European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution
Published online 19 October 2010, pages 1400 - 1433
- Electrolyte disorders
- Accidental hypothermia
- CA and cardiac surgery
- Traumatic CA
- Pregnancy CA
Poisoning rarely causes cardiac arrest, but is a leading cause of death in victims younger than 40 years of age. 22 x A.C. Bronstein, D.A. Spyker, L.R. Cantilena Jr., J.L. Green, B.H. Rumack, S.L. Giffin. 2008 annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 26th Annual Report. Clin Toxicol (Phila) 47 (2009) (911 - 1084) Evidence for treatment consists primarily of small case-series, animal studies and case reports. Poisoning by therapeutic or recreational drugs and by household products are the main reasons for hospital admission and poison centre calls. Inappropriate drug dosing, drug interactions and other medication errors can also cause harm. Accidental poisoning is commonest in children. Homicidal poisoning is uncommon. Industrial accidents, warfare or terrorism can also cause exposure to harmful substances.
Prevention of cardiac arrest
Assess using the ABCDE (Airway, Breathing, Circulation, Disability, Exposure) approach. Airway obstruction and respiratory arrest secondary to a decreased conscious level is a common cause of death after self-poisoning. 23 x Y. Yanagawa, T. Sakamoto, Y. Okada. Recovery from a psychotropic drug overdose tends to depend on the time from ingestion to arrival, the Glasgow Coma Scale, and a sign of circulatory insufficiency on arrival. Am J Emerg Med 25 (2007) (757 - 761) Pulmonary aspiration of gastric contents can occur after poisoning with central nervous system depressants. Early tracheal intubation of unconscious patients by a trained person decreases the risk of aspiration. Drug-induced hypotension usually responds to fluid infusion, but occasionally vasopressor support (e.g., noradrenaline infusion) is required. A long period of coma in a single position can cause pressure sores and rhabdomyolysis. Measure electrolytes (particularly potassium), blood glucose and arterial blood gases. Monitor temperature because thermoregulation is impaired. Both hypothermia and hyperthermia (hyperpyrexia) can occur after overdose of some drugs. Retain samples of blood and urine for analysis. Patients with severe poisoning should be cared for in a critical-care setting.
Interventions such as decontamination, enhanced elimination and antidotes may be indicated and are usually second line interventions. 24 x J.L. Zimmerman. Poisonings and overdoses in the intensive care unit: general and specific management issues. Crit Care Med 31 (2003) (2794 - 2801) Alcohol excess is often associated with self-poisoning.
Modifications to BLS/ALS
- Have a high index of personal safety where there is a suspicious cause or unexpected cardiac arrest. This is especially so when more than one casualty collapses simultaneously.
- Avoid mouth-to-mouth ventilation in the presence of chemicals such as cyanide, hydrogen sulphide, corrosives and organophosphates.
- Treat life-threatening tachyarrhythmias with cardioversion according to the peri-arrest arrhythmia guidelines (see Section 4, Advanced Life Support). 24a x European Resuscitation Council Guidelines for Resuscitation 2010: Section 4: Adult advanced life support. Resuscitation 2010; 81:1305–52. This includes correction of electrolyte and acid-base abnormalities.
- Try to identify the poison(s). Relatives, friends and ambulance crews can provide useful information. Examination of the patient may reveal diagnostic clues such as odours, needle marks, pupil abnormalities, and signs of corrosion in the mouth.
- Measure the patient's temperature because hypo- or hyperthermia may occur after drug overdose (see Sections 8d and 8e).
- Be prepared to continue resuscitation for a prolonged period, particularly in young patients, as the poison may be metabolized or excreted during extended life support measures.
- Alternative approaches which may be effective in severely poisoned patients include: higher doses of medication than in standard protocols; non-standard drug therapies; prolonged CPR.
- Consult regional or national poisons centres for information on treatment of the poisoned patient. The International Programme on Chemical Safety (IPCS) lists poison centres on its website: http://www.who.int/ipcs/poisons/centre/en/ .
- Online databases for information on toxicology and hazardous chemicals: ( http://toxnet.nlm.nih.gov/ ).
Specific therapeutic measures
There are few specific therapeutic measures for poisoning that are useful immediately and improve outcomes.25, 26, 27, 28, and 29 x A.T. Proudfoot, E.P. Krenzelok, J.A. Vale. Position paper on urine alkalinization. J Toxicol Clin Toxicol 42 (2004) (1 - 26) x S. Greene, C. Harris, J. Singer. Gastrointestinal decontamination of the poisoned patient. Pediatr Emerg Care 24 (2008) (176 - 186) quiz 87–9 x J.A. Vale. Position statement: gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 35 (1997) (711 - 719) x J.A. Vale, K. Kulig. Position paper: gastric lavage. J Toxicol Clin Toxicol 42 (2004) (933 - 943) x E.P. Krenzelok, M. McGuigan, P. Lheur. Position statement: ipecac syrup, American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 35 (1997) (699 - 709)
Therapeutic measures include decontamination, multiple-dose activated charcoal, enhancing elimination and the use of specific antidotes. Many of these interventions should be used only based on expert advice. For up-to-date guidance in severe or uncommon poisonings, seek advice from a poisons centre.
Activated charcoal adsorbs most drugs. Its benefit decreases over time after ingestion. There is no evidence that treatment with activated charcoal improves clinical outcome. Consider giving a single dose of activated charcoal to patients who have ingested a potentially toxic amount of poison (known to be adsorbed by activated charcoal) up to 1 h previously. 30 x P.A. Chyka, D. Seger, E.P. Krenzelok, J.A. Vale. Position paper: single-dose activated charcoal. Clin Toxicol (Phila) 43 (2005) (61 - 87) Give it only to patients with an intact or protected airway.
Multiple-dose activated charcoal significantly increases drug elimination, but no controlled study in poisoned patients has shown a reduction in morbidity and mortality and should only be used following expert advice. There is little evidence to support the use of gastric lavage. It should only be considered within 1 h of ingestion of a potentially life-threatening amount of a poison. Even then, clinical benefit has not been confirmed in controlled studies. Gastric lavage is contraindicated if the airway is not protected and if a hydrocarbon with high aspiration potential or a corrosive substance has been ingested.27 and 28 x J.A. Vale. Position statement: gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 35 (1997) (711 - 719) x J.A. Vale, K. Kulig. Position paper: gastric lavage. J Toxicol Clin Toxicol 42 (2004) (933 - 943)
Volunteer studies show substantial decreases in the bioavailability of ingested drugs but no controlled clinical trials show that whole-bowel irrigation improves the outcome of the poisoned patient. Based on volunteer studies, whole-bowel irrigation may be considered for potentially toxic ingestions of sustained-release or enteric-coated drugs. Its use for the removal of iron, lead, zinc, or packets of illicit drugs is a theoretical option. Whole-bowel irrigation is contraindicated in patients with bowel obstruction, perforation, ileus, and haemodynamic instability. 31 x Position paper: whole bowel irrigation. J Toxicol Clin Toxicol 42 (2004) (843 - 854)
Laxatives (cathartics) or emetics (e.g., ipecacuanha) have no role in the management of the acutely poisoned patient and are not recommended.26, 32, and 33 x S. Greene, C. Harris, J. Singer. Gastrointestinal decontamination of the poisoned patient. Pediatr Emerg Care 24 (2008) (176 - 186) quiz 87–9 x E.P. Krenzelok. Ipecac syrup-induced emesis…no evidence of benefit. Clin Toxicol (Phila) 43 (2005) (11 - 12) x Position paper: ipecac syrup. J Toxicol Clin Toxicol 42 (2004) (133 - 143)
Urine alkalinisation (urine pH of 7.5 or higher) by intravenous sodium bicarbonate infusion is a first line treatment for moderate-to-severe salicylate poisoning in patients who do not need haemodialysis. 25 x A.T. Proudfoot, E.P. Krenzelok, J.A. Vale. Position paper on urine alkalinization. J Toxicol Clin Toxicol 42 (2004) (1 - 26) Urine alkalinisation with high urine flow (approximately 600 ml h−1) should also be considered in patients with severe poisoning by the herbicides 2,4-dichlorophenoxyacetic acid and methylchlorophenoxypropionic acid (mecoprop). Hypokalaemia is the most common complication of alkalaemia.
