The Poison Control Center

Hydrocarbon Ingestion

Introduction
Pathophysiology
Treatment
Triage
References

Introduction

Hydrocarbons ranked sixth in substances most frequently involved in human exposures reported to the American Association of Poison Control Centers National Data Collection System in 1988. Roughly half of these cases involved children under the age of 6.¹ This is not surprising in view of the fact that hydrocarbon-based products are commonly found in the home. Children have access to kerosene during the winter months, and charcoal lighter fluid in the summer season. Often, the products are inappropriately stored in drinking glasses or unlabeled containers, and they may be attractive and pleasant-smelling, like furniture polishes. With adults, gasoline siphoning appears to be a source of accidental hydrocarbon exposure.

Hydrocarbons represent a diverse group of substances, and several classification systems have been used to describe them. Occasionally the terms "hydrocarbon" and "petroleum distillate" are used interchangeably. In fact, petroleum distillate refers to a type of hydrocarbon which results from the processing of crude oil, and may be aliphatic or aromatic. Turpentine, on the other hand, is an example of a hydrocarbon that is not a petroleum distillate since it is made from pine oil.

Probably the most useful means of classifying hydrocarbons is with respect to their clinical effects. Two groups may be described: (1) hydrocarbons which are easily aspirated following ingestion and (2) hydrocarbons that may produce systemic toxicity in addition to their aspiration potential. The first group includes aliphatic hydrocarbons such as kerosene, mineral spirits, gasoline, naphtha and mineral seal oil. They are poorly absorbed from the gastrointestinal tract, and therefore are not expected to produce systemic effects.^2-6

The second group of hydrocarbons, considered the more toxic of the two, includes halogenated and aromatic hydrocarbons. (Table 2) Halogenated hydrocarbons, such as the solvent trichloroethane and methylene chloride, can produce liver and renal toxicity following chronic exposure, as well as central nervous system (CNS) effects with acute exposure.

Toluene, xylene, and benzene belong to the cyclic, aromatic group of hydrocarbons. The solvents toluene and xylene are commonly abused for the euphoric effects produced by inhalation through techniques such as "huffing" or "bagging." Cardiac arrhythmias may result from this practice due to sensitization of the heart to catecholamines. Chronic exposure can cause peripheral neuropathies, electrolyte abnormalities and renal toxicity. Chronic exposure to benzene has been implicated in the development of aplastic anemia and leukemia.²

When considering hydrocarbons and the nature of their effects, it is important to remember that these substances may also be vehicles for highly toxic ingredients such as camphor, heavy metals and organophosphate insecticides.

Recently, several cases of injection of hydrocarbon insecticides in IV drug abusers have been reported. Chemical pneumonitis similar to that seen with aspiration has been noted.^7,8

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Pathophysiology

The physical properties of the hydrocarbons contribute to their ability to produce pulmonary effects. The risk for aspiration directly correlates with viscosity, which is measured in Saybolt Seconds Universal, the time required for a liquid to flow through a calibrated orifice.

Products with a low viscosity (<60 SSU) are associated with a high aspiration potential. Examples include gasoline, kerosene and naphtha (the ingredient in charcoal lighter fluid). Once aspirated, low viscosity allows for deeper penetration of the hydrocarbon into tissues of the distal airway. In conjunction with decreased viscosity, the physical properties of low surface tension and high volatility contribute to respiratory injury. Low surface tension enhances spreading of the liquid on lung tissue, while high volatility displaces alveolar gas and interferes with ventilation when aspiration has occurred.³

Aspiration of mineral seal oil, with a viscosity of 47 SSU, can result in surprisingly severe pulmonary complications. This may in part be attributable to the ability of mineral seal oil to cause a lipoid pneumonia component on top of chemical pneumonitis.²

On the other hand, products with a viscosity of >100 SSU, such as fuel oil, lubricating oil and mineral oil, present a low aspiration hazard.

Symptoms of aliphatic hydrocarbon ingestion, in the absence of toxic substituents, are confined to the gastrointestinal tract and the respiratory tract. Local effects include a burning sensation in the mouth and pharynx, nausea, gastric irritation, belching and diarrhea. These rarely require treatment and are considered fairly innocuous.^2-6

Pulmonary effects, when they do occur, are the result of aspiration. A severe necrotizing pneumonitis, with direct tissue destruction, can occur. Aspiration can occur at the time of ingestion, or during vomiting or gastric lavage.⁹ Aspiration can occur from minute amounts of hydrocarbon. Pulmonary toxicity represents the most common complication of hydrocarbon ingestion and accounts for the majority of fatalities.

When aspiration occurs, the patient may initially experience coughing, choking, gagging or grunting respirations. Dyspnea and cyanosis may be noted. Rales, rhonchi and decreased breath sounds may be present by auscultation. Fever and leukocytosis may also be present, but are not thought to correlate with an infectious process.^2,3

X-ray findings are usually significant at two to eight hours after ingestion. Pulmonary infiltrates or perihilar densities have commonly been seen. Following aspiration, deterioration of the patient may occur over the first 24-72 hours, with resolution of symptoms in three to six days.^3,5 The course may be prolonged with mineral seal oil exposure.² Reported complications of hydrocarbon aspiration include pneumatoceles, pleural effusion or pneumothorax. Bacterial superinfection is also possible. Hemorrhagic edema can rapidly lead to the patient's demise.

