Toxicology Emergencies CDEM


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Toxicology Emergencies CDEM

  1. 1. Toxicologic Emergencies Emergency Medicine Clerkship Lecture Series Primary Authors: Michael Levine, MD, Susan E. Farrell, MD Reviewer: Michael Beeson, MD
  2. 2. EPIDEMIOLOGY • In 2004, more than 2.4 million toxic exposures reported to U.S. Poison Control Centers • 1183 deaths • Over half of poisonings occur in children under 5 years of age
  3. 3. EVALUATION OF THE POISONED PATIENT • History • Physical Exam • Vital signs • Pupil exam • Skin findings • Mental status • Search for a toxidrome
  4. 4. MANAGEMENT OF THE POISONED PATIENT • A-B-C-D-E’s: ACLS measures as appropriate • IV, O2, cardiac monitoring, ECG • Determine blood glucose in all “intoxicated” patients. (Empiric dextrose administration is indicated for all patients with altered mental status if bedside glucose determination is not available) • Thiamine and naloxone empirically as indicated • Decontamination • Enhanced elimination • Antidotal therapy • Supportive care
  5. 5. HISTORY • Name and amount of agent(s) • Type of agent (immediate release, sustained release) • Time of ingestion/exposure • Route of ingestion/exposure • Any co-ingestants (including prescription, OTC’s, recreational drugs, herbals, chemicals, metals) • Reason for ingestion/exposure (e.g. accident, suicide attempt, therapeutic misuse, occupational) • Search exposure environment for pill bottles, drug paraphernalia, suicide note, chemical containers
  6. 6. PHYSICAL EXAM: VITAL SIGNS • Assess and manage the A-B-Cs: • Blood pressure • Heart rate • Respiratory rate • Tachypnea: Salicylates • Bradypnea: Opioids • Respiratory depth • Hyperpnea: Salicylates • Shallow respirations: Opioids • Temperature • Hyperthermia: Serotonin syndrome, NMS, malignant hyperthermia, anti-cholinergic toxidromes, salicylates • Hypothermia: Narcotic or sedative-hypnotic agents
  7. 7. PHYSICAL EXAM: PUPILS • Size • Large: Anticholinergic or sympathomimetic toxidrome • Small: Cholinergic toxidrome • Pinpoint: Opioid toxidrome • Nystagmus: Check for horizontal, vertical, or rotatory (ethanol, phenytoin, ketamine, PCP)
  8. 8. PHYSICAL EXAM: SKIN • Temperature: • Hyperpyrexia: Anticholinergic or sympathomimetic toxidromes, salicylates • Moisture: • Dry: Anticholinergic toxidrome • Moist: Cholinergic, sympathomimetic • Color: Cyanosis, pallor, erythema
  9. 9. PHYSICAL EXAM: OVERALL EXAM • Physiologic stimulation: Everything is “up”: • Elevated temperature, HR, BP, RR, agitated mental status • Sympathomimetics, anticholinergics, central hallucinogens, some drug withdrawal states • Physiologic depression: Everything is “down”: • Depressed temperature, HR, BP, RR, lethargy/coma • Sympatholytics, cholinergics, opioids, sedative-hypnotics • Mixed effects: Polysubstance overdose, metabolic poisons (hypoglycemic agents, salicylates, toxic alcohols)
  10. 10. TOXIDROMES • Anticholinergic • Cholinergic • Opioid • Sympathomimetic • Serotonin syndrome • Sympatholytic • Sedative-hypnotic
  11. 11. TOXIDROMES: ANTICHOLINERGIC • VS: Hyperthermia, tachycardia, elevated BP • CNS: Agitation, delirium, psychomotor activity, hallucinations, mumbling speech, unresponsive • Pupils: Mydriasis (minimally reactive to light) • Skin: Dry, warm, and flushed • GI/GU: Diminished BS, ileus, urinary retention • Examples: Atropine, antihistamines, CADs, cyclobenzaprine, phenothiazines, Datura spp. • Remember: “Dry as a bone, Red as a beet, Blind as a bat, Mad as a hatter, and hotter than hell”
