Hydrocarbon Poisoning



Hydrocarbon Poisoning


William J. Lewander

Alfred Aleguas Jr



Hydrocarbons are a group of organic compounds composed primarily of hydrogen and carbon. Although often mixtures, hydrocarbons may be divided into four basic types: aliphatic, halogenated, aromatic, and terpene.

Hydrocarbon exposures are frequent and account for an inordinate number of health care visits and hospital admissions. The American Association of Poison Control Centers reported 54,766 hydrocarbon exposures in 2007 [1,2]. Twenty-two percent were seen in a health care facility, and there were seven deaths. Nearly 32% of total exposures occurred in children younger than 6 years of age and involved ingestions, and most of these were accidental.

Storage in unmarked, readily accessible containers and an attractive color or aroma account for the high percentage of exposures in young children. In adolescents and adults, poisoning generally results from inhalational abuse, occupational exposure, intentional ingestion, or accidental aspiration during the siphoning of fuels. Cutaneous and even intravenous exposures have also been described. Ingestions in adults usually involve larger volumes, and there is a much greater likelihood of other coingested drugs or toxins. The majority of deaths are due to intentional inhalation abuse.


Aliphatic Hydrocarbons

Aliphatic hydrocarbons, known as petroleum distillates, are straight-chain compounds produced from the fractional distillation of natural petroleum (Table 134.1). They are the most common cause of hydrocarbon poisoning.

After ingestion, the major toxicity of petroleum distillates is their potential to cause a fulminant, and sometimes fatal, chemical pneumonitis. Aspiration of even small amounts may produce severe pulmonary toxicity. Although vomiting often precedes and precipitates aspiration, lack of vomiting does not preclude the possibility that aspiration has occurred. Little or no systemic toxicity occurs even with intragastric administration of large doses (12 to 18 mL per kg) [3,4].

The risk of aspiration increases with low viscosity, low surface tension, and high volatility. Viscosity, the tendency to resist flow, is the most important property determining aspiration potential [5]. Substances with low viscosity (e.g., gasoline, mineral seal oil, and kerosene) have a high aspiration potential, whereas those with high viscosity (e.g., mineral oil and fuel oil) have a low potential for aspiration. Reduced surface tension may also allow a substance to spread rapidly from the upper gastrointestinal (GI) tract to the trachea. High volatility (tendency of a liquid to become a gas) increases the likelihood of pulmonary absorption.

Aspirated petroleum distillates inhibit surfactant, resulting in alveolar collapse, ventilation–perfusion mismatch, and subsequent hypoxemia. In addition, bronchospasm and direct capillary damage lead to a chemical pneumonitis and hemorrhagic bronchitis–alveolitis [2,5,6]. In animals exposed to kerosene, acute alveolitis peaked at 3 days and resolved by 10 days [7]. Histologically, a chronic proliferative process occurred, peaking at 10 days and resolving over several weeks. When highly viscous petroleum distillates are aspirated, a less inflammatory but more localized and indolent lipoid pneumonia may occur [8].








Table 134.1 Common Petroleum Distillates




































Product Synonym Main use
Gasoline Petroleum spirits Fuel
Petroleum naphtha fluid Ligroin Cigarette lighter
VM and P naphtha thinner Varnish naphtha Paint or varnish
Mineral spirits Painter’s naphtha
Stoddard solvent
White spirits
Varsol
Mineral turpentine
Petroleum spirits
Dry cleaner Solvent Paint thinner
Kerosene fluid Coal oil Charcoal lighter Solvent
Fuel for stoves, lamps
Fuel oil Home heating oil Fuel
Diesel oil Gas oil Furniture polish


Central nervous system (CNS) manifestations result principally from hypoxia and acidosis caused by pulmonary toxicity [9]. Although systemic toxicity is uncommon, it may be seen if the petroleum distillate is a vehicle for more toxic substances (e.g., heavy metal and pesticide), if it contains additives, or if a concomitant or massive ingestion has occurred [10]. Cardiovascular, hepatic, renal, and hematologic toxicities depend on the specific toxic substance involved.

Use of aliphatic hydrocarbons as volatile substances of abuse (VSA) is a serious and growing problem. It is most often seen in adolescents who use VSA as an easily available, legal, and affordable substitute for other intoxicants [11,12]. The most common aliphatic VSA are n-hexane, n-butane, isobutane, and propane—seen in adhesives, aerosols, liquefied petroleum gas (i.e., cigarette lighter refills and camp stoves), and gasoline. Inhalation may involve sniffing, “huffing” (spraying the solvent onto a cloth held to the mouth and nose), “bagging” (spraying the solvent into a paper or plastic bag and repeatedly inhaling the vapors), or a variant of these techniques [11]. These highly lipid-soluble substances are rapidly absorbed through the lungs and distributed to the CNS and fatty tissues [13]. The onset of symptoms occurs in seconds to minutes, with peak effects occurring somewhat later due to slower diffusion into tissues. Elimination of aliphatic hydrocarbon VSA is primarily by pulmonary excretion, and successive oxidation and metabolism by hepatic cytochrome P450 mixed-function oxidases [13].

