Hydrocarbon toxicity: Difference between revisions

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==Background==
==Background==
* i.e gasoline, charcoal starter, lamp oil, petroleum jelly, paint, paint thinners, polish
*Typical exposures:
* usual exposures:
**Unintentional exposure (generally young children)
# kids with unintentional exposure
**Intentional abuse (generally adolescents, young adults)
# occupational exposure - dermal, inhalational
**Occupational exposure - dermal, inhalation
# adolescent, young adults - intentional abuse
*Intentional abuse methods:
* high volatility, low viscosity make them a set-up for aspiration, despite "simple ingestion"
**'''Huffing'''= hydrocarbon soaked into rag and placed over mouth and nose
**'''Bagging'''= hydrocarbon placed in a bag and fumes inhaled
**'''Sniffing'''= hydrocarbon inhaled directly
*High volatility, low viscosity → high risk for aspiration despite "simple ingestion"
*Easily washes out pulmonary surfactant if aspirated
 
===Examples===
*Gasoline
*Lighter fluid
*Lamp oil
*Petroleum jelly (Vaseline)
*Paint
*Paint thinners
*Polish
*Toluene


==Clinical Features==
==Clinical Features==
* pulm: aspiration
===Pulmonary===
# risk factors: high volume, vomiting, gagging, choking, coughing
*Aspiration
# CXR on presentation nonpredictive, but usually appear by 6hrs
**Low viscosity and surface tension of hydrocarbons make them high aspiration risk
**Additional risk factors: high volume, vomiting, gagging, choking, coughing
**[[CXR]] on presentation nonpredictive, but usually appear by 6hrs
*[[ARDS]]
 
===Cardiac===
*[[Arrhythmias]], [[Afib]], PVCs, [[Vtach]], [[torsades]]
*"Sudden sniffing death syndrome"= suspected cardiac sensitization to catecholamines
**Classic scenario: Sniffer is startled during use, collapses and dies
 
===CNS/PNS <ref> Tormoehlen L et al. Hydrocarbon toxicity: A review. Clinical toxicology 2014; 52: 479-489 </ref>===
*Stage 1: [[headache]], [[dizziness]], [[nausea]], tinnitus
*Stage 2: Slurred speech, confusion, [[hallucinations]], [[diplopia]], [[ataxia]]
*Stage 3: Obtundation, [[seizure]], death
 
===Renal===
*Toluene in particular may cause weakness secondary to severe [[hypokalemia]]
 
==Differential Diagnosis==
{{Drugs of abuse types}}
 
{{Toxic gas exposure DDX}}


*cardiac: arrhythmogenic, Afib, PVCs, Vtach, torsade, "sudden sniffing syndrome"
==Evaluation==
* 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
*Labs: as needed to evaluate for acidosis, anemia, renal/hepatic toxicity, coagulation, methemoglobinemia, carboxyhemoglobinemia depending on specific exposure
*[[ECG]]


==Workup==
===Evaluation===
* CXR: immediately if symptomatic, otherwise early CXR not predictive of pneumonitis. Observe for 4-6hrs then obtain CXR
*Clinical diagnosis, based on history and physical exam
* EKG: dysrhythmias
* labs: if toxic, to ascertain electrolytes, acid/base status


==Management==
==Management==
* antiobiotic prophylaxis show no benefit, but patients are at risk for superinfection
===Pulmonary===
* steroids not recommended and can lead to increased superinfection
*Secure airway, if needed.
* patients with severe toxicity will need intubation, high PEEP, possibly high frequency jet ventilation, and ECMO for refractory hypoxemia
*Beta2 agonist if wheezing (not proven benefit), consider [[BiPAP]]/[[CPAP]] (may further barotrauma)
*Severe toxicity will need [[intubation]], high PEEP, possibly high frequency jet ventilation, and ECMO for refractory hypoxemia
*Antibiotic prophylaxis show no benefit, but use if superinfection present
*Steroids not recommended for chemical pneumonitis and can lead to increased superinfection
 
===Cardiovascular===
*Treat hypotension with aggressive [[IVF]]
*Avoid [[dopamine]], [[epinephrine]], [[norepinephrine]] (may cause [[dysrhythmias]]), [[procainamide]] (may cause [[arrhythmias]]), and [[amiodarone]] ([[QT prolongation]])
*Treat ventricular dysrhythmias with [[propranolol]], [[esmolol]], or [[lidocaine]]
**Due to overstimulation of beta receptors by hydrocarbon
 