  12. 12. TOXIDROMES: CHOLINERGIC • VS: Bradycardia, high or low BP, tachypnea or bradypnea • CNS: Agitation, confusion, seizures, coma • Pupils: Miosis, eye pain, lacrimation • Skin: Diaphoresis • GI/GU: Salivation, vomiting, diarrhea, incontinence • Musculoskeletal: muscle fasciculations, weakness, paralysis • Examples: Organophosphate and carbamate insecticides, nerve agents, cholinesterase inhibitors (physostigmine, edrophonium), nicotine • Remember: “SLUDGE” Salivation, Lacrimation, Urinary incontinence, diarrhea, Gastrointestinal emesis
  13. 13. TOXIDROMES: OPIOID • VS: Hypothermia, bradycardia, normal or low BP, bradypnea • CNS: Lethargy, coma • Pupils: Miosis (exceptions: meperidine, DXM) • Skin: Cool, pale or moist, evidence of recent or remote needle injection possible • Misc: Hyporeflexia, pulmonary edema, seizures (meperidine and propoxyphene), ventricular dysrhythmias (propoxyphene) • Examples: Morphine and the synthetic opioids; (Note: clonidine can look like an opioid)
  14. 14. TOXIDROMES: SEDATIVE-HYPNOTIC • VS: Hypothermia, normal or bradycardic HR, hypotension, bradypnea • CNS: Drowsiness, dysarthria, ataxia, lethargy, coma • Pupils: Midsize or miosis, nystagmus • Misc: Hyporeflexia; (possible breath odors) • Examples: Alcohols, benzodiazepines, barbiturates, zolpidem, chloral hydrate, ethchlorvynol
  15. 15. TOXIDROMES: SEROTONIN SYNDROME • VS: Hyperthermia, tachycardia, hypertension, tachypnea • CNS: Confusion, agitation, lethargy, coma • Pupils: Mydriasis • Skin: Diaphoretic, flushed • Neuromuscular: Hyperreflexia, tremor, clonus, rigidity • Examples: Combinations that increase 5-HT stimulation (MAOIs, SSRIs, NSRIs, meperidine, L-tryptophan, dextromethorphan, trazadone, linezolid)
  16. 16. TOXIDROMES: SYMPATHOLYTICS • VS: Bradycardia, hypotension, bradypnea, hypopnea • CNS: Normal, lethargy, coma, seizures • Pupils: Mid size to miotic • Examples: Alpha1-adrenergic antagonists, beta-adrenergic antagonists, alpha2-adrenergic agonists, calcium channel blockers
  17. 17. TOXIDROMES: SYMPATHOMIMETICS • VS: Hyperthermia, tachycardia, hypertension, tachypnea, hyperpnea • CNS: Enhanced alertness, agitation, delirium, seizures, coma • Pupils: Mydriasis • Skin: Diaphoretic, hot • Neuromuscular: Hyperreflexia • Examples: Cocaine, phencyclidine, phenylethylamines (amphetamines)
  18. 18. SEIZURE-INDUCING DRUGS OTIS CAMPBELL • O – Organophosphates • T – TCAs • I – Insulin, Isoniazid (INH) • S – Sympathomimetics, salicylates, sulfonylureas • C – Cocaine, camphor, carbamazepine, carbamates, CO • A – Amphetamines, amantadine • M – Methylxanthines, meperidine, mushrooms (Gyromitra species) • P – Phenothiazines, propoxyphene, phencyclidine • B – Benzodiazepine/sedative-hypnotic withdrawal • E – Ethanol withdrawal • L – Lidocaine, lead • L – Lithium, Lindane® (hexachlorocyclohexane)
  19. 19. DECONTAMINATION • Activated charcoal: 1g/kg • The primary means of GI decontamination, IF it is warranted. • Some agents for which AC has reduced adsorptive capacity: metals (lead, iron), lithium, pesticides, hydrocarbons, alcohols, caustics, solvents • Contraindications: bowel obstruction/perforation, unprotected airway, caustics and most hydrocarbons • Whole bowel irrigation: PEG sol 1 – 2 l/h (adults); 500ml/h (ped) • Indications: toxic foreign bodies (e.g. body packers), sustained release products, lithium and metals • Contraindications: as for charcoal • Gastric lavage: • Indications: patients with life threatening ingestions (especially if no adequate antidote available) presenting within 1 hour of ingestion • Contraindications: corrosive ingestions, hydrocarbons • Syrup of ipecac: not recommended
