Hydrocarbon (HC) is widely used in our community where they are found in homes, they provide power for vehicles, and are widely used in every industrial process. In developing nations, kerosene is implicated in more than 33% of pediatric poisonings. Proportionately more fatalities are associated with children younger than 5 years, who often accidentally ingest hydrocarbons (HCs) and adolescents, who are more likely to abuse volatile HCs than any other age group.
HCs are organic compounds that are made primarily of carbon and hydrogen molecules. HCs are formed by distilling petroleum or wood and consist of aliphatic (carbon chain) or aromatic (carbon ring) molecules. Toxicity results from the volatility and viscosity of an HC product and the chemical characteristics of the HC and any additives.
HC toxicity is divided readily into clinical syndromes based on the organ system most severely affected. The lungs are affected most commonly, but instances of neurologic, cardiac, gastrointestinal, renal, hematologic, and skin pathology are well documented. The dose and route of exposure affect which systems are impacted and the severity of toxicity.
How does it cause toxicity?
The toxicity of HCs is a function of the individual compound's viscosity, volatility, surface tension, and the chemical activity of any side chains. Less viscous compounds spread more easily and, thus, are more toxic. A patient who ingests turpentine or gasoline is more likely to aspirate than a patient who has ingested grease or petroleum jelly. Similarly, a compound with low surface tension readily disperses itself, increasing the risk of aspiration. The substances with the highest volatility are readily inhaled and can displace oxygen. Side chains may include halogens, aromatic HCs, or heavy metals (e.g., arsenic).
Pulmonary toxicity usually results from aspiration or diffusion of ingested HC. Even small amounts of HC may cause a chemical pneumonitis; because many HCs have poor water solubility, they penetrate deep into the bronchopulmonary tree, causing bronchospasm followed by an inflammatory response. In the alveoli, volatile HCs may displace oxygen and surfactant, leading to hypoxia and a diffuse hemorrhagic exudative alveolitis. Alveolar dysfunction, in turn, leads to ventilation-perfusion ratio (V/Q) mismatch, hypoxemia, and, possibly, resultant respiratory failure.
Most HCs cause direct mucosal irritation and are absorbed quickly across tissue layers. Some can cause chemical burns. Ingestion causes burning pain in the mouth and throat, abdominal pain, nausea, and vomiting. Emesis increases the risk of aspiration. In animal studies, very large volumes of HC were required for significant absorption from the GI tract.
HCs are lipophilic and, thus, are attracted to lipid-rich neural tissue. Systemic absorption of HCs can cause acute and chronic central nervous system (CNS) and peripheral nervous system (PNS) toxicity. Demyelinating peripheral polyneuropathy is associated with exposure to certain 6-carbon aliphatic HCs (e.g., n-hexane, methyl n-butyl ketone) that are metabolized into a compound that interferes with axonal transport. Long-term workplace exposure to other HCs or volatile HC abuse may result in chronic headaches, cerebellar ataxia, and encephalopathic findings of cognitive and psychopathic impairment.
Certain volatile agents, such as butane, benzene, toluene, and xylene, are acute CNS depressants and have a disinhibiting euphoric effect. They often are agents of abuse. Patients present with symptoms of CNS disinhibition, such as dizziness, slurred speech, ataxia, and even obtundation. Ventilatory drive may be compromised. The initial presentation may mimic alcohol intoxication. In some patients, an initial component of CNS stimulation may present as agitation, tremor, or seizure. High concentrations of HC sensitize the myocardium to catecholamines, which predisposes the patient to ventricular tachycardia or fibrillation. This is the cause of "sudden sniffing death," which may occur when abusers suddenly exert themselves following HC intoxication.
HCs are abused through "sniffing" (directly inhaling vapors), "huffing" (placing a saturated rag over the mouth and nose and inhaling), or "bagging" (placing the HC in a plastic bag and repeatedly inhaling the vapors). Volatile HCs also are associated with atrioventricular block and bradycardia. Some agents may decrease cardiac contractility and peripheral vascular resistance.
What are the common signs and symptoms associated with hydrocarbon toxicity?
The information regarding the toxicity is very important. This information should include:
the specific agent and amount, co-ingestion, the time of exposure, and the symptoms of toxicity
Some of the most commonly occurring symptoms are respiratory distress, CNS abnormalities, cardiovascular complaints, GI distress, and local skin reactions.
The lung is the primary site of life-threatening toxicity in HC exposures. Pulmonary toxicity most often occurs following ingestion and aspiration of an HC. Respiratory symptoms generally, but not always, develop within 30 minutes of a significant ingestion. Coughing, choking, gasping, dyspnea, vomiting, tachypnea, grunting respirations, cyanosis, or coma suggests a history consistent with aspiration.
