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Hydrocarbons are a heterogenous group of organic substances that are primarily

composed of carbon and hydrogen molecules. They are quite abundant in
modern society. Some of the most commonly ingested hydrocarbons include
gasoline, lubricating oil, motor oil, mineral spirits, lighter fluid/naphtha, lamp oil,
and kerosene.[1] Other common sources of hydrocarbons include dry cleaning
solutions, paint, spot remover, rubber cement, and solvents. In addition, many
volatile substances that contain hydrocarbons (eg, glue, propellants) are
commonly abused for their euphoric effects.
Hydrocarbons can be classified as being aliphatic, in which the carbon moieties
are arranged in a linear or branched chain, or aromatic, in which the carbon
moieties are arranged in a ring. Halogenated hydrocarbons are a subgroup of
aromatic hydrocarbons, in which one of the hydrogen molecules is substituted by
a halogen group. The most important halogenated hydrocarbons include carbon
tetrachloride, trichloroethylene, tetrachloroethylene, trichloroethane, chloroform,
and methylene chloride.
The hydrocarbons can be derived from either petroleum or wood. Petroleum
distillates include kerosene, gasoline, and naphtha, whereas wood-derived
hydrocarbons include turpentine and pine oil. The length of the chains as well as
the degree of branching determine the phase of the hydrocarbon at room
temperature; most are liquid, but some short-chain hydrocarbons (eg, butane)
are gas at room temperature, whereas other long-chain hydrocarbons (eg,
waxes) are solid at room temperature.
Toxicity from hydrocarbon ingestion can affect many different organs, but the
lungs are the most commonly affected organ. The chemical properties of the
individual hydrocarbon determine the specific toxicity, while the dose and route
of ingestion affect which organs are exposed to the toxicity. Unlike the aromatic
or aliphatic hydrocarbons, the halogenated hydrocarbons tend to cause a wider
range of toxicity.
The recreational use of inhaling hydrocarbons and other volatile solvents for the
purposes of creating a euphoric state is becoming increasingly common. Several
methods are used for this abuse, including "sniffing" (directly inhaling vapors),
"huffing" (placing a hydrocarbon-saturated rag over the mouth and nose and
then inhaling), or "bagging" (inhaling via a plastic bag filled with hydrocarbon

The toxicity of hydrocarbons is directly related to their physical properties,
specifically the viscosity, volatility, surface tension, and chemical activity of the
side chains. The viscosity is a measure of resistance to flow and is measured in
Saybolt Seconds Universal (SSU). Substances with a lower viscosity (SSU < 60,
eg, turpentine, gasoline, naphtha) are associated with a higher chance of

aspiration. The surface tension is a cohesive force created by van der Waals
forces between molecules and is a measure of a liquid's ability to "creep." Like
the viscosity, the surface tension is also inversely related to aspiration risk; the
lower the viscosity, the higher the risk of aspiration. The viscosity is the single
most important chemical property associated with the aspiration risk. [2]
Volatility is the tendency for a liquid to change phases and become a gas.
Hydrocarbons with a high volatility can vaporize and displace oxygen, which can
lead to a transient state of hypoxia. Not surprisingly, the degree of volatility is
directly related with the risk of aspiration. The amount of hydrocarbon ingested
has not consistently been linked to the degree of aspiration and hence
pulmonary toxicity.
Toxicity from hydrocarbon exposure can be thought of as different syndromes,
depending on which organ system is predominately involved. Organ systems that
can be affected by hydrocarbons include the pulmonary, neurologic, cardiac,
gastrointestinal, hepatic, renal, dermatologic, and hematologic systems. The
pulmonary system is the most commonly involved system.[3]
Pulmonary complications, especially aspiration, are the most frequently reported
adverse effect of hydrocarbon exposure. While most aliphatic hydrocarbons have
little GI absorption, aspiration frequently occurs, either initially or in a
semidelayed fashion as the patient coughs or vomits, thereby resulting in
pulmonary effects. Once aspirated, the hydrocarbons can create a severe
Hydrocarbon pneumonitis results from a direct toxic affect by the hydrocarbon on
the lung parenchyma. The type II pneumocytes are most affected, resulting in
decreased surfactant production. This decrease in surfactant, results in alveolar
collapse, ventilation-perfusion mismatch, and hypoxemia. Hemorrhagic alveolitis
can subsequently occur, which peaks 3 days after ingestion. [4] The end result of
hydrocarbon aspiration is interstitial inflammation, intra-alveolar hemorrhage
and edema, hyperemia, bronchial necrosis, and vascular necrosis. Rare
pulmonary complications include the development a pneumothorax,
pneumatocele, or bronchopleural fistula.[5]
Nervous system
CNS toxicity can result from several mechanisms, including direct injury to the
brain or indirectly as a result of severe hypoxia or simple asphyxiation.
Many of the hydrocarbons that affect the CNS directly can make their way across
the blood-brain barrier because certain hydrocarbons are highly lipophilic. In
addition, for individuals who are huffing or bagging, the act of rebreathing can
result in hypercarbia, which can contribute to decreased level of arousal.
Prolonged abuse of hydrocarbons can result in white matter degeneration
(leukoencephalopathy) and atrophy. [6] [7] In addition, prolonged exposure to

