Hydrocarbon (HC) toxicity. Hydrocarbons are used as solvent bases for many toxic chemicals. In fact, 20% of pediatric aspiration accidents in children < 5 years of age are due to HCs.

Despite good intentions, by giving her daughter Ipecac (no longer recommended for ANY ingestion), the mother induced hydrocarbon aspiration – a much worse toxicity than simple ingestion. In fact, most of the toxicity from hydrocarbon ingestion is associated with aspiration. In general, absorption of and toxicity from hydrocarbons in the GI tract is typically low.

Three main properties are associated with toxicity in aspiration:

1) Viscosity: the capacity to resist flow. Low viscosity (<60 SSU) is associated with high toxicity (e.g. furniture polish, kerosene).

2) Volatility: the ease of a liquid to turn into a gas. High volatility associated with high toxicity (e.g. butane, gasoline).

3) Surface tension: the capacity to collect on a liquid surface. Low surface tension is associated with high toxicity (e.g. turpentine).

Moreover, HCs are lipophilic, allowing penetration into lower airways. This leads to bronchospasm and inflammation (pulmonary edema). Volatized HCs can displace oxygen in alveolar spaces, leading to hypoxia. HCs also directly injure alveoli and capillaries. Finally, HCs inhibit surfactant function, leading to alveolar collapse. These potential effects can lead to a chemical pneumonitis and potential respiratory failure.

1. Airway/Breathing: Oxygen, beta agonist trial (albuterol) (although no proven benefit), CPAP/BPAP if persistent hypoxemia. High-flow jet ventilation and ECMO have been anecdotally effective for refractory hypoxemia in children. Intubate if respiratory failure.

Note: Antibiotics, corticosteroids, and surfactant administration have NOT been proven to be of benefit for chemical aspiration. However, it can be difficult to differentiate pneumonia from chemical pneumonitis because both may present with fever, leukocytosis and infiltrates on CXR.

2. Circulation: Aggressive IVFs for hypotension. AVOID epinephrine and isoproterenol for treatment of hypotension. HCs can sensitize the heart to endogenous and exogenous catecholamines, leading to dysrhythmias and sudden death referred to as “sudden sniffing death”. Halogenated and aromatic HCs are more likely to lead to dysrhythmias, including V-Fib. For ventricular arrhythmias, AVOID type IA (procainamide) and type III (amiodarone) antiarrhythmics, as they may cause QT prolongation. Beta blockers and lidocaine are recommended in these instances.

3. Decontamination: GI decontamination is controversial. You can consider activated charcoal and stomach decompression with a small NG tube within 1 hour of ingestion although there is no proven benefit.

Only consider stomach decompression if the patient is alert and cooperative for the following cases:
C: Camphor (–>seizures)
H: Halogenated HCs (–>dysrhythmias, hepatotoxicity)
A: Aromatic HCs (–>bone marrow suppression, leukemia)
M: Metals (arsenic, mercury, lead)
P: Pesticides (–>cholinergic crisis, seizure, respiratory depression)

Check an ABG, CBC, BMP, LFTs, CXR, and abdominal x-ray (halogenated HCs are radiopaque).

Try to identify the causative hydrocarbon:
–Napthalene causes hemolytic anemia
–Amine-containing HCs can cause methemoglobinemia.
–Methylene chloride can cause a delayed carboxyhemoglobinemia.
–Benzene can cause aplastic anemia, AML and Multiple Myeloma.
–Halogenated HCs (i.e. carbon tetrachloride) can cause hepatic centrilobular necrosis
–Toluene can cause a renal tubular acidosis (hyperchloremic, hypokalemic NAGMA)

-Occupational: rarely life-threatening, non-specific symptoms
-Solvent-abusing adolescents/adults: “bagging” (inhaling from plastic bags), “huffing” (inhaling HC soaked cloth),“sniffing” (directly inhaled HC), “poppers” (vials of amyl nitrite crushed in tissue and inhaled)
-Most commonly abused HC is Toluene (gasoline, glue).
-Chronic use is associated with cognitive, behavioral and psychomotor deficits.
-MRI may show demyelination in periventricular and subcortical white matter.

-Anyone who remains symptomatic after 6 hours of exposure.
-Any child with wheezing, AMS or tachypnea within 2 hours of exposure.
-Any HC with delayed effects (e.g. halogenated HCs causing hepatotoxicity)
-Any exposure to HC with toxic additives (e.g. organophosphates, organic metal compounds)