Poisoning in Children

1. Poisoning in Children Presented by:Dr.Doaa Al-Masri. Moderated by:Dr J.Halazoun.

2. Introduction • Unintentional poisoning can occur following exposure to any of a large number of pharmaceutical or nonpharmaceutical products.

3. Acetaminophen • Definition: • It is the most common analgesic overdose in children younger than 6 years. • 99.8% of these exposures resulted in minor or no toxicity.

4. Acetaminophen • Clinical aspects: • The toxicity arises from the metabolism of the drug with the accumulation of a toxic metabolite in the hepatocyte and binds to intracellular molecules causing damage to the liver cells. • The minimum toxic dose is 140mg/kg. • A single ingestion of this quantity may cause transient reversible liver damage. • More severe toxicity results from ingestions in excess of 250mg/kg.

5. Acetaminophen • Clinical aspects • The initial symptoms and signs are nonspecific in the form of nausea and vomiting. • Within 18-24 hours after the dose , hepatic damage may become evident as transaminases begin to rise. • If not treated , hepatic damage may worsen over the next 2-3 days before gradually resolving. • Rarely fulminant hepatic failure can occur.

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7. Acetaminophen • The only accurate predictor is an acetaminophen serum level measured between 4 and 10 hours after the dose. • Hepatic toxicity has been defined by elevations in serum hepatic transaminases and prolongation of prothrombin time.

9. Acetaminophen • Diagnosis: history of an ingestion of at least 140mg/kg and serum level above the therapeutic range. • Toxicity is defined by serum level above the line in the nomogram or by positive history in association with increased liver enzymes. • If the patient is having the level in the toxic range ,treat by N-acetylcysteine.. • If the level cannot be determined,the therapy is based on the history . • The treatment should be initiated within 10 hours of the ingestion.

11. Acetaminophen • Prognosis: • In general it is good. • Few children develop hepatotoxicity and only occasional cases progress to serious liver damage and if the child recovers, the hepatic damage resolves completely. • Death is rare.

12. Ethanol • It is found in: • Beverages: wine,beer and liquor in different percentages. • Elixirs and cough preparations. • Personal care products:mouthwashes and aftershaves.

13. Ethanol • Clinical aspects:it is a dose related CNS depressant. • It also induces hypoglycemia by blockage of gluconeogenesis. • A single ingestion of 0.5mg/kg (1.5cc/kg) is sufficient to induce significant intoxication in a young child

14. Ethanol • Clinical aspects: • Dose related progressive CNS depression (inebiration,ataxia,vomiting and coma, respiratory depression, hypotension). • May mask toxicities from other coingested drugs. • May blunt the effect of CNS stimulants. • May potentiate the effects of other CNS depressants. • The clinical signs are nonspecific and can be masked by hypoglycemia and its severity is not related to ethanol level or the ingested dose.

15. Ethanol • Investigations: • serum electrolytes,glucose and ethanol. • Broad-spectrum drug screen if needed.

16. Ethanol • Diagnosis and management: • Any suspicion should be confirmed with measurement of the blood level. • Management is supportive and symptomatic. • Correction of electrolytes and hypoglycemia and administration of I.V. fluids. • No available antidote. • Extracorporeal removal techniques. • Good prognosis and recovery with supportive care.

17. Hydrocarbons: • Definition:they are substances comprised of hydrogen and carbon. • They are either aliphatic or aromatic or mixture of the two hydrocarbons.

19. Hydrocarbons • Gasoline was the most common, but Kerosene have the highest morbidity. • Lighter fluid was the only substance category that resulted in death.

20. Hydrocarbons • Clinical aspects:it irritates the gastrointestinal and respiratory tracts. • Chemical pneumonitis: spread over large areas of the lining of the lungs and destroying surfactant causing alveolar collapse, ventilation/perfusion mismatch and hypoxemia . • Direct capillary damage.

21. Hydrocarbons • Clinical aspects: • oropharyngeal and gastric irritation. • Vomiting,coughing and respiratory distress. • Petroleum smell , tachypnea, retractions, bronchospasm and wheezing and rales. • Fulminant chemical pneumonitis. • Fever within 6 hours. • The clinical peak of pulmonary damage is 3 days after aspiration.

