Pediatric emergency medicine trisk 4578 4578
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ion (Fe3+ ) and cobalt; in the body, the reaction of hydroxocobalamin with
cyanide yields cyanocobalamin, or vitamin B12 . The ability of the body to
metabolize small quantities of cyanide, given sufficient time, accounts for the
dependence of cyanide toxicity on conditions of concentration and exposure time.
The same amount of cyanide that will kill when given over a few minutes may be
successfully metabolized by the body if administered over several hours. Doses of
cyanide large enough to overwhelm normal metabolism inhibit electron transport
of the mitochondrial cytochrome chain. The inactivation of this enzyme site
results in cellular anoxia and a decreased arteriovenous oxygen difference (from
inability of cells to use delivered oxygen), increased lactic acid (from accelerated
glycolysis under anaerobic conditions), and metabolic acidosis.
Clinical Manifestations
Clinical manifestations of cyanide poisoning relate to cellular anoxia; thus the
heart and brain are most severely affected. High concentrations of cyanide vapor
initially produce tachypnea, hyperpnea, and hypertension within 10 to 15
seconds. Anoxic injury to the CNS and myocardium soon follow, with
unconsciousness and seizures (30 seconds after exposure), opisthotonus, trismus,
facial muscle spasm, decerebrate posturing, bradycardia, dysrhythmias,
hypotension, and eventually cardiac arrest (as early as 4 to 8 minutes after
exposure).
Exposure to low concentrations of vapor produces nonspecific effects such as
headache, light-headedness, nausea, and ataxia. “Classic” signs of cyanide
poisoning are said to include severe dyspnea without cyanosis, flushing from
increased oxygen content venous blood, and a bitter almond odor to breath and
body fluids. Noteworthy laboratory abnormalities in cyanide poisoning include an
abnormally high mixed venous oxygen saturation with a resultant decreased
arteriovenous oxygen content difference (one of the most useful laboratory
indicators of cyanide poisoning), a high anion gap metabolic acidosis, and
hyperlactatemia.
Both cyanide and nerve-agent casualties can collapse suddenly, stop breathing,
and convulse. Gasping, normal or dilated pupil size (as opposed to miosis), pink
skin (instead of cyanosis), and normal secretions (as opposed to increased
secretions) may lead to a clinical diagnosis of cyanide over nerve agent, but none
of these signs is pathognomic. The similarities between cyanide and nerve-agent
casualties may be more apparent than the differences.
Management
