Ingestion or aspiration of hydrocarbons mainly impairs the pulmonary system, but depending on the specific compound, the central nervous, peripheral nervous, GI, cardiovascular, renal, hepatic, dermal, and/or hematologic systems may be affected (Table 199-3).13
TABLE 199-3Clinical Manifestations of Hydrocarbon Exposure ||Download (.pdf) TABLE 199-3 Clinical Manifestations of Hydrocarbon Exposure
|System ||Clinical Manifestations |
|Pulmonary ||Tachypnea, grunting respirations, wheezing, retractions |
|Cardiac ||Ventricular dysrhythmias (may occur after exposure to halogenated hydrocarbons and aromatic hydrocarbons) |
|Central nervous ||Slurred speech, ataxia, lethargy, coma |
|Peripheral nervous ||Numbness and paresthesias in the extremities |
|GI and hepatic ||Nausea, vomiting, abdominal pain, loss of appetite (mostly with halogenated hydrocarbons) |
|Renal and metabolic ||Muscle weakness or paralysis secondary to hypokalemia in patients who abuse toluene |
|Hematologic ||Lethargy (anemia), shortness of breath (anemia), neurologic depression/syncope (carbon monoxide from methylene chloride), cyanosis (methemoglobinemia from amine-containing hydrocarbons) |
|Dermal ||Local erythema, papules, vesicles, generalized scarlatiniform eruption, exfoliative dermatitis, "huffer's rash," cellulitis |
Hydrocarbon aspiration causes chemical pneumonitis by direct toxicity to the pulmonary parenchyma and alteration of surfactant function. Destruction of alveolar and capillary membranes results in increased vascular permeability and edema. The clinical manifestations of pulmonary aspiration are usually apparent soon after exposure from irritation of the oral mucosa and tracheobronchial tree. Symptoms include coughing, choking, gasping, dyspnea, and burning of the mouth. Patients with these symptoms should be assumed to have aspirated.
Signs include tachypnea, grunting respirations, wheezing, or retractions depending on the severity of aspiration. An odor of the hydrocarbon may be noted on the patient's breath. Hyperthermia of ≥39°C (≥102.2°F) is likely and may occur initially or 6 to 8 hours after exposure. The fever is usually an inflammatory response due to pneumonitis. Necrotizing pneumonitis and hemorrhagic pulmonary edema may develop within minutes to hours in patients with severe aspiration. In most fatalities, these complications occur rapidly. With less severe damage, symptoms usually subside within 2 to 5 days, except in the case of pneumatoceles and lipoid pneumonias, the symptoms of which may persist for weeks to months.
Although in most patients with clinically significant aspiration chest radiographic results eventually are abnormal, the time course of radiographic changes varies, and correlation with physical examination findings may be poor. Changes may be seen as early as 30 minutes after aspiration, but the initial radiograph in a symptomatic patient may be deceptively clear. Conversely, an asymptomatic patient can still have abnormal chest radiographic findings later during the clinical course. Radiographic changes usually appear by 2 to 6 hours and are almost always present by 24 hours, if they are to occur (Figure 199-1). The most common radiologic finding is bilateral infiltrates at the bases with multilobar involvement more common than single-lobe involvement and right-sided involvement more common than left-sided involvement.14,15,16 Hydrocarbon-induced aspiration pneumonitis can lead to lung necrosis and the creation of a pneumatocele.17
Two chest radiographs of a child who aspirated lamp oil and developed aspiration pneumonitis. A. Day 1: intubated, left lower lobe infiltrates. B. Day 3: intubated, worsening perihilar and bibasilar patchy infiltrates and new right small pleural effusion.
Life-threatening dysrhythmias, such as ventricular tachycardia and ventricular fibrillation, may occur with systemic absorption. Dysrhythmias occur most commonly after exposure to halogenated hydrocarbons and aromatic hydrocarbons. Exposure to short-chain aliphatic hydrocarbons occasionally causes dysrhythmias (ventricular fibrillation).10 The most worrisome acute complication found in solvent abusers is "sudden sniffing death syndrome" and occurs within minutes of exposure.8 The mechanism of toxicity is believed to be catecholamine sensitization of the heart by hydrocarbons (especially halogenated hydrocarbons), resulting in ventricular dysrhythmias.8,10,18 Other mechanisms for sudden death include simple asphyxia, respiratory depression, and vagal inhibition. Ventricular akinesia and polymorphic ventricular dysrhythmias have also been described after overdose of chloral hydrate (a halogenated aliphatic hydrocarbon).18
CNS effects, primarily depression of consciousness, result from: (1) a direct toxic response to the systemic absorption of the hydrocarbon, (2) an indirect result of severe hypoxia secondary to aspiration, (3) simple asphyxiation due to the displacement of oxygen by the volatile hydrocarbon, and/or (4) volatile substance abuse with a plastic bag that prevents adequate oxygenation. Systemic effects occur through GI absorption, the inhalation of highly volatile petroleum distillates, or direct dermal penetration.
Signs of neurologic toxicity include slurred speech, ataxia, lethargy, and coma.13 Although hydrocarbons are central neurologic depressants, they often have an initial excitatory effect manifested as hallucinations, tremor, agitation, and convulsions. Individuals who abuse volatile solvents or workers who experience long-term hydrocarbon exposure may present to the ED complaining of recurrent headaches, ataxia, emotional lability, cognitive impairment, or psychomotor impairment.