Aliphatic VSA toxicity includes acute and chronic neurologic dysfunction; asphyxia; cardiovascular abnormalities; and pulmonary, GI, and cutaneous irritation. CNS toxicity ranges from stimulation at initial or low doses to a depressant effect, with general inhibition of cortical function at high doses [14]. Peripheral neuropathy and irreversible CNS damage have been reported [15,16,17,18]. Inhaled aliphatic hydrocarbons are asphyxiants (as well as pulmonary irritants) and may cause hypoxemia by decreasing the concentration of oxygen in inspired air. Their arrhythmogenic effects are thought to be due to their potentiation of endogenous catecholamines (“cardiac sensitization”), which may promote dysrhythmias (e.g., ventricular tachycardia or fibrillation) [19]. Additional factors such as hypoxia, acidosis, electrolyte abnormalities, and underlying cardiac conditions may contribute to arrhythmias. Dermal and mucosal irritation is due to their ability to dissolve lipids after prolonged or high-dose exposure [20]. Deaths associated with inhalational abuse may result from coma with respiratory depression, aspiration, or injuries incurred while intoxicated as well as from cardiac arrhythmias [21].


Clinical Manifestations

The clinical course after the ingestion of petroleum distillates primarily depends on the presence or absence of concomitant aspiration and its severity. Patients who aspirate generally demonstrate symptoms within 30 minutes; those who do not have symptoms within 6 hours of exposure remain asymptomatic [22]. Presenting signs and symptoms usually involve three main organ systems: pulmonary, CNS, and GI. Cardiovascular, renal, hematologic, and cutaneous toxicity have also been reported [23,24]. In most cases, symptoms resolve during the next 2 to 5 days with supportive care [22,25].

Initial coughing, gasping, and choking may progress and peak during the first 24 to 48 hours to tachypnea with grunting respirations, nasal flaring, retractions, and cyanosis [10,22]. The odor of petroleum distillates may be apparent on the breath. Wheezing, rhonchi, and rales may be heard on auscultation. In severe cases, pulmonary edema and hemoptysis occur. Arterial blood gases may demonstrate hypoxemia from ventilation–perfusion mismatch and early hypocarbia, which progresses to hypercarbia and acidosis. Abnormalities on chest radiographs occur in up to 75% of hospitalized patients, appearing within 2 hours in 88% of patients and by 12 hours in 98% [10,26], but may be delayed up to 72 hours. Early radiographic abnormalities include unilateral, but more commonly bilateral, basilar infiltrates and fine punctate perihilar densities. Localized areas of atelectasis are often present, whereas pleural effusions, pneumatoceles, and pneumothoraces occur infrequently [25,26]. Pneumatoceles generally occur 3 to 15 days after ingestion and resolve during 15 days to 21 months [2,27]. Radiographic findings correlate poorly with clinical symptoms and may persist for several days to weeks after symptoms have resolved [25,26,27]. Asymptomatic patients may have abnormal chest radiographs, whereas symptomatic patients may have minimal or no radiographic abnormalities early in the course [10].

Within the first 24 to 48 hours, fever (38°C to 39°C) and leukocytosis are common [22]. The persistence of fever beyond 48 hours suggests bacterial superinfection.

CNS involvement may occur in those with aspiration-induced hypoxemia, large intentional ingestions, or ingestions of mixtures that contain other toxic agents (e.g., aromatic hydrocarbons). Symptoms range from dizziness and lethargy (91%) to somnolence (5%) and, rarely, coma (3%) and convulsions (1%) [10,28]. The severity of CNS dysfunction often correlates with the severity of aspiration.

GI symptoms, such as local irritation of the oropharynx (e.g., burning), nausea, vomiting, and abdominal pain, are commonly reported. Hematemesis and melena occur rarely [10]. Vomiting appears to increase the likelihood of aspiration [25,29]. Cardiovascular toxicity is uncommon, but dysrhythmias and sudden death after gasoline siphoning have been reported [30].

Inhalation abuse may result in a range of acute CNS manifestations, including dizziness, incoordination, restlessness, excitement, euphoria, confusion, hallucinations, slurred speech, and coma with respiratory depression [31]. Peripheral neuropathy has been reported after chronic exposure [15,16]. Pulmonary toxicity may present as respiratory distress with cyanosis, or syncope with tachycardia or bradycardia. GI irritation may cause nausea, vomiting, and abdominal pain. Dermatologic manifestations range from perioral frost or pigmentation (after direct inhalation from a container) to local skin irritation [10].