Haemodialysis or haemoperfusion should be considered in specific life-threatening poisonings only. Haemodialysis removes drugs or metabolites that are water soluble, have a low volume of distribution and low plasma protein binding. Haemoperfusion can remove substances that have a high degree of plasma protein binding
These guidelines address only some causes of cardiorespiratory arrest due to acute poisoning.
Patients at risk of cardiac arrest
Overdose of benzodiazepines can cause loss of consciousness, respiratory depression and hypotension. Flumazenil, a competitive antagonist of benzodiazepines, should only be used only for reversal of sedation caused by a single ingestion of any of the benzodiazepines and when there is no history or risk of seizures. Reversal of benzodiazepine intoxication with flumazenil can be associated with significant toxicity (seizure, arrhythmia, hypotension, and withdrawal syndrome) in patients with benzodiazepine dependence or co-ingestion of proconvulsant medications such as tricyclic antidepressants.34, 35, and 36 x R.D. Pitetti, S. Singh, M.C. Pierce. Safe and efficacious use of procedural sedation and analgesia by nonanesthesiologists in a pediatric emergency department. Arch Pediatr Adolesc Med 157 (2003) (1090 - 1096) x Treatment of benzodiazepine overdose with flumazenil. The Flumazenil in Benzodiazepine Intoxication Multicenter Study Group. Clin Ther 14 (1992) (978 - 995) x P. Lheureux, M. Vranckx, D. Leduc, R. Askenasi. Flumazenil in mixed benzodiazepine/tricyclic antidepressant overdose: a placebo-controlled study in the dog. Am J Emerg Med 10 (1992) (184 - 188) The routine use of flumazenil in the comatose overdose patient is not recommended.
Modifications to BLS/ALS
There are no specific modifications required for cardiac arrest caused by benzodiazepines.36, 37, 38, 39, and 40 x P. Lheureux, M. Vranckx, D. Leduc, R. Askenasi. Flumazenil in mixed benzodiazepine/tricyclic antidepressant overdose: a placebo-controlled study in the dog. Am J Emerg Med 10 (1992) (184 - 188) x C. Beauvoir, D. Passeron, G. du Cailar, E. Millet. Diltiazem poisoning: hemodynamic aspects. Ann Fr Anesth Reanim 10 (1991) (154 - 157) x T. Gillart, S. Loiseau, K. Azarnoush, D. Gonzalez, D. Guelon. Resuscitation after three hours of cardiac arrest with severe hypothermia following a toxic coma. Ann Fr Anesth Reanim 27 (2008) (510 - 513) x S.P. Nordt, R.F. Clark. Midazolam: a review of therapeutic uses and toxicity. J Emerg Med 15 (1997) (357 - 365) x K.L. Machin, N.A. Caulkett. Cardiopulmonary effects of propofol and a medetomidine-midazolam-ketamine combination in mallard ducks. Am J Vet Res 59 (1998) (598 - 602)
Opioid poisoning causes respiratory depression followed by respiratory insufficiency or respiratory arrest. The respiratory effects of opioids are reversed rapidly by the opiate antagonist naloxone.
Patients at risk of cardiac arrest
In severe respiratory depression caused by opioids, there are fewer adverse events when airway opening, oxygen administration and ventilation are carried out before giving naloxone.41, 42, 43, 44, 45, 46, and 47 x J.J. Osterwalder. Naloxone – for intoxications with intravenous heroin and heroin mixtures – harmless or hazardous? A prospective clinical study. J Toxicol Clin Toxicol 34 (1996) (409 - 416) x K.A. Sporer, J. Firestone, S.M. Isaacs. Out-of-hospital treatment of opioid overdoses in an urban setting. Acad Emerg Med 3 (1996) (660 - 667) x K. Wanger, L. Brough, I. Macmillan, J. Goulding, I. MacPhail, J.M. Christenson. Intravenous vs subcutaneous naloxone for out-of-hospital management of presumed opioid overdose. Acad Emerg Med 5 (1998) (293 - 299) x R.A. Hasan, A.S. Benko, B.M. Nolan, J. Campe, J. Duff, G.Y. Zureikat. Cardiorespiratory effects of naloxone in children. Ann Pharmacother 37 (2003) (1587 - 1592) x K.A. Sporer. Acute heroin overdose. Ann Intern Med 130 (1999) (584 - 590) x J.L. Kaplan, J.A. Marx, J.J. Calabro, et al.. Double-blind, randomized study of nalmefene and naloxone in emergency department patients with suspected narcotic overdose. Ann Emerg Med 34 (1999) (42 - 50) x A.B. Schneir, T.F. Vadeboncoeur, S.R. Offerman, et al.. Massive OxyContin ingestion refractory to naloxone therapy. Ann Emerg Med 40 (2002) (425 - 428) The use of naloxone can prevent the need for intubation. The preferred route for giving naloxone depends on the skills of the rescuer: IV, intramuscular (IM), subcutaneous (SC) and intranasal (IN) routes can be used. The non-IV routes can be quicker because time is saved in not having to establish IV access, which can be extremely difficult in an IV drug abuser. The initial doses of naloxone are 400 μg IV, 43 x K. Wanger, L. Brough, I. Macmillan, J. Goulding, I. MacPhail, J.M. Christenson. Intravenous vs subcutaneous naloxone for out-of-hospital management of presumed opioid overdose. Acad Emerg Med 5 (1998) (293 - 299) 800 μg IM, 800 μg SC, 43 x K. Wanger, L. Brough, I. Macmillan, J. Goulding, I. MacPhail, J.M. Christenson. Intravenous vs subcutaneous naloxone for out-of-hospital management of presumed opioid overdose. Acad Emerg Med 5 (1998) (293 - 299) or 2 mg IN.48 and 49 x A.M. Kelly, D. Kerr, P. Dietze, I. Patrick, T. Walker, Z. Koutsogiannis. Randomised trial of intranasal versus intramuscular naloxone in prehospital treatment for suspected opioid overdose. Med J Aust 182 (2005) (24 - 27) x T.M. Robertson, G.W. Hendey, G. Stroh, M. Shalit. Intranasal naloxone is a viable alternative to intravenous naloxone for prehospital narcotic overdose. Prehosp Emerg Care 13 (2009) (512 - 515) Large opioid overdoses may require titration of naloxone to a total dose of 6–10 mg. The duration of action of naloxone is approximately 45–70 min, but respiratory depression can persist for 4–5 h after opioid overdose. Thus, the clinical effects of naloxone may not last as long as those of a significant opioid overdose. Titrate the dose until the victim is breathing adequately and has protective airway reflexes.
