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.