PEDIATRICS// //poisoning

POISONING

Poisoning in children is a common clinical problem & common cause of

hospital admission. Poisoning can occur with drugs, cleansing agents,
insecticides, paints, petroleum products, plants, & inhalation of toxic
gases or fumes.

- More than 90% of toxic exposure in children occurs at home, & most
involves only a single substance.
-Ingestion is the most common route of poisoning exposure (76% of
cases), with the dermal, ophthalmic, & inhalation routes each occurring in
about 8% of cases.
- Death due to unintentional poisoning in young children is uncommon
owing to increased product safety measures (e.g., child-resistant
packaging), increased poison prevention education, early recognition of
exposure, & improvements in medical management.

MANAGEMENT PLAN FOR POISONING

Identification of the poison is not the most critical aspect in the
management, & the time should not be lost trying to identify the
causative poison. Good supportive care is the backbone of any successful
therapy of poisoned children.

A-History: Obtaining an accurate problem-oriented history is of high

importance if a poisoning has occurred or is suspected. Precise history
should include the following:

1-Clinical manifestations: Due to the multiplicity of drugs & other

poisons, the pathophysiological changes can almost affect every system.
. Therefore, the possibility of poisoning should be considered in any child
: especially below 5 years, who acutely develops respiratory distress,
apnea, shock, cardiac arrhythmias, abnormal behaviors, abnormal
movements (like ataxia & dystonia), convulsions, disturbed
consciousness, or severe digestive or cutaneous manifestations.
2-Description of toxin: its name, ingredients & their concentrations.
Consultation of a poison control center usually provides important help.
3-Magnitude of exposure: The age & weight of the child.

1
 PEDIATRICS// //poisoning

4-Time of exposure: For some product, toxic manifestations may be

delayed for hours or days (important in therapy & prognosis).
5-Medical history: underlying diseases, concurrent drug therapy.

B- Medical care:

1. At home : If the poison is not so harmful, the patient can be treated at

home & follow-up assessment calls should be made approximately 0.5, 1,
& 4 hours after exposure.
2. At hospital:
1- Supportive measures: Once the patient has arrived in the appropriate
medical care setting, initial attention should focus on life support
(cardiorespiratory care). Initial treatment of apnea, shock, dysrrhythmias,
metabolic disturbances (dehydration, temperature abnormalities, acid-
base disorder rs, electrolyte disorders, blood sugar disorders). Repeated
assessment of the general condition, vital signs, blood counts, blood
gases, serum electrolytes, & blood sugar are important.
2- Investigations: All product containers thought to be related to
exposure should be collected & transported with the patient. If the patient
has vomited, the emesis should also be brought to the emergency
department for possible toxicologic analysis. For some intoxications (e.g.,
salicylates, acetaminophen, iron, methanol, ethylene glycol), blood levels
are integral in the treatment plan. Comprehensive qualitative "drug
screens" vary widely in their ability to detect toxins & generally add little
informations (urine is the best sample for drug screens).

3-Measures directed to the poison:

1-Antidote therapy: Unfortunately, only few drugs & poisons of which a

specific antidote is available. These include carbon monoxide (100% O2),
acetaminophen (N-Acetylcysteine), cyanide (Na nitrate & Na
thiosulphate), organophosphate &carbamate insecticide (atropine,
pralidoxime), methemoglobinemia (methylene blue), opiates & narcotics
(naloxone), iron (deferoxamine), lead (EDTA, DMSA), extrapyramidal
symptoms (diphenhydramine), digoxin (digoxin-specific Fab antidotes),
anticholinergic agents (physostigmine) & benzodiazepines (flumazenil).

2
 PEDIATRICS// //poisoning

2-Preventing absorption: Most toxins are rapidly absorbed from GIT or

through inhalation. Many may also be well absorbed upon dermal
contact. Prompt action to remove the toxin may prevent the development
of major toxicity. Dermal & ocular decontamination can be accomplished
by flushing the affected area with water. For inhaled toxin ,
decontamination is generally accomplished by moving the patient to fresh
air or, if necessary, administering O2.
Several procedures are used to prevent absorption of a toxin from GIT, &
each has limitations & risks. In general, most liquid drug products are
almost completely absorbed within 30 min of ingestion, & most solid
dosage forms within 1-2 hr, beyond this time, it is unlikely to be of value,
however, with some poisons , gastric lavage can be done within 12 hr of
ingestion (aspirin, opiate, tricyclic antidepressant).

