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Correspondence Critical Care and Resuscitation 2003; 5: 71-76 Correspondence Clinical toxicology: ‘bones’ of contention the renal excretion of aspirin and that forcing a diuresis was unnecessary and potentially dangerous as it may We refer to the two recent articles on diagnosis and precipitate cerebral and/or pulmonary oedema.10 management of poisoning published in the Journal.1,2 It is an enormous task to review all the literature regarding Tricyclic antidepressant (TCA) poisoning the diagnosis and management of deliberate self poison- The major cardiotoxic effect of TCA poisoning is ing, made all the more difficult by the considerable Na+ channel blockade. The ECG changes seen with a biases and conflicts within that literature. The European TCA overdose predict the risk of an adverse event. A association of poison control centres and clinical QRS width of > 0.16 s indicates a high risk of develop- toxicologists and American association of clinical ing ventricular dysrhythmias.11 As this QRS widening is toxicology have attempted this in the critical areas of a manifestation of the Na+ channel blockade it is decontamination3-8 and the American heart association illogical to use another Na+ channel blocking drug (e.g. has published a systematic review on the acute cardiac phenytoin), which may worsen the sodium channel resuscitation of the poisoned patient.9 These remain the blockade to control seizures. Bolus injection of sodium current consensus views of these bodies (and their bicarbonate is the treatment of choice for both dysrhyth- members); unfortunately some of the recommendations mias and seizures,9 and is superior to hyperventilation. in the two articles in the Journal are not supported by Physostigmine is no longer used in acute TCA over- these reviews. The authors of this letter, who provide dose, as there is no evidence that it is effective and its primary and tertiary toxicology consultative services use has produced fatal dysrhythmias12 and seizures.20 through a number of Australian poison information centres and toxicology treatment centres, also have Lithium toxicity problems with several aspects of these two articles. Significant acute lithium overdose presents with Whilst some of these disagreements could be perceived gastrointestinal symptoms. If renal function is normal as being ‘academic’, we believe that some of the even large overdoses rarely require haemodialysis. recommendations presented in the articles in the Journal Adequate crystalloid fluid resuscitation to maintain a have the potential to cause harm. In the interests of good urine output will manage most acute lithium patient care we have provided brief notes on some of the overdoses without further intervention. It is the clinical areas of these articles that concern us. condition of the patient, not the lithium level that will dictate the need for haemodialysis. Gastrointestinal decontamination Gastrointestinal decontamination is no longer per- Sympathomimetic drugs formed routinely, and should only be performed after an The delirious and agitated amphetamine intoxicated individual risk assessment of the poisoned patient.3-8 patient is almost always successfully managed with The indications for lavage, activated charcoal and whole appropriate doses of benzodiazepines. Beta-blockers are bowel irrigation in the two articles are contrary to the contraindicated because of resultant unopposed alpha consensus statements produced by the American and adrenoceptor mediated vasoconstriction.9 Severe hyper- European toxicology societies.3-8 There is no evidence tension refractory to benzodiazepines may be treated to support the indications for lavage detailed in table 4, with an alpha-blocker such as phentolamine or a direct and these recommendations fall outside current clinical smooth muscle relaxant agent but these are seldom toxicology practice. There is no evidence to suggest that required in the well-sedated patient.9 sorbitol added to activated charcoal increases efficacy5 nor is there any role for desferrioxamine in lavaging a Calcium channel blocker (CCB) overdose patient with iron overdose. The CCBs that are potentially lethal are those available in sustained release preparations with predom- Forced alkaline diuresis for aspirin overdose inately cardiac effects (e.g. verapamil and diltiazem).13 Forced alkaline diuresis is contraindicated in the A large (> 10 tablets) overdose seen early would be an management of aspirin overdose.10 This recommendat- indication for whole bowel irrigation and preparation for ion could potentially worsen the condition of a signif- early intubation and ICU admission.14 The doses of icantly poisoned patient. Prescott et al, demonstrated calcium chloride recommended in the article are too that it was the