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Toxicological Emergencies

Toxicological Emergencies. Dr. Shahid Aziz MBBS, MRCP (UK), MCEM (London) Assistant professor and consultant emergency medicine, DEM King Khalid University Hospital. Objectives. History and Physical Examination Toxicology Screening Three gaps are important in toxicology Treatment

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Toxicological Emergencies

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  1. Toxicological Emergencies Dr. Shahid Aziz MBBS, MRCP (UK), MCEM (London) Assistant professor and consultant emergency medicine, DEM King Khalid University Hospital

  2. Objectives • History and Physical Examination • Toxicology Screening • Three gaps are important in toxicology • Treatment • ICU Admission

  3. History and Physical Examination Difficulties • No reliable history in patients with profoundly altered metal status • Focused treatment decisions quite difficult. • Multiple substances

  4. History and Physical Examination • Separating patients who have suspected poisoning into broad categories that are based on vital signs, eye findings, mental status, and muscle tone, that helps to determine drug or toxin class i.e.“toxidromes.”

  5. Diagnosing toxicity from vital signs Bradycardia (PACED) Propranolol (beta-blockers), poppies (opiates), propoxyphene, physostigmine Anticholinesterase drugs, antiarrhythmics Clonidine, calcium channel blockers Ethanol or other alcohols Digoxin, digitalis

  6. Tachycardia (FAST) Free base or other forms of cocaine, freon Anticholinergics, antihistamines, antipsychotics, amphetamines, alcohol withdrawal Sympathomimetics (cocaine, caffeine, amphetamines, PCP), solvent abuse, strychnine Theophylline, TCAs, thyroid hormones

  7. Hypothermia (COOLS) Carbon monoxide Opioids Oral hypoglycemics, insulin Liquor (alcohols) Sedative-hypnotics

  8. Hyperthermia (NASA) Neuroleptic malignant syndrome, nicotine Antihistamines, alcohol withdrawal Salicylates, sympathomimetics, serotonin syndrome Anticholinergics, antidepressants, antipsychotics

  9. Hypotension (CRASH) Clonidine, calcium channel blockers Rodenticides (containing arsenic, cyanide) Antidepressants, aminophylline, antihypertensives Sedative-hypnotics Heroin or other opiates

  10. Hypertension (CT SCAN) Cocaine Thyroid supplements Sympathomimetics Caffeine Anticholinergics, amphetamines Nicotine

  11. Rapid respiration (PANT) PCP(phencyclidine), paraquat, pneumonitis (chemical), phosgene ASA and other salicylates Noncardiogenic pulmonary edema, nerve agents Toxin-induced metabolic acidosis

  12. Slow respiration (SLOW) Sedative-hypnotics (barbiturates, benzodiazepines) Liquor (alcohols) Opioids Weed (marijuana)

  13. COMA L: Lead, lithiumE: Ethanol, ethylene glycol, ethchlorvynolT: Tricyclic antidepressants, thallium, tolueneH: Heroin, hemlock, hepatic encephalopathy, heavy metals, hydrogen sulfide, hypoglycemicsA: Arsenic, antidepressants, anticonvulsants, antipsychotics, antihistaminesR: Rohypnol (sedative hypnotics), risperidoneG: GHB I: Isoniazid, insulinC: Carbon monoxide, cyanide, clonidine

  14. Agents that cause seizures (OTIS CAMPBELL) Organophosphates, oral hypoglycemicsTricyclic antidepressants Isoniazid, insulinSympathomimetics, strychnine, salicylatesCamphor, cocaine, carbon monoxide, cyanide, Amphetamines, anticholinergicsMethylxanthines (theophylline, caffeine), methanolPhencyclidine (PCP), propranololBenzodiazepine withdrawal,bupropion, GHBEthanol withdrawal, ethylene glycol Lithium, lidocaine Lead, lindane

  15. Agents that affect pupil size Miosis (COPS) Cholinergics, clonidine, carbamates Opiates, organophosphates Phenothiazines (antipsychotics), pilocarpine) Sedative-hypnotics Mydriasis (SAW) Sympathomimetics Anticholinergics Withdrawal

  16. Agents that cause skin signs Diaphoretic skin (SOAP) SympathomimeticsOrganophosphatesAcetylsalicylic acid or other salicylatesPhencyclidine Dry Skin Antihistamines, anticholinergics Bullae Barbiturates and other sedative-hypnotics,Bites: Snakes and spiders Acneiform rash BromidesChlorinated aromatic hydrocarbons (dioxin)

  17. Flushed or red appearance Anticholinergics, niacinBoric acidCarbon monoxide (rare)Cyanide (rare) Cyanosis ErgotamineNitratesNitritesAniline dyesPhenazopyridineDapsoneAny agent causing hypoxemia, hypotension, or methemoglobinemia.

