Common Poisoning among Children

1. Poisoning
Lutfi Abdallah

2. Epidemiology
• Data in sub-Saharan Africa is limited
• American Association of Poison Control
Centres > 2 million human poisoning
exposure reported annually
• > 50% in children 5 yr of age or younger
• Almost all are unintentional
• > 90% occur in the home - ingestion

3. • Ingestion
 It is the most common route of poisoning
exposure (77%) with dermal, inhalation,
ophthalmic route account 7.5%, 6%, 5%
respectively
 Common household products ie cosmetics,
person care item, cleaning solution

4. Pharmaceutical preparations ie analgesic,cough
and cold products,antimicrobial agent.
Plants, berries
In children 6-12 yr of age are much less common
• Adolescents – intentional suicide, abuse

5. Approach to the poisoned patient
• Approach is no different than that in any other
sick child
• Emergency assessment – A,B,C etc
• Emergency Treatment
• History
• Physical exam

6. know ;
• Clear cut history of poisoning
• A reliable person witnessed the event
• The substance is known
• Amount ingested ?
• Poisoning witnessed
• Substance unknown
• Amount ?
• Differential diagnosis in any unexplained illness in a
previously healthy child.

7. OVERVIEW OF COMMON ACCIDENTAL
INGESTION
INGESTION CLINICAL
MANIFESTATI
ON
NURSING
TREATMENT
INTERVENTION
S
Salicylate
(Aspirin)
Tinnitus
Hyperpyrexia
Seizures
Bleeding
Hyperventilation
Emesis
Hydration
Vitamin K
Activated
charcoal
Anticipatory
guidance
Bleeding
precautions
Counseling if
suicide attempt
Acetaminophen
(Tylenol)
Liver necrosis in
2-5 days; nausea;
vomiting; pain in
R upper
quadrant;
jaundice;
coagulation;
abnormalities,
hepatoxic
-Emesis
Mucomyst
(antidote)
-Counseling if
suicide attempt
- Liver
assessment

8. Lead (paint, also
in soil near
heavily trafficked
roadways,
household dust)
-Developmental
regression
-Impaired growth
(encelophalopath
y)
-Irritability
-Increased
clumsiness
-Chelation
therapy
-EDTA
-Bal
-Child must be
well hydrated
-Neuro
assessment
-Diet high in
calcium, iron
-Educate parents
to wash chuld’s
hands, toys
frequently to
remove lead dust
-Lead abatement
Hydrocarbons
(kerosene,
turpentine,
gasoline)
-Burning in mouth
- choking and
gagging
-CNS depression
-DO NOT INDUCE
EMESIS
-Activated
charcoal
-Gastric lavage
If vomiting,
reduce aspiration
Corrosives (drain
or oven cleanser,
chlorine bleach,
battery acid)
-Burning in mouth
-White swollen
mucous
membranes
-Violent vomiting
- DO NOT INDUCE
EMESIS
-Dilute toxin with
water
-Activated
charcoal
Keep warm and
inactive

9. Specific poisonings
• Acetaminophen

10. Specific poisonings
• 4 stages of Acetaminophen if left untreated
• Stage 1 – In the first 24 h after ingestion, the patient
develop nausea, vomiting and diaphoresis
• Stage 2 – During the next 24 -48 h, there is clinical
involvement. During this time serum AST, ALT, bilirubin, and
prothrombin increase. The patient develop right upper
quadrant pain.
• Stage 3 – From 72 to 96h after ingestion, the patient has
peak liver function abnormalities. GI symptoms may again
develop.
• Stage 4 – From 4 days to 2 weeks after ingestion, the
patient’s hepatic problems resolve.
<1% will develop fulminant hepatic necrosis.

11. Specific poisonings
If within 1 hour of ingestion give activated charcoal, if available, or induce
vomiting UNLESS an oral antidote may be required.
➤Decide if antidote is required to prevent liver damage: ingestions of
150mg/kg or more, or toxic 4 hour paracetamol level where this is available.
Antidote is more often required for older children who deliberately ingest
paracetamol or when parents overdose children by mistake.
➤If within 8 hours of ingestion give oral methionine or IV acetylcysteine.
Methionine can be used if the child is conscious and not vomiting (<6 years:
1 gram every 4 hours for 4 doses; 6 years or older: 2.5 grams every 4 hours
for 4 doses).
➤If more than 8 hours after ingestion, or the child cannot take oral
treatment,
give IV acetylcysteine.

12. Specific poisonings
Aspirin(Salicylates)

13. Specific poisonings
3 phases of salicylate ingestion
Phase 1 – The patient has respiratory alkalosis and potassium
and sodium bicarbonate are excreted in the urine. This phase
last approx. 12h in an adolescent but may not be evident in small
children.
Phase 2 – As alkalosis continues, a “paradoxical aciduria” occurs
approx. 12 – 24 h after salicylate ingestion in the adolescent. This
phase may begin shortly after salicylate ingestion in the young
child.
Phase 3 – Metabolic acidocic, dehydration and hypokalemia
appear 4-6h after ingestion of salicylates in an infant, and ≥ 24h
after ingestion in an adolescent.