  20. 20. ENHANCED ELIMINATION • Methods to increase the clearance of a substance from the body: • Multiple dose activated charcoal: phenobarbital, theophylline, carbamazepine, dapsone, quinine • Urinary alkalinization: salicylates • Hemodialysis: • Substance characteristics: water-soluble, low molecular weight (<500 D), low protein binding, small volume of distribution (< 1L/kg), low endogenous clearance • Charcoal hemoperfusion: similar to HD; in addition, substance adsorbed to AC
  21. 21. ANTIDOTES TOXIN ANTIDOTE Acetaminophen N-Acetylcysteine Anticholinergic agents Physostigmine Benzodiazepines Flumazenil Beta blockers or calcium IV fluids, calcium, glucagon, insulin (HIE) channel blockers Carbon monoxide O2 Cardiac glycosides Digoxin-specific Fab fragments Cocaine (or other Benzodiazepines sympathomimetics) Cyanide Amyl nitrate, sodium nitrate, sodium thiosulfate, hydroxycobalamin Ethylene glycol 4-Methylpyrazole, ethanol
  22. 22. ANTIDOTES TOXIN ANTIDOTE Heparin Protamine sulfate Hydrofluoric acid Calcium gluconate Iron Desferoxamine Isoniazid Pyridoxine Lead DMSA or BAL/CaNa2-EDTA Mercury BAL Methanol 4-Methylpyrazole, ethanol Opioids Naloxone Organophosphates/ Atropine + pralidoxime carbamates Sulfonylureas Glucose + octreotide (or meglitinides) Tricyclic antidepressants Sodium bicarbonate, benzodiazepines
  23. 23. TOXICOLOGY CASE 1 • A 23 year old female presents via EMS after ingesting 100 tablets of acetaminophen (APAP) immediate release preparation, 500mg tablets • The ingestion occurred 24 hours ago • She has had several episodes of non-bloody, non-biliary emesis • Serum acetaminophen level drawn on arrival: 40mg/dL
  24. 24. TOXICOLOGY CASE 1(cont’d) • Vital signs: T 98.5˚F, HR: 110 bpm, RR 20, BP 110/68, SaO2: 97% on RA • Labs include: • PT/INR/PTT: 14.2s/1.4; PTT: 80s • BUN/Creat: 47mg/dL/1.8mg/dL • Serum glucose: 80mg/dL • AST: 5,423 IU/L ALT: 6,087 IU/L
  25. 25. APAP TOXICITY • Four stages to toxicity: • I: 0-24 hours: Asymptomatic, or mild anorexia, nausea, vomiting, malaise • II: 24-48 hours: Transaminase levels start to rise at 12 hours; Abdominal pain, RUQ tenderness, vomiting, oliguria • III: 72-96 hours: Transaminases peak at 72 hours; PT rises, multi-system organ failure or recovery • IV: 4d-2 weeks: Resolution of hepatotoxicity • Toxicity results from accumulation of a toxic metabolite: N-acetyl-para-benzoquinoneimine (NAPQI) relative to endogenous glutathione • Toxic single ingestion is 150 mg/kg
  26. 26. APAP TOXICITY • At therapeutic doses: • 90% of APAP is conjugated and renally excreted • 2-4% is metabolized via P450 enzymes to NAPQI • NAPQI is quickly conjugated to glutathione to a non-toxic metabolite • In an overdose, glutathione stores are depleted, NAPQI accumulates leading to hepatotoxicity
  28. 28. N-Acetylcysteine • PO dosing: 140 mg/kg load, followed by 70mg/kg q4h x17 doses • IV dosing: 150 mg/kg load over 15 min, followed by 50mg/kg over 4 hours, followed by 100 mg/kg over 16 hours • Prolonging the initial loading period for IV NAC may reduce the incidence of anaphylactoid reactions
  29. 29. APAP TRANSPLANT GUIDELINES • King’s College guidelines • pH < 7.3 after fluid resuscitation or • PT > 100 • Creatinine > 3.4 • Grade III or IV encephalopathy • Lactate > 3.5mmol/L
