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HYDROCARBON
POISONING
A.SASIDHARAN
introduction
 Hydrocarbon (Kerosene) poisoning is one of the most common accidental poisoning in children in
developing countries due common use of kerosene in house-hold and unsafe storage practices.
 Hydrocarbons can cause rapid onset of CNS symptoms including CNS depression and seizures.
 Volatile hydrocarbons can be aspirated and cause chemical pneumonitis.
 Cardiac dysrhythmias are less common
 Poisoning can occur from accidental exposure (often younger children) or deliberate exposure (often
from inhalation e.g. from “sniffing” or “chroming”)
Hydrocarbon Compounds
 Hydrocarbons come in four structural classes.
 Aromatic - contain a benzene ring (most toxic) and are used in solvents and glues but also in paint and paint
remover.
 Aliphatic - petroleum distillates found in polishes, lamp oils, and lighter fluid.
 Halogenated - fluorinated, chlorinated, or brominated, and are used for refrigeration (Freon) and as
insecticides and herbicides.
 Terpene - found in turpentine and pine oil. Some of these hydrocarbons may be found in various mixed
forms and used as an aerosol spray propellant.
Hydrocarbon compounds
• Petrol
• Kerosene
• Lighter Fluid
• Paraffin Oil
• 2 Stroke Fuel
• Diesel Fuel
• Solvents
• White Spirit
• Lubricating Oil
• Furniture Polishes
• Essential oils
• Mineral Turpentine
Patient Requiring Assessment
 All patients with deliberate self-poisoning or significant accidental
exposure
 Any symptomatic patient
 Any patient whose developmental age is inconsistent with accidental
poisoning as non-accidental poisoning should be considered.
Risk Assessment
 History
Was exposure intentional or accidental?
Dose:
Type of compound
Quantity ingested
Duration of exposure in inhalation
Co-ingestants (e.g. paracetamol )
pathophysiology
 The toxicity of hydrocarbons is due to their low surface tension and vapour pressure which helps them
spread over large surface area of the lungs and cause chemical pneumonitis. While lower surface
tension helps in spreading over a large area, lower viscosity enhances penetration into distal airways
leading to severe necrotizing pneumonia.
 Thus compounds like kerosene, gasoline and naphtha with high volatility, low viscosity, and low surface
tension are more likely to be aspirated and cause severe lung injury.
Pathophysiology
Hydrocarbon aspiration
inhibit surfactant
Alveolar instability
early distal airway closure
ventilation perfusion mismatch
HYPOXIA
General Examination / Vitals
 PR
 BP
 SPO2
 TEMP
 Any smell of ingested hydrocarbon
Systemic Examination
 Respiratory
Coughing / gagging / choking indicates aspiration
Wheeze, tachypnoea, hypoxia, haemoptysis and pulmonary oedema are signs of evolving chemical
pneumonitis.
 Cardiovascular
Dysrhythmias occur early in exposure
Halogenated hydrocarbon abuse can cause a fatal malignant arrhythmia, termed "sudden sniffing death
cont.
 CNS
CNS depression (Acute exposure leads to an increase in gamma-amino butyric acid (GABA) and glycine function ),
but experimental evidence suggests effects on NMDA, dopamine, and GABA receptors.
coma and seizures may occur with large acute exposures. Onset is usually within 2 hours
 GIT
Nausea, vomiting and diarrhoea
Excessive burping, heartburn, epigastric pain
Conti
 Renal effects
Hydrocarbon toxicity can lead to metabolic acidosis, hypochloremia, and hypokalaemia
resulting from distal renal tubular acidosis. Anion gap acidosis occurs as the compounds are metabolized, and
sodium and potassium are lost via renal excretion along with these metabolites.
INVESTIGATIONS
 Asymptomatic children with small ingestions do not usually require investigation.
 For children with more significant ingestions, or who are symptomatic:
 12 lead ECG & cardiac monitoring for 4 hours
 CBC
 BUSE
 LFTs
 VBG
INV cont.
 CXR if respiratory symptoms ( some studies suggest CXR in asymptomatic also)
 CXR can be taken early or after 6 hrs of observation.
