CYANIDE (CN)

 

Etiology:

  1. Exposure can occur from food such as almond, apricot and cherry pits, medications ( IV Nitroprusside rarely seen before 24 hr treatment), paint removals, glue, burning synthetics (plastic, polyurethane, nylon), pesticides.
              
  2. CN binds to  Fe+++ in  mitochondria and interferes with oxidative phosphorylation producing  anaerobic milieu.
     
  3. Our body contains rhodanase, an enzyme that facilitates binding of cyanide to sulfur.  The compound formed, thiocyanate, is not toxic and is excreted renally.

S & S:

  1. Symptoms depend on amount of CN ingested and are 2ry to ¯ O2 & hypoxia except that pts are not cyanotic. Due to ¯ O2  pts will be confused, LOC, SZ, c/o chest pain, arrhythmia, SOB.
     
  2. Metabolic signs of hypoxia such as lactic acidosis with consequent AG met. acidosis.
  3. Cellular hypoxia causes the O2 not be utilized by cells and thus more O2 is found in venous bed. This causes the ratio between arterial and venous bed in [O2] to be decreased, i.e. the O2 % in vein is >40% and the AO2-VO2 gradient is decreased.
     
  4. Pts presumably have a smell of  bitter almonds on exam but only  a minority, 20%  of  the general  population, can detect this smell.

DX:

  1. Although the level of cyanide does not correlate with symptoms, its presence confirms the clinical suspicion. Cyanide has to be measured in whole blood since it is intracellular and intraerythrocyte.

Treatment:

  1. 100% O2, cardiac monitor.
     
  2. In USA a Cyanide Antidote Kit exists that contains  3  antidotes. See the kit for proper dosage.
     
    1. A vial  of amyl nitrates  is broken and pt  inhales it. It is used only if pt does not have  IV.
       
    2. If pt has IV, start sodium nitrate .
       
    3. After sodium nitrate, start  sodium thiosulfate.  Nitrates work by forming methemoglobin that binds to cyanide, preventing it  from binding to cytochrome oxidase. The therapeutic goal is to have methemoglobin level of 25%. Thiosulfate is a "bag" full of  sulfur which is utilized by  rhodonase as a magnet of cyanide from methemoglobin. In  this way thiocyanate is formed which is excreted renally.

[BACK]