PERIPHERAL NERVOUS SYSTEM TOXICITY
Exposure to n-hexane, methyl n-butyl ketone, and other six-carbon aliphatic hydrocarbons is associated with the development of a characteristic peripheral polyneuropathy caused by demyelinization and retrograde axonal degeneration.19 Onset of symptoms may be delayed for weeks, and toxicity is attributed to a metabolite, 2,5-hexanedione, produced by the cytochrome P-450–mediated biotransformation of the parent compounds. This neurotoxic metabolite is thought to inhibit glutaraldehyde-3-phosphate dehydrogenase, which supplies energy for axonal transport.
Clinically, the patient may complain of chronic numbness and paresthesias in the extremities. The key component in making the diagnosis is a history of exposure to solvents, usually through occupations and hobbies. The compound n-hexane is found in solvents used in the printing, shoemaking, textile, and furniture industries, as well as in gasoline, quick-drying glues, and rubber cement.20
GI AND HEPATIC TOXICITIES
Most hydrocarbons are GI irritants. Vomiting, which occurs in many patients with aliphatic hydrocarbon ingestions, increases the risk of pulmonary aspiration. Gastric perforation has been reported after accidental ingestion of chlorofluorocarbons.21
Hepatic damage resulting from ingestion of halogenated hydrocarbons is well described.22,23 Chlorinated hydrocarbons, such as carbon tetrachloride, methylene chloride, trichloroethylene, and tetrachloroethylene, are especially hepatotoxic. For example, carbon tetrachloride causes centrilobular liver necrosis similar to acetaminophen toxicity. Free radical metabolites of these agents that cause lipid peroxidation are apparently responsible for hepatocellular destruction. The time course of hepatic dysfunction with acute exposures appears similar to that of acetaminophen hepatotoxicity—within 24 to 48 hours after ingestion.
Clinically, patients may come to the ED complaining of nausea, vomiting, abdominal pain, or loss of appetite. Depending on the severity, the physical examination may reveal a patient with jaundice, lethargy, and/or abdominal tenderness, especially in the right upper quadrant. Results of serum transaminase tests and other hepatic synthetic function tests may be abnormal within 24 hours after ingestion.
RENAL AND METABOLIC TOXICITIES
Solvent abuse and occupational exposure to hydrocarbons may result in renal dysfunction. Chlorinated hydrocarbons, such as chloroform, carbon tetrachloride, and trichloroethylene, are also nephrotoxic. Toluene, an aromatic hydrocarbon that is commonly abused, may cause renal tubular acidosis in patients who inhale toluene-containing substances.8,24 The mechanism of toluene-induced renal tubular acidosis is not clear. The typical metabolic profile of renal tubular acidosis is a normal anion gap hyperchloremic acidosis with hypokalemia and a urine pH of >5.5. The metabolites of toluene (hippuric acid and benzoic acid) can be the cause of an elevated anion gap metabolic acidosis.25
Clinically, habitual toluene abusers may complain of muscle weakness caused by hypokalemia.26 The serum potassium level may be so low (<2 mEq/L) that severe weakness develops, occasionally resulting in muscle paralysis. Significant rhabdomyolysis may also result.27 Toluene abuse should be considered in individuals (especially young patients) who come to the ED with symptoms similar to hypokalemic periodic paralysis.24,26
Hydrocarbon-induced hemolysis rarely occurs after the acute ingestion of gasoline, kerosene, and tetrachloroethylene, and after inhalation of mineral spirits. Exposure to benzene (an aromatic hydrocarbon) is associated with an increased incidence of hematologic disorders, including aplastic anemia, acute myelogenous leukemia, and multiple myeloma.28 Naphthalene exposure is associated with hemolytic anemia. Delayed methemoglobinemia is associated with occupational exposure to hydrocarbons containing amine functional groups such as aniline (see chapter 207, "Dyshemoglobinemias").29 Delayed carboxyhemoglobinemia is associated with methylene chloride exposure due to its metabolism to carbon monoxide, which takes a few hours.30 This is unlike ordinary carbon monoxide exposure from exogenous sources in which the maximum carboxyhemoglobin level occurs at the time of the exposure. Clinically, patients may come to the ED with malaise, headache, dyspnea, or cyanosis depending on the exposure and the severity of the toxicity.
Dermal toxicity from exposure to hydrocarbons is most often associated with the short-chain aliphatic, aromatic, and halogenated hydrocarbons. These agents act as primary irritants and as sensitizers. Occasionally, highly permeable hydrocarbons can penetrate the skin, resulting in systemic toxicity. Skin findings can range from local erythema, papules, and vesicles to a generalized scarlatiniform eruption and an exfoliative dermatitis (Table 199-3). A "huffer's rash" may be noted over the face of patients who habitually abuse the volatile hydrocarbons.8 Frostbite of the face may develop during the inhalational abuse of fluorinated agents. A defatting dermatitis, similar to chronic eczematoid dermatitis, may occur.
Cellulitis and sterile abscesses have been associated with the injection of hydrocarbons, and even a small amount of injected hydrocarbon can cause significant injury.31 Hydrocarbon-induced soft tissue necrosis has recently been seen in patients using "krokodil," desomorphine synthesized from codeine with the use of hydrocarbon solvents.32 Dermal exposure to heated high-viscosity, long-chain aliphatics, such as tar, asphalt, or bitumen, presents a particularly challenging problem because of their association with thermal burns, hyperthermia, and difficulty with decontamination.33 Tar burns are discussed in the chapter 217, "Chemical Burns."