Hydrocarbons
Perspective
Human exposure to hydrocarbons (HCs) is a common problem. In 2010, U.S. poison centers reported 43,000 exposures to HCs, with the majority of cases managed in an outpatient setting.1 Exposure to HCs of patients who present to the emergency department (ED) can generally be classified into four types. The first is the accidental ingestion involving children younger than 5 years. This is the most common scenario causing fatality, and it usually involves significant pulmonary injury. Second is the intentional inhalational abuse of volatile HCs. Recreational abuse has been a medical problem since solvent inhalation became popular during the late 1800s. Fatalities in this group will typically occur within distinct demographic groups (Native Americans, homosexual men, and teenagers).1–3 Third is the accidental inhalational or dermal exposure to HCs in the household or workplace setting. The fourth type is massive oral ingestion of HCs in a suicide attempt.
Principles of Disease
HCs are a diverse group of organic compounds that contain hydrogen and carbon (Table 158-1). Most HCs (e.g., gasoline) are byproducts of crude oil and are therefore called petroleum distillates. Some products, such as turpentine, are derived from pine oil, not petroleum. HCs can also be classified by their structure. The two main categories are straight chain HCs (aliphatic, such as propane) and those containing a benzene ring structure (aromatic, such as toluene). HCs can also have multiple nonorganic side chains. For example, halogenated HCs usually will have one or more bromide, chloride, fluoride, or iodide moieties (e.g., carbon tetrachloride). Finally, HCs are used as the solvent base for many toxic chemicals, such as insecticides and metals, that in turn can cause a separate distinct syndrome of poisoning. Although the range of toxicity of HCs can vary widely, the majority of human exposures are confined to petroleum distillates.
Pathophysiology
Acute HC toxicity usually affects three main target organs: the lungs, the heart, and the central nervous system (CNS). Although certain HCs can enter the body through the skin or gastrointestinal tract, HCs cause the most damage through the lungs. Despite the fact that there are thousands of different types of HCs, their potential for acute toxicity depends on four characteristics4,5:
1. Viscosity is the capacity to resist flow or change. Low viscosity allows a substance to spread rapidly, and low-viscosity HCs spread easily into the airway and lungs. Viscosity is measured in Saybolt seconds universal (SSU), and substances with an SSU of less than 60 have the highest potential risk of aspiration. Lubricants and mineral oil have high viscosity and low toxicity, whereas furniture polish has low viscosity and high pulmonary toxicity.
2. Volatility is the ease for a liquid to turn into a gas. High volatility often has a detectable odor. HCs with high volatility can displace alveolar oxygen and cause hypoxia. Butane and propane are types of HCs with high volatility.
3. Surface tension is the capacity for a substance to collect on a liquid surface. Low surface tension enables a substance (e.g., turpentine) to disperse easily.
4. Chemical side chains often increase potential toxicity. These toxic side chains include metals (e.g., arsenic), halogens (e.g., carbon tetrachloride), and aromatic structures (e.g., toluene).
Pulmonary Pathophysiology
The primary target organ for toxicity is the lung. Fatalities after ingestion usually occur with an accompanying aspiration. A small amount of HC in the trachea can be devastating, whereas a much larger amount of the same compound in the stomach remains benign.1,5,6
HCs affect the lungs through several mechanisms. HCs are usually poorly water soluble and penetrate into the lower airways, producing bronchospasm and an inflammatory response. Second, volatized HCs can displace oxygen in the alveolar space, causing hypoxia. Third, HCs can cause direct injury to pulmonary alveoli and capillaries, producing distinct uniform lesions. Autopsy findings of these lesions include hyperemia, diffuse hemorrhagic exudative alveolitis with granulocytic infiltration, and microabscesses. Finally, HCs can inhibit surfactant function, leading to alveolar instability and collapse. These mechanisms lead to alveolar dysfunction, ventilation-perfusion mismatch, hypoxemia, and respiratory failure.5,6
Central Nervous System Pathophysiology
Certain HCs cause CNS depression (i.e., toluene, benzene, gasoline, butane, and chlorinated HCs). After respiratory exposure, most HCs passively diffuse through the pulmonary alveolus and are highly absorbed in blood and tissues. These HCs can cause euphoria, disinhibition, confusion, and obtundation. With an isolated single exposure, these effects usually have a rapid onset of intoxication and rapid recovery. For these reasons, substance abusers seek these HCs for recreational use. Inhalation of these substances avoids hepatic first-pass metabolism and generates high concentrations in the CNS. Chronic use of inhaled HCs can cause severe abnormalities in nervous system function, which include peripheral neuropathy, cerebellar degeneration, neuropsychiatric disorders, chronic encephalopathy, and dementia. More than 50% of patients who abuse toluene for more than 10 years will have cerebral cortical atrophy with histologic changes that include loss of neurons, diffuse gliosis, and axonal degeneration.3,7
Cardiac Pathophysiology
HCs can precipitate sudden death, especially after intentional inhalation. These compounds are thought to produce myocardial sensitization of endogenous and exogenous catecholamines, which then precipitates ventricular dysrhythmias and myocardial dysfunction. This is particularly true for halogenated and aromatic HCs (e.g., difluoroethane found in computer keyboard cleaning canisters).2,8
