This document summarizes information on several types of pediatric poisonings including paracetamol, iron, ethanol, methanol, and ethylene glycol. It describes the pathophysiology, signs and symptoms, toxicity levels, and treatment approaches for each type of poisoning. The key points are that paracetamol is metabolized by the liver and can cause liver damage/failure in overdose. Iron toxicity causes gastrointestinal and liver damage. Ethanol intoxication affects the central nervous system, liver, and metabolism. Methanol and ethylene glycol are metabolized to toxic compounds that can cause blindness, acidosis, and kidney damage. Activated charcoal and decontamination are not effective for methanol, while hemodial

1. Poisoning in Pediatrics
Supervised by Dr . Haytham dhomour
Done by : Ahmad AL-shurbaji

2. Paracetamol Poisoning

3. • Is also known by its chemical name, N -acetyl-p -aminophenol
• Acetaminophen toxicity is a common occurrence, particularly in
children .
• This drug is the most widely used analgesic-antipyretic
medication
• It is cited as a drug in over 50 brand-name products
(eg, Panadol , panda , Tempra, Feverall) .Numerous oral
preparations and include : liquids, tablets , capsules, and
suppositories .
INTRODUCTION

4. • acetaminophen poisoning is the most common cause of
nonfatal hepatic necrosis, acute liver failure and
overdose deaths.
• Overdose with acetaminophen can occur at any age.
Typically occurs in patients younger than 1 year when
caregivers give incorrect doses of a medication
containing acetaminophen to a child.
• An accidental poisoning can occur in toddlers and young
children with unsupervised access to medications. Older
patients (eg, teenagers and adults) may overdose with
intent to do self-harm

5. Pathophysiology
• Therapeutic oral doses of acetaminophen are rapidly absorbed by
the GI tract, with body serum level concentration peaking 1-2
hours postingestion
• The average elimination half-life of acetaminophen is 2 hours
(range, 0.9-3.25 h). In patients with hepatic dysfunction, the half-
life can be as long as 17 hours postingestion
• The liver metabolizes more than 90% of an acetaminophen dosage
to sulfate and glucuronide conjugates, which are both water-
soluble and are then eliminated in the urine

6. -When taken in overdose the liver conjugation becomes blocked,
causing paracetamol to be metabolized by an alternative pathway .
- This results in a toxic metabolite, N-acetyl-p-benzoquinone imine
(NAPQI), which is itself inactivated by glutathione.
- When glutathione stores are depleted, NAPQI reacts with
nucleophilic aspects of the cell, leading to necrosis

7. Toxicity
• The maximum daily dose of acetaminophen for children younger
than 12 years 80 mg/kg (10-15 mg/kg every 4-6 hours with a
maximum of 5 doses per 24-hour period)
• In children, the minimum toxic dose of acetaminophen for a single
acute ingestion is 150 mg/kg
• In adolescent and adult , the minimum toxic dose 7.5 – 10 g .
• Children who have acutely ingested 250 mg/kg or more significant
concern for acetaminophen-induced hepatotoxicity

8. History and physical examination
- Stage 1 (0 - 24) : These clinical signs are nonspecific (nausea,
vomiting) and usually asymptomatic , normal “LFT”
- Stage 2 (24-72 h ) : Patients present with pain and tenderness
in the right upper quadrant , decreased urinary output , tachycardia
and hypotension
“LFT” begin to increase ( INR, pt) .
-Stage 3 : (72 – 96 h : signs of hepatic failure with jaundice,
hypoglycemia, bleeding (coagulopathies) , Renal failure, multiorgan
failure are present.
- Stage 4 (4-14 d ) : Patients either have a complete recovery of
liver function and resolution of physical findings or they die

9. Treatment
• When a child with over dose give activated
charcoal(1g/kg)
• after 4 hours check level and use “Rumack- Matthew
nomogram” to determin toxicity .
• If toxicity is probable or possible start oral or IV
N-acetylcysteine
- Most effective within 8 h of ingestion
- 140 mg/kg PO initial dose, then 70 mg/kg PO q4 hr × 17 doses .
- 150 mg/kg IV over 1 hr, followed by 50 mg/ kg IV over 4 hr,
followed by 100 mg/kg IV over 16 hr