A -Emesis : Induction of vomiting by syrup of ipecac (10 ml for infants

6-12 mo of age, 15 ml for children 1-12 yr of age, & 30 ml for older
children & adults). This is followed by administration of at least 8 oz of
water or other clear fluid. The onset of vomiting is usually 20-30 min
after dosing in 90- 95% of patients.
Limitations:
- Ipecac should not be used in infant <6 mo of age .
- It is contraindicated after the ingestion of caustics &hydrocarbons
- It is contraindicated in coma.

B-Gastric lavage: This technique involves placing a tube into the

stomach to aspirate contents, followed by flushing of fluid (usually
normal saline) & its aspiration :
Limitations:
- Lavage is time consuming
- Removes only a fraction of gastric contents.
- It should only be used in older children & only in selected situations
(e.g., in large doses of aspirin, iron, opiates, & tricyclic
antidepressants). - It is contraindicated after the ingestion of caustics &
hydrocarbons and coma.

3
 PEDIATRICS// //poisoning

C-Activated charcoal: The use of activated charcoal to prevent

absorption of toxins has increased dramatically in the past 2 decades.
Many, but not all, toxins are adsorbed onto its surface, preventing
absorption from the GIT. The usual dose for a child is1 gm/kg & 30-100
g for an adolescent or adult, mixed with water. The dose may be repeated
every 2-4 hr until the first charcoal stool appears. Aspiration of activated
charcoal into the lungs occasionally occurs.
D-Cathartics: Cathartics are commonly used in conjunction with
activated charcoal to hasten the clearance of the charcoal-toxin complex,
although no evidence shows that this is of value. Commonly used
cathartics are sorbitol, magnesium sulfate, & magnesium citrate.
Cathartics should be used with care in young children because of the risk
of dehydration & electrolyte imbalance.

E-Whole bowel irrigation: Whole bowel irrigation involves instilling

large volumes of a polyethylene glycol electrolyte solution (Colyte) into
the stomach to cleanse the entire GIT. Whole bowel irrigation can be
combined with use of activated charcoal, if appropriate. It should be used
with caution in young children because of the possibility of fluid &
electrolyte imbalance.
3-Enhancing excretion: Enhancing excretion is useful for only a few
toxins & associated with risk.
A-Diuresis: It is a useful technique in drugs mainly excreted by the
kidney (e.g., salicylates & phenobarbital) & it is usually combined by
alkalanization of urine. 2-5 times the maintenance IV fluids are given to
establish a urine output of 2-5 ml/kg/hr. Concomitant use of diuretics as
furosemide & mannitol is indicated to ensure high urine flow rate.
B-Dialysis: Hemodialysis & peritoneal dialysis. They are not useful for
drugs that are either highly protein bound or have a large volume of
distribution. These techniques are also invasive
C-Hemoperfusion: Hemoperfusion is a dialytic technique in which
blood is passed through a column of activated charcoal or resin.

Acetaminophen:

The chief target organ of acetaminophen poisoning is the liver, with the
kidneys being involved in about 10 to 20% of those patients with
hepatotoxicity.
Rarely, nephrotoxicity may occur without significant hepatic
4
 PEDIATRICS// //poisoning

involvement. The dose required to produce significant hepatotoxicity in

adults is 7.5 to 10.0 g. The commonly stated hepatotoxic dose for
children is 150 mg/kg.

Stage I: 0-24 hrs

Early symptoms
Nausea, vomiting, malaise and diaphoresis.
Normal bilirubin Transaminases and PT.

Stage II: 24-48 hrs after ingestion.

