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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:
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,
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,
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
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
10 Continuing Education in Anaesthesia, Critical Care & Pain j Volume 10 Number 1 2010
Oral poisoning
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
Continuing Education in Anaesthesia, Critical Care & Pain j Volume 10 Number 1 2010 11