11. IRON Poisoning

12. INTRODUCTION
• Iron poisoning is a common toxicologic emergency in young
children. Contributing factors include the availability of iron
tablets and their candylike appearance
- Iron is used in pediatric for treatment of anemia
- Iron overload may develop chronically as well, especially in
patients requiring multiple transfusions of red blood cells (sickle
cell disease, thalassemia).
- Most exposures involve children younger than 6 years who have
ingested pediatric multivitamin preparations.

13. Pathophysiology
- Iron toxicity can be classified as corrosive or cellular.
- Ingested iron can have an extremely corrosive effect on the GI mucosa,
which can manifest as nausea, vomiting, abdominal pain, hematemesis, and
diarrhea; patients may become hypovolemic because of significant fluid and
blood loss.
- Cellular toxicity occurs with the absorption of excessive quantities of
ingested iron. overdose causes impaired oxidative phosphorylation and
mitochondrial dysfunction, which can result in cellular death.
- The liver is one of the organs most affected by cellular iron toxicity, but
other organs such as the heart, kidneys, lungs, and the hematologic
systems also may be impaired.
- With chronic iron overload, may cause death due to myocardial siderosis

14. Toxicity
• Different formulations of iron contain varying amounts of
elemental iron, as follows:
• Ferrous sulfate - 20% elemental iron
• Ferrous gluconate- 12% elemental iron
• Ferrous fumarate - 33% elemental iron
• Ferrous lactate - 19% elemental iron
• Ferrous chloride - 28% elemental iron
• (ingested iron for a 10-kg child who consumed ten 320-mg
tablets of ferrous gluconate (12% elemental iron per tablet):
• 10 tablets X 38.4 mg elemental iron per tablet = 384 mg/10 kg
38.4 mg/kg

15. • Children may show signs of toxicity with ingestions
of <20 mg/kg
• 20- 40mg/kg moderate toxicity
• >60mg/kg sever toxicity

16. Clinical features
- stage 1 (within 6 hours after the overdose), symptoms include vomiting,
hematemesis, diarrhea, abdominal pain, irritability, and drowsiness .
- stage 2 (6 to 12 hours after the overdose), the patient condition can
appear to recovery However, in serious ingestions, it may represent only a
temporary respite or may not occur at all; the patient may progress directly to phase
3.
- stage 3 (12 to 24 hours after the overdose), shock, jaundice, liver
failure , fever, bleeding,sever metabolic acidosis, and seizures , due to
mitochondrial damage and hepatocellular injury.
- stage 4 (2 to 6 weeks after the overdose), the stomach or intestine can
become blocked by scars. liver Cirrhosis can develop later
* X-rays: abdomen to detect radio-opaque tablets

17. Treatment
• Treatment including supportive care such as IV fluid , chelating
with IV deferoxamine(Infusion of 5–15 mg/kg/hr IV (max 6 g/24
hr) is recommended in the presence of moderate to sever
symptoms OR if serum iron >500mcg/dl .
• Some clinicians will consider whole bowel irrigation if large number
of pills remain in GI .
“Nasogastric polyethylene glycol 25–40 mL/kg/h for 4–6hr”
• Don’t use : gastric lavage or activated charcoal

18. ethanol Poisoning

19. • Ethanol is the most common psychoactive drug used by children and
adolescents in the United States and is one of the most commonly
abused drugs in the world.
• Is found in many household substances : liqour , perfume , Spirito
• Ehanol is primarily metabolized in the liver. Approximately 90% of
an ethanol load is broken down in the liver; the remainder is
eliminated by the kidneys and lungs. In children, ethanol is cleared
by the liver at the rate of approximately 30 mg/dL/h, which is more
rapid than the clearance rate in adults.
• Ethanol is rapidly absorbed, and peak serum concentrations typically
occur 30-60 minutes after ingestion. Its absorption into the body
starts in the oral mucosa and continues in the stomach and
intestine.

