POISONING IN CHILDHOOD Flashcards
What is poisoning?
Poisoning is exposure to a substance that is toxic to a human being.
Risk factors for poisoning (5)
1)Age:Most cases occur below 5 years of age. Poisoning in older children are often: Less common, Intentional (suicide,drug abuse)
2)Sex:Accidental poisoning is more common in males due to their more adventurous and inquisitive nature.
3)Poor parental supervision
4)Learning disability
5)Parents who abuse substances
Routes of poisoning (4)
1)Most poisoning occur through ingestion (77%)
Other routes of poisoning:
2)Dermal (8%)
3)Inhalation (6%)
4)Ophthalmic (5%)
Common poisons;
Approximately 50% of cases of poisoning involve non-drug substances like??? 50% are Pharmaceutical products like??
Approximately 50% of cases of poisoning involve non-drug substances like:
Hydrocarbons (kerosene),
cosmetics,
Caustic soda
personal care items,
cleaning solutions,
plants and foreign bodies.
50% are Pharmaceutical products like:
Analgesics (PCM, aspirin)
Haematinics (Iron tablets)
Cough & cold relievers,
Oral hypoglycaemic agents
Antimicrobials and
Vitamins supplements
ALCOHOL exists in form of?? (3)
The most frequently abused is?? And it’s sources??
Alcohol exists in form of:
ethanol
methanol and
isopropanol.
The most frequently abused is ethanol.
Sources of ethanol include locally brewed gin, refined alcohol e.g. brandy, whisky and wine.
Other alcohol containing items include ??
The most common mode of alcohol poisoning is??
Other alcohol containing items include perfumes, aftershave, mouth wash and paint removers.
The most common mode of alcohol poisoning is when children drink (usually out of the bottle) in the absence of their parents.
Pathophysiology of alcohol poisoning
Ethanol is rapidly absorbed from the stomach and small intestine reaching peak plasma levels within 30-60 minutes after ingestion.
Ethanol is metabolized predominantly by the liver.
Alcohol dehydrogenase converts ethanol to acetaldehyde which is further metabolized into acetic acid and then to carbondioxide and water.
Only 2-10% of ingested ethanol is excreted through the kidneys.
The lethal dose of ethanol in children is 3mg/kg compared to 5-8mg/kg in adults.
Signs of alcohol intoxication appear in children at blood alcohol levels of 50mg/dl.
Clinical features;
In severe alcohol poisoning, there is usually hypoglycaemia.
Other features include muscle incoordination, drowsiness, slurred speech, blurred vision and hypothermia.
In severe toxicity, there can be apnoeic attacks and coma.
There may be convulsions, resulting from hypoglycaemia.
Treatment
Since alcohol is rapidly absorbed, gastric aspiration is usually not useful.
Treatment of proven or suspected hypoglycaemia, is with IV 10% dextrose infusion.
Metabolic acidosis is treated with IV sodium bicarbonate
In patients with apnoeic attacks, ventilator support is useful.
Haemodialysis is indicated if there is severe metabolic acidosis or ethanol blood levels >50mg/dl
Hydrocarbon poisoning;
Hydrocarbons include:
most frequently available to children
Hydrocarbons include:
kerosene,
petrol,
lighter fluid,
paint thinner e.g. Turpentine
cleaning agents and
furniture polishes.
Of all these, the most frequently available to children is kerosene:
Pathophysiology of hydrocarbon poisoning
The most important toxic effect of hydrocarbons is aspiration pneumonitis.
•Aspiration usually occurs at the time of ingestion when coughing or gagging but can also result from induced vomiting after ingestion.
•Because of the low viscosity and high volatility of hydrocarbons, only a small quantity (<1ml) needs to be aspirated to cause significant lung injury.
•Most hydrocarbons have anesthetic property and can cause transient CNS depression.
•Pathologic changes in the lungs in kerosene inhalation include:
–bronchospasm,
–atelectasis,
–emphysema,
–bronchiolar oedema and
–necrosis.
•Secondary bacterial infection may be a complication.
Clinical/laboratory manifestations of hydrocarbon poisoning
Mild CNS depression.
•Aspiration pneumonitis manifests as cough, dyspnoea, wheezing, choking and chest retractions.
•GIT symptoms include nausea, vomiting, diarrhoea.
•Pneumatoceles may appear on the chest x-ray 2-3 weeks after exposure.
•CCF, headache, vertigo, ataxia, euphoria, and renal & hepatic damage may also be seen acutely
Treatment of hydrocarbon poisoning
All children who ingest kerosene must be observed for at least 6hrs in the hospital after which they can be let home if there are no symptoms.
•If there are signs of chemical pneumonitis, the child should be treated with antibiotics as the lungs can become secondarily infected. (Penicillins are helpful)
Oxygen and ventilation may be required for respiratory failure.
