should have continuous
Level 9
an ABC approach regardless of the agent used. ECG and invasive arterial pressure monitoring
Plymouth Hospitals NHS Trust
Plymouth Rare exceptions include patients poisoned with with regular blood gas analysis. Body tempera-
Devon PL6 8DH organophosphates, where health-care workers ture and serum glucose should be checked and
UK
first need to protect themselves from the agent, i.v. dextrose administered if required.
doi:10.1093/bjaceaccp/mkp039 Advance Access publication 15 December, 2009
6 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 10 Number 1 2010
& The Author [2009]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia.
All rights reserved. For Permissions, please email: journals.permissions@oxfordjournal.org
Oral poisoning

Table 1 Specific signs in poisoning and overdose

Toxidrome Drug Common Findings Other signs and symptoms Potential Treatments

Anticholinergic Scopolamine, atropine Altered mental status, dilated pupils, urinary Seizures, dysrrhythmias, Physostigmine; sedation with
retention, hyperthermia, dry mucous rhabdomyolysis benzodiazepines, cooling, supportive
membranes management
Cholinergic Organophosphates; Salivation, lacrimation, sweating, nausea, Bradycardia, dilated or constricted Airway protection and IPPV, atropine,
carbamates vomiting, urination, defaecation, muscle pupils, seizures, respiratory failure, pralidoxime
weakness, bronchorrhoea paralysis
Opioid Heroin, morphine CNS and respiratory depression, small pupils Hypothermia, bradycardia, respiratory Airway protection, IPPV naloxone
arrest, acute lung injury
Salicylates Aspirin Altered mental status, respiratory alkalosis, Low-grade fever, ketonuria, acute lung Multi-dose AC, alkalinization of urine,

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metabolic acidosis, tinnitus, hyperpnoea, injury Kþ repletion, haemodialysis,
tachycardia, sweating hydration
Serotonin Meperidine; MAOI, Altered mental status, increased muscle tone, Intermittent whole body tremor Cooling, benzodiazepines
Syndrome SSRI, TCA hyperreflexia, hyperthermia
Sympathomimetic Cocaine; amphetamine Agitation, dilated pupils, excessive sweating, Seizures, rhabdomyolysis, myocardial Cooling, sedation with
tachycardia, hypertension, hyperthermia infarction, cardiac arrest, benzodiazepines, hydration
hyperthermia

Investigations prolonged time in the Accident and Emergency Department and


increased incidence of aspiration pneumonitis. Its use is no longer
Acetaminophen levels are considered mandatory in all cases of recommended.5
adult overdose and should be taken 4 h post-exposure. Salicylate
levels are not recommended in the asymptomatic patient.
Screening for substances of abuse can be achieved quickly with Gastric lavage
readily available commercial urine kits. Other laboratory tests Gastric lavage is performed by placing a large-bore orogastric tube
include full blood count, urea and electrolytes, lactate, liver func- (30 –40 F), instilling and re-aspirating several litres of water to
tion tests, and coagulation studies. Where poisoning is caused by wash out the stomach contents. This is continued until no more
specific agents, for example, methanol or carbamazepine plasma pill fragments are identified in gastric contents.6 Patients must be
levels are taken 4 hourly to allow refinement of risk assessment able to protect their own airway. Drug absorption is not reduced if
and to gauge the response to enhanced elimination techniques. lavage is commenced 1 h or more after drug ingestion.
A chest radiograph may indicate pulmonary oedema, which is Paradoxically, one study suggested that gastric lavage promotes
suggestive of poisoning with narcotics or salicylates. Abdominal post-pyloric transfer of poison into the small intestine where it is
radiographs can identify packets of drugs smuggled in ‘body more rapidly absorbed. There are no data demonstrating improved
packers’. Radiological investigations are otherwise rarely required clinical outcome with gastric lavage and its use is associated with
in the setting of acute poisoning. significant morbidity and mortality. Complications include gastro-
intestinal tract perforation and aspiration.
Gastric decontamination
There is much debate regarding the use of the so-called ‘deconta- Activated charcoal
mination triangle’ of forced emesis, gastric lavage, and single-dose Most drugs and chemicals are absorbed by AC. It creates weak van
AC. Decontamination strategies are not without side-effects and der Waals forces that bind with the substance in the gastrointestinal
the risk:benefit ratio should be considered before administration. tract. The numerous charcoal particles provide a large enough
The American Academy of Clinical Toxicology and European surface area to prevent further absorption. AC should be adminis-
Association of Poisons Centres state that gastrointestinal deconta- tered orally or nasogastrically via a 16 F tube in the intubated
mination should not be administered routinely. patient. The charcoal to toxin ratio is 10:1 with a usual dose of
25 –50 g or 1 g kg21 in a child. This dose should be given within
1 h of poison ingestion.7 Its efficacy is time-dependent, with
Induced emesis
nearly 90% reduction in absorption 30 min after drug ingestion
Ipecac induces vomiting by both direct gastrointestinal effects and decreasing to 30% at 1 h.8 It has been shown to reduce acetamino-
central nervous system actions. It is administered at a dose of phen absorption up to 2 h after ingestion. AC is unpalatable and
30 ml in adults followed by water 240 ml. Emesis typically occurs can cause vomiting, thus in children it can be mixed with ice
within 20 min and persists for 30 –120 min. Several studies have cream. Patients should also be warned that it will make their stools
compared ipecac with single-dose AC. Ipecac conveys no benefit, black. It is not recommended in poisoning with lithium, iron,
whether given alone or combined with AC.4 Side-effects include alcohol, methanol, ethylene glycol, petroleum distillates,