Better, less symptoms.
Elevated bilirubin, transaminases and PT

Stage III :48-96 hrs ( 2- 4 days) after ingestion

Hepatic dysfunction (Rarely hepatic failure)
Peak elevations in:
Bilirubin
Transaminases may reach >
1000 IU/L
Prolonged PT

Stage IV :168- 192 hrs (7-8

days)
Clinical improvement
LFTs returning to normal

5
 PEDIATRICS// //poisoning

Iron Poisoning
Five Stages but variable
• Stage 1 : 30 min to 6 hr after ingestion
▪ GIT stage: within several hrs of ingestion:
▪ V/D, Hematochezia and abdominal pain
▪ significant volume losses leading to potential hypovolemic shock.
▪ Patients who do not develop GI symptoms within 6 hr of ingestion are
unlikely to develop serious toxicity.
Toxic doses occur at 10 -20mg/Kg of elemental iron

• Stage 2 : : 4 -48hrs
▪ Clinical improvement of GIT
▪ signs of hypoperfusion, including tachycardia, pallor, and fatigue ,
decreased U.O.

• Stage 3 : Circulatory collapse : 48 -96 hrs

▪ Metabolic acidosis, hypotension, Shock
▪ Coagulopathy
▪ Multi Organ Failure

• Stage 4 :
▪ Hepatic failure: 96 hrs
▪ Liver transplant can save lives

• Stage 5 : Bowel obstruction 2 -6 wks due to scarring

Management :
1. Gastric decontamination:
 WBI remains the decontamination strategy of choice
 No activated charcoal to be used!!!
2. Secure good IV
3. Get initial then 4hrs Iron levels and TIBC
4. Chelate with Deferoxamine if levels> 500mg/dL

6
 PEDIATRICS// //poisoning

HYDROCABONS
Hydrocarbons include a wide array of chemical substances. The most
important manifestation of hydrocarbon toxicity is aspiration
pneumonitis via inactivation of the type II pneumocytes and resulting
surfactant deficiency. Aspiration usually occurs during coughing and
gagging at the time of ingestion or vomiting after the attempted ingestion
of an aliphatic hydrocarbon. The propensity of a hydrocarbon to cause
aspiration pneumonitis is inversely proportional to its viscosity, and
directly proportional to its volatility. Compounds with low viscosity and
high volatility, such as kerosene, gasoline, and lamp oil, spread rapidly
across surfaces and cover large areas of the lungs when aspirated. Only
small quantities (<1 mL) of such chemicals need be aspirated to produce
significant injury. Pneumonitis does not result from dermal absorption of
hydrocarbons or from ingestion in the absence of aspiration. Gasoline and
kerosene are poorly absorbed, but they often cause considerable
irritation of the GI mucosa as they pass through the intestines.
All volatile hydrocarbons are lipid solvents producing local irritation
or, with prolonged exposure, chemical burns.
Certain hydrocarbons have unique toxicities and can cause symptoms
after ingestion, inhalation, or dermal exposures. These may include:
hepatic toxicity, renal toxicity. Methemoglobinemia, arrhythmias &
sudden death.
- Transient, mild CNS depression is common after hydrocarbon
ingestion or inhalation.

Clinical and Laboratory Manifestations of aspiration pneumonia

- Aspiration is characterized by coughing, which usually is the first
clinical finding.
- Respiratory symptoms may remain mild or may rapidly progress to
respiratory failure, chest retractions, grunting, cough, and fever may
occur as soon as 30 min after aspiration or may be delayed for several
hours.
- Ingestion of >30 mL (approximate volume of an adult swallow) of
hydrocarbon is associated with an increased risk of severe pneumonitis.
- Fever and leukocytosis are common accompanying signs in patients
with pneumonitis and don’t necessarily imply bacterial superinfection.
- Chest radiograph may initially be normal, but they often show
abnormalities within 6 hr of exposure in patients who have aspirated &
7
 PEDIATRICS// //poisoning

may remain abnormal long after a patient is clinically normal.

Pneumatoceles may appear on the chest radiograph 2-3 wk after
exposure.

Treatment
- Emesis & gastric lavage are contraindicated because of the risk of
aspiration, patients who ingest these compounds in volumes >30 mL,
such as might occur with intentional overdose, may benefit from gastric
emptying. This is still a high-risk procedure that can result in further
aspiration. If a cuffed endotracheal tube can be placed without inducing
vomiting, this procedure should be considered, especially in the presence
of altered mental status.