Acute withdrawal from opioids produces a state of sympathetic excess and may cause complications such as pulmonary oedema, ventricular arrhythmia and severe agitation. Use naloxone reversal of opioid intoxication with caution in patients suspected of opioid dependence.
Modifications for ALS
There are no studies supporting the use of naloxone once cardiac arrest associated with opioid toxicity has occurred. Cardiac arrest is usually secondary to a respiratory arrest and associated with severe brain hypoxia. Prognosis is poor. 42 x K.A. Sporer, J. Firestone, S.M. Isaacs. Out-of-hospital treatment of opioid overdoses in an urban setting. Acad Emerg Med 3 (1996) (660 - 667) Giving naloxone is unlikely to be harmful. Once cardiac arrest has occurred, follow standard resuscitation protocols.
This section addresses both tricyclic and related cyclic drugs (e.g., amitriptyline, desipramine, imipramine, nortriptyline, doxepin, and clomipramine). Self-poisoning with tricyclic antidepressants is common and can cause hypotension, seizures, coma and life-threatening arrhythmias. Cardiac toxicity mediated by anticholinergic and Na+ channel-blocking effects can produce a wide complex tachycardia (VT). Hypotension is exacerbated by alpha-1 receptor blockade. Anticholinergic effects include mydriasis, fever, dry skin, delirium, tachycardia, ileus, and urinary retention. Most life-threatening problems occur within the first 6 h after ingestion.50, 51, and 52 x G.F. Tokarski, M.J. Young. Criteria for admitting patients with tricyclic antidepressant overdose. J Emerg Med 6 (1988) (121 - 124) x B.F. Banahan Jr., P.H. Schelkun. Tricyclic antidepressant overdose: conservative management in a community hospital with cost-saving implications. J Emerg Med 8 (1990) (451 - 454) x B.A. Hulten, R. Adams, R. Askenasi, et al.. Predicting severity of tricyclic antidepressant overdose. J Toxicol Clin Toxicol 30 (1992) (161 - 170)
Patient at risk of cardiac arrest
A widening QRS complex (>100 ms) and right axis deviation indicates a greater risk of arrhythmias.53, 54, and 55 x B. Bailey, N.A. Buckley, D.K. Amre. A meta-analysis of prognostic indicators to predict seizures, arrhythmias or death after tricyclic antidepressant overdose. J Toxicol Clin Toxicol 42 (2004) (877 - 888) x H.K. Thanacoody, S.H. Thomas. Tricyclic antidepressant poisoning: cardiovascular toxicity. Toxicol Rev 24 (2005) (205 - 214) x A.D. Woolf, A.R. Erdman, L.S. Nelson, et al.. Tricyclic antidepressant poisoning: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila) 45 (2007) (203 - 233) Sodium bicarbonate should be considered for the treatment of tricyclic-induced ventricular conduction abnormalities.56, 57, 58, 59, 60, 61, 62, and 63 x J.R. Hoffman, S.R. Votey, M. Bayer, L. Silver. Effect of hypertonic sodium bicarbonate in the treatment of moderate-to-severe cyclic antidepressant overdose. Am J Emerg Med 11 (1993) (336 - 341) x C. Koppel, A. Wiegreffe, J. Tenczer. Clinical course, therapy, outcome and analytical data in amitriptyline and combined amitriptyline/chlordiazepoxide overdose. Hum Exp Toxicol 11 (1992) (458 - 465) x T.C. Brown. Tricyclic antidepressant overdosage: experimental studies on the management of circulatory complications. Clin Toxicol 9 (1976) (255 - 272) x J.R. Hedges, P.B. Baker, J.J. Tasset, E.J. Otten, W.C. Dalsey, S.A. Syverud. Bicarbonate therapy for the cardiovascular toxicity of amitriptyline in an animal model. J Emerg Med 3 (1985) (253 - 260) x K. Knudsen, J. Abrahamsson. Epinephrine and sodium bicarbonate independently and additively increase survival in experimental amitriptyline poisoning. Crit Care Med 25 (1997) (669 - 674) x S. Nattel, M. Mittleman. Treatment of ventricular tachyarrhythmias resulting from amitriptyline toxicity in dogs. J Pharmacol Exp Ther 231 (1984) (430 - 435) x P. Pentel, N. Benowitz. Efficacy and mechanism of action of sodium bicarbonate in the treatment of desipramine toxicity in rats. J Pharmacol Exp Ther 230 (1984) (12 - 19) x B.I. Sasyniuk, V. Jhamandas, M. Valois. Experimental amitriptyline intoxication: treatment of cardiac toxicity with sodium bicarbonate. Ann Emerg Med 15 (1986) (1052 - 1059) While no study has investigated the optimal target arterial pH with bicarbonate therapy, a pH of 7.45–7.55 has been commonly accepted and seems reasonable.
Intravenous lipid infusions in experimental models of tricyclic toxicity have suggested benefit but there are few human data.64 and 65 x G. Yoav, G. Odelia, C. Shaltiel. A lipid emulsion reduces mortality from clomipramine overdose in rats. Vet Hum Toxicol 44 (2002) (30) x M. Harvey, G. Cave. Intralipid outperforms sodium bicarbonate in a rabbit model of clomipramine toxicity. Ann Emerg Med 49 (2007) (178 - 185) 85e1–4 Anti-tricyclic antibodies have also been beneficial in experimental models of tricyclic cardiotoxicity.66, 67, 68, 69, 70, and 71 x G.J. Brunn, D.E. Keyler, S.M. Pond, P.R. Pentel. Reversal of desipramine toxicity in rats using drug-specific antibody Fab’ fragment: effects on hypotension and interaction with sodium bicarbonate. J Pharmacol Exp Ther 260 (1992) (1392 - 1399) x G.J. Brunn, D.E. Keyler, C.A. Ross, S.M. Pond, P.R. Pentel. Drug-specific F(ab’)2 fragment reduces desipramine cardiotoxicity in rats. Int J Immunopharmacol 13 (1991) (841 - 851) x M.J. Hursting, K.E. Opheim, V.A. Raisys, M.A. Kenny, G. Metzger. Tricyclic antidepressant-specific Fab fragments alter the distribution and elimination of desipramine in the rabbit: a model for overdose treatment. J Toxicol Clin Toxicol 27 (1989) (53 - 66) x P.R. Pentel, W. Scarlett, C.A. Ross, J. Landon, A. Sidki, D.E. Keyler. Reduction of desipramine cardiotoxicity and prolongation of survival in rats with the use of polyclonal drug-specific antibody Fab fragments. Ann Emerg Med 26 (1995) (334 - 341) x P.R. Pentel, C.A. Ross, J. Landon, A. Sidki, W.L. Shelver, D.E. Keyler. Reversal of desipramine toxicity in rats with polyclonal drug-specific antibody Fab fragments. J Lab Clin Med 123 (1994) (387 - 393) x R.C. Dart, A. Sidki, J.B. Sullivan Jr., N.B. Egen, R.A. Garcia. Ovine desipramine antibody fragments reverse desipramine cardiovascular toxicity in the rat. Ann Emerg Med 27 (1996) (309 - 315) One small human study 72 x K. Heard, R.C. Dart, G. Bogdan, et al.. A preliminary study of tricyclic antidepressant (TCA) ovine FAB for TCA toxicity. Clin Toxicol (Phila) 44 (2006) (275 - 281) provided evidence of safety but clinical benefit has not been shown.