certain hydrocarbons (eg, n -hexane or methyl-n -butyl ketone [MnBK]) can result
in peripheral neuropathy, blurred vision, sensory impairment, muscle atrophy,
and parkinsonism.[8]
Exposure to hydrocarbons can result in cardiotoxicity. [9]
Most importantly, the myocardium becomes sensitized to the effects of
catecholamines, which can predispose the patient to tachydysrhythmias, which
can result in syncope or sudden death.
Many of the hydrocarbons create a burning sensation because they are irritating
to the GI mucosa. Vomiting has been reported in up to one third of all
hydrocarbon exposures.


The chlorinated hydrocarbons, in particular carbon tetrachloride, are hepatotoxic.

Usually, the hepatotoxicity results after the hydrocarbon undergoes phase I
metabolism, thereby inducing free radical formation. These free radicals
subsequently bond with hepatic macromolecules and ultimately cause lipid
peroxidation. This metabolite creates a covalent bond with the hepatic
macromolecules, thereby initiating lipid peroxidation.
The common histopathologic pattern is centrilobular (zone III) necrosis.
Liver function test results can be abnormal within 24 hours after ingestion, and
clinically apparent jaundice can occur within 48-96 hours.
Methylene chloride, a hydrocarbon commonly found in paint remover, is
metabolized via the P450 mixed function oxidase system in the liver to carbon
monoxide (CO). Unlike other cases of CO exposure, with methylene chloride, CO
formation can continue for a prolonged period of time.
Chronic exposure to toluene, an aromatic hydrocarbon, can result in a distal renal
tubular acidosis and present with an anion gap acidosis. A patient may have
chronic exposure either via an occupational environment or by repeated
recreational inhalation.
Prolonged exposure to certain aromatic hydrocarbons (especially benzene) can
lead to an increased risk of aplastic anemia, multiple myeloma, and acute
myelogenous leukemia. In addition, hemolysis has been reported following the
acute ingestion of various types of hydrocarbons.

In cases of suspected hydrocarbon intoxication, it is important to determine the
agent ingested, the route of ingestion (eg, oral, dermal, inhalational) the amount
of substance ingested, and the time of the ingestion. In addition, the history
should include questions about co-ingestants, any vomiting or coughing prior to
arrival, and any attempt to treat the patient prior to arrival.
Respiratory distress
The lung is the primary site of most common toxicity following hydrocarbon
exposures. Pulmonary toxicity most often occurs following ingestion and
subsequent aspiration of hydrocarbon. Respiratory symptoms (eg, coughing,
gagging, choking) usually occur within 30 minutes of exposure but often can be
delayed several hours.
Many patients develop a transient cough. A prolonged cough and hypoxia,
however, is more concerning for aspiration. Lack of coughing does not exclude
the possibility of aspiration.
Nervous system
The most common CNS symptoms include headache, lethargy, and decreased
mental status. Nonspecific symptoms such as weakness and fatigue may also be
Because many of the solvents are highly lipophilic, solvent abuse causes a
transient euphoria.
With prolonged exposure to n -hexane, MnBK, and possibly toluene, an
axonopathy can occur. This peripheral neuropathy usually begins in the
extremities and then progresses more proximally.
The patient may complain of dyspnea or syncope.
In addition, because of sensitization of the myocardium to catecholamines, a
relatively young and previously healthy patient can present in full cardiac arrest
after being suddenly startled or following strenuous athletic events. A common
scenario for the cardiac arrest patient is the teenager who is huffing, or bagging
alone in a dark room, who then gets startled when a parent opens the door. This
"sudden sniffing death syndrome" results in ventricular fibrillation or ventricular
tachycardia, following a large catecholamine exposure to a myocardium that is
already sensitized to the effects of the catecholamines. This syndrome is more
common following exposure to the halogenated hydrocarbons, but it can occur
following exposure to aromatic hydrocarbons as well.

