HYDROCARBONS AND
VOLATILE
SUBSTANCES
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Hydrocarbons are a diverse group of organic compounds
consisting primarily of carbon and hydrogen atoms
arranged in various aliphatic and aromatic
configurations.
Products containing hydrocarbons are found in many
household and occupational settings:
fuels, lighter fluids, lamp oil, paints, paint removers,
pesticides, medications,cleaning and polishing agents,
spot removers, degreasers, lubricants,and solvents.
Hydrocarbon and volatile substance exposure may
cause life-threatening toxicity and, in some cases,
sudden death.
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
Most hydrocarbons are produced from
petroleum distillation:
aliphatic (open-chain) mixtures of hydrocarbons
& Short-chain& Intemediate-chain
 The wood distillates
 Aromatic hydrocarbons (containing a benzene ring)
 halogenated hydrocarbons

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Epidemiology
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Exposures to hydrocarbons and volatiles most
commonly occur in one of two settings: # Ingestion
#Inhalation.
3.5 to 10 percent of young people have experimented
with volatile substance inhalation to produce inebriation
The most commonly implicated volatiles were:
butane (39 percent),
aerosols (26 percent),
cleaners (16 percent),
glue (10 percent).
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CLINICAL FEATURES
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The toxic potential of hydrocarbons depends on:
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physical characteristics(volatility, viscosity, and surface tension)
chemical characteristics(aliphatic, aromatic, or halogenated), presence
of toxic additives (pesticidesor heavy metals),
route of exposure,
concentration,
dose.
Viscosity: the resistance to flow, and surface tension, ( a
major role in determining the aspiration potential.)

substances with viscosities less than60 SUS (e.g.,
gasoline, kerosene, mineral seal oil, turpentine, andaromatic and
halogenated hydrocarbons) are at greater risk for than are
those ingesting substances with viscosities
greater than 100 SUS (e.g., diesel oil, grease, mineral oil,
paraffin wax, and petroleum jelly)
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Low surface tension also increases the risk of aspiration.
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Volatility :denotes the ability of a substance to vaporize.
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A compound with high volatility evaporates easily and usually has low
viscosity and low surface tension.

Inhalation of volatile agents, )such as aromatic hydrocarbons, halogenated
hydrocarbons, or gasoline(, results in systemic absorption and the potential for
significant toxicity.
Dermal exposure to hydrocarbons: causes local toxicity, and occasionally
leads to systemic absorption.
 Intravenous administration of hydrocarbons :may cause pulmonary toxicity
by their first-pass exposure through the lungs (first capillary bed encountered).
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Characteristic presentations usually affect one or
more of the following
systems:
pulmonary,
Neurologic
:central
peripheral,
GI,
Cardiac,
Hepatic,
Renal,
Hematologic,
Dermal.
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Pulmonary Toxcity

Pulmonary complications, especially aspiration, are the
most frequent adverse effects of hydrocarbon exposure.
 Aliphatic hydrocarbons have a limited GI absorption;
toxicity usually results from aspiration of the low-viscosity
compounds or inhalation (with resulting systemic
absorption) of compounds with high volatility.
 Ingestion of aromatic or halogenated hydrocarbons may
also result in aspiration, GI absorption is greater.

That results in the development of lipoid
pneumonia. Deaths from hydrocarbon lipoid
pneumonia have been reported.
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The risk and degree of aspiration is not dependent on volume
ingested. ( 0.2 mL instilled intratracheally has caused pneumonitis.)

