Discussion
Early recognition of cyanide toxicity in the emergency department is of utmost importance. Patients with cyanide toxicity can present with a variety of manifestations based on the amount consumed, the time from consumption, and the route of exposure. In this manuscript we have presented a case of a 39 year old man who presented with acute cyanide poisoning and was treated with plasmapheresis in adjunct to other supportive measures.(6)
Although cyanide exposure can occur unintentionally and in occupational settings such as mining, agriculture, smoke, and metal industries, intentional ingestion of cyanide salts have been historically used for suicide and murder. Although the clinical presentations and laboratory data may not be specific at the time of presentation, some patients such as our case may confess of having intentionally ingested toxic cyanide salts.(3)
Patients with exposure to cyanide can present with altered levels of consciousness, seizures, respiratory compromise, nausea, vomiting, cardiac arrhythmias and arrest, blood pressure changes, altered body temperature, etc. All these symptoms arise secondary to cellular anoxia caused by cyanide, therefore organs with a high rate of oxygen consumption such as the brain, the heart, and the kidneys are prominently susceptible to damage. Although cherry red skin and bitter almond odor may be more specific of cyanide toxicity, they are only present in a minority of patients (~15%).(6,7)
Primary management of cyanide poisoning is similar to the management of other toxicities; supportive care. Oxygen supplementation, hydration, and removal of the toxic source are the mainstay of therapy. Patients’ vital signs and cardiac function should be monitored continuously. Intubation and vasopressors are inevitable if respiratory compromise or refractory hypotension occur, respectively. When available a cyanide antidote kit which consists of sodium thiosulfate, sodium nitrite, and amyl nitrite. Amyl nitrite and sodium nitrite cause the dissociation of cyanide from the cellular cytochrome oxidase, leading to cellular relief and the reversion to aerobic metabolism. The methemoglobinemia secondary to the use of nitrites will then be resolved by sodium thiosulfate. The end result is the excretion of thiocyanate in the urine.(6)
In our case, aside from vigilant supportive management, due to the unavailability of the cyanide antidote kit, we utilized plasmapheresis for intoxication. Plasmapheresis is not a common measure in cases of cyanide poisoning, however there have been seldom reports of plasmapheresis in such cases.
Z. Liu et al.(2) has reported a case of a 24 year old male patient who was diagnosed with concurrent methanol and cyanide poisoning. The patient has presented with bradycardia, hypotension, and decreased consciousness. Aside from supportive management, the patient was started on plasmapheresis 3 hours post-ingestion. The procedure was 2 hour in duration during which 2400 cc plasma was removed from the patient with 3000 cc of replacement solution consisting of 2000 cc of FFP and 1000 cc of NS. The patient had undergone hemodialysis after plasmapheresis. In our case the patient did not have any concurrent poisoning besides cyanide ingestion and did not undergo hemodialysis.
In another case Shatila et al.(8) has introduced a case of a young individual who presented to the emergency department with low oxygen saturation and increased methemoglobinemia. Supportive measures were taken and the patient was started on plasmapheresis on the second day of admission, however, primarily due to suspected thrombotic thrombocytopenic purpura (TTP). Plasmapheresis continued for six days during which after methemoglobin levels normalized. Although cyanide toxicity does not directly cause methemoglobinemia, the latter can be induced by the use of nitrites in such cases. In cases when the cyanide antidote kits may not be complete, induction of methemoglobinemia and subsequent plasmapheresis may be an option.