You are in: eMedicine Specialties > Emergency Medicine > TOXICOLOGY Toxicity, Hydrocarbon InsecticidesArticle Last Updated: Dec 10, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 10
  Author: Carlo L Rosen, MD, Assistant Professor of Medicine, Harvard Medical School; Program Director, Department of Emergency Medicine, Beth Israel Deaconess Medical Center/ Harvard Affiliated Emergency Medicine Residency program Carlo L Rosen is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine Coauthor(s): Jennifer Vyse Pope, MD, Staff Physician, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Morgan Skurky-Thomas, MD, Resident Physician, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School Editors: David C Lee, MD, Research Director, Department of Emergency Medicine, Assistant Professor, North Shore University Hospital and New York University Medical School; John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital; Michael J Burns, MD, Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center; John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center; Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital Author and Editor Disclosure Synonyms and related keywords: chlorinated hydrocarbon insecticides, organochlorines, solvents, fumigants, insecticide toxicity, hydrocarbon insecticide toxicity, hydrocarbon insecticide poisoning, dichlorodiphenyltrichloroethane, DDT, hexachlorocyclohexane, benzene hexachloride, lindane, gamma-hexachlorocyclohexane, cyclodienes, chlordane, heptachlor, aldrin, dieldrin, endrin, endosulfan, isobenzan, chlordecone, kelevan, mirex, toxaphene, dicofol, methoxychlor, organochlorine poisoning, pesticide poisoning, organochlorine insecticides, hydrocarbon solvents INTRODUCTIONSection 2 of 10
  BackgroundHydrocarbons are organic compounds made primarily of carbon and hydrogen atoms arranged in aliphatic and/or aromatic configurations. Chlorinated hydrocarbon (organochlorine) insecticides, solvents, and fumigants are widely used in the US. These compounds can be highly toxic and some agents, such as DDT, have been banned in the US because of their unacceptably slow degradation and subsequent bioaccumulation. The toxicity of these agents varies according to their molecular size, volatility, and effects on the CNS. In general, they cause either CNS depression or stimulation, depending upon the agent and dose.1 These compounds are separated into 6 groups, as follows:
PathophysiologyOrganochlorines are neurotoxins for insects and mammals. They are well absorbed orally and by inhalation. Transdermal absorption is variable. They are strongly lipid soluble and sequestered in body tissues with high lipid content, such as the brain and liver. Consequently, blood levels tend to be much lower than fatty tissue levels. The lipophilic tendency of organochlorines accounts for prolonged systemic effects in overdose. Toxicity in humans consists mainly of CNS, cardiac, and pulmonary effects. The organochlorines disturb the neuronal membrane causing hyperexcitability of the nervous system. Specifically, cyclodienes, hexachlorocyclohexanes, and toxaphene organochlorines inhibit the GABA receptor and prevent chloride influx in the CNS while DDT affects voltage-dependent Na channels. This effect results in agitation, confusion, and seizures. Cardiac effects have been attributed to sensitization of the myocardium to circulating catecholamines. Some of the more volatile hydrocarbons can be inhaled while in vapor form or swallowed while in liquid form. Inhalation of toxic vapors or aspiration of liquid after ingestion may lead to atelectasis, bronchospasm, hypoxia, and a chemical pneumonitis. In severe cases, this can lead to pulmonary edema, hemorrhage, and necrosis of lung tissue. In liquid form, they are easily absorbed through the skin and GI tract. Highly toxic organochlorines Moderately toxic hydrocarbons
FrequencyUnited StatesOrganochlorine pesticides are now only rarely used in the developed world, and poisonings have become correspondingly more rare. InternationalAn estimated 3 million cases of severe pesticide poisoning and 220,000 deaths occur each year worldwide. Organochlorine poisoning accounts for only a small fraction of pesticide poisoning. Approximately 95% of fatal pesticide poisonings occur in developing countries. Mortality/MorbidityToxic doses are variable, and reports of poisonings are limited. AgeAdults are most likely to have serious intentional poisonings and children are most likely to have accidental poisonings. CLINICALSection 3 of 10
HistoryThe history of exposure is by far the most important piece of information to obtain. In most cases, the exact history of pesticide exposure is known to the physician, and all efforts to resuscitate the patient can focus upon the specific hydrocarbon to which the patient was exposed. At times, the physician may not have the benefit of knowing the initiating event. CNS depression and excitation are the primary effects observed from organochlorine toxicity; therefore, the patient may appear agitated, lethargic, intoxicated, or even unconscious. Organochlorines lower the seizure threshold, which results in increased seizure activity. Initial euphoria with auditory or visual hallucinations and perceptual disturbances are common in the setting of acute toxicity. Patients may have pulmonary complaints or may be in severe respiratory distress. Cardiac dysrhythmias may complicate the initial clinical presentation.
PhysicalBecause of the high lipid solubility, duration of toxicity can be prolonged. Life-threatening complications are secondary to seizures or hypoxia secondary to prolonged CNS stimulation.