Pulmonary toxicity does not result from GI absorption but
occurs from direct aspiration of the hydrocarbon into the
pulmonary tree.
There is no evidence that hydrocarbons reflux from the
stomach into the airway.
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Spontaneous vomiting, however, does increase the risk of
aspiration.‘
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Pulmonary toxicity manifested as: acute bilateral pneumonitis
( from the inhalation of an aerosolized aliphatic hydrocarbon such as
gasoline)
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Hydrocarbon aspiration causes :
direct toxic injury to the pulmonary parenchyma
altered surfactant function.
increased vascular permeability and edema.
clinical bronchospasm
ventilation/perfusion mismatch.
CNS manifestations
Pneumatoceles,
pneumothoraces,
pneumomediastinum
bacterial superinfection,
acute respiratory distress syndrome,
death.
Long-term pulmonary dysfunction may occur.
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CNS manifestations seen after ingestion of a poorly GIabsorbed aliphatic hydrocarbon are thought to be
from :
hypoxia secondary to the hydrocarbon induced pneumonitis
and/or direct CNS toxicity following the pulmonary absorption
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19 percent had clinical or radiographic evidence of
pulmonary aspiration.
35 percent have initial symptoms,
only 3 percent have progressive pulmonary symptoms'
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
The clinical manifestations of pulmonary aspiration are
usually apparent almost immediately on ingestion.
The early effects result from irritation of the oral mucosa
and tracheobronchial tree.
Symptoms :
 coughing,
 choking,
 gasping,
 dyspnea,
 burning of the mouth.

Patients with these symptoms should be assumed to have
aspirated until proven otherwise.
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Physical examination :
 grunting respirations,
 retractions,
 tachypnea,
 tachycardia,
 cyanosis.
 An odor of the hydrocarbon may be noted on the
patient's breath.
 An elevated temperature of 39°C (I 02.2°F) or greater is
common ( may occur upon initial presentation or be
delayed for 6 to 8 h.)
 Auscultation may be normal,or reveal wheezing and
decreased or absent breath sounds.
 Arterial blood gas analysis may demonstrate a widened
alveolar-arterial oxygen gradient or frank hypoxemia.
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The development of a necrotizing pneumonitis and
hemorrhagic pulmonary edema usually occurs within
hours in severe aspiration.
Most fatalities from these complications occur within 24
to 48 h.
With less-severe damage, symptoms usually subside
within 2 to 5 days

pneumatoceles and lipoid, pneumonias
whose symptoms may persist for weeks to months.
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
most patients with clinically significant aspiration have
abnormal chest x-rays,
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radiographic changes varies and correlation with physical
examination may be poor.
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Changes may be seen as early as 30 min after aspiration, but
the initial radiograph in the symptomatic patient may be
deceptively clear.

Radiographic changes usually appear by 2 to 6 h and are
almost always present by18 to 24 h, if they are to occur.
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Radiographic changes limited to bilateral perihilar
regions with clear lung bases are also common,
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mild radiographic changes do not automatically mean
the patient will become symptomatic.

right-sided involvement is more common than left-sided
involvement.

Multilobar involvement is more common than single-lobe
involvement
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Central Nervous System Toxicity
Result from:
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a direct toxic response to the systemic absorption of the hydrocarbon,
indirect result of severe hypoxia secondary to aspiration,
a result of simple asphyxiation due to either loss of ventilatory drive,
the use of a plastic bag or other device during "bagging."
Through:
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GI absorption,
the inhalation of highly volatile petroleum distillates,
direct dermal penetration, usually by prolonged contact with
chlorinated hydrocarbons.
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Volatile solvent abuse most often occurs in teenagers
and younger adults,
 These patients are described as "huffers" or "baggers"
depending on whether they inhale through a rag soaked
with the hydrocarbon held to the mouth or rebreathe into
a plastic bag containing the hydrocarbon.
 The act of rebreathing to facilitate inhalation may also
contribute to toxicity by producing significant hypercarbia
and hypoxia.
 They behave similarly to the inhalational anesthetic agents.
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Hydrocarbon intoxication may be confused with ethanol inebriation.
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CNS depression ranges in severity from :
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These effects are usually dose-dependent.
Although hydrocarbons are CNS depressants, they often
have an initial excitatory effect manifested as :
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euphoria,
exhilaration,
giddiness,.
More severe excitatory features include:
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dizziness,
slurred speech,
ataxia,
lethargy to obtundation,
coma and apnea.
tremor,
agitation,
convulsions.
Perceptual changes, such as confusion, hallucinations,
and psychosis, may occur.
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Chronic CNS sequelae:
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Recurrent headaches,
cerebellar ataxia,
chronic encephalopathy consisting of tremors,
emotional lability,
mental status changes,
cognitive impairment,
psychomotor impairment,
These effects may be transitory or permanent.
The development of encephalopathy, ataxia,
tremor, chorea, and myoclonus also is
associated with the habitual sniffing of leaded
gasoline.
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Peripheral Nervous System Toxicity
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Exposure to aliphatic hydrocarbons is associated with
the development of a characteristic peripheral
polyneuropathy caused by demyelinization and
retrograde axonal degeneration.
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Onset of symptoms may be delayed for months to
years after initial exposure.
Toxicity is attributed to a metabolite, 2,5-hexanedione,
produced by the cytochrome P450-mediated
biotransformation of the parent compounds.
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Long, distal nerves seem to be most vulnerable,
characteristically producing foot and wrist drop with
numbness and paresthesias.

