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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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objectives
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
GI DECONTAMINATION
  • Ipecac
  • Gastric Lavage
  • Activated charcoal
  • Cathartics
  • Whole-Bowel irrigation
ipecac
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
gastric lavage
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
activated charcoal
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
cathartics
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
whole bowel irrigation
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
rch poisonings 1997 2001
RCH POISONINGS (1997-2001)
  • 2637 ER visits for poisoning
  • 730 hospital admissions (28%)
  • 53 ICU admissions
    • 2% of all poisonings
    • 7% of all admissions
pathophysiology
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

clinical presentation
CLINICAL PRESENTATION
  • Quinidine-like effects depress myocardial conduction
    • Prolonged QRS, QT or PR intervals
    • Torsade de pointes
  • Ataxia, hallucinations, coma, seizures
  • Other anticholinergic effects
management
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?
cardiac drugs

CARDIAC DRUGS

Beta-Adrenergic Blockers and Calcium Channel Blockers

presentations
PRESENTATIONS
  • Bradycardia
  • Hypotension
  • Coma
  • Convulsions
  • Hypoglycemia: Beta-blockers
  • Hyperglycemia: Calcium channel blockers
management1
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
clinical presentation1
CLINICAL PRESENTATION
  • Coma
  • Respiratory depression
  • Seizures
  • Ventricular arrhythmias
  • Other anticholinergic effects (Ileus, hyperthermia, urinary retention)
management2
MANAGEMENT
  • Supportive
  • Seizures:
    • Benzodiazepines
    • Phenobarbital
    • Not phenytoin.
  • Charcoal hemoperfusion and hemodialysis have reduced [serum] by 25-50%
pathophysiology1
PATHOPHYSIOLOGY
  • Metabolites cause the poisoning
  • Ethylene glycol  glycoaldehyde  glycolic oxalic acids
  • Methanol  formaldehyde  formic acid
  • These cause metabolic acidosis, blindness, and cardiovascular instability
traditional treatment
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
fomepizole
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
fomepizole vs etoh
FOMEPIZOLE VS ETOH
  • Does not require separate preparation
  • Adverse effects: HA, nausea and vertigo vs altered mental status and hypoglycemia
  • Hemodialysis still useful
pathophysiology2
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
clinical stages
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)
management3
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
dfo indications
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

pathophysiology3
PATHOPHYSIOLOGY
  • Benzodiazepines act on the CNS by potentiating gamma-aminobutyric acid which renders the postsynaptic receptor sites to be less excitable
clinical presentation2
CLINICAL PRESENTATION
  • Most commonly; ataxia, lethargy and slurred speech
  • Respiratory depression and coma
  • Hypotension and hypothermia are rare
management4
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
background
BACKGROUND
  • Sulfonylureas stimulate insulin secretion which results in hypoglycemia
  • Most common are glyburide, glipizide and chlorpropamide
  • Relatively uncommon poisoning but high morbidity and mortality
traditional treatment1
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
octreotide
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
pathophysiology4
PATHOPHYSIOLOGY
  • Metabolized in 3 ways:
    • Glucuronidation
    • Sulfation
    • Via cytochrome P450 pathway to a toxic intermediate that conjugates with glutathione
  • In OD glutathione becomes depleted
management5
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)