Hydrocarbon toxicity: Difference between revisions
 
(13 intermediate revisions by 4 users not shown)
Line 9: Line 9:
**'''Sniffing'''= hydrocarbon inhaled directly
**'''Sniffing'''= hydrocarbon inhaled directly
*High volatility, low viscosity → high risk for aspiration despite "simple ingestion"
*High volatility, low viscosity → high risk for aspiration despite "simple ingestion"
*Easily washes out pulmonary surfactant if aspirated


===Examples===
===Examples===
Line 18: Line 19:
*Paint thinners
*Paint thinners
*Polish
*Polish
*Toluene


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


*Cardiac: arrhythmias, Afib, PVCs, Vtach, torsades
===Cardiac===
*[[Arrhythmias]], [[Afib]], PVCs, [[Vtach]], [[torsades]]
*"Sudden sniffing death syndrome"= suspected cardiac sensitization to catecholamines
*"Sudden sniffing death syndrome"= suspected cardiac sensitization to catecholamines
**Classic scenario: Sniffer is startled during use, collapses and dies
**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
===CNS/PNS <ref> Tormoehlen L et al. Hydrocarbon toxicity: A review. Clinical toxicology 2014; 52: 479-489 </ref>===
**Stage 2: Slurred speech, confusion, hallucinations, diplopia, ataxia
*Stage 1: [[headache]], [[dizziness]], [[nausea]], tinnitus
**Stage 3: Obtundation, seizure, death
*Stage 2: Slurred speech, confusion, [[hallucinations]], [[diplopia]], [[ataxia]]
*Renal: Toluene in particular may cause weakness secondary to severe hypokalemia
*Stage 3: Obtundation, [[seizure]], death
 
===Renal===
*Toluene in particular may cause weakness secondary to severe [[hypokalemia]]


==Differential Diagnosis==
==Differential Diagnosis==
{{Drugs of abuse types}}
{{Drugs of abuse types}}
{{Toxic gas exposure DDX}}


==Evaluation==
==Evaluation==
Line 49: Line 59:
===Pulmonary===
===Pulmonary===
*Secure airway, if needed.  
*Secure airway, if needed.  
*Beta2 agonist if wheezing (not proven benefit), consider [[Bipap]]/[[Cpap]] (may further barotrauma)
*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
*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
*Antibiotic prophylaxis show no benefit, but use if superinfection present
Line 56: Line 66:
===Cardiovascular===
===Cardiovascular===
*Treat hypotension with aggressive [[IVF]]
*Treat hypotension with aggressive [[IVF]]
*Avoid dopamine, epinephrine, norepinephrine (may cause dysrhythmias)
*Avoid [[dopamine]], [[epinephrine]], [[norepinephrine]] (may cause [[dysrhythmias]]), [[procainamide]] (may cause [[arrhythmias]]), and [[amiodarone]] ([[QT prolongation]])
*Treat ventricular dysrhythmias with [[propranolol]], [[esmolol]], or [[lidocaine]]
*Treat ventricular dysrhythmias with [[propranolol]], [[esmolol]], or [[lidocaine]]
**Due to overstimulation of beta receptors by hydrocarbon


===Dermal===
===Dermal===
Line 68: Line 79:


==Disposition==
==Disposition==
*Discharge after 6 hour observation if:
===Discharge===
**Asymptomatic
After 6 hour observation if:
**Normal vital signs (including SpO2)
*Asymptomatic
**No abnormal pulmonary findings
*Normal vital signs (including SpO2)
**Normal CXR at 6hrs post exposure
*No abnormal pulmonary findings
***If asymptomatic but radiographic evidence of pneumonitis, consider discharge with 24-hour follow-up.
*Normal CXR at 6hrs post exposure
*Admit:
**If asymptomatic but radiographic evidence of pneumonitis, consider discharge with 24-hour follow-up.
**Clinical evidence of toxicity
 
===Admit===
*Clinical evidence of toxicity


==See Also==
==See Also==

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
Retrieved from "https://www.wikem.org/w/index.php?title=Hydrocarbon_toxicity&oldid=371944"