20. Krebs cycle
CO2 water
alcohol
dehydrogenase
acetaldehyde
dehydrogenase

21. • Ethanol ingestion and intoxication can lead to a marked hypoglycemic
state in infants and young children
• CNS depressant : respiratory depression and hypoxia
• The classic triad of signs of ethanol intoxication includes coma,
hypoglycemia, and hypothermia. These signs usually occur when the
Ethanol level in the blood exceeds 100 mg/dL
• Flushed skin
• Diuresis .
• Acute pancreatitis
• Loss of gross muscle control (ataxia, slurred speech)
• Sudden death
Acute ethanol intoxication

22. Chronic ethanol use can lead to the following:
• Chronic pancreatitis
• Hepatic dysfunction
• Hematologic disorders
• Numerous electrolyte abnormalities
• Hypertension
• Cardiomyopathy
• Malnutrition
• Obesity

23. Toxicity
• Ethanol level :
-Intoxication 100-150 mg/dL
- Loss of muscle coordination - 150-200 mg/dL
- Decreased level of consciousness - 200-300 mg/dL
- Death - 300-500 mg/dL

24. Tretment
• The main treatment of patients with ethanol toxicity is supportive care .
• Assess the airway
• Obtain intravenous (IV) access and replace any fluid deficit or use a
maintenance fluid infusion.
• Quickly correct hypoglycemia. In children, 2-4 mL/kg of 25% dextrose
solution
• Correct any electrolyte abnormalities
• If the ingestion occurred within 1 hour of presentation, placing a
nasogastric tube and evacuating the stomach contents can be helpful.

25. • In patients with chronic ethanol abuse, administer thiamine 100 mg IV
to prevent neurologic injury.
• Hemodialysis

26. Methanol

27. • Methanol is found in windshield fluid , deicer and as fuel additive.
• Can cause blindness and death .
• It is metabolize by alcohol dehydrogenase and ultimately to formic
acid this toxic metabolite , toxicity can be delayed if congestion
with ethanol due to competition of both on AD.

28. SYMPTOMS
• Malaise
• Headache
• Abdominal discomfort
• N/V
• Visual disturbance and blurred vision
• CNS depression
• Metabolic acidosis

29. • Because Rapid absorption gastric decontamination and activated
charcoal do not work
• Do methanol level and blood gasses and electrolytes
• Treat metabolic acidosis with sodium bicarbonate
• Antidote is IV 4-methylpyrazole (fomepizole)
• Folate to enhance the metabolism of formic acid to less toxic
• Hemodialysis should be considered is sever poising (visual
symptoms , significant acidosis )

30. Ethylene glycol

31. • ETHYLENE GLYCOL INGESTION Ethylene glycol is sweet-tasting
and found in antifreeze and other coolants.
• Once ingested, it is metabolized via alcohol dehydrogenase to
glycolate, glyoxylate, and oxalic acid.
• The kidney is most affected by ethylene glycol ingestion

32. • There are 3 stages of intoxication:
- Stage 1: CNS., vomiting, drowsiness, slurred speech, lethargy
- Stage 2 :renal damage, coma, and cardiorespiratory findings
including tachypnea from metabolic acidosis .
- Stage 3 (after 24-72 hours): renal failure.

33. • Because of rapid absorption, gastric decontamination and activated
charcoal are not effective.
• Treatment is similar to methanol poisoning, including sodium bicarbonate
for metabolic acidosis inhibition of alcohol dehydrogenase with IV
fomepizole
• Give thiamine and pyridoxine, which are cofactors in the metabolism of
ethylene glycol.
• Hypocalcemia is common and may also require therapy.
• Hemodialysis is done for significant ethylene glycol poisoning

34. References
• Medscape
• Medstudy 7th edition
• Nelson 7th edition