Nausea, vomiting, and sore throat are frequent but are relatively mild.
Local reactions such as a burning sensation in the mouth, pruritus, or a perioral
rash are not uncommon and are usually mild.
Diarrhea, melena, and hematemesis are rare.

Prior to instituting the physical examination, the patient should be appropriately
decontaminated, if indicated.
The physical examination should focus on the patient's airway, breathing, and
circulation (ABCs).
Patients who are experiencing any respiratory compromise should be placed on
supplemental oxygen. For those patients who are in severe respiratory distress,
or who are too lethargic to be able to adequately protect their airway, advanced
airway management may be required.



















Lethargy to coma


GI - Nausea/vomiting




Nasal dermatitis or perioral dermatitis (with chronic abuse)

Skin irritation (with single use) at an intravenous, intramuscular, or

subcutaneous injection site

Hydrocarbon exposure can be divided into the following 4 broad categories:

Nonintentional nonoccupational exposure: Accidental ingestions are the most frequent type
and commonly involve young children tasting a hydrocarbon. Typically, children do not drink large
quantities, as hydrocarbons generally taste bad. Adults and older children occasionally consume a
hydrocarbon if liquid is placed in an unlabeled can or bottle resulting in accidental ingestion.
Recreational exposure: Inhaling of hydrocarbons or other volatile solvents for the purpose of
producing a transient state of euphoria is becoming more common. This pattern of use is most
common in junior high and high-school aged children.
Occupational exposure: This type of exposure is most often industrial, where a worker has
either a dermal exposure to the liquid or an inhalational exposure to the vapors.
Intentional: This type of exposure usually involves consuming a large amount of the
hydrocarbon as an oral ingestion during a suicide attempt.


Respiratory Distress Syndrome, Adult

Toxicity, Alcohols

Toxicity, Barbiturate

Toxicity, Benzodiazepine

Toxicity, Toluene

Laboratory Studies
The workup depends on the exposure.

Pulse oximetry should be performed on all patients to evaluate oxygenation.

Complete blood count

Chronic benzene exposure may produce either acute myelogenous leukemia or aplastic anemia.
In the acute ingestion, leukocytosis can occur.
Anemia can occur as a result of intravascular hemolysis.
A CBC should be ordered if there is concern for any of the above findings. However, it is not
necessary to routinely obtain a CBC in all hydrocarbon exposures.

A routine basic metabolic panel should be performed to determine the BUN, creatinine, glucose,
electrolytes, and anion gap.
Any patient appearing intoxicated should have the serum glucose level checked expeditiously.
The anion gap will most likely be normal, but in acute toluene intoxication, an elevated anion gap can
be present. The presence of an anion gap, especially if associated with a profound acidosis in a
patient appearing intoxicated, however, should prompt an evaluation for other etiologies (eg,
methanol,ethylene glycol, salicylates).
Acute renal failure following massive hydrocarbon ingestion can occur but is rare.
Testing of the hepatic transaminase levels should be performed, as these can be elevated following
hydrocarbon ingestion (particularly the halogenated hydrocarbons).
A serum creatine kinase (CK) level should be obtained, as acuterhabdomyolysis has been reported in
association with isolated hydrocarbon intoxication.
Specific diagnostic testing for hydrocarbon poisonings is available, but it is unlikely to be clinically
helpful, as these tests are not routinely available

Imaging Studies
Chest radiography
All symptomatic patients should have a chest x-ray performed.
Patients who are asymptomatic (eg, no coughing or signs/symptoms of respiratory distress) should
not have a chest radiograph obtained immediately. Rather, asymptomatic patients should have chest
radiography performed at the end of a 6-hour observation period.
See the image below.

Anteroposterior view of the chest of 14-month-old boy 30 hours after ingesting

lamp oil. Note the central right lower lobe infiltrate obscuring the right heart border.

Other Tests

An electrocardiogram should be obtained to assess for arrhythmias, especially in those

individuals with suspected hydrocarbon abuse (ie, individuals who were huffing or bagging).

