Transcript 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
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Ipecac
Gastric Lavage
Activated charcoal
Cathartics
Whole-Bowel irrigation
IPECAC
• 21% to 38% of drug is removed from the
stomach if given in first hour
• Average child presents 1.5 hours postingestion, 3.5 hours for adults
• No evidence that ipecac improves outcome
• Use in the ED should be abandoned
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
• 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
• 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
• 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)
• 2637 ER visits for poisoning
• 730 hospital admissions (28%)
• 53 ICU admissions
– 2% of all poisonings
– 7% of all admissions
RCH ICU ADMISSIONS
Antidepressants
Antihypertensives
Anticonvulsants
Alcohols
Iron
Benzodiazipines
Others
TRICYCLIC
ANTIDEPRESSANTS
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
• Quinidine-like effects depress myocardial
conduction
– Prolonged QRS, QT or PR intervals
– Torsade de pointes
• Ataxia, hallucinations, coma, seizures
• Other anticholinergic effects
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
Beta-Adrenergic Blockers and
Calcium Channel Blockers
PRESENTATIONS
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Bradycardia
Hypotension
Coma
Convulsions
Hypoglycemia: Beta-blockers
Hyperglycemia: Calcium channel blockers
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
CARBAMAZEPINE
CLINICAL PRESENTATION
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Coma
Respiratory depression
Seizures
Ventricular arrhythmias
Other anticholinergic effects (Ileus,
hyperthermia, urinary retention)
MANAGEMENT
• Supportive
• Seizures:
– Benzodiazepines
– Phenobarbital
– Not phenytoin.
• Charcoal hemoperfusion and hemodialysis
have reduced [serum] by 25-50%
METHANOL AND ETHYLENE
GLYCOL
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
• 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
• 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
• Does not require separate preparation
• Adverse effects: HA, nausea and vertigo vs
altered mental status and hypoglycemia
• Hemodialysis still useful
IRON
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
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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)
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
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
BENZODIAZEPINES
PATHOPHYSIOLOGY
• Benzodiazepines act on the CNS by
potentiating gamma-aminobutyric acid
which renders the postsynaptic receptor
sites to be less excitable
CLINICAL PRESENTATION
• Most commonly; ataxia, lethargy and
slurred speech
• Respiratory depression and coma
• Hypotension and hypothermia are rare
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
SULFONYLUREAS
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 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
• 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
ACETAMINOPHEN
PATHOPHYSIOLOGY
• Metabolized in 3 ways:
– Glucuronidation
– Sulfation
– Via cytochrome P450 pathway to a toxic
intermediate that conjugates with glutathione
• In OD glutathione becomes depleted
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)