Modifications to BLS/ALS
There are no randomised controlled trials evaluating conventional versus alternative treatments for cardiac arrest caused by tricyclic toxicity. One small case-series of cardiac arrest patients, showed improvement with the use of sodium bicarbonate. 73 x P. Pentel, C.D. Peterson. Asystole complicating physostigmine treatment of tricyclic antidepressant overdose. Ann Emerg Med 9 (1980) (588 - 590)
Sympathetic overstimulation associated with cocaine toxicity can cause agitation, tachycardia, hypertensive crisis, hyperthermia and coronary vasoconstriction causing myocardial ischaemia with angina.
Patients at risk of cardiac arrest
In patients with severe cardiovascular toxicity, alpha blockers (phentolamine), 74 x R.A. Lange, R.G. Cigarroa, C.W. Yancy Jr., et al.. Cocaine-induced coronary-artery vasoconstriction. N Engl J Med 321 (1989) (1557 - 1562) benzodiazepines (lorazepam, diazepam),75 and 76 x B.M. Baumann, J. Perrone, S.E. Hornig, F.S. Shofer, J.E. Hollander. Randomized, double-blind, placebo-controlled trial of diazepam, nitroglycerin, or both for treatment of patients with potential cocaine-associated acute coronary syndromes. Acad Emerg Med 7 (2000) (878 - 885) x T. Honderick, D. Williams, D. Seaberg, R. Wears. A prospective, randomized, controlled trial of benzodiazepines and nitroglycerine or nitroglycerine alone in the treatment of cocaine-associated acute coronary syndromes. Am J Emerg Med 21 (2003) (39 - 42) calcium channel blockers (verapamil), 77 x B.H. Negus, J.E. Willard, L.D. Hillis, et al.. Alleviation of cocaine-induced coronary vasoconstriction with intravenous verapamil. Am J Cardiol 73 (1994) (510 - 513) morphine, 78 x K.E. Saland, L.D. Hillis, R.A. Lange, J.E. Cigarroa. Influence of morphine sulfate on cocaine-induced coronary vasoconstriction. Am J Cardiol 90 (2002) (810 - 811) and sublingual nitroglycerine79 and 80 x W.C.I. Brogan, R.A. Lange, A.S. Kim, D.J. Moliterno, L.D. Hillis. Alleviation of cocaine-induced coronary vasoconstriction by nitroglycerin. J Am Coll Cardiol 18 (1991) (581 - 586) x J.E. Hollander, R.S. Hoffman, P. Gennis, et al.. Nitroglycerin in the treatment of cocaine associated chest pain – clinical safety and efficacy. J Toxicol Clin Toxicol 32 (1994) (243 - 256) may be used as needed to control hypertension, tachycardia, myocardial ischaemia and agitation. The evidence for or against the use of beta-blocker drugs,81, 82, 83, and 84 x P.B. Dattilo, S.M. Hailpern, K. Fearon, D. Sohal, C. Nordin. Beta-blockers are associated with reduced risk of myocardial infarction after cocaine use. Ann Emerg Med 51 (2008) (117 - 125) x W. Vongpatanasin, Y. Mansour, B. Chavoshan, D. Arbique, R.G. Victor. Cocaine stimulates the human cardiovascular system via a central mechanism of action. Circulation 100 (1999) (497 - 502) x R.A. Lange, R.G. Cigarroa, E.D. Flores, et al.. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med 112 (1990) (897 - 903) x I.C. Sand, S.L. Brody, K.D. Wrenn, C.M. Slovis. Experience with esmolol for the treatment of cocaine-associated cardiovascular complications. Am J Emerg Med 9 (1991) (161 - 163) including those beta-blockers with alpha blocking properties (carvedilol and labetolol).85, 86, and 87 x M. Sofuoglu, S. Brown, D.A. Babb, P.R. Pentel, D.K. Hatsukami. Carvedilol affects the physiological and behavioral response to smoked cocaine in humans. Drug Alcohol Depend 60 (2000) (69 - 76) x M. Sofuoglu, S. Brown, D.A. Babb, P.R. Pentel, D.K. Hatsukami. Effects of labetalol treatment on the physiological and subjective response to smoked cocaine. Pharmacol Biochem Behav 65 (2000) (255 - 259) x J.D. Boehrer, D.J. Moliterno, J.E. Willard, L.D. Hillis, R.A. Lange. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans. Am J Med 94 (1993) (608 - 610) is limited. The best choice of anti-arrhythmic drug for the treatment of cocaine-induced tachyarrhythmias is not known.
Systemic toxicity of local anaesthetics involves the central nervous system, the cardiovascular system. Severe agitation, loss of consciousness, with or without tonic–clonic convulsions, sinus bradycardia, conduction blocks, asystole and ventricular tachyarrhythmias can all occur. Toxicity can be potentiated in pregnancy, extremes of age, or hypoxaemia. Toxicity typically occurs in the setting of regional anaesthesia, when a bolus of local anaesthetic inadvertently enters an artery or vein.
