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It is suggested in the passage that lactic acidosis in patients suffering from smoke inhalation ----.
The most common cause of cyanide poisoning is
smoke inhalation. A source to the public is
acetonitrile in the form of artificial fingernail remover.
Cyanide poisoning produces cellular hypoxia by
binding with the ferric iron of mitochondrial
cytochrome oxidase, disrupting the electron transport
chain and the ability of cells to use oxygen. Patients
who inhale cyanide may rapidly develop coma,
shock, seizures, lactic acidosis, and respiratory and
cardiac arrest. Mild exposures following smoke
inhalation are now being described. Diagnosis may
be difficult in these patients, and emergency
administration of an antidote may be lifesaving.
Patients with smoke inhalation who show evidence of
lactic acidosis should be suspected of cyanide
poisoning. The body has a natural enzyme, called
“rhodanese”, which can complex cyanide and sulphur
to form mildly toxic thiocyanate. Intravenous
administration of sodium thiosulphate provides the
sulphur necessary to produce thiocyanate and is
relatively safe. Sodium nitrite may also be
administered, but its use is reserved for the most
critical cases only, because it causes hypertension
and methemoglobinemia.