ACCIDENTAL POISONING IN CHILDREN

I often wonder if it was the same God that watched over adults that watched over kids and to my surprise it’s the same big God. Children seem to get away with a lot of accidents especially when they put all sorts of things in their mouth.

In primary school, kids would put lead (from pencils) on biscuit and eat it and nothing would happen, some kids would play with sand and even eat some sand and nothing would happen. Have you ever tried to do same as an adult? Yea, I thought so.....

Most cases of poisoning exposures occur in children  less than the age of 5 yrs. Almost all are accidental, reflecting the propensity for children in this age group to put virtually everything in their mouths. Majority occur in the home, & most involve only a single substance.

Ingestion is the most common route. Others are the dermal (skin), ophthalmic (the eyes), & inhalational routes (the nose). Poisoning in older children are much less common and are primarily intentional (suicide or abuse) or occupational in adolescents.

Most cases involve non-drug products e.g. household cosmetics, hydrocarbons (kerosene) & caustic soda. The remainder are pharmaceutical preparations e.g. analgesics (Paraceutamol, Aspirin), Iron tablets, cold & cough mixtures. Few children have ingested their parents’ oral hypoglycaemic agents and organophate-based pesticides (e.g. Gamalin-20^®).

More than 75% of poisoning exposures can be managed at home without direct medical intervention, because either the product involved is not inherently very toxic or the quantity of the material involved is not sufficient to produce toxic effects.

1.      History: Name/ type of toxin, Amounts taken/ duration of exposure, Determine the age, Progression of Symptoms & Pre-hospital/ Home treatment protocol.

2.      Examination: Weight of the victim, Vital signs, State of hydration, Urine output & Features of cardio-respiratory disturbances, shock, dysrhythmias, altered sensorium & seizures.

3.      Management:

a.       Stop further contact: Dermal (skin), ocular & oral decontamination by flushing the affected area with tepid (room temperature) water over a minimum of 10 minutes. For dermal exposures, mild soap & water can be used.

b.      Prevent further Absorption:

                    i.      Emesis (vomit) induction: with syrup of ipecac or concentrated salt solution (e.g. 3%). The onset of emesis is usually 20–30 min. For infants (6-12 months); 10 mL, children 1-12 yrs (15 mL) & 30 mL for older children & adults. Avoid if < 6 months.

                  ii.      Gastric lavage.

                iii.      Activated charcoal.

                iv.      Cathartics: are commonly used in conjunction with activated charcoal to hasten the clearance of the charcoal-toxin complex e.g. sorbitol (max: 1g/ kg), magnesium sulphate (max dose: 250 mg/ kg), & magnesium citrate (max: 250 mL/ kg).

                  v.      Whole Bowel Irrigation: involves instilling large volumes of a colonic lavage solution (e.g. Colyte) into the stomach to cleanse the entire GI tract.

c.       Enhance elimination.

                    i.      Diuresis.

                  ii.      Ion trapping: alkalinisation (hpH) of the urine with IV bicarbonate increases the elimination of weak acids, such as salicylates & phenobarbital (phenobab). Alternately, acidifying the urine to increase the elimination of weak bases such as amphetamine.

                iii.      Dialysis. (Haemodialysis, peritoneal dialysis & haemoperfusion).

                iv.      Exchange blood transfusion.

4.      Laboratory Evaluation.

For specific instances (e.g. salicylates, PCM, iron & alcohols) laboratory/ toxicological measurement is integral to the treatment plan. RBS, PCV (pack cell volume), E/ U + Cr (electrolyte/Urea/Creatinine), LFTs (liver function tests), clotting profiles & CXR (chest X-ray) are often helpful.

Hydrocarbon Poisoning (e.g. Kerosene)

This occurs at some homes because of the storage of kerosene (which looks like water) in bottles.

Aspiration usually occurs at the time of ingestion or following coughing, gagging or induction of vomiting. Little quantities aspirated (<1 mL) may produce significant injury. Pneumonitis does not follow dermal absorption or from ingestion without aspiration.

Aspiration Pneumonitis is characterised by coughing, which usually is the first clinical finding. Transient, mild CNS depression is common. CCF, headache, vertigo, ataxia, euphoria, & renal & hepatic damage may also be seen acutely.

CXR (chest X-ray); an initial film is usually normal but subsequent films may show features of Pneumonitis & much later, pneumatocoeles.

Emesis (vomit) or instillations of vegetable oils or mineral oil into the stomach in an attempt to prevent absorption are contraindicated. In hydrocarbon-induced (lipoid) Pneumonitis, corticosteroids may be harmful & should be avoided. Likewise, antibiotics should not be given prophylactically.

However, for superimposed bacterial pneumonia which occurs in only a small percentage of cases, antibiotics (penicillin) are helpful. Respiratory failure has been successfully treated with both standard ventilation & with ECMO.

Acetaminophen (Paraceutamol, PCM, Acetaminophen sodium)

PCM is the most widely used analgesic & antipyretic. Consequently, it is commonly available in the home, where it can be accidentally ingested by young children or taken in an intentional overdose by adolescents (in suicide attempts).

The acute toxic dose of PCM is > 150 mg/kg in children younger than 12 yr or > 7.5 g in adolescents & adults. In adults, renal damage & failure are also associated with long-term ingestion. Repeated doses of PCM at doses exceeding those recommended may lead to hepatic injury or failure in some children.

If untreated, patients who have acutely overdosed pass through four stages of toxicity. Early symptoms are non-specific.

Stages in the Clinical Course of PCM Toxicity

Stage	Time Following Ingestion	Characteristics
I	½ – 24 hrs	Anorexia, nausea, vomiting, malaise, pallor, diaphoresis.
II	24 – 48 hrs	Resolution of above; right upper quadrant abdominal pain & tenderness; ↑bilirubin, ↑Prothrombin time, ↑hepatic enzymes; oliguria.
III	72 – 96 hrs	Peak liver function abnormalities; anorexia, nausea, vomiting, malaise.
IV	4 days –2 wks	Resolution of hepatic dysfunction or complete liver failure.

Children younger than 6 yr fair better than adolescents. The mortality rate is < 0.5%. Most children survive without sequelae but severely affected patients may require liver transplantation. Prognosis worsens with concomitant alcohol use.

Please contact the nearest Hospital or clinic as soon as possible if your child or sibling has an accidental poisoning.