Poisoning in children

Epidemiology and routes of entry

In pediatric practice, there are two fundamentally different age peaks of exogenous intoxications. In early and preschool children (1–5 years old), poisonings are accidental, which is associated with their high exploratory activity or iatrogenic errors by parents in dosing medications. In adolescence (11–17 years old), intentional poisonings predominate — conscious ingestion of toxicants with suicidal intent or to achieve a state of intoxication (alcohol, drugs).

In the International Classification of Diseases, this pathology belongs to the class of injuries and consequences of external causes. The primary and dominant route of poison entry into the body is oral (via the gastrointestinal tract). Inhalation, percutaneous (through intact skin), transmucosal, and parenteral routes are also encountered.

Pathogenesis and age-related features

The basic mechanism of action of most toxins lies in damaging cellular enzyme systems. This triggers a cascade of metabolic disorders that lead to severe multiple organ failure. In children, poisonings proceed significantly more severely than in adult patients.

This is explained by a number of anatomical and physiological features:

• High lability and instability of metabolic processes.
• Increased permeability of blood-tissue barriers, due to which toxins penetrate tissues more easily, including the central nervous system.
• Initially reduced tolerance of the child's body to the effects of chemical xenobiotics.

Stages of the clinical course

The pathological process in acute intoxications develops sequentially, passing through four mandatory stages:

1. Preliminary (latent) period. The time from contact with the xenobiotic to the appearance of the first symptoms. Duration varies from a few seconds to several days.
2. Toxic period. The phase of full-blown clinical manifestations of the specific action of the poison, lasting about 2–5 days.
3. Post-toxic period. The stage of secondary somatogenic disorders and target organ damage (from 2 to 5 weeks).
4. Recovery period. The stage of long-term consequences with persistent changes (lasting from 6 months to several years).

Specific toxicromes and markers

For rapid diagnosis, the assessment of unique clinical markers characteristic of specific poisons is extremely important. First of all, pupillary reactions, skin condition, and mucous membranes are evaluated.

Ophthalmological markers:

• Miosis (pupillary constriction): typical for poisoning with organophosphates, toadstools, opiates, and barbiturates.
• Mydriasis (pupillary dilation): indicates poisoning with methanol or anticholinergics.

Skin and respiratory changes:

• Pronounced cyanosis occurs due to methemoglobinemia (nitrates, aniline).
• Hyperemia is characteristic of the effects of atropine and pilocarpine.
• Specific breath odor (acetone, gasoline, alcohol) allows for the rapid detection of volatile toxins.
• Hemolysis and erythrocyte destruction occur in poisoning with acetic acid, arsenic, snake venom, and mushroom toxins.

Diagnostic algorithm

Diagnosis is based on five complementary stages:

1. Clinical and anamestic: inspection of the accident scene and collection of toxicological history.
2. Clinical and instrumental: assessment of the severity of the condition and identification of organ dysfunctions in the toxic period.
3. Chemical and toxicological: laboratory identification of the substance and determination of its concentration in biological fluids.
4. Biological: testing the degree of toxicity on laboratory animals (in vivo).
5. Forensic: conducting specialized expertise.

Class and exam questions

What else to study on this topic

• Mechanisms of hepatotoxic action (paracetamol, alcohol)
• Clinical presentation of hallucinatory syndrome
• Hematological complications: hemolysis and coagulopathies
• Symptoms of poisoning complications (shock, acute kidney injury, cerebral edema)
• Differential diagnosis of poisoning and neuroinfections

Other topics in "Chapter 13. Main syndromes requiring emergency care"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.