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HIGHLIGHTS IN PEDIATRICS TOXICOLOGYDr. Manal Al MaskatiOct, 2011 - Kuwait
OBJECTIVES
Few words about poisoning in Pediatrics.
Key points in poisoning history and physical
examination.
Some important Toxidromes.
Common cases of poisoning in Pediatric age
group.
INTRODUCTION
Poisonings too common in pediatric world.
Around 6,000,000 children ingest potentially toxic substance each year nationwide.
Most frequently in children ages 1-5 years old.
Most common exposures are substances found around the house (makeup, household chemicals, over the counter medicines, and houseplants).
Substances either nontoxic or, if toxic, in insufficient amounts to cause significant problems.
Second peak of exposures in adolescent population, most are suicide attempts.
Drug or Poison Potentially Lethal Dose In 10 kg Child
Camphor 1 teaspoon of 20% oil
Chloroquine 1 tablet (500 mg)
Codeine 3 tablets (60 mg each)
Desipramine 2 tablets (75 mg each)
Hydrocarbons (e.g. gasoline)
One swallow (if aspirated)
Oral Hypoglycemics 2 Glyburide tablets (5mg each)
Imipramine 1 tablet (150 mg)
Iron 10 tablets (Full Adult Strength)
Lindane 2 teaspoons
Methyl Salicylate Less that 1 teaspoon of Oil of Wintergreen
Theophylline 1 tablet (500 mg)
Verapamil 1 tablet (240 mg)
HISTORY
Three key questions in all poisoning cases:
1) WHAT substance(s) was ingested?
2) WHEN did the ingestion occur?
3) HOW MUCH was ingested?
HISTORY Answers to questions will provide valuable
information about:
a) Severity of the ingestion.
b) Potential benefits/efficacy of GI
decontamination.
c) Whether or not therapeutic interventions
necessary.
d) Accurate interpretation of specific drug levels.
e) Disposition of the patient.
TOXICOLOGIC PHYSICAL EXAMINATIONa) Eyes: pupillary size, symmetry and response to light
presence of nystagmus (vertical or horizontal).
b) Oropharynx: moist or dry mucus membranes, presence/absence of the gag reflex, presence of any particular or distinctive odors.
c) Abdomen: presence/absence and quality of bowel sounds.
d) Skin: warm/dry, warm/sweaty or cool.
e) Neurologic: level of consciousness and mental status, presence of tremors, seizures or other movement disorders, presence/absence and quality of deep tendon reflexes.
TOXIDROMES Refer to specific constellation of signs and symptoms
specific class or type of toxic substance.
1. Anticholinergics (atropine, antihistamines, cyclic antidepressants):
Tachycardia, hypertension, tachypnea (red as a beet).
Mydriasis (blind as a bat).
Agitation, hallucinations/delirium, seizures, hypoactive bowel sounds( mad as a hatter).
Warm/dry skin, dry mouth (hot as a hare ,dry as a bone).
TOXIDROMES 2. Sympathomimetics (cocaine,
amphetamines, PCP, decongestants, beta-
agonists, theophylline):
Tachycardia, hypertension, tachypnea.
Mydriasis.
Agitation, hallucinations, delirium, seizures,
hypoactive bowel sounds.
Warm/sweaty skin.
TOXIDROMES
3.Cholinergics (organophosphate and
carbamate insecticides):
"D-U-M-B3-E-L-S"
Defecation, Urinary incontinence, Miosis.
Bradycardia/Bronchospasm/Bronchorrhea.
Emesis, Lacrimation, Salivation.
TOXIDROMES 4. Opioids (codeine, morphine, meperidine, heroin):
Bradycardia, hypotension, bradypnea.
Hypothermia, hyporeflexia, pinpoint pupils.
5.Sedative-hypnotics (ethanol, benzodiazepines,
barbiturates):
Bradycardia, hypotension, bradypnea.
Hypothermia, hyporeflexia, miosis.
PYRAMID OF TOXICOLOGY
A two year olds brought to the Pediatric Emergency Department by his mother following an ingestion of 20-22 cyproheptadine HCL tablets (4mg Periactin) 1-1.5 hours prior to presentation. According to his mother, the patient was acting "bizarre".
VS: BP:130/70 P :160 T :98.4
Skin: Warm, dry, not flushed
Neck: Supple
Lungs: CTAB
Heart: Tachycardic, otherwise WNL
Abdomen: soft, NT
Neurologic: Delerious. Patient grasping objects on the floor that were not present Unable to recognize mother, gait ataxic. DTR's normal, no focal findings.
CASE 1
ANTIHISTAMINE TOXICITY (ANTICHOLINERGIC TOXIDROME)Management
ABC's + supportive care.
Sedation with benzodiazepines.
Give false positive tricyclic immunoassay on
urine screen hamper accurate diagnosis.
Physostigmine not indicated unless
patient's condition deteriorated.
If hemodynamically stable, likely to respond
well to sedation.
A three year-old male is brought to the Emergency Department in severe respiratory distress. The mother states that she was polishing her dining room table and left to answer the phone. She subsequently found he child several minutes later drenched in the furniture polish solution. The child was noted to be coughing violently, and was anxious and irritable.
