HIGHLIGHTS IN
PEDIATRICS
TOXICOLOGY
Dr. Manal Al Maskati
Oct, 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
Chloroquine
Codeine
Desipramine
Hydrocarbons (e.g. gasoline)
Oral Hypoglycemics
1 teaspoon of 20% oil
Imipramine
Iron
Lindane
Methyl Salicylate
Theophylline
Verapamil
1 tablet (500 mg)
3 tablets (60 mg each)
2 tablets (75 mg each)
One swallow (if aspirated)
2 Glyburide tablets (5mg each)
1 tablet (150 mg)
10 tablets (Full Adult Strength)
2 teaspoons
Less that 1 teaspoon of Oil of Wintergreen
1 tablet (500 mg)
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 EXAMINATION
a) 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.
CASE 1

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.
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.
CASE 2


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
HYDROCARBON ASPIRATION
Management
 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 Compounds
Risk of
Systemic
Toxicity
Risk of
Aspiration
Treatment
No Systemic Toxicity, High Viscosity
(Petrolatum Jelly, motor oil)
Low
Low
None
High
Observe for
pneumonia; do
not empty
stomach
High
Observe for
pneumonia,
Empty stomach if
ingestion is > 2
mL/kg
No Systemic Toxicity, Low Viscosity
(Gasoline, kerosene, mineral seal oil,
petroleum ether)
Unknown of Uncertain Systemic
Toxicity
(Turpentine, pine oil)
Systemic Toxins
(Camphor, phenol, halogenated or
aromatic compounds)
Low
Uncertain
High
High
Observe for
pneumonia;
perform gastric
lavage or give AC
CASE 3

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
ACETAMINOPHEN TOXICITY
OPIOID 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
ingestions.
intentional overdoses often polydrug
ACETAMINOPHEN TOXICITY
OPIOID 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), redosing 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 TOXICITY
OPIOID 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.
CASE 4

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
LAB WORK
Sodium: 148
Potassium: 3.2
Chloride: 101
Bicarbonate: 13
ABG on Room Air
pH: 7.21
pCO2: 10
pO2: 80
Urinalysis
U/O over 1st hour: 5cc
Specific Gravity: 1.029 with microscopic hematuria
Radiographic
Chest X-Ray: Bilateral hilar infiltrates
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.
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
 Anticholinergic  Tachycardia
 Hypertension
 Alpha1
Blockade
 Peripheral Vasodilation
 Flushing
 Hypotension (tends to predominate over
HTN)
 Na Channel
Blockade




Membrane Depression
Conduction Disturbances
Prolonged PR, QRS
Arrhythmias (tachy, VF)
CNS Effects




Hyperthermia
Agitation
Delerium
Coma
 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 BLOCKERS
CALCIUM 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
Vascular
Smooth
Muscle
+
++
+++
Cardiac
+++
++
+
Diltiazem Dihydropyridines
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

Most common features of overdose of both classes
hypotension + bradycardia.

ECG's show simply sinus bradycardia, with vaiable PR
prolongation.

Beta blockers
blockers not.
within therapeutic range.
QRS prolongation, but calcium channel
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.