  30. 30. TOXICOLOGY CASE 2 • A 20 year old male presents via EMS after his neighbor found him unresponsive. The patient is comatose • The neighbor developed a headache and nausea after spending 10 minutes in the patient’s house • It is winter, and the patient had been using a camp stove for heat
  31. 31. TOXICOLOGY CASE 2 (cont’d) • VS: T: 98.9˚F, HR: 110 bpm, RR: 6, BP: 150/100 mmHg, SaO2: 99%. • Moans to painful stimuli with no focal neurologic deficits • Pupils 4mm, sluggishly reactive • Skin notable for central cyanosis • Blood glucose: 90mg/dL • ECG: Sinus tachycardia, normal intervals,no evidence of acute ischemia • Labs include: COHb: 60%
  32. 32. CO TOXICITY • 17,115 cases of CO exposure reported to US Poison Control Centers in 2004 • CO is a colorless, odorless, non-irritating gas • Sources of CO exposure include: • Smoke • Car exhaust • Propane powered vehicles or engines • Hibachi grills and kerosene heaters • Methylene chloride
  33. 33. CO TOXICITY • CO combines with Hgb to form carboxyhemoglobin (COHb) • COHb has 240 X the affinity for O2 • CO + Hgb  shifts the O2 dissociation curve to the left: oxygen delivery to tissues is reduced • CO can cause hypotension via CO-induced cGMP production and increased NO production • CO can inhibit electron transport which limits ATP production • CO is associated with microvascular damage and inflammation in the CNS
  34. 34. CLINICAL EFFECTS OF CO COHb% Signs/Symptoms <5% None or mild HA 10% Slight HA, dyspnea on vigorous exertion 20% Throbbing headache, dyspnea with moderate exertion 30% Severe HA, irritability, fatigue, dim vision 40-50% Tachycardia, confusion, lethargy, syncope 50-70% Coma, seizures, death > 70% Rapidly fatal
  35. 35. CO TOXICITY • CO poisoning is frequently misdiagnosed: symptoms are nonspecific • Need a high index of suspicion • Consider CO poisoning: • Multiple patients with similar complaints, especially from the same household • Vague, flu like symptoms without fever or lymphadenopathy • Winter, environmental history and exposures • Uncommon presentation of syncope • Normal COHb levels • 0-5% in non-smokers • up to 10% in smokers > 1ppd
  36. 36. PULSE OXIMETRY • Noninvasive measure of functional hemoglobin oxygen saturation • Does not measure hemoglobin species that cannot carry oxygen • MetHb • COHb • Co-oximeter measures fractional hemoglobin oxygen saturation
  37. 37. PULSE OXIMETRY GAP Severe CO poisoning • Significant dyshemoglobinemia results in a divergence between functional and fractional hemoglobin oxygen saturation • In patients with markedly elevated COHb levels, pulse oximetry can overestimate O2Hb% • In severe CO poisoning, the pulse oximetry gap approaches the COHb level
  38. 38. CO TREATMENT • Oxygen!! • The half life of COHb decreases with inspired O2 concentration: • t1/2 at room air: 4-6 hours • t1/2 at “100%” O2 via NRB at 1 ATM: 90 min • t1/2 at 100% O2 via ETT at 1 ATM: 60 min • t1/2 at 100% O2 at 3 ATM (HBO): 23 minutes
  39. 39. HYPERBARIC OXYGEN • The rationale behind HBO therapy for CO: • Decrease the incidence of delayed neurologic sequelae • Should be started within 6 hours • HBO indications are controversial, but generally include: • COHgb > 25-40% • Altered Mental Status or history of same (syncope) • Arrhythmias • Symptoms of cardiac ischemia • COHgb > 15% if pregnant