Unleaded gasoline sniffing has produced a similar
clinical picture as well.
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Gastrointestinal Toxicity
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Most hydrocarbons act as intestinal irritants.
resulting in burning in the mouth and throat,
abdominal pain,
belching,
nausea,
vomiting,
diarrhea.
Vomiting, which occurs in approximately one-third of the
patients with aliphatic hydrocarbon ingestions, is
particularly trouble some because of the increased risk
of pulmonary aspiration.
Corrosive GI injury, as well as pancreatitis, has been reported with
ingestion of some chlorinated hydrocarbons.
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Cardiac Toxicity
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Life-threatening dysrhythmias, such as ventricular
tachycardia and ventricular fibrillation, sudden
Death may occur with systemic absorption
(gastrointestinal or inhalational) of a variety of
hydrocarbon compounds.
Most commonly, dysrhythmias occur after exposure to
halogenated hydrocarbons and aromatic hydrocarbons.

The term "sudden sniffing death" describes solvent
abusers who die suddenly after exertion, panic, or fright.
(The sudden release of catecholamines,asphyxia, respiratory depression,
and vagal inhibition.)
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The use of exogenous catecholamines, such as
epinephrine, may precipitate sudden
dysrhythmias and should be avoided except if
required for cardiac resuscitation.

Decreases in myocardial contractility and peripheral vascular
resistance as well as bradycardia and atrioventricular
conduction blocks have also been associated with volatile
solvent abuse.
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Hepatic Toxicity
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Halogenated hydrocarbons is well described.
Carbon tetrachloride toxicity has been used as a model
for toxin-induced hepatic dysfunction. As little as 3 mL
of carbon tetrachloride has been associated with the
development of fatal liver injury.“
Chloroform and methylene chloride, are also associated
with liver dysfunction. (Free-radical metabolites)
Pathologic examination reveals acute fatty
degeneration of the liver with areas of centrilobular
necrosis.
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Liver function tests may be elevated within 24 h after
ingestion,with the development of liver tenderness and
jaundice in 48 to 96 h.
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Chronic exposure to carbon tetrachloride may be
associated with the development of cirrhosis and
hepatomas.
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Renal and Metabolic Toxicity
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Solvent abuse and occupational exposure to
hydrocarbons may result in renal dysfunction.
Exposure to hepatotoxic halogenated hydrocarbons,
such as carbon tetrachloride, trichloroethylene, and
chlorinated paraffins, have caused acute renal failure,
Renal tubular acidosis may occur in patients who
abuse toluene containing substances.(Patients present with
a non-anion gap metabolic acidosis, hypokalemia, and
hypophosphatemia.)
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Significant rhabdomyolysis may also result.
Toluene toxicity may also cause a high anion gap
metabolic acidosis as a result of the accumulation of
hippuric acid and benzoic acid metabolites.
Proteinuria and renal insufficiency can occur in patients
who abuse toluene.
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Hematologic Toxicity
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Chronic exposure to benzene, the prototypical aromatic
hydrocarbon,is associated with an increased incidence
of hematologic disorders including aplastic anemia,
acute myelogenous leukemia, and multiple myeloma.
Although aplastic anemia is associated with glue sniffing,
this is most likely a result of the benzene fraction of the
glue, and not the toluene.
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Dermal Toxicity
Dermal exposure to hydrocarbons may also result in
toxicity.
 Cutaneous injury is most often associated with the
short-chain aliphatic,aromatic, and halogenated
hydrocarbons.
 Clinically, skin findings can range from local erythema,
papules, and vesicles to a generalized scarlatiniform
eruption and an exfoliative dermatitis.
 A "huffer's rash" may be noted over the face of patients
who chronically abuse the volatile hydrocarbons.
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Pruritus may also be present.
 Extensive partial-thickness and full-thickness
bums following immersion in hydrocarbons may also occur.
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TREATMENT
Prehospital
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Not all patients who have ingested hydrocarbons
require emergency department evaluation.
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patients who are asymptomatic or who quickly become
asymptomatic after ingestion can be watched safely at
home. (reliable follow-up can be ensured.)
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All symptomatic patients and intentional
exposures should be referred to the hospital for
further evaluation.
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Patients who ingest hydrocarbons that may
cause significant systemic toxicity (e.g.,
aromatic, halogenated hydrocarbons, or toxic
additives), whether or not symptomatic, should
also be referred to the hospital.

