INTRODUCTION — Cyanide is a mitochondrial toxin that is among the most rapidly lethal poisons known to man. Used in ancient times as a method of execution, cyanide causes death within minutes to hours of exposure. Though significant cyanide poisoning is uncommon, it must be recognized rapidly to ensure prompt administration of life-saving treatment
CLINICAL PRESENTATION — Clinical features of cyanide poisoning are dependent upon the route, duration, and amount of exposure. Central nervous system and cardiovascular system dysfunction are most prominent. Symptoms and signs can include the following:

Central nervous system - Headache, anxiety, confusion, vertigo, coma, seizures
Cardiovascular - Initial tachycardia and hypertension, then bradycardia and hypotension, atrioventricular block, ventricular dysrhythmias
Respiratory - Initial tachypnea then bradypnea, pulmonary edema
Gastrointestinal - Vomiting, abdominal pain
Skin - Flushing, cherry-red color, cyanosis (late finding)
Renal - Renal failure
Hepatic - Hepatic necrosis
Miscellaneous - Rhabdomyolysis, bright red venules seen on fundoscopy [22]
Symptoms depend on the route of cyanide poisoning. After inhaling hydrogen cyanide (HCN), the victim may detect a bitter, almond odor (discernible to approximately 60 percent of the population) [22]. Initially, inhalation of small amounts of HCN causes headache, anxiety, nausea, and a metallic taste [8]. In contrast, cyanogen chloride (CClN) exposure predominantly results in eye and mucous membrane irritation and then pulmonary symptoms, namely bronchorrhea, cough, and dyspnea [20]. Inhalation of 100 ppm for 30 minutes or 300 ppm for five minutes is usually fatal [8].

While toxicity from parenteral exposure begins within seconds, toxicity from ingestion or dermal exposure is delayed from minutes to hours, depending on the extent of exposure. Ingestion of cyanide salts results in gastric irritation, frequently causing vomiting and abdominal pain [15]. The lethal oral dose of cyanide is 50 mg of HCN and 200 mg of potassium cyanide (KCN) in an adult [8,20]. The lethal dermal exposure is estimated to be 100 mg/kg (show table 3) [6].

Delayed sequelae — Survivors of severe cyanide poisoning may develop delayed-onset Parkinsonism or other neurologic sequelae. The basal ganglia in particular are sensitive to cyanide toxicity [22]. Basal ganglia injury may be due to either direct cellular injury or secondary hypoxic effects. Computed tomography (CT) and magnetic resonance imaging (MRI) of the brain usually demonstrate radiologic changes several weeks after the exposure. Resolution of symptoms is variable, and treatment is supportive.

Chronic cyanide exposure — Chronic cyanide exposure results in vague symptoms, such as headache, dysgeusia (abnormal taste), vomiting, chest pain, abdominal pain, and anxiety [8]. There are at least three insidious syndromes associated with chronic, low-level cyanide exposure: tobacco amblyopia, tropical ataxic neuropathy, and Leber hereditary neuropathy.