  40. 40. TOXICOLOGY CASE 3 • A 22 year old male brought via EMS after being found “drunk.” He was found near an empty bottle of window-washer fluid • The patient had threatened suicide earlier in the day
  41. 41. TOXICOLOGY CASE 3 (cont’d) • Labs include: • Serum glucose: 124 mg/dL • Sodium: 130 mEq/L; K: 3.7 mEq/L; Cl: 88 mEq/L; Bicarbonate: 12 mEq/L; BUN: 22 mg/dL; Creatinine 1.5 mg/dL • Anion gap of 30 • Serum ethanol: non-detectable • Serum APAP/ASA: non-detectable • Serum osmolality: 324 mOsm/kg
  42. 42. TOXIC ALCOHOLS • Most commonly: methanol, isopropanol, and ethylene glycol (EG) • Should be suspected based on: • history, physical exam, lab abnormalities • The degree of intoxication correlates with the number of carbons in the alcohol: • Methanol < ethanol or ethylene glycol < isopropanol
  43. 43. TOXIC ALCOHOL LABS • All toxic alcohols cause an osmolar gap • Methanol and EG cause an increased anion gap acidosis • Isopropanol causes ketosis without acidosis • Osmolar gaps can be present early after ingestion, but will be absent after the alcohol is metabolized • Anion gap acidosis can be absent early after ingestion, but will develops after methanol or EG metabolism
  44. 44. “GAPS” Anion gap Gap’s Osmolar gap Time
  45. 45. METHANOL • Methanol (CH3OH): • window-washer fluid, anti-icing agents, solvents, varnish/paint removers, some anti-freezes • Methanol intoxication: • “Snow storm” blindness (edema of the optic disk/nerve) • Abdominal pain, nausea, vomiting • Lethargy, coma
  46. 46. METHANOL METABOLISM Methanol Alcohol dehydrogenase* Formaldehyde Aldehyde dehydrogenase Formic acid Folate CO2 + H2O * Inhibited by 4-methylpyrazole or ethanol
  47. 47. ISOPROPANOL • Isopropanol (CH3-CHOH-CH3): • The most intoxicating alcohol • Osmolar gap, followed by ketosis • Metabolized to acetone by alcohol dehydrogenase
  48. 48. ETHYLENE GLYCOL • Ethylene glycol C(OH2) – C(OH2) sources: • Antifreeze, brake fluid, anti-icing solutions, solvents • If fluorescein has been added to an EG- containing antifreeze, the patient’s urine may fluoresce under Wood’s lamp • Metabolized to: • Glycolic acid: anion gap acidosis • Oxalic acid, combines with calcium, causing calcium oxylate crystal deposition and hypocalcemia • Calcium oxylate deposition in the renal tubules causes acute renal failure
  49. 49. ETHYLENE GLYCOL METABOLISM Ethylene glycol Alcohol dehydrogenase* Glycoaldehyde Aldehyde dehydrogenase Glycolic acid Lactate dehydrogenase Glyoxylic acid Pyridoxine, Mg Thiamine Glycine + α-OH-β- Benzoic acid Oxalic acid ketoadipic acid *Inhibited by 4-methylpyrazole or ethanol Pyridoxine, Mg, and thiamine are co-factors for their respective reactions
  50. 50. TREATMENT • Methanol or EG: 4-methyl-pyrazole (4-MP, fomepizole) • 4-MP inhibits alcohol dehydrogenase activity • Ethanol also competes for active sites on alcohol dehydrogenase and inhibits methanol and EG metabolism • Potential adverse effects of ethanol infusion: • Intoxication, hypotension, pancreatitis, gastritis, hypoglycemia, or phlebitis • Hemodialysis clears the toxic alcohol and corrects acid/base abnormalities
  51. 51. TREATMENT (cont’d) • EG: Other cofactors to enhance nontoxic metabolism: • thiamine, pyridoxine, magnesium • Methanol: Other cofactors to enhance nontoxic metabolism: • folic acid (or folinic acid) • Treatment of Isopropanol ingestion: • Supportive care • H2 blockers or proton-pump inhibitors • Ensure that no other toxic alcohol is present