•Avoid corticosteroid
•Contraindicated:
–Gastric lavage
–forced emesis
–Mineral oil
these can lead to more aspiration of the hydrocarbon.
What is considered the toxic dose of IRON POISONING?
•The severity of toxicity is based on the amount of elemental iron ingested:
–Greater than 60mg/kg of elemental iron is considered the toxic dose.
Pathophysiology of iron poisoning
Iron is corrosive to the gastrointestinal mucosa and may lead to:
•intestinal ulceration, oedema and occasionally melena,
•haematemesis and
•possible perforation.
•Iron also accumulates in mitochondria thus it can produce systemic effects
Iron causes:
•venodilation and
•increased capillary permeability leading to
•Hypotension
•Metabolic acidosis.
•Hepatic necrosis develops after serious poisoning resulting in:
•abnormal liver function tests
•Coagulopathies
•Altered sensorium.
Clinical & laboratory manifestations of iron poisoning
Nausea, vomiting, diarrhoea and abdominal pain usually develop within 30 minutes to 6 hour after ingestion.
•In severe toxicity, there may be drowsiness and hypotension.
•Since iron is radiopaque, an abdominal radiograph may confirm ingestion.
–A negative result however, does not rule out ingestion as only undissolved tablets can be seen.
Gastric scarring, pyloric stenosis and intestinal strictures can develop 2-4 weeks after ingestion of large doses.
•Serum iron concentration >500mg/dl 4hrs after ingestion indicates significant toxicity.
Treatment of iron poisoning
•Ipecac-induced emesis & whole bowel irrigation may be used to remove iron tablets from the stomach
•Oral bicarbonate (2%), dilute phosphosoda (1: 4) & magnesium hydroxide (milk of magnesia) may also be beneficial
•Endoscopic removal of tablets adherent to the gastric mucosa is beneficial
Intravenous Desferoxamine infusion:
–This Iron chelator is the “antidote” for moderate-severe poisoning.
–Desferoxamine-iron complex colours the urine red.
•In markedly elevated blood levels of iron, exchange blood transfusion or haemodialysis can be done.
•Gastric lavage and activated charcoal are ineffective in children
Pathophysiology of acetaminophen poisoning?
The toxic dose of acetaminophen:?
Toxicity results from the formation of a highly reactive intermediate metabolite; N-acetyl-p-benzoquinoneimine (NAPQI) which combines with hepatic macromolecules to produce hepatocellular damage.
•Renal damage & failure may follow long term use
•The toxic dose of acetaminophen:
–≥ 200mg/kg in children younger than 12 years
–≥ 7.5g in adolescent and adults
Repeated administration of acetaminophen at doses exceeding 60mg/kg/day for consecutive days may lead to hepatic injury or failure.
•In infants who are not eating well as a result of illness, hepatic glutathione stores are low leading to a higher risk of acetaminophen hepatotoxicity.
Clinical & laboratory Features;
the 4 stages of acetaminophen toxicity?
Stages-Time after ingestion-characteristics
I). 0.5-24hrs; Anorexia, nausea, vomiting, malaise, pallor, diaphoresis
II). 24-48hrs; Resolution of earlier symptoms, right upper quadrant abdominal pain and tenderness, elevated bilirubin, Prothrombin Time, hepatic enzymes, oliguria
III). 72-96hrs; Peak liver function abnormalities, anorexia, vomiting and malaise may reappear
IV). 4days -2wks; Resolution of hepatic dysfunction or complete liver failure
Treatment of acetaminophen poisoning
Treatment is better started within 1-2hrs after ingestion of a large overdose.
•The antidote for acetaminophen poisoning is N-acetylcysteine (NAC).
•A precursor for glutathione synthesis.
•Replenishes glutathione stores &
•Prevents reaction of NAPQI with hepatocytes
•NAC therapy (P.O. or I.V.) should begin very early post-intoxication
•Oral administration of activated charcoal can be given to reduce absorption.
Prognosis of Acetaminophen poisoning
Children younger than 6 yr fair better than adolescents.
•The mortality rate is < 0.5%.
•Most children survive without sequelae.
•Severe cases may need liver transplantation.
•Prognosis worsens with concomitant alcohol use
SALICYLATE POISONING
Toxic dose?
Salicylates (e.g Aspirin) are gastric irritants:
–nausea and vomiting usually occur early after overdose
•Salicylates also decreases platelet adhesiveness
•Toxic dose: >150 mg/kg
•Salicylates affects most organ system by:
•Uncoupling oxidative phosphorylation
•Inhibiting Kreb’s cycle enzyme
•Inhibiting amino acid synthesis
Clinical features of Aspirin poisoning?