DIFFERENTIALSSection 4 of 10
Anxiety Sedation Shock, Septic Toxicity, Alcohols Toxicity, Antihistamine Toxicity, Arsenic Toxicity, Barbiturate Toxicity, Benzodiazepine Toxicity, Hydrocarbons Toxicity, Lead Toxicity, Local Anesthetics Toxicity, Rodenticide Toxicity, Toluene Toxicity, Valproate Toxicity, Vitamin
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| Drug Name | Lorazepam (Ativan) |
|---|---|
| Description | Sedative hypnotic with short onset of effects and relatively long half-life. DOC because of its long duration of seizure control. Rate of injection should not exceed 2 mg/min. May be IM if unable to obtain IV access. By increasing the action of GABA, a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation. Important to monitor patient's blood pressure after administering dose. Adjust prn. |
| Adult Dose | 0.04 mg/kg (eg, 2-4 mg) IV; titrate to effect Status epilepticus: 4 mg/dose IV slowly over 2-5 min; repeat in 10-15 min prn; not to exceed 8 mg/dose |
| Pediatric Dose | Children: 0.05 mg/kg IV (range 0.02-0.1 mg/kg) Adolescents: Administer as in adults Status epilepticus: Neonates: 0.05 mg/kg IV over 2-5 min; may repeat in 10-15 min prn Infants and children: 0.1 mg/kg IV over 2-5 min; second dose of 0.05 mg/kg IV at 10-15 min prn; not to exceed 4 mg Adolescents: 0.7 mg/kg IV slowly over 2-5 min; not to exceed 4 mg; second dose in 10-15 min prn |
| Contraindications | Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma |
| Interactions | Alcohol, phenothiazines, barbiturates, and MAOIs increase CNS toxicity |
| Pregnancy | D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus |
| Precautions | Monitor for respiratory depression with high or repeated doses; contains benzyl alcohol, which may be toxic to infants in high doses; caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, Parkinson disease, or patients who may have inhibition of benzodiazepine metabolism and clearance (eg, using nicotine, taking cimetidine) |
| Drug Name | Midazolam (Versed) |
|---|---|
| Description | Used as alternative in termination of refractory status epilepticus. Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects. Thus, clinician must wait 2-3 min to fully evaluate sedative effects before initiating procedure or repeating dose. |
| Adult Dose | 0.05 mg/kg IV; not to exceed 2.5 mg |
| Pediatric Dose | Administer as in adults |
| Contraindications | Documented hypersensitivity; preexisting hypotension; narrow-angle glaucoma; sensitivity to propylene glycol (diluent) |
| Interactions | Sedative effects may be antagonized by theophyllines; narcotics and erythromycin may accentuate sedative effects of because of decreased clearance |
| Pregnancy | D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus |
| Precautions | Caution in congestive heart failure, pulmonary disease, renal impairment, and hepatic failure; monitor for respiratory depression with high or repeated doses |
| Drug Name | Diazepam (Valium) |
|---|---|
| Description | Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. |
| Adult Dose | 0.2 mg/kg IV at 2 mg/min, not to exceed 20 mg/dose; may repeat |
| Pediatric Dose | 0.2-0.5 mg/kg IV <5 years: Not to exceed 5 mg >5 years: Not to exceed 10 mg |
| Contraindications | Documented hypersensitivity; narrow-angle glaucoma; altered mental status; low BP or RR |
| Interactions | Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, cimetidine, barbiturates, alcohols, and MAOIs |
| Pregnancy | D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus |
| Precautions | Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity); monitor for altered mental status, respiratory depression, and hypotension |
Adsorbs GI toxins, which are then fecally excreted. May not adsorb hydrocarbons and other toxins. Besides adsorbing toxins, activated charcoal also creates a diffusion gradient in the GI circulation, a "sink" effect, which draws absorbed drug into the GI tract for binding and elimination.
| Drug Name | Activated charcoal (Liqui-Char) |
|---|---|
| Description | Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water. For maximum effect, administer within 30 min of ingesting poison. Multiple dose activated charcoal (MDAC) may be administered as 10-20 g q2-4h without a cathartic. |
| Adult Dose | 1 g/kg PO usually with a cathartic (eg, sorbitol) in the first dose |
| Pediatric Dose | 1-2 g/kg PO <2 years: Cathartic not recommended |
| Contraindications | Documented hypersensitivity; poisoning or overdose of mineral acids and alkalies; unprotected airway |
| Interactions | May inactivate ipecac syrup if used concomitantly; effectiveness of other medications decreases with coadministration; do not mix with sherbet, milk, or ice cream (decreases adsorptive properties) |
| 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 | Ensure airway protection during administration; monitor for bowel sounds before administration to avoid ileus complication; not very effective in poisonings of ethanol, methanol, and iron salts; induce emesis before administration; after emesis with ipecac syrup, patient may not tolerate activated charcoal for 1-2 h; can administer in early stages of gastric lavage; without sorbitol, gastric lavage returns are black |
Binding agents are used in the treatment of hypercholesterolemia and have been noted to bind certain lipid-soluble drugs and enterohepatically-recycled drugs.
| Drug Name | Cholestyramine (Questran) |
|---|---|
| Description | Forms a nonabsorbable complex with bile acids in the intestine, which, in turn, inhibits enterohepatic reuptake of intestinal bile salts. |
| Adult Dose | 4 g PO qid initial; generally administered with a cathartic (eg, sorbitol) |
| Pediatric Dose | 80 mg/kg PO tid |
| Contraindications | Documented hypersensitivity; biliary obstruction |
| Interactions | Inhibits absorption of numerous drugs and fat-soluble vitamins |
| 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 | Caution in constipation and phenylketonuria; nausea, abdominal discomfort, constipation, steatorrhea, and diarrhea may occur |
The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Kevin Ban, MD, to the development and writing of this article.
The authors and editors of eMedicine gratefully acknowledge the assistance of Lada Kokan, MD, with the literature review and referencing for this article.
Toxicity, Hydrocarbon Insecticides excerpt
Article Last Updated: Dec 10, 2007
