Young children are frequently poisoned by agents that are attractive and readily available to them. The combination of curiosity, desire to mimic parental behavior (such as drinking from a bottle or can), newly acquired developmental milestones, and access to household products, makes children younger than 6 years particularly vulnerable to hazardous household chemicals. Thus, these substances represent the third most common poisoning exposure in young children.¹

Most concerning household chemicals fall into three main categories: hydrocarbons, alcohols, and caustics. Table 167-1 lists some common products and their potentially toxic components. Among children for whom medical attention is sought for poisoning from such agents, ingestion is by far the most common route of exposure.

Hydrocarbon compounds include petroleum distillates (lighter fluid, kerosene, mineral oil, naphtha, gasoline, butane); plant extract oils, also referred to as terpenes (turpentine, lamp oil, menthol, eucalyptus oil); camphor; inhalants (toluene, chlorofluorocarbons); and organic solvents (toluene, xylene, benzene).

PATHOPHYSIOLOGY

After ingestion, hydrocarbon compounds enter the esophagus but also spread into the tracheobronchial tree, and the lungs are the primary target of injury. The potential for a given substance to cause direct lung injury is influenced by its (1) viscosity, (2) surface tension, and (3) volatility. Low-viscosity liquids with high volatility and low surface tension have the highest potential for pulmonary injury. Highly viscous hydrocarbons (motor oil, paraffin) very seldom cause lung injury, whereas low-viscosity substances (gasoline, kerosene) easily enter the lungs. The chemical can cause alveolar collapse and damage surfactant, which can lead to pneumonitis and in some cases can progress to respiratory failure.

In addition, lipid-soluble hydrocarbons, such as terpenes and aromatics can easily cross the blood-brain barrier and cause central nervous system (CNS) depression. Other organ damage may result from a particular compound’s inherent toxicity. Table 167-2 offers a mnemonic, which lists the hydrocarbons and their specific systemic toxicity. Inhalant abuse of organic solvents is associated with a sudden death syndrome via sensitization of the myocardium to catecholamines and can also cause a chronic encephalopathy. Because petroleum distillates and terpenes account for the majority of pediatric hydrocarbon exposures, the remainder of this discussion will focus on pulmonary toxicity.

CLINICAL PRESENTATION

Children may be brought to medical attention for a witnessed or suspected ingestion, even if asymptomatic. Patients with severe ingestion may have signs of lung injury promptly after ingestion, including tachypnea, hypoxia, cough, wheezing, or evidence of increased work of breathing. A child who develops respiratory distress within the first hours is very concerning and may progress quickly to respiratory failure. Fever develops in about 50% of patients with chemical pneumonitis and reflects the inflammatory response to the noninfectious lung injury. An aroma of the hydrocarbon may remain on the skin, clothing, or breath and suggests ingestion or exposure. Some hydrocarbon compounds may produce mild mucosal irritation as well.

DIAGNOSTIC EVALUATION

Evaluation of a child after hydrocarbon ingestion or exposure should focus on the patient’s respiratory status. Careful physical examination with measurement of the respiratory rate and work of breathing as well as pulse oximetry should be performed immediately and repeated frequently. A chest radiograph should be performed on initial assessment and repeated with clinical deterioration or as part of clinical reassessment (e.g. consideration for admission or discharge). One large review of 950 children found that all patients who were both asymptomatic and had normal chest radiographs at 6 hours after exposure were suitable for discharge and did not deteriorate. In contrast, patients who have initial symptoms and infiltrates on chest radiographs usually worsen and require hospitalization.²

An elevation of the white blood count (WBC) and neutrophil count may be seen in patients with significant chemical pneumonitis. Such leukocytosis early after ingestion reflects the noninfectious inflammation associated with the lung injury.

Further evaluation may be indicated, depending on the toxicities of the particular substance involved (see Table 167-2). For example, serum transaminase studies should be considered for patients exposed to halogenated compounds.

MANAGEMENT

The mainstay of treatment for these patients involves supportive care with careful monitoring of respiratory status as well as respiratory support and treatment of other concomitant organ dysfunction as necessary. Endotracheal intubation and ventilation or extracorporeal support may be needed with profound lung injury.

Corticosteroids do not improve the course of hydrocarbon pneumonitis and have been associated with increased bacterial superinfection in animal studies.³ Antibiotics have also failed to show any benefits, may increase infection with resistant organisms, and are indicated only for patients in whom fever and leukocytosis persist and bacterial infection seems likely. Of note, several animal studies and a recent case report in humans suggest that the use of exogenous surfactant therapy early in the course of acute respiratory failure secondary to hydrocarbon ingestion may dramatically improve the patient’s course and should be considered as a reasonable therapeutic intervention based on pathophysiologic rationale.⁴

CONSULTATION

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  Involvement of critical care specialists may be warranted in patients whose clinical condition is deteriorating and when there is an anticipated need for increasing respiratory support or level of monitoring.

  
  
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  Social work or social services consultation may be indicated if the circumstances surrounding the ingestion raise suspicion of abuse or neglect.

  
  
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  Consultation with a regional poison control center is appropriate, especially for children with severe or atypical symptoms or when the compound involved is highly toxic.

ADMISSION CRITERIA

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  Any patient with respiratory symptoms should be admitted for monitoring and support. Patients who remain asymptomatic for 6 hours after exposure may be candidates for outpatient follow-up with parental supervision.

DISCHARGE CRITERIA

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  Patients whose respiratory symptoms have resolved sufficiently to be discharged have no further risk from hydrocarbon pneumonitis and can be sent home.

The major compounds involved in pediatric alcohol exposure include ethylene glycol, methanol, isopropanol, and most commonly, ethanol. Ethanol is readily available for adult consumption in most households and may also be found in toiletries such as mouthwash and antibacterial soap. Isopropanol is the active ingredient in rubbing alcohol. Ethylene glycol has a sweet taste and is found in antifreeze, while methanol can be found in windshield washer fluid and Sterno fuel.

PATHOPHYSIOLOGY

All mentioned alcohols act to some degree on the CNS to cause intoxication, CNS depression, and hypothermia, and all are metabolized by the enzyme alcohol dehydrogenase (Figure 167-1). The mechanism of hypothermia is complex and not entirely elucidated; however, it stems from the depth of CNS depression and resultant loss of behavioral responses to cold. In young children, ethanol metabolism suppresses gluconeogenesis and ingestion may cause hypoglycemia hours after exposure. Isopropanol is metabolized to acetone, which causes ketonemia and ketonuria without acidosis; in addition, isopropanol is a gastrointestinal irritant that often causes bleeding, although it is not usually life threatening.

Ethylene glycol and methanol are referred to as “toxic alcohols” because of their conversion through alcohol dehydrogenase to highly toxic metabolites (see Figure 167-1). Ethylene glycol is metabolized to glycolic and oxalic acid, which cause profound acidosis and renal failure, partially as a result of oxalate crystalluria. In addition, oxalate forms complexes with calcium, which can lead to systemic hypocalcemia and its attendant complications (e.g. seizures, tetany, dysrhythmia). Methanol is metabolized to formic acid, which also causes severe metabolic acidosis as well as unique retinal toxicity.