  52. 52. TOXICOLOGY CASE 4 • A 3 year old male is brought by his parents 1 hour after he is found with one of his grandmother’s sustained – release verapamil tablets in his mouth • A pill count shows 1 additional tablet might be missing • The child is asymptomatic
  53. 53. TOXICOLOGY CASE 4 (cont’d) • Vital signs: T: 98.6˚F, HR: 80 bpm, RR: 22, BP:100/60, SaO2: 99% • Initial labs: • Na: 140 mEq/L; K: 3.7 mEq/L; Cl: 113 mEq/L; Bicarbonate: 22 mEq/L; BUN: 12 mg/dL; Creatinine 0.8 mg/dL. Serum glucose: 120mg/dL • ECG: normal sinus rhythm, normal intervals. • Two hours later: the patient is less arousable • Vital signs: HR: 50 bpm, RR: 18, BP: 70/40 SaO2: 99% • ECG: junctional bradycardia, normal QRS and QTc intervals • Serum glucose: 190 mg/dL
  54. 54. CALCIUM CHANNEL BLOCKER (CCB) • Classes of CCB approved in the US: • Phenylalkylamines: Verapamil • Verapamil: Effects cardiac myocytes and electrical conduction system ( decreased contractility, AV nodal conduction delay and block) • Benzothiazepines: Diltiazem • Benzothiazepines: Effects cardiac myocytes, electrical conduction system, and peripheral vascular smooth muscle cells • Dihydropyridines: Nifedipine, amlodipine, nicardipine • Dihydropyridines: Effects peripheral vascular smooth muscle cells ( peripheral vasodilation, decreased peripheral vascular resistance) • In overdose, the selectivity of the CCB classes may be lost
  55. 55. CCB TOXICITY • CCBs: • Block L-type calcium channels • Inhibit intracellular calcium influx • In overdose: • Verapamil or diltiazem: Bradycardia and hypotension • Dihydropyridines: Hypotension and tachycardia • Insulin release from pancreatic β-cells depends on L- type calcium channels; hyperglycemia can occur after CCB overdose • The degree of hyperglycemia may correlate with the severity of the overdose
  56. 56. CCBs versus BETA BLOCKERS • β1 antagonism: • Decreased cardiac contractility • Reduced AV nodal conduction • β2 antagonism: • Increased smooth muscle tone…bronchospasm • Labetolol: • 7:1 β:α antagonist activity • Βeta adrenergic antagonists: • Inhibit gluconeogenesis and glycogenolysis • Hypoglycemia can occur in overdose • Seizures can occur in overdose (propranolol)
  57. 57. CCB and BETA BLOCKER TREATMENT • Ensure ABCs • Improve heart rate and blood pressure: • Atropine: Often fails to improve HR • Calcium: Used in both CCB and Beta blocker toxicity; Improves HR and contractility • Glucagon: Improves myocardial contractility • Direct α agonist agents: Increase peripheral vascular resistance • (Epinephrine has both β1 and α1 agonist effects)
  58. 58. CCB/BETA BLOCKER TX • Therapies unique to CCB or β blocker involve: • IV fluids – Offsets hypotension induced by peripheral vasodilation • Calcium – Calcium competitively overcomes blockade of the voltage-sensitive calcium channels • Glucagon: Acts on adenylate cyclase independently of the β receptor to convert ATP into cAMP • Epinephrine: Binds to β receptors to convert adenylate cyclase into cAMP • Insulin: Promotes increased uptake and utilization of carbohydrates by cardiac myocytes (primarily used only for CCB toxicity
  59. 59. Hyperinsulinemic Euglycemia (HIE) • Normally: Cardiac myocytes preferentially metabolize glucose; in shock states, metabolism is dependent on free fatty acids • Hyperinsulinemic euglycemic (HIE) therapy: shifts myocardial metabolism from FFA to carbohydrates • HIE: • Insulin (0.5-1 unit/kg bolus, followed by 0.5-1 unit/kg/hr) • Dextrose (1 amp D50, or continuous D10 infusion) • Watch for hypokalemia and hypophosphatemia • HIE therapy: Associated with rapid, dramatic improvement in cardiovascular hemodynamics