Volatile substance abusers and others exposed
to volatiles should have immediate cardiac
monitoring and advanced life support transport,
if available,because of the potential for lifethreatening dysrhythmias.
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Emergency Department

Establishing the airway and maintaining ventilation is the
critical first maneuver in any patient who presents with
respiratory depression and/or significant CNS
depression.
The detection of a sweet odor:
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Certain halogenated hydrocarbon exposures (especially chloroform
or trichloroethylene)
petrol odor suggests gasoline or some other petroleum derivative.
Continuous cardiac monitoring should be initiated,
and an electrocardiogram should be obtained.
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Hydrocarbon induced dysrhythmias, if present, would generally
occur shortly after the exposure, especially with inhalational use
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
Hypotension should be treated with aggressive fluid
resuscitation.
Catecholamines, such as dopamine,
norepinephrine, or epinephrine, should be
avoided to prevent precipitating dysrhythmias,
especially following exposure to halogenated
hydrocarbons and aromatic hydrocarbons.

The administration of glucose, thiamine, and naloxone
should be considered in cases of altered mental status

The patient needs to be fully undressed to prevent
ongoing contamination from hydrocarbon-soaked
clothes.
Dermal decontamination with soap and water,
eye decontamination with saline irrigation,should be
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Prehospital decontamination is preferable.
It is important for staff to wear protective gloves and aprons to
prevent possible secondary exposure, especially for
organophosphate containing mixtures.
Useful diagnostic tests include the chest x-ray and
arterial blood gas to detect pulmonary aspiration and
hypoxemia.
Abdominal radiographs may show evidence of
chlorinated hydrocarbon ingestions,such as carbon
tetrachloride, because ofthe radiopaque nature of these
polyhalogenated substances
Tests of liver and renal function should be obtained for
the development of hepatic and renal injury.
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
A carboxyhemoglobin level is useful to evaluate the
extent of endogenous carbon monoxide production
following methylene chloride exposure.

