Toxaphene Toxicity Treatment & Management

• Establish the ABCs. Protect the airway at all times. Do not induce emesis because the patient may have a sudden change in mental status and could aspirate gastric contents.
• Avoid strong external stimuli to the patient, which may precipitate convulsions.
• Remove the patient from source of exposure and prevent contamination of others.
• Consider skin decontamination by washing with soap and water and removing clothing (place in plastic bags) as early as possible; it is performed best in the field.
• With massive exposure or multiple victims, contact a hazardous materials (HAZMAT) team for assistance.
• Initiate cooling measures (eg, wetting, fanning, ice bath) if the patient is hyperthermic.

Early (preventive) and aggressive supportive measurements are required for a good outcome. No specific antidote is available for toxaphene poisoning.

Continue ABCs. Consider early and gentle rapid sequence intubation with prophylactic use of a benzodiazepine to control agitation and theoretically reduce possibility of seizures. Seizures may begin without any prodromal signs or symptoms. If paralyzed, EEG monitoring is warranted.

If ingested, do not induce emesis. Carefully perform orogastric lavage with suction, especially for recent liquid ingestion. Always secure the airway well before executing lavage. GI decontamination with aqueous-based oral activated charcoal (AC) is indicated to limit drug absorption from the GI tract. Never use oral oil-based cathartics because they may facilitate absorption of toxaphene. Avoid sorbitol-based AC because it may induce vomiting.

Regardless of the route of exposure, consider multiple dose activated charcoal (MDAC) because it may enhance fecal elimination of toxaphene by interrupting its biliary-enterohepatic and enteroenteric recirculation. Induced diuresis, hemodialysis, and hemoperfusion have not been shown to be effective enhanced elimination techniques. In contrast, cholestyramine resin is a selective oral binding agent that has been successfully used to enhance fecal elimination of chlorinated hydrocarbons by interrupting the biliary-enterohepatic and enteroenteric recirculation.

Dysrhythmias may occur because of increased myocardial sensitization to catecholamines induced by chlorinated hydrocarbon. If at all possible, avoid use of epinephrine and other sympathomimetic drugs possessing beta1-agonist properties to avoid increased risk of developing ventricular dysrhythmias. Use of beta-blockers is reported to control ventricular dysrhythmias because of sensitized myocardium. If the patient is hypotensive and unresponsive to fluids, intravenous administration of a pure alpha-adrenergic agonist agent (eg, phenylephrine) is the therapy of choice.

Because of a theoretical benefit from using N -acetylcysteine (NAC) if liver abnormalities or necrosis is suspected in the patient (elevated serum levels of liver enzymes), administration of the drug is suggested to prevent irreversible hepatic injury. Favorable outcomes following use of NAC have been reported in cases of carbon tetrachloride and chloroform poisonings (not proven). Suspected mechanism of hepatic injury appears similar to that of acetaminophen and empiric use of NAC may be justified, especially in significant poisoning. Generally, the only significant adverse event associated with oral use of NAC is pulmonary aspiration (although one case of an anaphylactoid reaction to oral NAC has been reported); therefore, ensure proper protection of the airway.

Aggressive cooling measures may be required if the patient presents with or develops hyperthermia.

• In all cases, seek consultation with the regional poison control center and a medical toxicologist (certified through the American Board of Medical Toxicology or the American Board of Emergency Medicine).