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Toxicity, Hydrocarbons: Treatment & Medication
Updated: Apr 30, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Prehospital Care
- Prehospital care should focus on decontamination, followed by immediate transport to a medical facility capable of managing such a patient. GI decontamination has no role in prehospital care. Decontamination should focus on removing any remaining hydrocarbon that might be on the clothes or skin, in the correct clinical setting.
- Patients should be kept calm to prevent arrhythmia as a result of myocardial sensitization.
- All patients should have their airway, breathing, and circulation managed per routine advanced life support protocols.
- Symptomatic patients should receive intravenous access and cardiac monitoring.
- The hydrocarbon agent should be transported with the patient to the hospital, if this can be done in a safe manner. Bringing the substance to the hospital can permit identification.
Emergency Department Care
Management for hydrocarbon intoxication is largely supportive.
- Asymptomatic patients should be observed with continual pulse-oximetry for a period of at least 6 hours. If the patient remains asymptomatic (eg, no coughing, vomiting, tachypnea, or other evidence of respiratory difficulties), then a chest radiograph may be obtained to evaluate for aspiration.
- Other etiologies of altered mental status should be investigated as deemed clinically appropriate by the treating clinician.
- Patients who show signs of impending respiratory failure despite supplemental oxygen may require rapid sequence intubation for definitive airway management. Intubation and positive pressure ventilation may be required for evidence of on-going respiratory distress.
- If arrhythmias occur, electrolytes, including magnesium and potassium, should be replaced.
- If ventricular fibrillation occurs, and the thought is that the arrhythmia is because of myocardial sensitization, catecholamines, including epinephrine, should be avoided. In this setting, lidocaine or beta-blockers can be used.
- Decontamination of the GI tract remains controversial.
- The use of ipecac-induced emesis is contraindicated, and activated charcoal does not absorb hydrocarbons well.
- Gastric lavage should not be routinely performed.
- The hydrocarbons with significant systemic toxicity for which the benefits of gastric decontamination may outweigh the real risks of inducing aspiration follow the mnemonic CHAMP:
- Camphor (toxicity is seizures)
- Halogenated hydrocarbons (toxicity is arrhythmias and hepatotoxicity)
- Aromatic hydrocarbons (toxicity is CNS toxicity, myelosuppression, and malignancy)
- Metals (heavy metals)
- Pesticides (cholinergic symptoms, seizures)
- Antibiotics are frequently given to patients who develop a pneumonitis following hydrocarbon aspiration. In animal models, the empiric administration of antibiotics altered the lung flora compared with controls and did not yield any benefit. Clinically, superinfection can definitely occur. Because the pneumonitis itself can create abnormal lung sounds, fever, and leukocytosis, distinguishing if these effects are because of a superimposed infection or if they are the result of the pneumonitis itself is often difficult. Any finding on a chest radiograph within a few hours of the exposure, however, is unlikely to be pneumonia, and much more likely to be a pneumonitis.
- Steroids have not been proven to be beneficial.
- Several commercial surfactant preparations are available for use with other conditions, such as hyaline membrane disease (HMD). Animal data on its use demonstrate conflicting results, and currently no human data exist to support its routine use.
Consultations
- All hydrocarbon ingestions should be discussed with the regional poison control center (800-221-1222) or a medical toxicologist.
- Psychiatry consultation should be performed if deemed clinically relevant.
Medication
Medications are used for treatment of hydrocarbon-induced ventricular dysrhythmias.
Antiarrhythmic Agent, Class II
These agents inhibit chronotropic, inotropic, and vasodilatory response to beta-adrenergic stimulation.
Propranolol (Betachron E-R, Inderal, InnoPran XL)
Class II antiarrhythmic, nonselective, beta-adrenergic, receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.
Effective for treating aggression resulting from head injury. Also used for reducing restlessness and disinhibition. Treatment for persistent agitation and aggression in organic brain syndromes.
Adult
1-3 mg (under careful monitoring) IV; not to exceed 1 mg/min to avoid lowering blood pressure and causing cardiac standstill
Allow time for drug to reach site of action (particularly if slow circulation); administer second dose after 2 min prn; thereafter, do not give additional drug in <4 h
Do not continue doses after desired alteration in rate or rhythm achieved; switch to PO ASAP; 10-30 mg tid/qid (usual)
Pediatric
2-4 mg/kg/d PO divided bid (ie, 1-2 mg/kg bid)
IV use is not recommended; however, for arrhythmias, a dose of 0.01-0.1 mg/kg, not to exceed 1 mg/dose by slow push has been recommended; change to PO ASAP
Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol
Documented hypersensitivity; uncompensated congestive heart failure; bradycardia, cardiogenic shock; AV conduction abnormalities
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm (withdraw drug slowly and monitor closely)
Esmolol (Brevibloc)
Short-acting IV cardioselective beta-adrenergic blocker with no membrane depressant activity. Half-life of 8 min allows for titration to effect and quick discontinuation prn.
Adult
Loading dose: 250-500 mcg/kg IV for 1 min
Maintenance infusion: 50-100 mcg/kg/min IV for 4 min; repeat if inadequate; if still inadequate, repeat loading dose, then increase maintenance dose by increments of 50 mcg/kg/min IV
Pediatric
Not established: 100-300 mcg/kg/min IV with continuous heart rate and blood pressure monitoring to determine onset of beta-blockade (equal to >10% reductions); titrate upward in 50-100 mcg/kg/min increments IV q10min prn
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents
Documented hypersensitivity; asthma; COPD; CHF; moderate-to-severe left ventricular dysfunction; hypotension <90 mm Hg; bradycardia <60/min, second- and third-degree AV block
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication is abruptly withdrawn (withdraw drug slowly and monitor patient closely)
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| Overview: Toxicity, Hydrocarbons |
| Differential Diagnoses & Workup: Toxicity, Hydrocarbons |
 Treatment & Medication: Toxicity, Hydrocarbons |
| Follow-up: Toxicity, Hydrocarbons |
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References
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Garrettson LK. n-Hexane and 2-Hexanone. In: Sullivan JB, Krieger GR, eds. Clinical Environmental Health and Toxic Exposure. 2nd ed. Philadelphia, Pa: Lippincott Williams and Wilkins; 2001:1211-14; chap110.
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Palmer RB, Phillips SD. Chlorinated hydrocarbons. In: Shannon MW, Borron SW, Burns MJ, eds. Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose. 4th ed. Philadelphia, Pa: Saunders; 2007:1347-61.
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Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Heard SE. 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 25th Annual Report. Clin Toxicol (Phila). Dec 2008;46(10):927-1057. [Medline]. [Full Text].
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Further Reading
Keywords
hydrocarbon toxicity, hydrocarbon poisoning, hydrocarbon exposure, hydrocarbon, hydrocarbon ingestion, inhaling hydrocarbons, hydrocarbon inhalation, halogenated hydrocarbons, carbon tetrachloride, trichloroethylene, tetrachloroethylene, trichloroethane, chloroform, methylene chloride, kerosene, gasoline, naphtha, wood-derived hydrocarbons, turpentine, pine oil, petroleum distillates, short-chain hydrocarbons, butane, long-chain hydrocarbons