  18. Common toxidromes Cholinergic (Examples: organophosphates, carbamates, pilocarpine) (DUMBELLS) Diarrhea, diaphoresisUrinationMiosisBradycardia, bronchosecretionsEmesisLacrimationLethargicSalivation

  19. Nicotinic (recalled by the days of the week) Monday: Miosis Tuesday: Tachycardia Wednesday: Weakness Thursday: Tremors Friday: Fasciculations Saturday: Seizures Sunday: Somnolent

  20. Anticholinergic (Examples: antihistamines, cyclic antidepressants, atropine, benztropine, phenothiazines, scopolamine) Hyperthermia (HOT as a hare) Flushed (RED as a beet) Dry skin (DRY as a bone) Dilated pupils (BLIND as a bat) Delirium, hallucinations (MAD as a hatter) Tachycardia Urinary urgency and retention

  21. Sympathomimetic (Examples: cocaine, amphetamines, ephedrine, phencyclidine, pseudoephedrine) Mydriasis Tachycardia Hypertension Hyperthermia Seizures

  22. Opioid (Examples: heroin, morphine, codeine, methadone, fentanyl, oxycodone, hydrocodone) Miosis Bradycardia Hypotension Hypoventilation Coma

  23. Table  --  Antidotes and their indications

  24. Enhanced elimination by charcoal hemoperfusion

  25. History and Physical Examination Treat Toxidrome Yes No • vital signs • ocular findings • mental status • muscle tone determine drug or toxin class

  26. History and Physical Examination • Initially, a rapid survey for ABCs & life-threatening nature • Then, a more focused examination for Physical examination A rapid but careful physical examination of the patient is performed in stages. • Signs of trauma • Neurologic findings • Skin changes • Odors • Eyes

  27. History and Physical Examination Physical examination Patients may present with • hypotension or hypertension • bradyarrhythmias or tachyarrhythmias. • The pathogenesis of hypotension varies and may include • Hypovolemia • Myocardial depression • Cardiac arrhythmias • Systemic vasodilation.

  28. Urine Drug Screens • Detect only natural opiates • Do not detect synthetic or semisynthetic products • morphine • codeine • heroin • Oxycodone • Hydrocodone • Fenanyl • Propoxyphene • Meperidine • methadone.

  29. Laboratories Investigation • Most hospital laboratories have the capability to rapidly identify and quantify only a small fraction of the substances commonly encountered in clinical practice.

  30. Toxicology Screening Check acetaminophen levels in all cases of suspected intoxication

  31. Supportive serum toxicology assays AcetaminophenLithiumSalicylateValproic acidCarbamazepineCo-oximetry (carboxyhemoglobin, methemoglobin) DigoxinPhenobarbitalIronEthanolMethanolEthylene glycol Theophylline • Data from Wu AH, McKay C, Broussard LA, et al. National Academy of Clinical Biochemistry Laboratory Medicine practice guidelines: recommendations for the use of laboratory tests to support poisoned patients who present to the emergency department. Clin Chem 2003;49:357–79. • SkeltonH.,DannL.M.,et al. Drug screening of patients who deliberately harm themselves admitted to the emergency department. Ther Drug Monit (1998) 20 : pp 98-103.

  32. GENERAL TREATMENT • ABCs. • Protection of the cervical spine (unless trauma has been excluded). • A rapid assessment of the need of endotracheal intubation • Attention to any abnormalities of the vital signs. • Discontinuing the offending • Any life-threatening abnormalities • A 12-lead EKG is obtained along with continuous cardiac monitoring. • ABG

  33. Initial supportive measures Endotracheal intubation is indicated • when there is concern regarding airway protection and clinical deterioration • acute respiratory failure. • the need for high levels of supplemental oxygen It decreases (but does not eliminate) the risk of aspiration (which is approximately 11% in the comatose patient with drug overdose).

