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ACUTE EXPOSURE INFORMATION

  1. Lactonitrile is an cyanogenic aliphatic nitrile compound. Its toxicity is thought to be mainly due to the metabolic release of cyanide by hepatic biotransformation after absorption. However, some acute toxicity may be due to the parent compound itself. At least one human fatality has been reported from lactonitrile poisoning.
  1. Although the aliphatic nitrile compounds in general cause the same signs and symptoms as seen in cyanide poisoning, the onset of toxicity is likely to be delayed for up to several hours after exposure as some time is required for sufficient hepatic metabolism of the parent compound with release of sufficient amounts of cyanide.
    1. The implication of this slow onset is that PROLONGED OBSERVATION in a CONTROLLED SETTING where cyanide poisoning can be treated is required following exposure.
  1. Chronic occupational exposure to other similar nitrile compounds such as acetonitrile has resulted in interference of iodine uptake by the thyroid and some cases of goiter, presumably by interference of thiocyanate produced during normal cyanide detoxification by the endogenous rhodanese enzyme. Whether this occurs with lactonitrile exposure has not been reported.
  1. HYDROGEN CYANIDE may be released from lactonitrile in the presence of alkali. Both cyanide and oxides of nitrogen fumes may be evolved during thermal decomposition.
  1. The remainder of this discussion relates to CYANIDE POISONING and TREATMENT. The possibility of DELAYED ONSET of SYMPTOMS, up to SEVERAL HOURS AFTER LACTONITRILE EXPOSURE must be kept in mind. PROLONGED OBSERVATION is usually required for initially asymptomatic individuals with aliphatic nitrile exposure.
  1. RELEASED CYANIDE -
    1. Hydrogen cyanide gas exposure may produce death within minutes. Lesser exposures may produce nausea, vomiting, palpitations, confusion, hyperventilation, anxiety, and vertigo. Severe hypoxic signs in the absence of cyanosis suggest the diagnosis. Cyanide release after systemic lactonitrile absorption may take a considerable period, with SYMPTOM ONSET DELAYED for SEVERAL HOURS after exposure.
    1. Patients have survived potentially lethal cyanide exposures with supportive care only, and the absence of a rapidly deteriorating course does not exclude the diagnosis.
    1. Cyanosis is generally a late finding and does not occur until the stage of circulatory collapse and apnea. The patient's clinical state will depend on the extent and time since exposure. Initially the patient may experience flushing, tachycardia, tachypnea, headache, and dizziness. This may progress to agitation, stupor, coma, apnea, generalized convulsions, pulmonary edema, bradycardia, hypotension, and death.
  1. If systemic CYANIDE POISONING is suspected, IMMEDIATELY BEGIN ADMINISTERING 100% OXYGEN. OBTAIN THE CYANIDE ANTIDOTE KIT AND PREPARE IT FOR USE.
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