14. Specific poisonings
Diagnostic tests
- WBC, Hct, platelets ↑
- BUN, cratinine ↑
- Hypernatremia or hyper- or hypokalemia
- Hyper- or hypoglycemia
- The arterial blood gas will show a metabolic acidosis and
respiratory compensation in children and a respiratory alkalosis
alone in adolescents.

15. Give activated charcoal if available.
Note that salicylate tablets tend to form a concretion in the stomach leading to
delayed absorption, so it is worthwhile giving several doses of charcoal. If charcoal is
not available and a severely toxic dose has been given, then perform gastric lavage or
induce vomiting.
➤Give IV sodium bicarbonate 1 mmol/kg over 4 hours to correct acidosis and to raise
the pH of the urine to above 7.5 so that salicylate excretion is increased. Give
supplemental potassium too. Monitor urine pH hourly.
➤Give IV fluids at maintenance requirements unless child shows signs of
dehydration in which case give adequate rehydration.
➤Monitor blood glucose every 6 hours and correct as necessary.
➤Give vitamin K 10mg IM or IV.

16. Specific poisonings
Complications/Follow-up:
Some causes of death from salicylate ingestion
include respiratory failure, cerebral edema,
hemorrhage and cardiovascular collapse.

17. Specific poisonings
Iron
■ Check for clinical features of iron poisoning: nausea, vomiting, abdominal pain and
diarrhoea. The vomit and stools are often grey or black. In severe poisoning there may
be gastrointestinal haemorrhage, hypotension, drowsiness, convulsions and metabolic
acidosis. Gastrointestinal features usually appear in the first 6 hours and a child who
has remained asymptomatic for this time probably does not require antidote
treatment.
➤Activated charcoal does not bind to iron salts, therefore consider giving a gastric
lavage if potentially toxic amounts of iron were taken.
➤Decide whether to give antidote treatment. Since this can have side-effects it
should only be used if there is clinical evidence of poisoning.
➤If you decide to give antidote treatment, give deferoxamine (50 mg/kg IM up to a
maximum of 1 g) by deep IM injection repeated every 12 hours; if very ill, give IV
infusion 15 mg/kg/hour to a maximum of 80 mg/kg in 24 hours.

18. Specific poisonings
Carbon Monoxide
A 5 year old is brought to the Emergency centre for the first time
seizure. The child was previously well, and has never had a seizure.
His father states that the child was travelling cross-country in an older
model vehicle when the seizure occurred. The child was sleeping on
the floor of the vehicle, and there were five adults who were smoking
tobacco at the time of the event. On physical examination the child
appears drowsy, but otherwise, the physical examination is
unremarkable. The pulse oximetry reads 97%

19. Specific poisonings
Definition: CO is colorless, odorless gas produced from the
combustion of carbon-containing fuel.
Risk factors/ Etiology: The affinity of CO to hemoglobin is 250 times
that of oxygen. This results in the formation of caboxyhemoglobin,
decreasing the oxygen carrying capacity of blood.

20. Specific poisonings
Presentation:
Symptom depend on the carboxyhemoglobin levels
0-10% None
11-20% Mild headache
21-30% Throbbing headache, irritability
31-40% Severe headache, lethargy, nausea, vomiting
41-50% Confusion, syncope, tachycardia, tachypnea
51-60% Syncope, coma, seizure
61-70% Coma, hypertension, respiratory failure, death
>70% Death

21. Specific poisonings
➤Give 100% oxygen to accelerate removal of carbon monoxide (note
patient can look pink but still be hypoxaemic) until signs of hypoxia
disappear.
➤Monitor with pulse oximeter but be aware that these can give
falsely high readings. If in doubt, be guided by presence or absence of
clinical signs of hypoxaemia.

22. Specific poisonings
Caustics(Acids and Alkalis)
A 2 year- old boy present to the emergency centre with his parent who
say that they found the patient drinking some Caustic Soda Beads. The
patient was crying profusely, and has blisters and burns in his mouth.
The patient is drooling.
Defn:
Caustics include both acids and alkali(base)

23. Specific poisonings
Acids cause tissue necrosis, and the alkali produce liqufaction necrosis
with the risk of perforation if the burn is located in the intestinal tract.
Serious injuries tend to occur with a pH <2 or >2
Presentation:
Burns mucous membranes may be visualized.
The patient may drool and refuse to swallow secondary to pain.
Esophageal stricture may be found.
Acids may be responsible for delayed gastric emptying from pylorus
scarring.
Diagnostic Test: CBC, Abdominal radiograph

24. Specific poisonings
Treatment:
• Do not induce vomiting or use activated charcoal when corrosives
have been ingested as this may cause further damage to the
mouth, throat, airway, oesophagus and stomach.
• Give milk or water as soon as possible to dilute the corrosive agent.
• Then give the child nothing by mouth and arrange for surgical
review to check for oesophageal damage/rupture, if severe.

25. Specific poisonings
• Petroleum compounds e.g. kerosene, turpentine substitutes,
petrol
➤Do not induce vomiting or give activated charcoal as inhalation can
cause respiratory distress with hypoxaemia due to pulmonary oedema
and lipoid pneumonia. Ingestion can cause encephalopathy.