===Dermal===
*Pre-arrival decontamination, remove clothing
*Soap and water, saline for eye exposure
 
===GI===
*[[GI decontamination]] controversial
*Majority do not benefit


==Disposition==
==Disposition==
* home: 6hrs of obs, no abnormal lung findings, adequated O2, not tachypneic and nl CXR at 6hrs
===Discharge===
* admit: clinical e/o toxicity or intentional ingestion
After 6 hour observation if:
*asymptomatic BUT radiographic e/o pneumonitis, home with follow up next day
*Asymptomatic
*Normal vital signs (including SpO2)
*No abnormal pulmonary findings
*Normal CXR at 6hrs post exposure
**If asymptomatic but radiographic evidence of pneumonitis, consider discharge with 24-hour follow-up.
 
===Admit===
*Clinical evidence of toxicity


==See Also==
==See Also==
*[[Toxicology (Main)]]
*[[Inhalants]]


==Sources==
==References==
Goldfrank's Toxicologic Emergencies
<references/>
<references/>
[[Category:Toxicology]]

Latest revision as of 20:58, 8 November 2023

Background

  • Typical exposures:
    • Unintentional exposure (generally young children)
    • Intentional abuse (generally adolescents, young adults)
    • Occupational exposure - dermal, inhalation
  • Intentional abuse methods:
    • Huffing= hydrocarbon soaked into rag and placed over mouth and nose
    • Bagging= hydrocarbon placed in a bag and fumes inhaled
    • Sniffing= hydrocarbon inhaled directly
  • High volatility, low viscosity → high risk for aspiration despite "simple ingestion"
  • Easily washes out pulmonary surfactant if aspirated

Examples

  • Gasoline
  • Lighter fluid
  • Lamp oil
  • Petroleum jelly (Vaseline)
  • Paint
  • Paint thinners
  • Polish
  • Toluene

Clinical Features

Pulmonary

  • Aspiration
    • Low viscosity and surface tension of hydrocarbons make them high aspiration risk
    • Additional risk factors: high volume, vomiting, gagging, choking, coughing
    • CXR on presentation nonpredictive, but usually appear by 6hrs
  • ARDS

Cardiac

  • Arrhythmias, Afib, PVCs, Vtach, torsades
  • "Sudden sniffing death syndrome"= suspected cardiac sensitization to catecholamines
    • Classic scenario: Sniffer is startled during use, collapses and dies

CNS/PNS [1]

Renal

  • Toluene in particular may cause weakness secondary to severe hypokalemia

Differential Diagnosis

Drugs of abuse

Toxic gas exposure

Evaluation

Workup

  • CXR: immediately if symptomatic, otherwise early CXR not predictive of pneumonitis. Observe for 4-6hrs then obtain CXR
  • Labs: as needed to evaluate for acidosis, anemia, renal/hepatic toxicity, coagulation, methemoglobinemia, carboxyhemoglobinemia depending on specific exposure
  • ECG

Evaluation

  • Clinical diagnosis, based on history and physical exam

Management

Pulmonary

  • Secure airway, if needed.
  • Beta2 agonist if wheezing (not proven benefit), consider BiPAP/CPAP (may further barotrauma)
  • Severe toxicity will need intubation, high PEEP, possibly high frequency jet ventilation, and ECMO for refractory hypoxemia
  • Antibiotic prophylaxis show no benefit, but use if superinfection present
  • Steroids not recommended for chemical pneumonitis and can lead to increased superinfection

Cardiovascular

Dermal

  • Pre-arrival decontamination, remove clothing
  • Soap and water, saline for eye exposure

GI

Disposition

Discharge

After 6 hour observation if:

  • Asymptomatic
  • Normal vital signs (including SpO2)
  • No abnormal pulmonary findings
  • Normal CXR at 6hrs post exposure
    • If asymptomatic but radiographic evidence of pneumonitis, consider discharge with 24-hour follow-up.

Admit

  • Clinical evidence of toxicity

See Also

References

  1. ↑ Tormoehlen L et al. Hydrocarbon toxicity: A review. Clinical toxicology 2014; 52: 479-489
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