Patients at risk of cardiac arrest
Evidence for specific treatment is limited to case reports involving cardiac arrest and severe cardiovascular toxicity and animal studies. Patients with both cardiovascular collapse and cardiac arrest attributable to local anaesthetic toxicity may benefit from treatment with intravenous 20% lipid emulsion in addition to standard advanced life support.89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, and 103 x R.J. Litz, M. Popp, S.N. Stehr, T. Koch. Successful resuscitation of a patient with ropivacaine-induced asystole after axillary plexus block using lipid infusion. Anaesthesia 61 (2006) (800 - 801) x M.A. Rosenblatt, M. Abel, G.W. Fischer, C.J. Itzkovich, J.B. Eisenkraft. Successful use of a 20% lipid emulsion to resuscitate a patient after a presumed bupivacaine-related cardiac arrest. Anesthesiology 105 (2006) (217 - 218) x P.C. Marwick, A.I. Levin, A.R. Coetzee. Recurrence of cardiotoxicity after lipid rescue from bupivacaine-induced cardiac arrest. Anesth Analg 108 (2009) (1344 - 1346) x H.M. Smith, A.K. Jacob, L.G. Segura, J.A. Dilger, L.C. Torsher. Simulation education in anesthesia training: a case report of successful resuscitation of bupivacaine-induced cardiac arrest linked to recent simulation training. Anesth Analg 106 (2008) (1581 - 1584) table of contents x J.A. Warren, R.B. Thoma, A. Georgescu, S.J. Shah. Intravenous lipid infusion in the successful resuscitation of local anesthetic-induced cardiovascular collapse after supraclavicular brachial plexus block. Anesth Analg 106 (2008) (1578 - 1580) table of contents x G.L. Foxall, J.G. Hardman, N.M. Bedforth. Three-dimensional, multiplanar, ultrasound-guided, radial nerve block. Reg Anesth Pain Med 32 (2007) (516 - 521) x S. Shah, S. Gopalakrishnan, J. Apuya, T. Martin. Use of Intralipid in an infant with impending cardiovascular collapse due to local anesthetic toxicity. J Anesth 23 (2009) (439 - 441) x C. Zimmer, K. Piepenbrink, G. Riest, J. Peters. Cardiotoxic and neurotoxic effects after accidental intravascular bupivacaine administration. Therapy with lidocaine propofol and lipid emulsion. Anaesthesist 56 (2007) (449 - 453) x R.J. Litz, T. Roessel, A.R. Heller, S.N. Stehr. Reversal of central nervous system and cardiac toxicity after local anesthetic intoxication by lipid emulsion injection. Anesth Analg 106 (2008) (1575 - 1577) table of contents x H. Ludot, J.Y. Tharin, M. Belouadah, J.X. Mazoit, J.M. Malinovsky. Successful resuscitation after ropivacaine and lidocaine-induced ventricular arrhythmia following posterior lumbar plexus block in a child. Anesth Analg 106 (2008) (1572 - 1574) table of contents x G. Cave, M.G. Harvey, T. Winterbottom. Evaluation of the Association of Anaesthetists of Great Britain and Ireland lipid infusion protocol in bupivacaine induced cardiac arrest in rabbits. Anaesthesia 64 (2009) (732 - 737) x G. Di Gregorio, D. Schwartz, R. Ripper, et al.. Lipid emulsion is superior to vasopressin in a rodent model of resuscitation from toxin-induced cardiac arrest. Crit Care Med 37 (2009) (993 - 999) x G.L. Weinberg, T. VadeBoncouer, G.A. Ramaraju, M.F. Garcia-Amaro, M.J. Cwik. Pretreatment or resuscitation with a lipid infusion shifts the dose–response to bupivacaine-induced asystole in rats. Anesthesiology 88 (1998) (1071 - 1075) x G. Weinberg, R. Ripper, D.L. Feinstein, W. Hoffman. Lipid emulsion infusion rescues dogs from bupivacaine-induced cardiac toxicity. Reg Anesth Pain Med 28 (2003) (198 - 202) x G.L. Weinberg, G. Di Gregorio, R. Ripper, et al.. Resuscitation with lipid versus epinephrine in a rat model of bupivacaine overdose. Anesthesiology 108 (2008) (907 - 913) Give an initial intravenous bolus of 20% lipid emulsion followed by an infusion at 15 ml kg−1 h−1. Give up to three bolus doses of lipid at 5-min intervals and continue the infusion until the patient is stable or has received up to a maximum of 12 ml kg−1 of lipid emulsion. 104 x Management of severe local anaesthetic toxicity. (Association of Anaesthetists of Great Britain and Ireland, 2010) [accessed 28.06.10]
Modifications to BLS/ALS
Standard cardiac arrests drugs (e.g., adrenaline) should be given according to standard guidelines, although animal studies provide inconsistent evidence for their role in local anaesthetic toxicity.100, 103, 105, 106, and 107 x G. Di Gregorio, D. Schwartz, R. Ripper, et al.. Lipid emulsion is superior to vasopressin in a rodent model of resuscitation from toxin-induced cardiac arrest. Crit Care Med 37 (2009) (993 - 999) x G.L. Weinberg, G. Di Gregorio, R. Ripper, et al.. Resuscitation with lipid versus epinephrine in a rat model of bupivacaine overdose. Anesthesiology 108 (2008) (907 - 913) x V.D. Mayr, L. Mitterschiffthaler, A. Neurauter, et al.. A comparison of the combination of epinephrine and vasopressin with lipid emulsion in a porcine model of asphyxial cardiac arrest after intravenous injection of bupivacaine. Anesth Analg 106 (2008) (1566 - 1571) table of contents x S.D. Hicks, D.D. Salcido, E.S. Logue, et al.. Lipid emulsion combined with epinephrine and vasopressin does not improve survival in a swine model of bupivacaine-induced cardiac arrest. Anesthesiology 111 (2009) (138 - 146) x D.B. Hiller, G.D. Gregorio, R. Ripper, et al.. Epinephrine impairs lipid resuscitation from bupivacaine overdose: a threshold effect. Anesthesiology 111 (2009) (498 - 505)
Beta-blocker toxicity causes bradyarrhythmias and negative inotropic effects that are difficult to treat, and can lead to cardiac arrest.