 For all children with deliberate poisoning, perform further screening for co-ingestants
CXR
Acute Management
 1. Resuscitation
 Standard procedures and supportive care
 Intubate early for progressive CNS depression
 Ventricular dysrhythmias:
 Commence advance life support
 Intubate, hyperventilate, correct hypoxia
 Correct electrolyte disturbances
 Withhold catecholamine inotropes if possible
Decontamination
 Activated charcoal is specifically contraindicated in hydrocarbon poisoning as they do not bind
hydrocarbons and increase the risk of hydrocarbon aspiration
 Gastric lavage / emetic is contraindicated as worsens the condition
Conti.
 Seizures – Benzodiazepines remain standard first line treatment.
 Ongoing care and monitoring
Asymptomatic children with normal vital signs should be observed for 6 hours post exposure before
discharge
Patients with milder respiratory or CNS symptoms should be admitted for a longer period of observation
+/- supportive care
Chemical Pneumonitis
 Chemical pneumonitis is managed supportively (Oxygen & bronchodilators – may require non invasive
ventilation or intubation if severe). Corticosteroids and prophylactic antibiotics are not indicated. Fever
is common following aspiration with pneumonitis – antibiotics should be withheld until there is objective
evidence of bacterial infection
Prognosis
 Prognosis
Pulmonary toxicity is the major cause of morbidity and mortality.
 Aspiration pneumonitis is the most common complication of hydrocarbon ingestion, followed by CNS
and cardiovascular complications. The major respiratory complications are aspiration and lung injury
secondary to pneumonitis. Pneumothorax and barotrauma are potential complications of mechanical
ventilation. Most patients improve after 24 hours, and symptoms resolve within 1 week.
Discharge Criteria
Normal GCS
Normal ECG
No respiratory symptoms (cough, dyspnoea, wheeze)
Normal observations including pulse oximetry
Period of observation as above
For deliberate ingestion a risk assessment should indicate that the patient is at low risk of further self harm in the
discharge setting
Prevention
 Patient Education
 Patient education is crucial in the prevention of unnecessary or accidental exposure. Most exposures in
young children are accidental and can be prevented. Teaching points include the following:
 Parents should teach young children about the dangers of poisons, beginning at an early age
 Advise the parents about the proper storage and labelling of harmful chemicals
 Inform parents about common household products that may be dangerous, and recommend steps that
they can take to minimize the possibility of an accidental exposure
 Educate parents that they need to supervise their children when they are in high-risk areas (eg, kitchen,
garage, laundry room) where toxic substances may be present
 THANK YOU

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Hydrocarbon poisoning

  • 2. introduction  Hydrocarbon (Kerosene) poisoning is one of the most common accidental poisoning in children in developing countries due common use of kerosene in house-hold and unsafe storage practices.  Hydrocarbons can cause rapid onset of CNS symptoms including CNS depression and seizures.  Volatile hydrocarbons can be aspirated and cause chemical pneumonitis.  Cardiac dysrhythmias are less common  Poisoning can occur from accidental exposure (often younger children) or deliberate exposure (often from inhalation e.g. from “sniffing” or “chroming”)
  • 3. Hydrocarbon Compounds  Hydrocarbons come in four structural classes.  Aromatic - contain a benzene ring (most toxic) and are used in solvents and glues but also in paint and paint remover.  Aliphatic - petroleum distillates found in polishes, lamp oils, and lighter fluid.  Halogenated - fluorinated, chlorinated, or brominated, and are used for refrigeration (Freon) and as insecticides and herbicides.  Terpene - found in turpentine and pine oil. Some of these hydrocarbons may be found in various mixed forms and used as an aerosol spray propellant.
  • 4. Hydrocarbon compounds • Petrol • Kerosene • Lighter Fluid • Paraffin Oil • 2 Stroke Fuel • Diesel Fuel • Solvents • White Spirit • Lubricating Oil • Furniture Polishes • Essential oils • Mineral Turpentine
  • 5. Patient Requiring Assessment  All patients with deliberate self-poisoning or significant accidental exposure  Any symptomatic patient  Any patient whose developmental age is inconsistent with accidental poisoning as non-accidental poisoning should be considered.
  • 6. Risk Assessment  History Was exposure intentional or accidental? Dose: Type of compound Quantity ingested Duration of exposure in inhalation Co-ingestants (e.g. paracetamol )
  • 7. pathophysiology  The toxicity of hydrocarbons is due to their low surface tension and vapour pressure which helps them spread over large surface area of the lungs and cause chemical pneumonitis. While lower surface tension helps in spreading over a large area, lower viscosity enhances penetration into distal airways leading to severe necrotizing pneumonia.  Thus compounds like kerosene, gasoline and naphtha with high volatility, low viscosity, and low surface tension are more likely to be aspirated and cause severe lung injury.
