COMMON INTOXICATIONS IN KIDS

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COMMON INTOXICATIONS IN KIDS

• Blake Bulloch, MD

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OBJECTIVES

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

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GI DECONTAMINATION

• Ipecac
• Gastric Lavage
• Activated charcoal
• Cathartics
• Whole-Bowel irrigation

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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

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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

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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

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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

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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

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RCH POISONINGS (1997-2001)

• 2637 ER visits for poisoning
• 730 hospital admissions (28)
• 53 ICU admissions
• 2 of all poisonings
• 7 of all admissions

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RCH ICU ADMISSIONS
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TRICYCLIC ANTIDEPRESSANTS
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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

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CLINICAL PRESENTATION

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

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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?

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CARDIAC DRUGS

• Beta-Adrenergic Blockers and Calcium Channel
  Blockers

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PRESENTATIONS

• Bradycardia
• Hypotension
• Coma
• Convulsions
• Hypoglycemia Beta-blockers
• Hyperglycemia Calcium channel blockers

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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

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CARBAMAZEPINE
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CLINICAL PRESENTATION

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

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MANAGEMENT

• Supportive
• Seizures
• Benzodiazepines
• Phenobarbital
• Not phenytoin.
• Charcoal hemoperfusion and hemodialysis have
  reduced serum by 25-50

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METHANOL AND ETHYLENE GLYCOL
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PATHOPHYSIOLOGY

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

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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

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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

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FOMEPIZOLE VS ETOH

• Does not require separate preparation
• Adverse effects HA, nausea and vertigo vs
  altered mental status and hypoglycemia
• Hemodialysis still useful

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IRON
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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

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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)

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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

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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 gt 300
  ug/dl

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BENZODIAZEPINES
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PATHOPHYSIOLOGY

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

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CLINICAL PRESENTATION

• Most commonly ataxia, lethargy and slurred
  speech
• Respiratory depression and coma
• Hypotension and hypothermia are rare

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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

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SULFONYLUREAS
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BACKGROUND

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

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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

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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

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ACETAMINOPHEN
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PATHOPHYSIOLOGY

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

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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)