Hydrocarbon toxicity
Revision as of 17:31, 15 May 2014 by Rossdonaldson1 (talk | contribs)
Background
- usual exposures:
- kids with unintentional exposure
- occupational exposure - dermal, inhalational
- adolescent, young adults - intentional abuse
- high volatility, low viscosity make them a set-up for aspiration, despite "simple ingestion"
Examples
- Gasoline
- Charcoal starter
- Lamp oil
- Petroleum jelly
- Paint
- Paint thinners
- Polish
Clinical Features
- pulm: aspiration
- risk factors: high volume, vomiting, gagging, choking, coughing
- 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
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.