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COMMON INTOXICATIONS IN KIDS

COMMON INTOXICATIONS IN KIDS. Blake Bulloch, MD. OBJECTIVES. Review new recommendations for GI decontamination Review the common types of intoxications seen in children with recommendations on non-dialytic detoxifying therapies. GI DECONTAMINATION. Ipecac Gastric Lavage Activated charcoal

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COMMON INTOXICATIONS IN KIDS

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  1. COMMON INTOXICATIONS IN KIDS Blake Bulloch, MD

  2. OBJECTIVES • Review new recommendations for GI decontamination • Review the common types of intoxications seen in children with recommendations on non-dialytic detoxifying therapies

  3. GI DECONTAMINATION • Ipecac • Gastric Lavage • Activated charcoal • Cathartics • Whole-Bowel irrigation

  4. IPECAC • 21% to 38% of drug is removed from the stomach if given in first hour • Average child presents 1.5 hours post-ingestion, 3.5 hours for adults • No evidence that ipecac improves outcome • Use in the ED should be abandoned

  5. GASTRIC LAVAGE • 32% of drug removed if performed  1 hour • In ED studies no difference in outcomes versus charcoal alone • Complication rate of 3% and includes: • aspiration pneumonia • dysrhythmias • hypoxia and hypercapnia / laryngospasm

  6. ACTIVATED CHARCOAL • Mean  in drug absorption is 89% if given within 30 min and 37% if given at 1 hour • Complications minimal • Insufficient data to support or exclude its use after 1 hour post-ingestion

  7. CATHARTICS • Two reasons cited for use of cathartics which are NOT true: • 1) Prevent charcoal induced constipation • 2) Decrease bioavailability of the ingestant • Not recommended for GI decontamination

  8. WHOLE-BOWEL IRRIGATION • At 1 hour or longer after ingestion WBI decreases bioavailability 70% • Long procedure and labor-intensive • Limit to poisons not adsorbed by charcoal and to sustained release pharmaceuticals • Should not be used routinely in poisonings

  9. RCH POISONINGS (1997-2001) • 2637 ER visits for poisoning • 730 hospital admissions (28%) • 53 ICU admissions • 2% of all poisonings • 7% of all admissions

  10. RCH ICU ADMISSIONS

  11. TRICYCLIC ANTIDEPRESSANTS

  12. PATHOPHYSIOLOGY Most toxic reactions are due to: (1) Anticholinergic effects (2) Excessive blockade of norepinephrine reuptake at the postganglionic synapse (3) Direct quinidine-like effects on the myocardium

  13. CLINICAL PRESENTATION • Quinidine-like effects depress myocardial conduction • Prolonged QRS, QT or PR intervals • Torsade de pointes • Ataxia, hallucinations, coma, seizures • Other anticholinergic effects

  14. MANAGEMENT • Sodium bicarbonate: • Increases the plasma protein binding of TCAs • May help overcome sodium channel blockade • If hypotensive may consider norepinephrine infusion (0.1-0.3 ug/kg/min) • Less ventricular arrhythmias than with dopamine?

  15. CARDIAC DRUGS Beta-Adrenergic Blockers and Calcium Channel Blockers

  16. PRESENTATIONS • Bradycardia • Hypotension • Coma • Convulsions • Hypoglycemia: Beta-blockers • Hyperglycemia: Calcium channel blockers

  17. MANAGEMENT • Atropine, fluid boluses and pressors to treat bradycardia and hypotension • Glucagon 3-5 mg/kg IV bolus up to 10 mg followed by an infusion of 2-5 mg/h • CCB: 10% Ca gluconate 0.6 ml/kg or 10% Ca chloride 0.2 ml/kg • Pacemaker

  18. CARBAMAZEPINE

  19. CLINICAL PRESENTATION • Coma • Respiratory depression • Seizures • Ventricular arrhythmias • Other anticholinergic effects (Ileus, hyperthermia, urinary retention)

  20. MANAGEMENT • Supportive • Seizures: • Benzodiazepines • Phenobarbital • Not phenytoin. • Charcoal hemoperfusion and hemodialysis have reduced [serum] by 25-50%