Cases of acute renal tubular necrosis [32,33], hemoglobinuria secondary to intravascular hemolysis [34,35], severe burns after prolonged immersion in gasoline [36], and supraglottitis [37] have been reported. Aliphatic hydrocarbons are highly flammable, especially gasoline, and accidental thermal burns may occur during recreational use [38]. Therefore, patients with unexplained burns should be questioned regarding possible inhalation abuse. Chronic gasoline inhalation may also be accompanied by organo-lead poisoning [20,21,39]. Parenteral administration of petroleum distillates has caused local cellulitis, thrombophlebitis, and necrotizing myositis, with resultant compartment syndromes. Associated systemic effects include febrile reactions, hemorrhagic pneumonitis, pulmonary edema, seizures, and CNS depression [23,40,41].


Diagnostic Evaluation

After ingestion, diagnostic evaluation includes a thorough history (e.g., identity, amount, and concentration of toxin; time of ingestion; and symptoms before presentation at health care facility) and a physical examination (focusing on vital signs and the respiratory, CNS, and GI systems). Pulse oximetry should be monitored and a chest radiograph obtained in all symptomatic patients and in cases in which aspiration is suspected.
In symptomatic patients or those who have ingested concomitant toxins or toxic additives, laboratory evaluation should include an arterial blood gas determination; complete blood cell count; electrolyte, blood urea nitrogen, creatinine, and glucose measurements; liver function tests; and urinalysis.


Management

Patients with ingestions who remain or become asymptomatic with a normal chest radiograph (obtained 2 hours or more after exposure) may be discharged after 6 hours of observation. All symptomatic patients, those with abnormal chest radiographs, arterial blood gases, or pulse oximetry, and patients with suicidal intent should be hospitalized. Gastric decontamination is not recommended in petroleum distillate ingestion because absorption and systemic toxicity are minimal, and spontaneous or induced vomiting increases the risk of aspiration and pneumonitis [28,42]. Gastric decontamination is recommended only if potentially toxic amounts of aromatic or halogenated hydrocarbons, pesticides, heavy metals, or other substances have been ingested. Ipecac syrup is not recommended for GI decontamination. Patients who are unconscious, unable to protect the airway (e.g., poor or absent gag reflex), or deteriorating should be intubated with a cuffed endotracheal tube (in patients older than 6 years of age) and then have gastric aspiration or lavage performed. Activated charcoal and cathartic are indicated only if a toxic additive is present or concomitant ingestion has occurred. If cutaneous exposure has occurred, contaminated clothing should be removed and the skin thoroughly washed with soap and water [10].

All patients with respiratory symptoms should be given oxygen, placed on a cardiac monitor, and have intravenous access established. An arterial blood gas determination and chest radiograph should be obtained. The need for intubation should be based on clinical assessment of respiratory distress and objective data from arterial blood gases or pulse oximetry. Chest radiographs do not always correlate with clinical status and should not be used as the sole determinant for respiratory interventions. Continuous positive airway pressure may be necessary to maintain oxygenation, but the patient should be carefully monitored for the development of a pneumothorax. Bronchospasm should be treated with β2-agonist bronchodilators because of potential myocardial sensitization to catecholamines [43].

Supportive care of pneumonitis includes careful monitoring of acid–base, fluid, and electrolyte balance (e.g., cautious hydration to avoid pulmonary edema), serial arterial blood gases or pulse oximetry, and chest radiograph evaluation. Complete blood cell counts with differential, serial sputum, or tracheal aspirate Grams stains and cultures assist in determining if bacterial superinfection has occurred. Baseline renal and liver function studies and a toxic screen should be obtained if toxic additives or concomitant ingestion is suspected. Animal and clinical investigations have failed to demonstrate any beneficial effect of steroid treatment [44,45]. Two animal studies indicate that they may be harmful [46,47,48]. In addition, prophylactic antibiotics have not been shown to be helpful [42,45,46]. Fever and leukocytosis secondary to chemical pneumonitis are common during the first 24 to 48 hours in the absence of superimposed bacterial pneumonia [10]. Antibiotics (e.g., penicillin or clindamycin) should be given only to patients with documented bacterial pneumonias (e.g., Grams stain or culture of sputum or tracheal aspirate) or worsening chest radiograph, leukocytosis, and fever after the first 40 hours [10]. Successful use of high-frequency jet ventilation and extracorporeal membrane oxygenation for the treatment of respiratory failure has been reported [49,50,51]. Other measures such as cardiopulmonary bypass, partial liquid fluorocarbon ventilation, and exogenous surfactant have been suggested for refractory cases, but the data to support their use are limited. [52,53].

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Sep 5, 2016 | Posted by in CRITICAL CARE | Comments Off on Hydrocarbon Poisoning

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