Aspiration of aliphatic hydrocarbons may result in lethargy, tremors, and, rarely, convulsions or coma. These effects are more likely due to severe pulmonary injury or hypoxia. Death from CNS depression following aliphatic hydrocarbon ingestion has not been reported.³

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Treatment

Hydrocarbon ingestion presents a challenge to emergency room physicians as well as poison control center specialists. Many controversies surround the proper management of the exposure. Issues include indications and preferred methods for gastric decontamination, use of oil-based cathartics, and the use of steroids or antibiotics. In part, the debate stems from a relative lack of reliable toxicity data and good controlled studies evaluating treatment modalities.

Certain recommendations can be made based on properties of the ingested hydrocarbon.

Regardless of the amount involved, gastric emptying is not indicated for accidental ingestion of a hydrocarbon lacking systemic toxicity. This represents the majority of cases. The risk of aspiration during vomiting or lavage far outweighs any benefit from removal of the substance. The frequently cited amount of >1mL./kg. as the indication for gastric emptying is not supported by animal studies.^2,4

In the case of ingestion of a hydrocarbon capable of causing systemic toxicity, or, when coingestion is suspected, gastrointestinal (GI) decontamination would be warranted. The mnemonic CHAMP has been proposed for delineation of toxic hydrocarbons — Camphorated, Halogenated, Aromatic, heavy Metals and Pesticides. The primary toxicity of these agents relates to their systemic effects, and treatment should be based on expected effects.

Gastric emptying is not without risk. Both ipecac-induced emesis and emesis from insertion of a lavage tube can increase the risk of aspiration. In addition, aspiration may occur as the result of re-exposure of the larynx to hydrocarbon from the tip of the tube during removal. An endotracheal tube cuff is not protective against aspiration.² For these reasons, Syrup of Ipecac is the preferred method of gastric emptying, provided the patient has a gag reflex, is alert, and is likely to remain so, and provided the substance is not expected to cause seizures.^2,10

Activated charcoal does not effectively adsorb hydrocarbons, and, in the absence of coingestants, has no role in therapy. Oils, such as mineral or olive oil, once advocated to increase the viscosity of the hydrocarbon, are no longer recommended because of the risk for lipoid pneumonia.⁹

If hydrocarbon aspiration occurs, oxygen and aggressive respiratory support are indicated. With severe pulmonary complications, CPAP or PEEP may be required. Steroids have not been shown to be useful, and antibiotics should be reserved for documented infection. A beta-2 selective agonist can be given for bronchospasm, while epinephrine should be avoided as it may precipitate dysrhythmias.

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Triage

With respect to initial management of hydrocarbon ingestion, certain suggestions can be made. If the patient has no symptoms following accidental ingestion of a "nontoxic" hydrocarbon, he or she can be observed at home. If, on the other hand, the patient initially experiences coughing, choking, or vomiting, or if the ingestion is intentional, referral to a health care facility for evaluation is necessary.¹¹

All symptomatic patients should have a chest X-ray taken no sooner than two hours post- ingestion, and should be observed in the emergency department for a period of six hours. The patient may be discharged with observation at home if asymptomatic throughout and X-ray is negative. In the presence of a positive two-hour X-ray, the patient should be admitted for monitoring of blood gases, repeat chest X-rays, and respiratory support if required.^2,12

*CXR taken no sooner than two hours post-ingestion
**May opt to observe for six hours and discharge if still asymptomatic

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References

1. 1. Litovitz TL, Schmitz BF, Holm KC. 1988 annual report of the American Association of Poison Control Centers National Data Collection System. Am J Emerg Med 1989 Sep;7(5):495-545.
2. Litovitz T. Hydrocarbon ingestions. Entechnology. 1983 Mar;62(3):142-7.
3. Arena JM. Hydrocarbon poisoning—current management. Pedtr Ann. 1987 Nov;16(11):879- 83.
4. Dice WH, Ward G, Kelley J, Kilpatrick WR. Pulmonary toxicity following gastrointestinal ingestion of kerosene. Ann Emerg Med 1982 Mar; 11(3):138-42.
5. Eade NR, Taussig LM, Marks MI. Hydrocarbon pneumonitis. Pediatrics. 1974 Sep;54(3): 351- 7.
6. Karlson KH Jr. Hydrocarbon poisoning in children. South Med J 1982 Jul;75(7):839-840.
7. Beck DE, Freeman B, Moore CR. Toxicities with intravenous and subcutaneous administration of a petroleum distillate. Drug Intell Clin Pharm 1981 Sep;15(9):693-694.
8. Neeld EM, Limacher MC. Chemical pneumonitis after the intravenous injection of hydrocarbon. Radiology 1978 Oct;129(1):36
9. Beamon RF, Siegel CJ, Landers G, Green V. Hydrocarbon ingestion in children: a six-year retrospective study. JACEP 1976 Oct;5(10):771-5.
10. Ng RC, Darwish H, Steward DA. Emergency treatment of petroleum distillate and turpentine ingestion. Can Med Assoc J 1974 Sep 21;111(6):537-538.
11. Machado B, Cross K, Snodgrass WR. Accidental hydrocarbon ingestion cases telephoned to a regional poison center. Ann Emerg Med 1988 Aug;17(8):804-807.
12. Anas N, Namasonthi V, Ginsburg CM. Criteria for hospitalizing children who have ingested products containing hydrocarbons. JAMA 1981 Aug 21;246(8):840-3.

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