Introduction
Cyanide poisoning is a well known intoxication and a historically
recognized cause of suicide.(1) Cyanide salts are widely used in the
jewelry industry and are not readily available to the public. Ten
percent of the causes of intoxication and suicide involve cyanide
salts.(2,3) By disrupting the enzymatic pathways involved in cellular
respiration, cyanide hinders utilization of oxygen by cells leading to
their rapid dysfunction. Cyanide-induced hypoxia ultimately leads to
neurologic and cardiovascular compromise. (4)
Rapid diagnosis of cyanide poisoning may not be possible due to the
nonspecific presentations and the limited availability of blood cyanide
level kits and their time consuming nature. Headache, confusion,
vertigo, palpitations, respiratory distress and hyperventilation are
among the manifestations of acute cyanide intoxication. Rapid
development of hypotension, shock, bradycardia, and ultimately death may
ensue. (4) Cellular hypoxia leads to acid-base disorders, and lactic
acidosis is a hallmark of cyanide intoxication. Several studies have
pointed to lactate levels as a sensitive marker in cyanide poisoning.
(4)
Management of cyanide poisoning mainly comprises of supportive measures
for preserving organ perfusion and maintaining proper homeostasis by
correction of acid-base disorders and use of vasopressors and hydration
in cases of severe hypotension. Specific antidote kits are used in
emergency settings however, these kits may not readily be available at
all centers. Other measures such as hemodialysis and plasmapheresis may
be used on a case by case basis to eliminate toxic substances from the
circulation.(2,5)
In this report we present a case of an intentional cyanide ingestion who
was brought to our emergency department. Aside from supportive measures
taken, due to the unavailability of cyanide antidote kits at our center,
plasmapheresis was initiated.