Hydrocarbon toxicity

Background

• i.e gasoline, charcoal starter, lamp oil, petroleum jelly, paint, paint thinners, polish
• usual exposures:

1. kids with unintentional exposure
2. occupational exposure - dermal, inhalational
3. adolescent, young adults - intentional abuse

• high volatility, low viscosity make them a set-up for aspiration, despite "simple ingestion"

Clinical Features

• pulm: aspiration

1. risk factors: high volume, vomiting, gagging, choking, coughing
2. CXR on presentation nonpredictive, but usually appear by 6hrs

• cardiac: arrhythmogenic, Afib, PVCs, Vtach, torsade, "sudden sniffing syndrome"
• CNS/PNS: excitation, followed by depression, ataxia, neuropathy

Workup

• CXR: immediately if symptomatic, otherwise early CXR not predictive of pneumonitis. Observe for 4-6hrs then obtain CXR
• EKG: dysrhythmias
• labs: if toxic, to ascertain electrolytes, acid/base status

Management

• antiobiotic prophylaxis show no benefit, but patients are at risk for superinfection
• steroids not recommended and can lead to increased superinfection
• patients with severe toxicity will need intubation, high PEEP, possibly high frequency jet ventilation, and ECMO for refractory hypoxemia

Disposition

• home: 6hrs of obs, no abnormal lung findings, adequated O2, not tachypneic and nl CXR at 6hrs
• admit: clinical e/o toxicity or intentional ingestion
• asymptomatic BUT radiographic e/o pneumonitis, home with follow up next day

See Also

Toxicology (Main) Inhalants

Sources

Goldfrank's Toxicologic Emergencies Bass M. Sudden sniffing death. JAMA. 1970;212:2075-2079 Bysani BK et al. Treatment of hydrocarbon pneumonitis: high frequency jet ventilation as an alternative to extracorporeal membrane oxygenation. Chest. 1994;106:300-303. Brock WJ et al. Cardiac sensitization: methadology and interpretation in risk assessment. Toxicol Pharmacol. 2003;38:78-90.