History
Key historical features for suspected hydrogen cyanide (HCN) casualties include the following [5, 4] :
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Onset, severity, and time course of symptoms
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Time, nature, and route of exposure
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Presence of smoke; odors and colors of gas
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Odor of bitter almonds (noted by approximately 40% of patients exposed to cyanide)
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Effects on surroundings (eg, dead animals or other human casualties)
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Evidence of exposure to other chemicals or co-ingestants
The delay between exposure and the onset of symptoms depends on the type of cyanide involved, the route of entry, and the dose. Rapidity of symptom onset, depending on the type of cyanide exposure, occurs in the following order (most rapid to least rapid): gas, soluble salt, insoluble salt, and cyanogens.
A history of recent depression in the patient with sudden collapse or altered mental status, metabolic acidosis, and tachyphylaxis in an intensive care unit patient who is receiving nitroprusside should evoke suspicion of the diagnosis.
Symptoms may include the following:
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General weakness, malaise, and collapse
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Neurologic symptoms (reflecting progressive hypoxia) - Headache, vertigo, dizziness, giddiness, inebriation, confusion, generalized seizures, coma
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Gastrointestinal symptoms - Abdominal pain, nausea, vomiting
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Cardiopulmonary symptoms - Shortness of breath, possibly associated with chest pain, apnea
Symptoms after exposure to high vapor concentrations may include the following:
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Transient hyperpnea and hypertension 15 seconds after inhalation
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Convulsions in 30-45 seconds
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Loss of consciousness in 30 seconds
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Respiratory arrest in 3-5 minutes
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Bradycardia, hypotension, and cardiac arrest within 5-8 minutes of exposure
Symptoms after exposure to lower vapor concentrations or after ingestion or liquid exposure may include the following:
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Delayed onset of symptoms of several minutes
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Feelings of apprehension or anxiety
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Vertigo
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Feeling of weakness
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Nausea, with or without vomiting
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Muscular trembling
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Loss of consciousness
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Headache
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Dyspnea
Patients exposed to cyanogen chloride experience severe eye and mucous membrane irritation. [23] Low-dose exposure results in rhinorrhea, bronchorrhea, and lacrimation. Inhalational exposure results in dyspnea, cough, and chest discomfort. Onset of symptoms after exposure to nitriles (acetonitrile and/or propionitrile) may be significantly delayed.
Physical Examination
Physical findings of cyanide exposure are generally nonspecific, yet the onset of illness may be dramatic. Findings can include the following:
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Vital signs are variable
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Initial bradycardia and hypertension - May rapidly give way to hypotension with reflex tachycardia, with resulting final bradycardia and hypotension
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Cardiac dysrhythmias may be followed by cardiac arrest
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Tachypnea - May be transient, with subsequent bradypnea followed by apnea
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High, falsely reassuring pulse oximetry - Oxygen is present in the blood as oxyhemoglobin but cannot be effectively used in oxidative phosphorylation
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Cherry-red skin color - Reflecting absent tissue oxygen extraction
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Soot in the mouth and nose after smoke inhalation
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The smell of bitter almonds on the breath (cannot be detected by 60% of the population)
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Normal or dilated pupils
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Diaphoresis
Neurologic symptoms may include the following:
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Altered mental status - Confusion, drunken behavior
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Mydriasis
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Ataxia
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Generalized convulsions
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Coma
Classically, the skin of a cyanide-poisoned patient is described as cherry red in color due to elevated venous oxygen content resulting from failure of tissues to extract oxygen. In addition, arterialization of the venous blood may also be noted during phlebotomy or examination of the retinal veins. Alternatively, patients may be cyanotic after prolonged respiratory failure and shock. Despite its name, cyanosis is not a prominent finding of cyanide poisoning. Finally, many patients with cyanide poisoning have normal-appearing skin.