Transient coughing is common in HC ingestion because of volatilization. Prolonged cough usually indicates aspiration; however, the absence of cough does not rule out aspiration.
Lethargy and depressed sensorium are the most common CNS symptoms. They may be associated with significant aspiration pneumonitis or caused by toxic additives from large intestinal ingestions.
Solvent abuse (deliberate concentration and inhalation of vapors) causes a transient euphoria because of CNS effects.
Dyspnea, syncope, and sudden cardiac death may result from arrhythmias. This is believed to be caused by HCs sensitizing the myocardium to catecholamines.
A relatively young healthy patient may present in full arrest after engaging in strenuous athletic events following solvent abuse.
Nausea, vomiting, and sore throat are frequent with large ingestions but are relatively mild. GI complaints are more common with furniture polish than with other HC ingestions.
Diarrhea, melena, and hematemesis are rare.
Local reactions such as burning of the mouth, pruritus, or rash are common and generally mild.
Physical examination is crucial and should focus on the patient’s airway, breathing, and circulation (ABCs). Urgently triage patients with signs of respiratory distress and place them in a room where airway management equipment is readily available.
Odor on breath or clothes from HCs is a common finding.
Fever often is present but does not correlate with clinical symptoms.
Tachypnea, grunting respirations, accessory muscle use, riles, wheezing indicates pulmonary toxicity. Hypoxia is observed with severe aspiration pneumonia and may lead to cardiac and CNS dysfunction.
Cardiac toxicity is rare with acute ingestion. Evidence of cardiac toxicity includes tachycardia, cardiac dysrhythmias, and hypotension.
Coma is uncommon. It is present in fewer than 3% of hospitalized patients. Depressed sensorium and lethargy are observed with serious aspiration pneumonias.
Skin lesions, such as erythema, blistering, and pain, are common after dermal exposures. Chronic solvent abusers may have perioral and nasal irritant dermatitis or conjunctivitis from repeated contact with HCs. Patients may present with dermal irritation and destruction following injection of HC either subcutaneously or intravenously from suicide attempts or for recreational purposes.
What are the main reasons for hydrocarbon toxicity?
Causes of HC exposure can be divided into 4 main categories, as follows:
Accidental ingestion is the most common cause of HC exposure.
Typically observed in children younger than 5 years who have access to HCs without supervision
Also observed in adults and older individuals when HCs are placed in unlabeled containers (e.g., beverage cans)
Intentional abuse for recreational purposes is observed most commonly in adolescents and young adults. It is common in minority populations and adolescents with a history of polysubstance abuse, adjustment disorders, and rebellion.
Accidental exposures in the household or workplace are generally limited and involve dermal and inhalational exposure.
Massive oral ingestions are associated with suicide attempts.
What are the laboratory studies that should be done for hydrocarbon toxicity?
Laboratory evaluation should be done in order to rule out some of the other possibilities. These studies are:
Arterial blood gases
Abnormalities include hypoxemia and hypocarbia caused by V/Q mismatch.
Methemoglobinemia may be observed following exposure to nitrite-containing HCs (e.g., aniline, nitrobenzene).
Complete blood count
Leukocytosis is common within the first 48 hours.
Anemia and thrombocytopenia from intravascular hemolysis and consumptive coagulopathy is rare.
Chronic exposure to benzene is linked to aplastic anemia and acute myelogenous leukemia.
Electrolytes, blood urea nitrogen, creatinine
Hypomagnesemia, hypophosphatemia potassium abnormalities, and anion gap acidosis are observed with toluene exposure.
Acute renal failure in massive HC exposure is rare.
Hepatic function: Elevated aminotransferases may be observed with HC ingestions. The halogenated HCs are particularly hepatotoxic.
Urinalysis: Urinalysis usually is normal; however, renal failure is documented with HC exposure and a baseline urinalysis may be helpful for substantial exposures.
Creatine kinase: Acute rhabdomyolysis reported in association with isolated HC exposure, particularly toluene exposures, is rare.
Chest x-ray: Radiographic abnormalities generally occur within 30 minutes of significant aspiration but may be delayed for up to 12 hours. Approximately 75% of patients hospitalized for suspected HC aspiration have radiographic abnormalities. Radiographic abnormalities may lag behind clinical evaluation and often do not correlate with clinical presentation. A right lower lobe infiltrate is classic for aspiration pneumonia, but consider any evidence of an alveolar infiltrate as evidence of aspiration in an HC exposure. Radiographic abnormalities progressively worsen for the first 72 hours and then resolve over several days.
Obtain an ECG on all substantial HC ingestions. Individuals with solvent abuse are particularly prone to arrhythmias. Observe patients on cardiac monitors.
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