Patients at risk of cardiac arrest
Evidence for treatment is based on case reports and animal studies. Improvement has been reported with glucagon (50–150 μg kg−1),108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120, and 121 x B. Bailey. Glucagon in beta-blocker and calcium channel blocker overdoses: a systematic review. J Toxicol Clin Toxicol 41 (2003) (595 - 602) x S. Fahed, D.F. Grum, T.J. Papadimos. Labetalol infusion for refractory hypertension causing severe hypotension and bradycardia: an issue of patient safety. Patient Saf Surg 2 (2008) (13) x C.M. Fernandes, M.R. Daya. Sotalol-induced bradycardia reversed by glucagon. Can Fam Physician 41 (1995) (659 - 660f) 63–5 x W. Frishman, H. Jacob, E. Eisenberg, H. Ribner. Clinical pharmacology of the new beta-adrenergic blocking drugs. Part 8. Self-poisoning with beta-adrenoceptor blocking agents: recognition and management. Am Heart J 98 (1979) (798 - 811) x A.L. Gabry, J.L. Pourriat, T.D. Hoang, C. Lapandry. Cardiogenic shock caused by metoprolol poisoning. Reversibility with high doses of glucagon and isoproterenol. Presse Med 14 (1985) (229) x E. Hazouard, M. Ferrandiere, V. Lesire, F. Joye, D. Perrotin, B. de Toffol. Peduncular hallucinosis related to propranolol self-poisoning: efficacy of intravenous glucagon. Intensive Care Med 25 (1999) (336 - 337) x M.I. Khan, M.T. Miller. Beta-blocker toxicity – the role of glucagon. Report of 2 cases. S Afr Med J 67 (1985) (1062 - 1063) x B.H. Moller. Letter: massive intoxication with metoprolol. Br Med J 1 (1976) (222) x D. O’Mahony, P. O’Leary, M.G. Molloy. Severe oxprenolol poisoning: the importance of glucagon infusion. Hum Exp Toxicol 9 (1990) (101 - 103) x C.J. Wallin, J. Hulting. Massive metoprolol poisoning treated with prenalterol. Acta Med Scand 214 (1983) (253 - 255) x R.S. Weinstein, S. Cole, H.B. Knaster, T. Dahlbert. Beta blocker overdose with propranolol and with atenolol. Ann Emerg Med 14 (1985) (161 - 163) x F. Alderfliegel, M. Leeman, P. Demaeyer, R.J. Kahn. Sotalol poisoning associated with asystole. Intensive Care Med 19 (1993) (57 - 58) x C.J. Kenyon, G.E. Aldinger, P. Joshipura, G.J. Zaid. Successful resuscitation using external cardiac pacing in beta adrenergic antagonist-induced bradyasystolic arrest. Ann Emerg Med 17 (1988) (711 - 713) x S. Freestone, H.M. Thomas, R.K. Bhamra, E.H. Dyson. Severe atenolol poisoning: treatment with prenalterol. Hum Toxicol 5 (1986) (343 - 345) high-dose insulin and glucose,122, 123, and 124 x W. Kerns 2nd, D. Schroeder, C. Williams, C. Tomaszewski, R. Raymond. Insulin improves survival in a canine model of acute beta-blocker toxicity. Ann Emerg Med 29 (1997) (748 - 757) x J.S. Holger, K.M. Engebretsen, S.J. Fritzlar, L.C. Patten, C.R. Harris, T.J. Flottemesch. Insulin versus vasopressin and epinephrine to treat beta-blocker toxicity. Clin Toxicol (Phila) 45 (2007) (396 - 401) x C. Page, L.P. Hacket, G.K. Isbister. The use of high-dose insulin-glucose euglycemia in beta-blocker overdose: a case report. J Med Toxicol 5 (2009) (139 - 143) phosphodiesterase inhibitors,125 and 126 x M.H. Kollef. Labetalol overdose successfully treated with amrinone and alpha-adrenergic receptor agonists. Chest 105 (1994) (626 - 627) x J. O’Grady, S. Anderson, D. Pringle. Successful treatment of severe atenolol overdose with calcium chloride. CJEM 3 (2001) (224 - 227) calcium salts, 127 x F. Pertoldi, L. D’Orlando, W.P. Mercante. Electromechanical dissociation 48 hours after atenolol overdose: usefulness of calcium chloride. Ann Emerg Med 31 (1998) (777 - 781) extracorporeal and intra-aortic balloon pump support,128, 129, and 130 x F.K. McVey, C.F. Corke. Extracorporeal circulation in the management of massive propranolol overdose. Anaesthesia 46 (1991) (744 - 746) x A.S. Lane, A.C. Woodward, M.R. Goldman. Massive propranolol overdose poorly responsive to pharmacologic therapy: use of the intra-aortic balloon pump. Ann Emerg Med 16 (1987) (1381 - 1383) x M. Rooney, K.L. Massey, F. Jamali, M. Rosin, D. Thomson, D.H. Johnson. Acebutolol overdose treated with hemodialysis and extracorporeal membrane oxygenation. J Clin Pharmacol 36 (1996) (760 - 763) and calcium salts. 131 x J.R. Brimacombe, M. Scully, R. Swainston. Propranolol overdose – a dramatic response to calcium chloride. Med J Aust 155 (1991) (267 - 268)
Calcium channel blockers
Calcium channel blocker overdose is emerging as a common cause of prescription drug poisoning deaths.22 and 132 x A.C. Bronstein, D.A. Spyker, L.R. Cantilena Jr., J.L. Green, B.H. Rumack, S.L. Giffin. 2008 annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 26th Annual Report. Clin Toxicol (Phila) 47 (2009) (911 - 1084) x K.R. Olson, A.R. Erdman, A.D. Woolf, et al.. Calcium channel blocker ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila) 43 (2005) (797 - 822) Overdose of short-acting drugs can rapidly progress to cardiac arrest. Overdose by sustained-release formulations can result in delayed onset of arrhythmias, shock, and sudden cardiac collapse. Asymptomatic patients are unlikely to develop symptoms if the interval between the ingestion and the call is greater than 6 h for immediate-release products, 18 h for modified-release products other than verapamil, and 24 h for modified-release verapamil.
Patients at risk of cardiac arrest
Intensive cardiovascular support is needed for managing a massive calcium channel blocker overdose. While calcium chloride in high doses can overcome some of the adverse effects, it rarely restores normal cardiovascular status. Haemodynamic instability may respond to high doses of insulin given with glucose supplementation and electrolyte monitoring in addition to standard treatments including fluids and inotropic drugs.133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 144, 145, 146, 147, and 148 x E.W. Boyer, P.A. Duic, A. Evans. Hyperinsulinemia/euglycemia therapy for calcium channel blocker poisoning. Pediatr Emerg Care 18 (2002) (36 - 37) x V. Cohen, S.P. Jellinek, L. Fancher, et al.. Tarka(R) (Trandolapril/Verapamil Hydrochloride Extended-Release) overdose. J Emerg Med (2009) x S.L. Greene, I. Gawarammana, D.M. Wood, A.L. Jones, P.I. Dargan. Relative safety of hyperinsulinaemia/euglycaemia therapy in the management of calcium channel blocker overdose: a prospective observational study. Intensive Care Med 33 (2007) (2019 - 2024) x N.S. Harris. Case records of the Massachusetts General Hospital. Case 24-2006. A 40-year-old woman with hypotension after an overdose of amlodipine. N Engl J Med 355 (2006) (602 - 611) x J. Herbert, C. O’Malley, J. Tracey, R. Dwyer, M. Power. Verapamil overdosage unresponsive to dextrose/insulin therapy. J Toxicol Clin Toxicol 39 (2001) (293 - 294) x K.K. Johansen, B. Belhage. A 48-year-old woman's survival from a massive verapamil overdose. Ugeskr Laeger 169 (2007) (4074 - 4075) x K. Kanagarajan, J.M. Marraffa, N.C. Bouchard, P. Krishnan, R.S. Hoffman, C.M. Stork. The use of vasopressin in the setting of recalcitrant hypotension due to calcium channel blocker overdose. Clin Toxicol (Phila) 45 (2007) (56 - 59) x M. Marques, E. Gomes, J. de Oliveira. Treatment of calcium channel blocker intoxication with insulin infusion: case report and literature review. Resuscitation 57 (2003) (211 - 213) x M. Meyer, E. Stremski, M. Scanlon. Successful resuscitation of a verapamil intoxicated child with a dextrose-insulin infusion. Clin Intensive Care 14 (2003) (109 - 113) x C. Morris-Kukoski, A. Biswas, M. Para. Insulin “euglycemia” therapy for accidental nifedipine overdose. J Toxicol Clin Toxicol 38 (2000) (557) x L. Ortiz-Munoz, L.F. Rodriguez-Ospina, M. Figueroa-Gonzalez. Hyperinsulinemic-euglycemic therapy for intoxication with calcium channel blockers. Bol Asoc Med P R 97 (2005) (182 - 189) x N.P. Patel, M.E. Pugh, S. Goldberg, G. Eiger. Hyperinsulinemic euglycemia therapy for verapamil poisoning: case report. Am J Crit Care 16 (2007) (18 - 19) x R. Place, A. Carlson, J. Leikin, P. Hanashiro. Hyperinsulin therapy in the treatment of verapamil overdose. J Toxicol Clin Toxicol (2000) (576 - 577) x L. Rasmussen, S.E. Husted, S.P. Johnsen. Severe intoxication after an intentional overdose of amlodipine. Acta Anaesthesiol Scand 47 (2003) (1038 - 1040) x S.W. Smith, K.L. Ferguson, R.S. Hoffman, L.S. Nelson, H.A. Greller. Prolonged severe hypotension following combined amlodipine and valsartan ingestion. Clin Toxicol (Phila) 46 (2008) (470 - 474) x T.H. Yuan, W.P.I. Kerns, C.A. Tomaszewski, M.D. Ford, J.A. Kline. Insulin-glucose as adjunctive therapy for severe calcium channel antagonist poisoning. J Toxicol Clin Toxicol 37 (1999) (463 - 474) Other potentially useful treatments include glucagon, vasopressin and phosphodiesterse inhibitors.139 and 149 x K. Kanagarajan, J.M. Marraffa, N.C. Bouchard, P. Krishnan, R.S. Hoffman, C.M. Stork. The use of vasopressin in the setting of recalcitrant hypotension due to calcium channel blocker overdose. Clin Toxicol (Phila) 45 (2007) (56 - 59) x C.R. Dewitt, J.C. Waksman, Pharmacology. Pathophysiology and management of calcium channel blocker and beta-blocker toxicity. Toxicol Rev 23 (2004) (223 - 238)
Although cases of digoxin poisoning are fewer than those involving calcium channel and beta-blockers, the mortality rate from digoxin is far greater. Other drugs including calcium channel blockers and amiodarone can also cause plasma concentrations of digoxin to rise. Atrioventricular conduction abnormalities and ventricular hyperexcitability due to digoxin toxicity can lead to severe arrhythmias and cardiac arrest.
Patients at risk of cardiac arrest
Standard resuscitation measures and specific antidote therapy with digoxin-specific antibody fragments should be used if there are arrhythmias associated with haemodynamic instability.150, 151, 152, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, and 163 x M. Eddleston, S. Rajapakse, Rajakanthan, et al.. Anti-digoxin Fab fragments in cardiotoxicity induced by ingestion of yellow oleander: a randomised controlled trial. Lancet 355 (2000) (967 - 972) x T.W. Smith, V.P. Butler Jr., E. Haber, et al.. Treatment of life-threatening digitalis intoxication with digoxin-specific Fab antibody fragments: experience in 26 cases. N Engl J Med 307 (1982) (1357 - 1362) x T.L. Wenger, V.P.J. Butler, E. Haber, T.W. Smith. Treatment of 63 severely digitalis-toxic patients with digoxin-specific antibody fragments. J Am Coll Cardiol 5 (1985) (118A - 123A) x E.M. Antman, T.L. Wenger, V.P. Butler Jr., E. Haber, T.W. Smith. Treatment of 150 cases of life-threatening digitalis intoxication with digoxin-specific Fab antibody fragments: final report of a multicenter study. Circulation 81 (1990) (1744 - 1752) x A.D. Woolf, T. Wenger, T.W. Smith, F.H.J. Lovejoy. The use of digoxin-specific Fab fragments for severe digitalis intoxication in children. N Engl J Med 326 (1992) (1739 - 1744) x A.R. Hickey, T.L. Wenger, V.P. Carpenter, et al.. Digoxin Immune Fab therapy in the management of digitalis intoxication: safety and efficacy results of an observational surveillance study. J Am Coll Cardiol 17 (1991) (590 - 598) x T.L. Wenger. Experience with digoxin immune Fab (ovine) in patients with renal impairment. Am J Emerg Med 9 (1991) (21 - 23) discussion 33–4 x U. Wolf, D. Bauer, W.H. Traub. Metalloproteases of Serratia liquefaciens: degradation of purified human serum proteins. Zentralbl Bakteriol 276 (1991) (16 - 26) x P. Taboulet, F.J. Baud, C. Bismuth, E. Vicaut. Acute digitalis intoxication – is pacing still appropriate?. J Toxicol Clin Toxicol 31 (1993) (261 - 273) x F. Lapostolle, S.W. Borron, C. Verdier, et al.. Digoxin-specific Fab fragments as single first-line therapy in digitalis poisoning. Crit Care Med 36 (2008) (3014 - 3018) x T.J. Hougen, B.L. Lloyd, T.W. Smith. Effects of inotropic and arrhythmogenic digoxin doses and of digoxin-specific antibody on myocardial monovalent cation transport in the dog. Circ Res 44 (1979) (23 - 31) x R.F. Clark, B.S. Selden, S.C. Curry. Digoxin-specific Fab fragments in the treatment of oleander toxicity in a canine model. Ann Emerg Med 20 (1991) (1073 - 1077) x J.R. Brubacher, D. Lachmanen, P.R. Ravikumar, R.S. Hoffman. Efficacy of digoxin specific Fab fragments (Digibind) in the treatment of toad venom poisoning. Toxicon 37 (1999) (931 - 942) x P. Lechat, M. Mudgett-Hunter, M.N. Margolies, E. Haber, T.W. Smith. Reversal of lethal digoxin toxicity in guinea pigs using monoclonal antibodies and Fab fragments. J Pharmacol Exp Ther 229 (1984) (210 - 213) Antibody-specific therapy may also be effective in poisoning from plants as well as Chinese herbal medications containing digitalis glycosides.150, 164, and 165 x M. Eddleston, S. Rajapakse, Rajakanthan, et al.. Anti-digoxin Fab fragments in cardiotoxicity induced by ingestion of yellow oleander: a randomised controlled trial. Lancet 355 (2000) (967 - 972) x A. Dasgupta, K.A. Szelei-Stevens. Neutralization of free digoxin-like immunoreactive components of oriental medicines Dan Shen and Lu-Shen-Wan by the Fab fragment of antidigoxin antibody (Digibind). Am J Clin Pathol 121 (2004) (276 - 281) x G.M. Bosse, T.M. Pope. Recurrent digoxin overdose and treatment with digoxin-specific Fab antibody fragments. J Emerg Med 12 (1994) (179 - 185) Digoxin-specific antibody fragments interfere with digoxin immunoassay measurements and can lead to overestimation of plasma digoxin concentrations.