  60. 60. CARDIAC GLYCOSIDES • Digoxin: A cardiac glycoside used for the treatment of CHF and atrial fibrillation • Mechanism of action: • Inhibits Na/K/ATPase, leading to: • Increased intracellular sodium/calcium exchange • Increased intracellular calcium • Increased extracellular potassium • Digoxin • Increases excitability and automaticity of cardiac myocytes • Decreases conduction velocity at the AV node
  61. 61. CARDIAC GLYCOSIDE TOXICITY • Cardiac glycosides: • Foxglove, oleander, lily of the valley, red squill • Secretions of Bufo toads (e.g. Colorado river toad) • Symptoms of toxicity: • Nausea and vomiting • Weakness, lethargy, confusion • Visual disturbances • Acute toxicity: • Serum potassium is elevated, predictive of mortality. • Chronic toxicity: • Precipitated by hypokalemia, hypomagnesemia, renal failure • Digoxin toxicity can occur with therapeutic digoxin levels
  62. 62. CARDIAC GLYCOSIDE TOXICITY: THE ECG • Nearly every dysrhythmia has been associated with digoxin toxicity • PVCs are the most common ECG abnormality • Bidirectional ventricular tachycardia and accelerated junctional rhythms with nodal block are relatively specific for cardiac glycoside toxicity, but are less common
  63. 63. CARDIAC GLYCOSIDE TOXICITY: TREATMENT • Digoxin-specific Fab fragments indications: • Hyperkalemia (K > 5.0) • Life-threatening arrhythmias • Phenytoin or lidocaine: • May suppress ventricular dysrhythmias if digoxin-specific Fab is unavailable • Correct hypokalemia, hypomagnesemia • Calcium therapy for hyperkalemia should be avoided with concomitant digoxin toxicity
  64. 64. TOXICOLOGY CASE 5 • A 42 year old woman presents via EMS after she was found unresponsive at home • Vital signs: T 99.8˚ F, HR: 121 bpm, RR: 14; BP: 97/52; SaO2: 93% on RA • PE: Disheveled, minimally responsive female; pupils: 8 mm, minimally reactive; dry lips and mucous membranes; tachycardia, absent bowel sounds; skin warm and flushed
  65. 65. TOXICOLOGY CASE 5 (cont’d) • The patient is placed on a cardiac monitor and IV access is obtained • Shortly after an ECG is performed, the patient has a brief, generalized tonic-clonic seizure
  66. 66. TCA ingestion Note the tachycardia, QRS prolongation, tall R wave in aVR, and the rightward deflection of the terminal 40 msec of aVR.
  67. 67. TRICYCLIC ANTIDEPRESSANT TOXICITY • TCA toxicity: • Sodium channel blockade: conduction delay • Alpha1 adrenergic blockade: hypotension • Cholinergic (muscarinic) blockade: mydriasis, dry mucous membranes, tachycardia, ileus, urinary retention • Histamine blockade • Treatment: • Sodium bicarbonate • Direct alpha1 adrenergic agents as pressors • Benzodiazepines as seizure prophylaxis/treatment • NaHCO3 is indicated for any QRS > 100 ms
  68. 68. TRICYCLIC ANTIDEPRESSANT TOXICITY • The risk of ventricular dysrhythmias and seizures correlates with QRS prolongation • ECG findings suggestive of TCA toxicity include: Tachycardia Prolonged PR, QRS intervals Tall R wave in aVR Rightward deflection of terminal 40 msec in aVR • NaHCO3 is indicated for any QRS > 100 ms
  69. 69. In Summary Approach all patients in a systematic fashion Toxic exposures most often only require supportive care Be aware of toxic exposures that require specific antidotes Most toxic exposures are unintentional Consider contacting a regional poison control center for all but the most straight forward cases