0071643192.pdf

TOXICOLOGY

MECHANISM/TOXICITY

■ Inhibits cytochrome oxidase, disrupting oxidative phosphorylation →cellular
hypoxia and lactic acidosis

SYMPTOMS/EXAM

■ Effects are very rapid following CN inhalation or absorption.
■ In contrast, toxicity due to amygdalin may be delayed by hours as CN is
released by metabolism.
■ Early symptoms of N/V, headache, and confusion are followed rapidly by
seizures and coma.
■ Cardiovascular findings include hypertension and tachypnea (initially),
dysrhythmias, pulmonary edema, and cardiac arrest.
■ Skin may appear flushed or cyanotic.

DIFFERENTIAL

Any other cause of coma, shock, or lactic acidosis

DIAGNOSIS

■ CN poisoning should be considered in any patient presenting with rapid
onset of coma, shock, and marked lactic acidosis.
■ ABG findings are similar to severeCO poisoning.
■ Clues to the diagnosis include:
■ A history of smoke inhalation or occupational access to CN
■ Evidence of decreased tissue extraction of O 2 :
■ Arterial appearance of venous blood
■ Elevated measured venous O 2 saturation (>90%)
■ Marked lactic acidosis
■ Patient has a distinct, almond-like smell. Many individuals are geneti-
cally incapable of detecting this odor.
■ Blood CN levels can be directly measured, but are not available in a
timely manner.

TREATMENT

■ Acute stabilization as required
■ Surface decontamination, if indicated
■ Antidote = cyanide antidote kit; three components:
■ Amyl nitrite pearls (for inhalation)
■ Use until IV access is obtained.
■ Induces methemoglobinemia
■ Methemoglobin strongly binds CN, pulling it away from cellular
enzymes.
■ Is used illicitly as “poppers”
■ IV sodium nitrite
■ Induces methemoglobinemia
■ IV sodium thiosulfate
■ Binds to CN to form thiocyanate, a much less toxic compound that
is renally excreted
■ A smoke inhalation victim with suspected CN poisoning should only
receive sodium thiosulfate. There is the potential for worsening tissue oxy-
genation from nitrite-induced methemoglobinemia.
■ Antidote = hydroxycobalamin.

Laboratory clues to CN

poisoning: Marked lactic

acidosis, arterial appearance

of venous blood, elevated

measured venous O 2

saturation

Suspect CN poisoning if

patient presents with rapid

onset of coma, shock, and

severe metabolic acidosis.

Sodium thiosulfate should be

administered empirically if CN

poisoning is considered.

Avoid using sodium nitrite in

smoke inhalation victims with

suspected CO poisoning. Use

sodium thiosulfate alone.