Pulse oximetry will not differentiate between oxyhemoglobin and
carboxyhemoglobin.
Routine drug screens are not useful for the detection of
hydrocarbons,
 In all intentional ingestions, an acetaminophen
level, ethanol level, anion gap, and osmolality may be
helpful in assessing for the presence of other
coingestants.
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Gastrointestinal Decontamination
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For most hydrocarbon ingestions, gastrointestinal decontamination
would provide little benefit;
The necessity for GI decontamination depends on the type of
hydrocarbon and route of exposure.
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supportive care and appropriate treatment of coexisting ingestions
are all that is required.
The majority of hydrocarbon ingestions, which consist of aliphatic
hydrocarbons mixtures do not require GI decontamination.
Gl decontamination may be warranted when the ingested
hydrocarbon is known to have good Gl absorption and may cause
significant systemic toxicity (e.g., toluene, chloroform, wood
distillates)or an additive in the toxic agent (e.g., organophosphate
pesticidesare often mixed in petroleum distillates).
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If the patient presents to the ED shortly after the
ingestion of these toxic hydrocarbons, aspiration with a
small nasogastric tube may be useful.
 In patients who present with an altered mental status,
the airway should be protected with a cuffed
endotracheal tube,
 In smaller children younger than 8 years of age, the cuff
should be kept inflated only during the period of lavage
because of cuff-related injury from prolonged inflation.
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Ipecac induced Emesis is contraindicated

Although activated charcoal may adsorb
somehydrocarbon compounds, its use is not
recommended for most hydrocarbon ingestions
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Charcoal instillation may distend the stomach increasing
the risk for vomiting and aspiration.
The use of charcoal should only be considered if one
of the CHAMP-type hydrocarbons has been ingested,
and extreme caution should be exercised because of
aspiration risk.
Many patients will already have diarrhea from the
hydrocarbon, and further catharsis is not required.
Oil-based cathartics, which had been used in the past
to thicken the ingested hydrocarbon to increase its
viscosity and decrease the subsequent risk of aspiration,
are contraindicated.
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Pulmonary Treatment
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Nebulized oxygen is helpful in the treatment of
pulmonary aspiration.
Inhaled B-agonists may also be useful, especially in the
setting of bronchospasm,( but their role in the treatment of
hydrocarbon pneumonitis has not been studied)
Positive end-expiratory pressure (PEEP) or continuous
positive-airway pressure (CPAP) may sometimes be
required, but because of the potential for further injury
from barotrauma,one should observe for the
development of pneumatoceles or pneumothorax.
In cases of severe pulmonary aspiration resulting in
refractory hypoxemia, treatment with extracorporeal
membrane oxygenation and high-frequency jet
ventilation has proved successful.
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Corticosteroids are contraindicated because they
impair the cellular immune response and increase the
chance of bacterial superinfection remains.
Antibiotics have no proven role in prophylaxis and
are usually not required except in cases of continued
pulmonary deterioration because of the risk of a
superimposed bacterial pneumonitis.
Nacetyl cysteine and hyperbaric oxygen may have a
role in preventing hepatic toxicity after carbon
tetrachloride (and possibly chloroform)exposure, but
more studies are needed.
Hyperbaric oxygen therapy may be indicated for
patients who develop significant carbon monoxide
toxicity after exposure to methylene chloride,
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B-blockers may be useful in the treatment of
hydrocarboninduced malignant dysrhythmias.
Although extracorporeal removal with hemodialysis,
hemoperfusion, or peritoneal dialysis has been
attempted for severe intoxications, clinically controlled
evidence of efficacy is lacking.
Specific antidotal treatment directed at the complications
of toxic additives, such as organophosphates, pyrethrins
or heavy metals, may also be needed.
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DISPOSITION
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Hospitalization is required for patients who have
ingested aliphatic hydrocarbons who are symptomatic at
the time of evaluation, and patients exposed to
significant amounts of methemoglobinemia-producing
hydrocarbons.
After a 6-h observation period, asymptomatic patients
with a normal chest x-ray may be discharged
home, but follow up should be assured as delayed
toxicity (18+ h) has been reported.
Similar disposition of asymptomatic patients, with
abnormal chest x-rays has also been suggested if
reliable follow-up can be ensured. Some physicians,
however, prefer to observe these patients for 24 h in the
hospital.
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
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Hospitalization is recommended for those who
ingest hydrocarbons capable of producing
delayed complications (e.g., halogenated
hydrocarbons causing hepatic toxicity) and
those with toxic additives (organophosphates
and organic metal compounds).
All patients taking ingestions with suicidal intent
or presenting with complications of solvent
abuse should have psychiatric evaluation.
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‫شاد باشید‬
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