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.