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