Prehospital Care

Prehospital care should focus on decontamination, followed by immediate transport to a

medical facility capable of managing such a patient. GI decontamination has no role in prehospital
care. Decontamination should focus on removing any remaining hydrocarbon that might be on the
clothes or skin, in the correct clinical setting.
Patients should be kept calm to prevent arrhythmia as a result of myocardial sensitization.
All patients should have their airway, breathing, and circulation managed per routine
advanced life support protocols.
Symptomatic patients should receive intravenous access and cardiac monitoring.
The hydrocarbon agent should be transported with the patient to the hospital, if this can be
done in a safe manner. Bringing the substance to the hospital can permit identification.

Emergency Department Care

Management for hydrocarbon intoxication is largely supportive.
Asymptomatic patients should be observed with continual pulse-oximetry for a period of at least 6
hours. If the patient remains asymptomatic (eg, no coughing, vomiting, tachypnea, or other evidence
of respiratory difficulties), then a chest radiograph may be obtained to evaluate for aspiration.
Other etiologies of altered mental status should be investigated as deemed clinically appropriate by
the treating clinician.
Patients who show signs of impending respiratory failure despite supplemental oxygen may
require rapid sequence intubation for definitive airway management. Intubation and positive pressure
ventilation may be required for evidence of on-going respiratory distress.
If arrhythmias occur, electrolytes, including magnesium and potassium, should be replaced.
If ventricular fibrillation occurs, and the thought is that the arrhythmia is because of myocardial
sensitization, catecholamines, including epinephrine, should be avoided. In this setting, lidocaine or
beta-blockers can be used.

Decontamination of the GI tract remains controversial.

The use of ipecac-induced emesis is contraindicated, and activated charcoal does not absorb
hydrocarbons well.
Gastric lavage should not be routinely performed.
The hydrocarbons with significant systemic toxicity for which the benefits of gastric decontamination
may outweigh the real risks of inducing aspiration follow the mnemonic CHAMP:

Camphor (toxicity is seizures)

Halogenated hydrocarbons (toxicity is arrhythmias and hepatotoxicity)
Aromatic hydrocarbons (toxicity is CNS toxicity, myelosuppression, and malignancy)
Metals (heavy metals)
Pesticides (cholinergic symptoms, seizures)
Antibiotics are frequently given to patients who develop a pneumonitis following hydrocarbon
aspiration. In animal models, the empiric administration of antibiotics altered the lung flora compared
with controls and did not yield any benefit. Clinically, superinfection can definitely occur. Because the
pneumonitis itself can create abnormal lung sounds, fever, and leukocytosis, distinguishing if these
effects are because of a superimposed infection or if they are the result of the pneumonitis itself is
often difficult. Any finding on a chest radiograph within a few hours of the exposure, however, is
unlikely to be pneumonia, and much more likely to be a pneumonitis.
Steroids have not been proven to be beneficial.
Several commercial surfactant preparations are available for use with other conditions, such as
hyaline membrane disease (HMD). Animal data on its use demonstrate conflicting results, and
currently no human data exist to support its routine use.

Further Inpatient Care

Following a 6-hour observation period during which a patient has a normal chest radiograph
and never developed any symptoms (including coughing, vomiting, respiratory difficulty) of
hydrocarbon exposure, the patient can be safely discharged home with close follow-up (reevaluation
in 24 h).
Patients who develop any symptoms of hydrocarbon exposure during the 6-hour observation
should be admitted to a unit capable of continuous pulse oximetry.
Patients should be closely observed for any evidence of respiratory deterioration.
Patients with radiographic evidence of pneumonitis should receive repeat chest radiographs
every 24 hours (or sooner, if clinically indicated) to ensure the pneumonitis is not progressing.

Antiarrhythmic Agent, Class II

Class Summary

These agents inhibit chronotropic, inotropic, and vasodilatory response to beta-adrenergic


View full drug information

Propranolol (Betachron E-R, Inderal, InnoPran XL)

Class II antiarrhythmic, nonselective, beta-adrenergic, receptor blocker with membranestabilizing activity that decreases automaticity of contractions.

Effective for treating aggression resulting from head injury. Also used for reducing
restlessness and disinhibition. Treatment for persistent agitation and aggression in organic
brain syndromes.

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Esmolol (Brevibloc)

Short-acting IV cardioselective beta-adrenergic blocker with no membrane depressant

activity. Half-life of 8 min allows for titration to effect and quick discontinuation prn.