Continuing Education in Anaesthesia, Critical Care & Pain j Volume 10 Number 1 2010 7
Oral poisoning

corrosives, acids, or alkalis. Repeated doses of 25 g per 4–6 Treatment for specific poisons
hourly can be of benefit for poisoning with slow release formu-
lations, for example, salicylate, barbiturates, theophylline, quinine, Acetaminophen
digoxin, carbamazepine, phenytoin, and dapsone. Multiple doses Acetaminophen is responsible for 30 000 UK hospital admissions
interrupt the enterohepatic circulation of the drug, reducing the a year and results in 345 deaths per annum. It is often one com-
plasma levels, and there are data that this reduces the duration of ponent of a mixed overdose. Acetaminophen produces the toxic
toxicity. A major but rare adverse effect from repeat doses is acute metabolite N-acetyl-p-benzoqinone imine (NAPQI) which is neu-
bowel obstruction from charcoal concretions, which is particularly tralized by glutathione (Fig. 1). Depletion of glutathione results in
likely in the presence of an anticholinergic ileus. NAPQI toxicity to hepatocytes. Patients particularly at risk are
chronic alcoholics, those taking antiepileptic drugs, for example,

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carbamazepine and phenytoin (i.e. enzyme inducers) and patients
Whole bowel irrigation receiving anti-tuberculous treatment, since they produce more
NAPQI. Other patients at risk include those who have reduced glu-
Whole bowel irrigation (WBI) aims to reduce the time for ingested tathione stores due to such conditions as HIV, malnutrition, or
substances to be absorbed. It requires the administration of poly- terminal malignancy.
ethylene glycol (PEG) 1.5–2 litres solution per hour and is best A recent Cochrane review concluded that AC was more effec-
administered through a 12 F feeding tube. The head of the bed tive than gastric lavage or ipecac in reducing acetaminophen
should be elevated to 45º to prevent aspiration. If emesis occurs, absorption.
then the infusion should be discontinued for 30 min and restarted N-acetylcysteine (NAC) should be given, but the optimum
at half the normal rate. Metoclopramide can be helpful as an anti- dosing regimen remains uncertain. NAC may reduce the mortality
emetic due to its prokinetic effects. Current recommendations are of patients with fulminant liver failure. The superiority of NAC
that the PEG is administered until the effluent is clear. The tech- over methionine is unproven and 5% of patients receiving it will
nique is not used routinely but may be considered where poisoning develop anaphylactoid reactions. Current advice from Toxbase is
includes sustained release or enteric coated tablets.9 It may also be that high-risk patients should receive NAC at lower plasma aceta-
used for drugs for which charcoal is known to be ineffective, for minophen concentrations (Fig. 2).
example, alcohols, boric acid, cyanide, iron, lithium, hydrocarbons, Patients who develop fulminant liver failure may be offered
acids, and alkalis. It has been used with some success in the treat- life-saving liver transplantation, but the selection criteria are in
ment of body packers, heavy metal, and battery ingestion. WBI is need of refinement based on long-term outcome data.11
contraindicated in patients with an unprotected airway, haemo-
dynamic instability, bowel obstruction, bowel perforation, or an
ileus.

Increased elimination
Alkaline diuresis enhances the elimination of weak acids such as
salicylates and some herbicides. Sodium bicarbonate is adminis-
tered and the pH of the urine measured to keep the urinary pH
7.5–8.5. Weak acids become charged in alkaline urine resulting in
a concentration gradient drawing more toxin into the renal tubular
system. Hypokalaemia can result from this technique and should
be corrected aggressively. Alkaline diuresis should be used with
caution in patients with renal impairment or cardiac disease.