  • 8. Pathophysiology Hydrocarbon aspiration inhibit surfactant Alveolar instability early distal airway closure ventilation perfusion mismatch HYPOXIA
  • 9. General Examination / Vitals  PR  BP  SPO2  TEMP  Any smell of ingested hydrocarbon
  • 10. Systemic Examination  Respiratory Coughing / gagging / choking indicates aspiration Wheeze, tachypnoea, hypoxia, haemoptysis and pulmonary oedema are signs of evolving chemical pneumonitis.  Cardiovascular Dysrhythmias occur early in exposure Halogenated hydrocarbon abuse can cause a fatal malignant arrhythmia, termed "sudden sniffing death
  • 11. cont.  CNS CNS depression (Acute exposure leads to an increase in gamma-amino butyric acid (GABA) and glycine function ), but experimental evidence suggests effects on NMDA, dopamine, and GABA receptors. coma and seizures may occur with large acute exposures. Onset is usually within 2 hours  GIT Nausea, vomiting and diarrhoea Excessive burping, heartburn, epigastric pain
  • 12. Conti  Renal effects Hydrocarbon toxicity can lead to metabolic acidosis, hypochloremia, and hypokalaemia resulting from distal renal tubular acidosis. Anion gap acidosis occurs as the compounds are metabolized, and sodium and potassium are lost via renal excretion along with these metabolites.
  • 13. INVESTIGATIONS  Asymptomatic children with small ingestions do not usually require investigation.  For children with more significant ingestions, or who are symptomatic:  12 lead ECG & cardiac monitoring for 4 hours  CBC  BUSE  LFTs  VBG
  • 14. INV cont.  CXR if respiratory symptoms ( some studies suggest CXR in asymptomatic also)  CXR can be taken early or after 6 hrs of observation.  For all children with deliberate poisoning, perform further screening for co-ingestants
  • 15. CXR
  • 16.
  • 17. Acute Management  1. Resuscitation  Standard procedures and supportive care  Intubate early for progressive CNS depression  Ventricular dysrhythmias:  Commence advance life support  Intubate, hyperventilate, correct hypoxia  Correct electrolyte disturbances  Withhold catecholamine inotropes if possible
  • 18. Decontamination  Activated charcoal is specifically contraindicated in hydrocarbon poisoning as they do not bind hydrocarbons and increase the risk of hydrocarbon aspiration  Gastric lavage / emetic is contraindicated as worsens the condition
  • 19. Conti.  Seizures – Benzodiazepines remain standard first line treatment.  Ongoing care and monitoring Asymptomatic children with normal vital signs should be observed for 6 hours post exposure before discharge Patients with milder respiratory or CNS symptoms should be admitted for a longer period of observation +/- supportive care
  • 20. Chemical Pneumonitis  Chemical pneumonitis is managed supportively (Oxygen & bronchodilators – may require non invasive ventilation or intubation if severe). Corticosteroids and prophylactic antibiotics are not indicated. Fever is common following aspiration with pneumonitis – antibiotics should be withheld until there is objective evidence of bacterial infection
  • 21. Prognosis  Prognosis Pulmonary toxicity is the major cause of morbidity and mortality.  Aspiration pneumonitis is the most common complication of hydrocarbon ingestion, followed by CNS and cardiovascular complications. The major respiratory complications are aspiration and lung injury secondary to pneumonitis. Pneumothorax and barotrauma are potential complications of mechanical ventilation. Most patients improve after 24 hours, and symptoms resolve within 1 week.
  • 22. Discharge Criteria Normal GCS Normal ECG No respiratory symptoms (cough, dyspnoea, wheeze) Normal observations including pulse oximetry Period of observation as above For deliberate ingestion a risk assessment should indicate that the patient is at low risk of further self harm in the discharge setting
  • 23. Prevention  Patient Education  Patient education is crucial in the prevention of unnecessary or accidental exposure. Most exposures in young children are accidental and can be prevented. Teaching points include the following:  Parents should teach young children about the dangers of poisons, beginning at an early age  Advise the parents about the proper storage and labelling of harmful chemicals  Inform parents about common household products that may be dangerous, and recommend steps that they can take to minimize the possibility of an accidental exposure  Educate parents that they need to supervise their children when they are in high-risk areas (eg, kitchen, garage, laundry room) where toxic substances may be present