Cyanide is generally considered to be a rare cause of acute poisoning; however, cyanide exposure occurs relatively frequently in patients with smoke inhalation from residential or industrial fires. Its main toxicity results from inactivation of cytochrome oxidase (at cytochrome a3), thus uncoupling mitochondrial oxidative phosphorylation and inhibiting cellular respiration, even in the presence of adequate oxygen supply. Tissues with the highest oxygen needs (brain and heart) are the most severely affected by acute cyanide poisoning.
Patients at risk of cardiac arrest
Patients with severe cardiovascular toxicity (cardiac arrest, cardiovascular instability, metabolic acidosis, or altered mental status) caused by known or suspected cyanide poisoning should receive cyanide antidote therapy in addition to standard resuscitation, including oxygen. Initial therapy should include a cyanide scavenger (either intravenous hydroxocobalamin or a nitrite – i.e., intravenous sodium nitrite and/or inhaled amyl nitrite), followed as soon as possible by intravenous sodium thiosulphate.166, 167, 168, 169, 170, 171, 172, 173, 174, and 175 x S.W. Borron, F.J. Baud, P. Barriot, M. Imbert, C. Bismuth. Prospective study of hydroxocobalamin for acute cyanide poisoning in smoke inhalation. Ann Emerg Med 49 (2007) (794 - 801) e1–2 x J.L. Fortin, J.P. Giocanti, M. Ruttimann, J.J. Kowalski. Prehospital administration of hydroxocobalamin for smoke inhalation-associated cyanide poisoning: 8 years of experience in the Paris Fire Brigade. Clin Toxicol (Phila) 44 (2006) (37 - 44) x F.J. Baud, P. Barriot, V. Toffis, et al.. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med 325 (1991) (1761 - 1766) x S.W. Borron, F.J. Baud, B. Megarbane, C. Bismuth. Hydroxocobalamin for severe acute cyanide poisoning by ingestion or inhalation. Am J Emerg Med 25 (2007) (551 - 558) x O.B. Espinoza, M. Perez, M.S. Ramirez. Bitter cassava poisoning in eight children: a case report. Vet Hum Toxicol 34 (1992) (65) x P. Houeto, J.R. Hoffman, M. Imbert, P. Levillain, F.J. Baud. Relation of blood cyanide to plasma cyanocobalamin concentration after a fixed dose of hydroxocobalamin in cyanide poisoning. Lancet 346 (1995) (605 - 608) x P. Pontal, C. Bismuth, R. Garnier. Therapeutic attitude in cyanide poisoning: retrospective study of 24 non-lethal cases. Vet Hum Toxicol 24 (1982) (286 - 287) x M.A. Kirk, R. Gerace, K.W. Kulig. Cyanide and methemoglobin kinetics in smoke inhalation victims treated with the cyanide antidote kit. Ann Emerg Med 22 (1993) (1413 - 1418) x K.K. Chen, C.L. Rose. Nitrite and thiosulfate therapy in cyanide poisoning. J Am Med Assoc 149 (1952) (113 - 119) x D. Yen, J. Tsai, L.M. Wang, et al.. The clinical experience of acute cyanide poisoning. Am J Emerg Med 13 (1995) (524 - 528) Hydroxocobalamin and nitrites are equally effective but hydroxocobalamin may be safer because it does not cause methaemoglobin formation or hypotension.
Modifications to BLS/ALS
In case of cardiac arrest caused by cyanide, standard ALS treatment will fail to restore spontaneous circulation as long as cellular respiration is blocked. Antidote treatment is needed for reactivation of cytochrome oxidase.
Carbon monoxide poisoning is common. There were about 25,000 carbon monoxide related hospital admissions reported in the US in 2005. 176 x S. Iqbal, J.H. Clower, T.K. Boehmer, F.Y. Yip, P. Garbe. Carbon monoxide-related hospitalizations in the U.S.: evaluation of a web-based query system for public health surveillance. Public Health Rep 125 (2010) (423 - 432) Patients who develop cardiac arrest caused by carbon monoxide rarely survive to hospital discharge, even if return of spontaneous circulation is achieved; however, hyperbaric oxygen therapy may be considered in these patients as it may reduce the risk of developing persistent or delayed neurological injury.177, 178, 179, 180, 181, 182, 183, 184, and 185 x N.B. Hampson, J.L. Zmaeff. Outcome of patients experiencing cardiac arrest with carbon monoxide poisoning treated with hyperbaric oxygen. Ann Emerg Med 38 (2001) (36 - 41) x E.P. Sloan, D.G. Murphy, R. Hart, et al.. Complications and protocol considerations in carbon monoxide-poisoned patients who require hyperbaric oxygen therapy: report from a ten-year experience. Ann Emerg Med 18 (1989) (629 - 634) x K.J. Chou, J.L. Fisher, E.J. Silver. Characteristics and outcome of children with carbon monoxide poisoning with and without smoke exposure referred for hyperbaric oxygen therapy. Pediatr Emerg Care 16 (2000) (151 - 155) x L.K. Weaver, R.O. Hopkins, K.J. Chan, et al.. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 347 (2002) (1057 - 1067) x S.R. Thom, R.L. Taber, I.I. Mendiguren, J.M. Clark, K.R. Hardy, A.B. Fisher. Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Ann Emerg Med 25 (1995) (474 - 480) x C.D. Scheinkestel, M. Bailey, P.S. Myles, et al.. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial. Med J Aust 170 (1999) (203 - 210) x J.C. Raphael, D. Elkharrat, M.C. Jars-Guincestre, et al.. Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication. Lancet 2 (1989) (414 - 419) x D.N. Juurlink, N.A. Buckley, M.B. Stanbrook, G.K. Isbister, M. Bennett, M.A. McGuigan. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev (2005) (CD002041) x N.A. Buckley, G.K. Isbister, B. Stokes, D.N. Juurlink. Hyperbaric oxygen for carbon monoxide poisoning: a systematic review and critical analysis of the evidence. Toxicol Rev 24 (2005) (75 - 92) The risks inherent in transporting critically ill post-arrest patients to a hyperbaric facility may be significant, and must be weighed against the possibility of benefit on a case-by-case basis. Patients who develop myocardial injury caused by carbon monoxide have an increased risk of cardiac and all-cause mortality lasting at least 7 years after the event; it is reasonable to recommend cardiology follow-up for these patients.186 and 187 x D. Satran, C.R. Henry, C. Adkinson, C.I. Nicholson, Y. Bracha, T.D. Henry. Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. J Am Coll Cardiol 45 (2005) (1513 - 1516) x C.R. Henry, D. Satran, B. Lindgren, C. Adkinson, C.I. Nicholson, T.D. Henry. Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning. JAMA 295 (2006) (398 - 402)
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|Y. Yanagawa, T. Sakamoto, Y. Okada.||Recovery from a psychotropic drug overdose tends to depend on the time from ingestion to arrival, the Glasgow Coma Scale, and a sign of circulatory insufficiency on arrival.||Am J Emerg Med 25 (2007) (757 - 761)||2007|
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