  34. Initial supportive measures • Rapid IV normal saline solution infusion is indicated in most instances. • Vasopressors may be required for refractory hypotension. • The vasopressor of choice depends on the type of intoxication • Hypertension-induced (reflex) bradycardia generally should not be treated.

  35. Coma Cocktail Initial supportive measures • Dexrtrose, flumazenil, naloxone, thiamine. .

  36. Coma Cocktail Initial supportive measures There is no evidence that dextrose should be withheld until thiamine is administered. • Reuler JB, Girard DE, Cooney TG. Wernicke's encephalopathy. N Engl J Med 1985; 312:1035–1039

  37. Coma Cocktail Initial supportive measures Naloxone • rapidly reverses coma, respiratory depression, and hypotension induced by opioids. • An initial dose of 0.2 to 0.4 mg is administered IV (or endotracheally). • If there is no response after 2 to 3 min, repeated up to 10 mg as required. • lack of response to 10 mg of naloxone generally excludes opioid toxicity.

  38. Coma Cocktail Initial supportive measures Naloxone • a higher dose may precipitate large cardiovascular changes in opioid dependent patients. • Observe for • acute pulmonary edema • opioid withdrawal • seizures

  39. Coma Cocktail Initial supportive measures Flumazenil • Its use in undifferentiated ED patients is not recommended • Withdrawal seizures in mixed overdoses or in patients with long-term use of benzodiazepines. HoffmanR.S.,GoldfrankL.R., The poisoned patient with altered consciousness: controversies in the use of a coma cocktail. JAMA (1995) 274 : pp 562 SpiveyW.H., Flumazenil and seizures: analysis of 43 cases. Clin Ther (1991) 14 : pp 292-305.

  40. Coma Cocktail Initial supportive measures Flumazenil • Case reports have cautioned clinicians of the risk of precipitating seizures with flumazenil when there is a suspicion of benzodiazepine plus TCA overdose • 0.2 mg of IV flumazenil over 30 s followed by another 0.3-mg dose if necessary. • Doses beyond 3 mg generally do not provide additional benefit.

  41. GASTRIC LAVAGE Decontamination • Patients must be able to maintain their airways or be intubated. • Should not be performed on patients who have ingested medications that may cause seizures or abrupt central nervous system deterioration.

  42. GASTRIC LAVAGE Decontamination • There is no clear definition of when to end the procedure.

  43. GASTRIC LAVAGE Decontamination • One study using radiographic markers suggested that GL may actually propel gastric contents past the pylorus, moving the poison into the small intestine, where most of the drug will be absorbed SaettaJ.P.,MarchS.,GauntM.E.,et al. Gastric emptying procedures in the self-poisoned patient: are we forcing contents beyond the pylorus?. J R Soc Med (1991) 84 : pp 274-276.

  44. GASTRIC LAVAGE Decontamination • three clinical trials have failed to demonstrate improved outcomes when GL is added to AC for the management of undifferentiated symptomatic poisoning patients. KuligK.,Bar-OrD.,CantrillS.V.,et al. Management of acutely poisoned patients without gastric emptying. Ann Emerg Med (1985) 14 : pp 562-567. PondS.M.,Lewis-DriverD.J.,WilliamsG.M.,et al. Gastric emptying in acute overdose: a prospective randomised trial. Med J Aust (1995) 163 : pp 345-349. SaettaJ.P.,MarchS.,GauntM.E.,et al. Gastric emptying procedures in the self-poisoned patient: are we forcing contents beyond the pylorus?. J R Soc Med (1991) 84 : pp 274-276

  45. GASTRIC LAVAGE Decontamination • GI tract perforation • hypoxia • aspiration. • esophageal perforation • Arterial oxygen tension dropped 17% during GL • pneumothorax Complications associated with GL include

  46. GASTRIC LAVAGE Decontamination • Based on the available data, the American Academy of Clinical Toxicology does not recommend gastric lavage unless a patient has ingested a potentially life-threatening amount of a poison and the procedure can be undertaken within 60 minutes of ingestion

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