VS: BP :100/60 P :120 RR :30 T :101.2 rectally.
Gen: Anxious, dyspneic, crying infant, coughing violently. Mild cyanosis noted during coughing episodes. Use of accessory muscles and nasal flaring noted. Kerosene-like odor noted on patient's breath.
Lungs: Diffuse crackles bilaterally.
Heart: Tachycardia.
Abd: soft, NT.
Neuro: Unable to obtain adequate exam due to poor cooperation
CASE 2
HYDROCARBON ASPIRATIONManagement Most hydrocarbon ingestions of small volume. ABC's to prevent further aspiration, may need
intubation for airway protection and /or progressive respiratory distress.
Skin decontamination is needed, by removing his clothing and washing with gentle soap and water.
Observe for signs of pneumonia , aspiration cause aseptic chemical pneumonitis does not require antibiotics.
Secondary bacterial pneumonia may need treatment Prophylactic antibiotics NOT indicated.
Steroids also NOT indicated. Supportive treatment with oxygen and
bronchodilators to counteract bronchospasm.
Common CompoundsRisk of
Systemic Toxicity
Risk of Aspirati
onTreatment
No Systemic Toxicity, High Viscosity (Petrolatum Jelly, motor oil)
Low Low None
No Systemic Toxicity, Low Viscosity (Gasoline, kerosene, mineral seal oil, petroleum ether)
Low High
Observe for pneumonia;
do not empty stomach
Unknown of Uncertain Systemic Toxicity (Turpentine, pine oil)
Uncertain High
Observe for pneumonia,
Empty stomach if
ingestion is > 2 mL/kg
Systemic Toxins (Camphor, phenol, halogenated or aromatic compounds)
High High
Observe for pneumonia;
perform gastric
lavage or give AC or do
both
A 50 kg 14 year old female is brought to the Emergency Department in a comatose state. History, as obtained from the distraught parents, reveals that their daughter was very upset recently following the termination of her relationship with her closest friend. The child was found in a lethargic state when the parents returned home from the theater. An empty bottle of Darvocet N-100 was found in the bedroom near the patient. The mother confirms that the medication was prescribed by her family physician for back pain, and the prescription for 100 tablets had been filled one week ago. The parents last saw the patient approximately 5 hours ago.
VS: BP: 80/40 P: 110 R :8 T :98.6 rectally
Gen: Comatose female, responsive only to deep sternal pressure, vomitus on clothing, diaphoretic.
HEENT: Pupils equal at 3mm bilaterally, sluggish.
Lungs: CTAB
Heart: WNL
Abdomen: soft, NT
Neurologic: Absent DTR's
CASE 3
ACETAMINOPHEN TOXICITYOPIOID TOXICITY Darvocet N-100 is a combination analgesic that
contains propoxyphene, a synthetic opioid, and
650mg of acetaminophen.
Synthetic opioids that do not cause significant
miosis (others Demerol and Dextromethorphan)
Many of synthetic opioids do not show up on
routine urine tox screens.
This scenario carries high possibility of additional
unknown coingestants intentional
overdoses often polydrug ingestions.
ACETAMINOPHEN TOXICITYOPIOID TOXICITY
Management
Close attention to ABC's.
Intubation if there risk of aspiration.
For opioid toxicity:
Naloxone (Narcan) to be given at initial dose of 2mg.
Further doses given until adequate effect achieved.
Naloxone provide rapid (1-2 minutes) reversal of symptoms.
Due to short duration of naloxone action (60 minutes), re-dosing will likely be necessary ,if opioid symptoms persist.
Lack of response to narcan might point to coingestion of another CNS depressant (benzodiazepines or barbiturates).
ACETAMINOPHEN TOXICITYOPIOID TOXICITY For acetaminophen toxicity APAP level should be sent. 4 hour post ingestion level key in
determining need for treatment. If level is toxic based on nomogram ,treatment
with NAC should be initiated. If level is subtoxic, then to be repeated within
4 hours to confirm it . Initial loading dose of NAC within 8 hrs of
ingestion, good effect if given within 24 hrs of ingestion.
NAC Loading dose 140 mg, followed by 70 mg q4h X 17 doses.
Rumack-Matthew Nomogram
A 15 year old female is brought to the Emergency Department in a confused state by her sister. Following an argument, the patient ingested an unknown amount of medication during the early morning hours. Her sister who was, awakened in the morning to find the patient mumbling incoherently. She brought her to the Emergency Department and quickly left. The patient herself can give no additional history.
VS: BP:70/50 P:120 R:32 T:102.6
GEN: Disoriented, somewhat restless female
HEENT: NCAT, TM's clear bilat., Pt c/o "noise in her ears", PERRLA, Pt. complains of blurred vision.
Lungs: Crackles 2/3 of the way up bilat.