- Decontamination of skin & clothes.

- Activated charcoal also is not useful, because it does not bind to
hydrocarbons.
- If hydrocarbon-induced pneumonitis develops, respiratory treatment
is supportive. consisting of oxygen, fluids, and ventilator support.
- The child who has no symptoms and normal chest radiograph findings
should be observed for 6-8 hr to ensure safe discharge.
- Neither corticosteroids nor prophylactic antibiotics have shown any
clear benefit.

ORGANOPHOSPHATES & CARBAMATES

The most commonly used insecticides are either organophosphates or
carbamates. Both of these classes are inhibitors of cholinesterase
enzymes. Most pediatric poisonings occur as the result of accidental
exposure to insecticides in & around the home or farm.
Clinical manifestations
Clinical manifestations of organophosphates & carbamates toxicity relate
to the accumulation of acetylcholine at peripheral nicotinic & muscarinic
synapses & in the CNS.
- Muscarinic signs & symptoms include diaphoresis, emesis, urinary &
fecal incontinence, tearing, drooling, bronchorrhea & bronchospasm,
miosis, & hypotension & bradycardia .
- Nicotinic signs & symptoms include muscle weakness, fasciculation,
tremors, hypoventilation, hypertension, tachycardia, & dysrhythmias.

8
 PEDIATRICS// //poisoning

- CNS effect includes malaise, confusion, delirium, seizures, & coma.

Symptoms caused by carbamate toxicity are usually less severe than those
seen with organophosphates.

Treatment
- Decontamination should be done; activated charcoal can be used for
gastric decontamination.
- Basic supportive care should be provided, including fluid & electrolyte
replacement & intubation with artificial ventilation if necessary.
- Tow antidotes are useful in treatment: atropine &pralidoxime.
Atropine, which blocks the acetylcholine receptors, is useful for both
organophosphates &carbamates. It is most effective at reversing the
muscarinic & CNS effects. Often, large doses of atropine must be
administered by continuous infusion (0.05 mg/kg slow IV, repeated every
5-10 min as needed, dilute in 1-2 ml of NS for ET instillation).
Pralidoxime chemically breaks the bond between the organophosphates
& the enzyme, liberating the enzyme & degrading the organophosphates.
Without treatment, the patient may die or the symptoms may persist for
weeks, requiring continous supportive care.

TRICYCLIC ANTIDEPRESSANTS
e.g amitriptyline
Anticholinergic effects cause most of the following presenting symptoms
:
Dry mouth
Flushed skin
Blurred vision
Urinary retention
Constipation
Dizziness
Emesis

Physical Signs of TCA toxicity include the following:

Anticholinergic effects
Altered mental status (agitation, confusion, lethargy)
Resting sinus tachycardia
Dry mucous membranes
Mydriasis
Fever
9
 PEDIATRICS// //poisoning

Cardiac effects
Hypertension (early and transient, should not be treated)
Tachycardia
Orthostasis and hypotension
Arrhythmia/ECG changes
CNS effects
Coma
Seizure
Myoclonic twitches/tremor
Hyperreflexia
Pulmonary effects - Hypoventilation resulting from CNS depression
GIT effects - Decreased or absent bowel sounds

Lab Studies:
Rapid bedside glucose level determination
Serum pH, electrolytes, calcium, Urine toxicology screening
The single most important test to guide therapy and prognosis remains the
12 -lead surface ECG.
Important ECG changes include the following:
1. Prolongation of the QRS complex
2. Prolongation of the QT interval
3. Tachycardia and arrhythmia

Medical Care:
Careful attention to ABC , and neurologic parameters are of most
importance because of the risk of rapid deterioration in patients.
Decontamination strategies should be used carefully in selected
patients(usually charcoal) Sodium bicarbonate given in doses to achieve
PH level 7.45 -7.55 to treat and prevent dysrhythmias
Lidocain is used to treat dysrhythmias that are unresponsive to serum
alkalization

10