Haemodialysis
Haemodialysis is helpful in ethylene glycol, methanol, lithium,
theophylline, and salicylate poisoning. The usefulness of this tech-
nique depends on the pharmacological properties of the ingested
drug. The drug or poison should have a low volume of distribution
(,1 litre kg21), a low molecular weight (,500 Da), low protein
binding, and low water solubility.10 Fig 1 Acetaminophen metabolism.

8 Continuing Education in Anaesthesia, Critical Care & Pain j Volume 10 Number 1 2010
Oral poisoning

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Fig 2 Acetaminophen nomogram ( permission from Prof. P.A. Routledge, Therapeutics and Toxicology Centre, Cardiff University).

Salicylates Table 2 Common antidotes

Indicated in poisoning with Antidote


Patients with salicylate poisoning may present with tinnitus, deaf-
ness, hyperventilation, epigastric pain, vomiting, hyperthermia, Benzodiazepines Flumazenil
sweating, dehydration, respiratory alkalosis, metabolic acidosis, Ethylene glycol, methanol Fomepizole and ethanol (10% for i.v. use)
and electrolyte disturbances. Agitation and confusion may indicate Organophosphates Atropine
Warfarin Factor II, VII, IX, X concentrate
the development of cerebral oedema which can be fatal. Treatment Cyanide Dicobalt edetate, hydroxycobalamin
includes rehydration, treatment of acid –base disturbance, and close Digoxin Digibind
monitoring of plasma levels. AC should be administered as soon as b-Blockers Glucagon
Methaemoglobinaemia Methylene blue
possible even in delayed presentations. The use of multidose AC is Acetaminophen N-acetylcysteine
debatable, but should be considered if the plasma salicylate level Opiate Naloxone
continues to increase or if a slow release preparation has been
taken. Alkalinization of the urine may increase the elimination of
salicylate and should be considered in patients with signs of dysarthria, and ataxia. Coma is not common but is most often seen
toxicity or in patients with plasma levels more than 300 mg in the elderly or patients who have ingested alcohol or other drugs.
litre21. In patients with levels more than 700 mg litre21, haemo- Treatment is supportive. The use of flumazenil is controversial as
dialysis should be considered. it has many side-effects and is rarely indicated. Adverse effects
include ventricular tachycardia, raising intracranial pressure, with-
drawal in chronic abusers, and seizures if used in the presence of
Benzodiazepines tricyclic antidepressants. It can be used to reverse benzodiazepine
Deaths associated with benzodiazepine overdose are due to mixed coma so as to avoid intubation, but this should be limited to situ-
overdoses, especially alcohol and other drugs. Clinical manifes- ations of benzodiazepine overdose where no other drugs have been
tations are associated with drowsiness, respiratory depression, taken (Table 2).

Continuing Education in Anaesthesia, Critical Care & Pain j Volume 10 Number 1 2010 9
Oral poisoning

Opiates there are no controlled trials to support the use of either agent. If
rhabdomyolysis is suspected, urinary alkalinization and volume
Increasing doses of opioids progressively produce euphoria, pin-
replacement may be helpful to reduce renal failure. Fluid resuscita-
point pupils, sedation, respiratory depression, and apnoea.
tion including 225 mmol of 8.4% sodium bicarbonate over 2 h is
Complications include hypotension, convulsions, non-cardiogenic
administered to increase urine pH to .7. If renal failure occurs,
pulmonary oedema, and compartment syndrome from prolonged
haemodialysis or haemofiltration is required.
immobility. Where this is suspected, serum CK and urinary myo-
globin should be measured to look for evidence of rhabdomyolysis.
Naloxone should be given in 100 mg boluses i.v. to a maximum of Methanol and ethylene glycol
2 mg with the aim of reversing the opiate effect and reversing res- Methanol and ethylene glycol poisoning results in a severe high

