Hydrocarbon toxicity: Difference between revisions
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**'''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 | ||
**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=== | ||
* "Sudden sniffing death syndrome"= suspected cardiac sensitization to catecholamines | *[[Arrhythmias]], [[Afib]], PVCs, [[Vtach]], [[torsades]] | ||
*"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 | |||
*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== | ==Differential Diagnosis== | ||
{{Drugs of abuse types}} | {{Drugs of abuse types}} | ||
== | {{Toxic gas exposure DDX}} | ||
==Evaluation== | |||
===Workup=== | ===Workup=== | ||
*CXR: immediately if symptomatic, otherwise early CXR not predictive of pneumonitis. Observe for 4-6hrs then obtain CXR | *[[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 | *Labs: as needed to evaluate for acidosis, anemia, renal/hepatic toxicity, coagulation, methemoglobinemia, carboxyhemoglobinemia depending on specific exposure | ||
*ECG | *[[ECG]] | ||
===Evaluation=== | ===Evaluation=== | ||
| Line 46: | Line 57: | ||
==Management== | ==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=== | |||
*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== | ||
===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== | ==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]
- 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
- 25C-NBOMe
- Alcohol
- Amphetamines
- Bath salts
- Cocaine
- Ecstasy
- Gamma hydroxybutyrate (GHB)
- Heroin
- Inhalant abuse
- Hydrocarbon toxicity
- Difluoroethane (electronics duster)
- Marijuana
- Kratom
- Phencyclidine (PCP)
- Psilocybin ("magic mushrooms")
- Synthetic cannabinoids
- Chloral hydrate
- Body packing
Toxic gas exposure
- Carbon monoxide toxicity
- Chemical weapons
- Cyanide toxicity
- Hydrocarbon toxicity
- Hydrogen sulfide toxicity
- Inhalant abuse
- Methane toxicity
- Smoke inhalation injury
- Ethylene dibromide toxicity
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
- 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
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
- ↑ Tormoehlen L et al. Hydrocarbon toxicity: A review. Clinical toxicology 2014; 52: 479-489