Heart: Tachycardia, otherwise WNL
Abd: 2+ Mid-epigastric tenderness with diminished bowel sound
Skin: Warm and moist
CASE 4
Sodium: 148Potassium: 3.2Chloride: 101Bicarbonate: 13ABG on Room AirpH: 7.21pCO2: 10pO2: 80UrinalysisU/O over 1st hour: 5ccSpecific Gravity: 1.029 with microscopic hematuriaRadiographicChest X-Ray: Bilateral hilar infiltrates
LAB WORK
SALICYLATE TOXICITY Elevated anion gap metabolic acidosis (AG=34). A combination of primary AG metabolic acidosis +
primary respiratory alkalosis highly suggestive of salicylate poisoning.
A serum salicylate level > 60, indicates major exposure.
Level > 100, indicates severe poisoning. Mental status + acid/base status more important
than serum concentration. Bedside, quick urine test ferric chloride
test. Presence of salicylates purple color change.
Click icon to add picture
10% Ferric Chloride Test
MANAGEMENT ABC's.
Activated charcoal should be administered.
Bicarbonate, both to correct the acidemia, and alkalinize
the urine facilitate excretion of salicylates.
Important to maintain serum potassium in normal range
hypokalemia hamper efforts to alkalinize the urine.
Dialysis to be considered for refractive acidosis or
severe hypokelemia.
TRICYCLIC ANTIDEPRESSANTS
Significant source of poisonings.
Toxic effects of TCA’s mediated through
anticholinergic, alpha1 blockade, and quinidine-like Na
channel blockade effects.
TCA’s have low therapeutic to toxic ratio, doses < 10
times therapeutic sufficient to cause toxicity.
Symptoms appear rapidly (within 1 hr of ingestion).
Asymptomatic person for 6 hrs post ingestion unlikely
to develop life-threatening events.
Mechanism Cardiovascular Effects CNS Effects Anticholinergic
Tachycardia Hypertension
Hyperthermia Agitation Delerium Coma
Alpha1 Blockade
Peripheral Vasodilation Flushing Hypotension (tends to predominate over HTN)
Na Channel Blockade
Membrane Depression Conduction Disturbances Prolonged PR, QRS Arrhythmias (tachy, VF)
Seizures (may be related to serotonin or norepinephrine mediated effects)
DIAGNOSIS Urine screens can detect many of TCA’s, but a
negative screen doesn’t rule out exposure.
ECG key element to diagnose TCA toxicity.
QRS prolongation + seizures + lethargy or coma ,
highly suggestive of TCA poisoning.
Degree of QRS prolongation severity of CNS +
cardiovascular toxicity.
QRS >0.10 associated with seizures and >0.16
associated with arrhythmias.
MANAGEMENT ABC’s Activated charcoal. Unlike pure anticholinergic toxicity, physostigmine
should NOT be used in TCA overdose worsen seizures + conduction disturbances + increased risk for asystole.
Most important therapy for TCA overdose sodium bicarbonate, QRS prolongation or hypotension.
Initial dose 1 mEq/kg, repeated as boluses to maintain QRS < 0.10.
Asymptomatic pts monitored for at least 6 hours, symptomatics should be admitted to ICU for at least 24 hours.
BETA BLOCKERSCALCIUM CHANNEL BLOCKERS Beta Blockers
Have negative inotropic + chronotropic effects.
In toxic doses, myocardial depressant effects
predominate (hypertension, ventricular
arrhythmias).
Calcium Channel Blockers
Have negative inotropic + chronotropic effects ,
and/or vasodilation, depends on site of action.
Site of Action
Verapimil Diltiazem Dihydropyridines
Vascular Smooth Muscle
+ ++ +++
Cardiac +++ ++ +
Site of Action
MANIFESTATIONS Toxic doses for both classes varies from agent to
agent.
Both beta blockers and calcium channel blockers have very small therapeutic to toxic ratio.
Signs of toxicity within therapeutic range.
Most common features of overdose of both classes hypotension + bradycardia.
ECG's show simply sinus bradycardia, with vaiable PR prolongation.
Beta blockers QRS prolongation, but calcium channel blockers not.
MANIFESTATIONS
MANAGEMENT ABC’s Activated charcoal . Gastric lavage for significant
ingestions( within 1/2 -1 hr of ingestion). Sustained release preparations may need
whole bowel irrigation. No place for dialysis. Focused Therapy -- Beta Blockers Glucagon is antidote. Has positive inotropic
+ chronotropic. Given as bolus followed by continuous
infusion. Epinephrine also effective. QRS prolongation treated with sodium
bicarbonate.
MANAGEMENT Focused Therapy -- Calcium Channel
Blockers Calcium is antidote, helps to overcome the
blockade of calcium channels. Given either as calcium chloride or calcium
gluconate, repeated as needed. Calcium gluconate preferable (tissue
damage with calcium chloride) 30 mL of calcium gluconate approximately 1 gram of calcium.
Leads to rapid improvement in contractility, but no effect on conduction disturbances, sinus node depression or peripheral vasodilation.
Glucagon and epinephrine beneficial in treating severe hypotension and/or bradycardia.
TAKE HOME MESSAGE
Prevention is always better than treatment.
As early as the diagnosis and intervention as
better as the results.
Detailed history + Thorough examination +
Reliable source + Little knowledge about
toxicology Successful management.
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