  21. METHANOL AND ETHYLENE GLYCOL

  22. PATHOPHYSIOLOGY • Metabolites cause the poisoning • Ethylene glycol  glycoaldehyde  glycolic oxalic acids • Methanol  formaldehyde  formic acid • These cause metabolic acidosis, blindness, and cardiovascular instability

  23. TRADITIONAL TREATMENT • Ethanol administration to occupy binding sites on alcohol dehydrogenase and prevent generation of toxic metabolites • Hemodialysis to eliminate parent compound • Sodium bicarbonate to treat metabolic acidosis

  24. FOMEPIZOLE • Competitively inhibits alcohol dehydrogenase • Loading dose 15 mg/kg followed by 10 mg/kg q12h for 4 doses then 15 mg/kg q12h • Doses given intravenously over 30 minutes

  25. FOMEPIZOLE VS ETOH • Does not require separate preparation • Adverse effects: HA, nausea and vertigo vs altered mental status and hypoglycemia • Hemodialysis still useful

  26. IRON

  27. PATHOPHYSIOLOGY • Excess iron is directly caustic to the GI mucosa  hypovolemia and shock • Free unbound iron: • Increases capillary permeability • Accumulates mainly in the liver and concentrates in mitochondria disrupting oxidative phosphorylation  lactic acidosis

  28. CLINICAL STAGES • Stage 1: GI phase (within hours) • Stage 2: Latent (6 - 24 hours) • Stage 3: Shock phase (variable) • Stage 4: GI tract scarring (days to weeks)

  29. MANAGEMENT • WBI unless ileus, obstruction, perforation or GI hemorrhage • Deferoxamine mesylate is a chelating agent that removes iron from tissues and free iron from plasma • Dose: 15 mg/kg/hour

  30. DFO INDICATIONS 1) Symptomatic patients with more than transient minor symptoms 2) Patients with lethargy, abdominal pain, hypovolemia or acidosis 3) Positive AXR 4) Any symptomatic patient with iron level > 300 ug/dl

  31. BENZODIAZEPINES

  32. PATHOPHYSIOLOGY • Benzodiazepines act on the CNS by potentiating gamma-aminobutyric acid which renders the postsynaptic receptor sites to be less excitable

  33. CLINICAL PRESENTATION • Most commonly; ataxia, lethargy and slurred speech • Respiratory depression and coma • Hypotension and hypothermia are rare

  34. MANAGEMENT • Flumazenil • Competitive BDZ receptor antagonist • Adult dose is 0.2 mg IV every minute until response achieved (maximum 3 mg) • Literature to support higher doses • Pediatric dose recommendation: • 10 ug/kg for 2 doses

  35. SULFONYLUREAS

  36. BACKGROUND • Sulfonylureas stimulate insulin secretion which results in hypoglycemia • Most common are glyburide, glipizide and chlorpropamide • Relatively uncommon poisoning but high morbidity and mortality

  37. TRADITIONAL TREATMENT • Routine treatments are often ineffective because they stimulate endogenous insulin secretion (dextrose and glucagon) • Corticosteroids are unreliable • Diazoxide (antihypertensive) is an inhibitor of insulin secretion and is effective • Concern exists over possible hypotension

  38. OCTREOTIDE • Inhibits the secretion of insulin • Stabilizes blood glucose levels and prevents rebound hypoglycemia • Dose is 50 ug subcutaneously q8-12h • Recommendation: Octreotide to all patients who remain hypoglycemic after a 1 g/kg dose of dextrose

  39. ACETAMINOPHEN

  40. PATHOPHYSIOLOGY • Metabolized in 3 ways: • Glucuronidation • Sulfation • Via cytochrome P450 pathway to a toxic intermediate that conjugates with glutathione • In OD glutathione becomes depleted

  41. MANAGEMENT • GI decontamination • Obtain 4 hour level • N-Acetylcysteine (NAC): • United States: 140 mg/kg P.O. then 70 mg/kg q4h for 17 doses (Total time 72 h) • Everywhere else: I.V. infusion x 3 (Total time: 21 h)

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