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Pathophysiology
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
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
pneumonitis.
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]
Cardiovascular
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.
Gastrointestinal
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.
Hepatic
[10]
History
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
reported.
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.
Cardiovascular
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.
Gastrointestinal
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.
Physical
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.
Respiratory
Coughing
Gagging
Choking
Tachypnea
Hemoptysis
Rales
Rhonchi
Wheezes
Hypoxia
Cyanosis
Cardiovascular
Tachycardia
Dysrhythmias
Hypotension
CNS
Headache
Ataxia
Weakness
Lethargy to coma
Seizures
GI - Nausea/vomiting
Dermal
Erythema
Blistering
Pain
Causes
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.
Differentials
Toxicity, Alcohols
Toxicity, Barbiturate
Toxicity, Benzodiazepine
Toxicity, Toluene
Laboratory Studies
The workup depends on the exposure.
Chemistries
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.
Other Tests
Prehospital 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.
Class Summary
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.
Esmolol (Brevibloc)