alkalinisation of the urine that increased low.9 71 Critical Care and Resuscitation 2003; 5: 71-76 Toxic alcohols G. Braitberg As intravenous ethanol is sometimes not available, it Department of Medicine, Austin and Repatriation is important that oral (via nasogastric tube) ethanol be Medical Centre, Heidelberg, Victoria 3084 considered for blocking alcohol dehydrogenase. Ethanol prevents further production of toxic metabolites and REFERENCES should be administered early whilst haemodialysis is 1. Worthley LIG. Clinical Toxicology: Part 1. Diagnosis being prepared. Haemodialysis is indicated whenever and management of common drug overdosage. Critical there is evidence of an osmolar and anion gap metabolic Care and Resuscitation 2002;4:192-215. acidosis. As most toxic alcohol assays are “sent out” and 2. Worthley LIG. Clinical Toxicology: Part 2. Diagnosis and management of uncommon poisonings. Critical the results unavailable in a timely manner, a decision to Care and Resuscitation 2002;4:216-230. treat must be made on clinical grounds. Fomepizole also 3. American Academy of Clinical Toxicology, European blocks alcohol dehydrogenase but is not available in Association of Poisons Centres and Clinical Australia. Toxicologists. Position statement: ipecac syrup. J Toxicological problems are common in clinical Toxicol Clin Toxicol 1997;35:699-709. practice. Between 100 - 400 patients per 100 000 4. American Academy of Clinical Toxicology, European population present to emergency departments per year Association of Poisons Centres and Clinical with deliberate self poisoning.17 Up to 30% will require Toxicologists. Position statement: gastric lavage. J intensive care. The care of these patients is usually Toxicol Clin Toxicol 1997;35:711-719. 5. American Academy of Clinical Toxicology, European undertaken by emergency physicians, general physic- Association of Poisons Centres and Clinical ians and intensivists. For some patients, specific toxicol- Toxicologists. Position statement: single-dose activated ogical expertise is required for safe and effective care charcoal. J Toxicol Clin Toxicol 1997;35:721-741. while for many others such expertise can make manage- 6. American Academy of Clinical Toxicology, European ment much more efficient.18,19 Several Australian cities Association of Poisons Centres and Clinical have hospital based toxicology treatment services and Toxicologists. Position statement: cathartics. J Toxicol there is a 24 hour a day, 7 day a week consultant Clin Toxicol 1997;35:743-752. toxicologist available through the poisons information 7. American Academy of Clinical Toxicology, European centres (131126) to assist in the management of the Association of Poisons Centres and Clinical Toxicologists. Position statement: whole bowel poisoned patient. irrigation. J Toxicol Clin Toxicol 1997;35:753-762. In summary, although these articles have attempted 8. American Academy of Clinical Toxicology, European to provide an overview of the field of clinical Association of Poisons Centres and Clinical toxicology, we believe there are a considerable number Toxicologists, Vale JA, Krenzelok EP, Barceloux DG. of recommendations presented that are not in keeping Position statement and practice guidelines on the use of with current toxicological advice or practice and have multi-dose activated charcoal in the treatment of acute the potential to negatively impact on patient care. poisoning. J Toxicol Clin Toxicol 1999;37:731-751. 9. Albertson TE, Dawson A, De Latorre F, et al. TOX-ACLS: toxicologic-oriented advanced cardiac life support. Ann Emerg Med 2001;37(4 Suppl):S78-S90. M. Little, L. Murray, J. Armstrong 10. Prescott LF, Balali-Mood M, Critchley JA, Johnstone Department of Emergency Medicine, Sir Charles AF, Proudfoot AT. Diuresis or urinary alkalinisation for Gairdner Hospital, Nedlands, Western Australia salicylate poisoning? BMJ 1982;285:1383-1386. 6009 11. Boehnert MT, Lovejoy FH, Jr. Value of the QRS duration versus the serum drug level in predicting A. H. Dawson, I. M. Whyte, G. K. Isbister seizures and ventricular arrhythmias after an acute Department of Clinical Toxicology and overdose of tricyclic antidepressants. N Engl J Med Pharmacology, Newcastle Mater Misericordiae 1985;313:474-479. 12. Dziukas LJ, Vohra J. Tricyclic antidepressant poisoning. Hospital, New South Wales 2300 Med J Aust 1991;154:344-350. 13. Oakley PW, Whyte IM, Carter GL. Lithium toxicity: an R. Dowsett, A. Graudins iatrogenic problem in susceptible individuals. Aust NZ J Department of Emergency Medicine, Westmead Psychiatry 2001;35:833-840. Hospital, Westmead, New South Wales 2145 14. Dawson AH, Whyte IM. The assessment and treatment of theophylline poisoning. Med J Aust F. Daly 1989;151:689-693. Department of Emergency Medicine, Royal Perth 15.
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