22. Hydrocarbons • Management: • Asymptomatic patients should be observed. • Symptomatic patients should be investigated by ABG and CXR.

23. Hydrocarbons • Diagnosis by history, symptoms and signs of respiratory involvement and CXR . • Management: • Asymptomatic patients with normal CXR. • Asymptomatic patients with abnormal CXR. • Symptomatic patients. • Role of prophylactic antibiotics and corticosteroids.

24. Hydrocarbons • Prognosis: • Most ingestions will result in no or minor clinical effects. • Most patients with chemical pneumonitis will recover completely. • Rarely it is complicated by prolonged bronchospastic tendencies or pneumatoceles.

25. Theophylline • Definition: it is used as a bronchodilator and it is widely available in different clinical forms. • It is uncommon. • Children younger than 4 years appear to be at a higher risk of developing serious toxicity than are older children.

26. Theophylline • Clinical aspects: the acute ingestion of a dose exceeding 10mg/kg may result in some degree of clinical toxicity. • Nausea/vomiting/abdominal discomfort. • Restlesssness/agitation/tremors/peripheral vasodilation/sinus tachycardia. • Convulsions/hypotension/arrhythmia.

27. Theophylline • Investigations : • Serum levels correlate well with clinical toxicity and levels may not peak for many hours after ingestion of a sustained release product. • Minor toxicity:20-40 mcg/ml. • Moderate toxicity:40-60 mcg/ml. • Severe toxicity:70-80 mcg/ml. • Levels above 100 mcg/ml are associated with death. • Serum electrolytes and sugar, ABG, ECG.

28. Theophylline • Diagnosis/management • If the ingestion was within the previous 2 hours: give activated charcoal (1g/kg) • Monitor theophylline level. • If the patient is having more severe or worsening toxicity and serum levels more than 60mcg/ml,he must be admitted for careful monitoring, supportive care and multiple doses of activated charcoal. • If serum levels more than 80mcg/ml,the patient should be transferred to a facility where extracorporeal clearance can be performed.

29. Tricyclic Antidepressants • These drugs are used in children to treat enuresis. • They cause toxicity by blockage of the cholinergic neurotransmitter acetylcholine,preventing reuptake of the adrenergic neurotransmitter norepinephrine and by blocking sodium channels in the myocardium.

30. Tricyclic Antidepressants • Clinical toxicity begins within 6 to 8 hours after ingestion and peaks within 24 hours of presentation. • The potentially toxic dose is 5-20mg/kg. • Dry mouth,ileus, dilated pupils, urinary retention and mild sinus tachycardia. • CNS effects- which are more common than the cardiovascular system involvement- include delirium,agitation,restlessness, hallucinations and convulsions. • Cardiac arrhythmia and hypertension but hypotension is a poor prognostic sign.

31. Tricyclic Antidepressants • Serum levels do not contribute to treatment decisions. • ECG changes: • Conduction defects. • Ventricular arrhythmia. • The single most useful predictor of convulsions or cardiac arrhythmia is QRS duration on a limb-lead ECG.

33. Tricyclic Antidepressants • TCA overdose should be suspected in any child with acute onset of nonfocal neurologic abnormalities and lives in a house in which TCA are present. • Gastrointestinal decontamination with activated charcoal. • Convulsions are treated with benzodiazepines. • Cardiac arrhythmia: sodium bicarbonates. • Prognosis: generally it is good.

34. Methanol • It is present in automobile windshield washing fluid. • It has an unpleasant taste. • Potentially toxic amount of 0.15 cc/kg or 3 cc in 20 kg child.So a very small quantity is needed to result in serious toxicity.

35. Methanol • Clinical aspects • Inebiration • Metabolic acidosis( due to formation of formic acid) and compensatory respiratory alkalosis. • Ocular findings( blurred vision,snow field vision, hyperemia and edema of optic disks). • Nausea/vomiting/abdominal discomfort. • Investigate by measuring serum methanol level and ABG.

36. Methanol • Management: • Sodium bicarbonate. • Ethanol. • Leucovorin or folate. • Hemodialysis.

37. Methanol • Prognosis: • If treated early,recovery is expected. • Permanent ocular damage.