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piratory depression. This antidote can precipitate an acute agitated anion gap metabolic acidosis. Both are metabolized via the
withdrawal state and when giving it staff should be mindful of enzyme alcohol dehydrogenase resulting in formation of acids
their own safety. Naloxone can be administered i.v., i.m., s.c., or (formic, glycolic, and oxalic, respectively) which accumulate in
via the tracheal route. It has a short half-life (20 min if given i.v.) the body and are responsible for neurological damage and death.
and therefore may be needed as an infusion since respiratory Overdose with these agents can be treated with oral or nasogastric
depression may reoccur. It can rarely cause ventricular dysrhyth- ethanol because of its greater affinity for alcohol dehydrogenase.
mias and hypertension and drowsiness at very high doses. However, maintaining plasma alcohol levels in the correct range is
difficult and time-consuming, particularly if the patient is under-
Tricyclic antidepressants going dialysis. Fomepizole blocks the metabolism of methanol and
ethanol and can be injected 12 hourly. It is expensive and not
Tricyclic antidepressants cause 250 fatalities each year in the UK.
widely available. Folate deficiency in primates is predictive of
The predominant cause of death is cardiac depression by sodium
poor outcome in methanol toxicity and it is suggested that folate
channel blockade with resultant decrease in cardiac output.
be given in a dose of 1 mg kg21 day21 for 48 h.12
Overdose presents with a sinus tachycardia, mydriasis, coma,
hyperreflexia, convulsions, ECG changes, and hypotension.
A QRS interval of .120 ms indicates cardiac toxicity and is pre- Summary
dictive of ventricular arrhythmias and seizures. Treatment includes Acute poisoning is relatively common and is the cause of signifi-
prevention of absorption using AC. Sodium bicarbonate is given as cant morbidity and mortality. NPIS and Toxbase provide a 24 h
a loading dose (8.4% 1–2 ml kg21) followed by an infusion or information service for all aspects of poisoning. Treatment of poi-
intermittent bolus. Sodium bicarbonate should be administered soning remains largely supportive. Few drugs have antidotes and
even in the absence of a significant metabolic acidosis as it helps therefore treatment is aimed at reducing further absorption of the
to stabilize the Na channels in the myocardium and prevent cardio- drug, increasing its elimination, and treating the side-effects.
toxicity. Convulsions can be treated with benzodiazepines initially, Gastric decontamination with AC is time-dependent, but can sig-
but anaesthesia with propofol may be required. Phenytoin is the nificantly reduce drug absorption. Forced emesis and gastric lavage
anti-arrhythmic of choice and glucagon can be helpful if there is are no longer recommended.
evidence of myocardial depression.
References
Selective serotonin reuptake inhibitors
1. Greene SL, Dargan PI, Jones AL. Acute poisoning: understanding 90% of
These drugs include citalopram, fluoxetine, flovoxamine, paroxe- case in a nutshell. Postgrad Med J 2005; 81: 204– 16
tine, and sertraline. Nausea, vomiting, agitation, tremor, nystag- 2. Jones A, Dargan P, Greene S et al. Guy’s and St Thomas’ Poisons Unit
Annual Report 2005– 2006.
mus, drowsiness, dysrhythmias, and mild hypertension are the
most common features of overdose. Convulsions have been 3. Good AM, Bateman DN. National Poisons Information Service Annual
Report, 2005/2006.
reported up to 10 h post-ingestion. If administered with other
4. Heard K. The changing indications of the gastrointestinal decontamina-
drugs like cocaine, tricyclics MAOIs, or MDMA which release ser- tion in poisonings. Clin Lab Med 2006; 26: 1 –12
otonin or affect its reuptake, this may result in serotonin syndrome.
5. Krenzelok EP, McGuigan M, Lheur P. Position Paper: Ipecac Syrup
Serotonin syndrome consists of a triad of altered mental status, American Academy of Clinical Toxicology, European Association of
neuromuscular hyperactivity, and autonomic instability, similar in Poisons Centres and Clinical Toxicologists. Clin Toxicol 2004; 42: 133– 43
presentation to neuroleptic malignant syndrome—hyperpyrexia, 6. Vale JA. Position statement: gastric lavage. American Academy of Clinical
acidosis, arrythmias, and rhabdomyolysis are seen. Treatment is Toxicology; European Association of Poisons Centres and Clinical
Toxicologists. J Toxicol Clin Toxicol 1997; 35: 711– 9
supportive but should include AC up to 1 h post-ingestion.
7. Chyka PA, Seger D. Position statement: single dose activated charcoal.
Convulsions should be treated with benzodiazepines and pheny-
American Academy of Clinical Toxicology; European Association of
toin. Cryoheptadine and chlorpromazine are 5HT-2A antagonists Poisons Centres and Clinical Toxicologists. J Toxicol Clin 1997; 35:
and have successfully been used to treat serotonin syndrome, but 721–41

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8. Green R, Grierson R, Sitar DS, Tenenbein M. How long after drug inges- 11. Brok J, Buckley N, Gluud C. Interventions for Paracetamol
tion is activated charcoal still effective? J Toxicol Clin Toxicol 2001; 39: (Acetaminophen) Overdose (Review), The Cochrane Library, Issue 3,
601–5 Wiley, 2008; 1– 57
9. Lapatto-Reiniluoto O, Kivisto KT, Neuvonen PJ. Activated charcoal alone 12. Brent J, Mcmartin K, Philips S, Aaron C, Kulig K. Fomepizole in the
and followed by whole bowel irrigation in preventing the absorption of treatment of methanol poisoning. N Engl J Med 2001; 344: 24–2
sustained release drugs. Clin Pharmacol Ther 2001; 70: 255– 60
10. Jones LO. Poisoning. Anaesth Intensive Care Med 2006; 7: 132 –4 Please see multiple choice questions 5– 7

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