Acrylonitrile toxicity

Background

• Industrial chemical used in production of plastics, rubber, and acrylic fibers
• Structure: Nitrile group linked to a vinyl group (CH2=CHCN)
• Dual toxicity mechanism: direct irritant/hepatotoxin AND metabolized to form cyanide
• Exposure routes: inhalation (most common occupational), dermal absorption, ingestion
• Also released in combustion of synthetic materials (house fires)

Clinical Features

• Early: Mucous membrane irritation, headache, nausea, vomiting, dizziness
• Cyanide effects: Altered mental status, seizures, lactic acidosis, hypotension, cardiovascular collapse
• Hepatotoxicity: Elevated transaminases, potential fulminant hepatic failure (delayed 1-3 days)
• Dermal exposure: erythema, blistering, chemical burns

Differential Diagnosis

• Cyanide toxicity
• Hydrogen sulfide toxicity
• Carbon monoxide toxicity
• Other nitrile compound exposures

Evaluation

• Labs: CBC, BMP, hepatic panel, lactate, VBG/ABG
• Cyanide levels (often not available rapidly)
• High anion gap metabolic acidosis with elevated lactate suggests cyanide component
• Monitor serial hepatic panels for delayed hepatotoxicity

Management

• Cyanide antidotes: hydroxocobalamin (preferred) or sodium thiosulfate
• N-Acetylcysteine (NAC) for hepatoprotection
• Aggressive decontamination: remove clothing, copious water irrigation for dermal exposure
• Supportive care: IV fluids, vasopressors for hypotension, benzodiazepines for seizures

Disposition

• Admit all symptomatic patients for monitoring (hepatotoxicity may be delayed)
• Asymptomatic exposures: observe minimum 4-6 hours with serial labs

See Also

• Cyanide
• Smoke inhalation