Case 21 – A Little Oil Goes a Long Way

Case #21 – A Little Oil Goes a Long Way
Author: Tara Kamath, MD
Peer Reviewer: Michael Christian, MD

A 3-year old girl, Lucy, is brought in by her mother for accidental ingestion. The mother states that she was folding laundry, while Lucy was playing in the other room. Lucy had opened up a box in the closet and found a tiki torch. The mother thought that she may have drunk some of the torch oil, so she decided to give Lucy Syrup of Ipecac to induce vomiting and then bring her to the ED. Lucy vomited what the mother thought was all of the torch oil prior to leaving the house. Shortly after, she had a coughing fit, followed by noisy breathing and grunting and the mother states that her mouth looked “blue”.

On exam, the patient is obtunded. She is tachypneic and using accessory muscles to breathe.

Vitals: Temp: 101.0, HR: 150, BP: 80/40, RR: 40, O2 Sat: 88% on RA

What toxicity is of main concern in the clinical scenario described above?
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.
Why is the patient presenting with the symptoms described above?
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.

What is the appropriate initial management of this patient?
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)

What further work-up could be considered?
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)

What are other common means of HC exposure?
-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.
What are the indications for admission?
-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)


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Khalade A, Jaakkola MS, Pukkala E, et al. Exposure to benzene at work and the risk of leukemia: a systematic review and meta-analysis. Environ Health. 2010 Jun 28;9:31.

Lubman DI, Yücel M, Lawrence AJ. Inhalant abuse among adolescents: neurobiological considerations. Br J Pharmacol. 2008 May;154(2):316-26.

Yücel M, Takagi M, Walterfang M, et al. Toluene misuse and long-term harms: a systematic review of the neuropsychological and neuroimaging literature. Neurosci Biobehav Rev. 2008 Jul;32(5):910-26.

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