Cyanide poisoning Source of Cyanide , Mechanism of toxisity , Clinical manifistatin , Diagnosis and treatment prepared by : Hardi S. Muhemmed

1. Cyanide poisoning
Hardi Sdiq
Collage of pharmacy
University of sulaimani
1

2. cyanide
It is a rapidly acting lethal agent that is limited in its
military usefulness by its high LCt50 and high
volatility.
Physical characteristics:
cyanides are in liquid state in
munitions, but rapidly vaporize
upon detonation of the munitions.
The major threat is from the vapor .

3.  Cyanide is hazardous by:
 Inhalation
 Rapid onset: seconds to minutes
 Ingestion
 Delayed onset: 15 to 30 minutes
 Skin contact
 Delayed onset: 15 to 30 minutes
Death occurs in 6 to 8 minutes after inhalation of a
high Concentration .
2 to 5 mg/kg of it is lethal .

4. Plant source
almond
250 mg CN/100g plant tissue
Cassava Wild Cherries
104 mg CN/ 100 g plant 140-370 mg CN/ 100 g
tissue plant material

5. Mechanism of toxicity
 It produce cellular hypoxia
 by binding to ferric iron
 specially that present in
 cytochrom oxidase system .
 When it bind to this enzyme
complex electron transport is inhibited
( ATP will not produced ) this is result in decrease
cellular utilization of oxygen ( hypoxia ) .

6. Clinical manifestations
• Common final pathway for cyanide intoxication
is cellular hypoxia
 Metabolic acidosis: nonspecific symptoms
 CNS: dizziness, nausea, vomiting, drowsiness,
tetany, trismus, hallucations
 CV: arrhythmia, hypotension. Tachycardia and
hypertension
 Respiratory: dyspnea, initial hyperventilation
followed by hypoventilation and pulmonary
edema.

7. Sign and symptom of its toxicity
 Mild Toxicity
 Nausea
 Dizziness
 Drowsiness
 Moderate Toxicity
 Loss of consciousness for a short period
 Convulsion
 Vomiting
 Cyanosis
 Severe Toxicity
 Deep coma
 Dilated non-reactive pupils
 Deteriorating cardio-respiratory function

8. diagnosis
 Case history
 suspicion of exposure
 Clinical presentation
 metabolic acidosis, multisystem involvement
 odor of bitter almonds
 Laboratory diagnosis
 blood cyanide levels can be drawn .
 high anion gap metabolic acidosis
 arterial and venous pO2 may be elevated .

9. treatment
 Treatment regimen depends on : severity of
symptoms, route of exposure ,and what is available
 Treatment options are:
1) Sodium nitrite
2) Sodium thiosulfate
3) Amyl nitrite
4) Activated charcoal
5) Supplemental oxygen
6) Hydroxocobalamin

10. Commercial cyanide antidote kits
contain Sodium nitrite & sodium thiosulfate
First step :
 use Sodium nitrite : converts a portion of the
hemoglobin into methemoglobin.
 effectively pulling the cyanide off the cells and
onto the methemoglobin. Once bound with the
cyanide, the Methemoglobin becomes
cyanomethemoglobin.

11. Second step :
use sodium thiosulfate : which is administered IV.
The sodium thiosulfate and cyano-methemoglobin
become thiocyanate, releasing the hemoglobin, and
the thiocyanate excreted by the kidneys .

12. Amyl nitrite :
-An inhaled drug, similar to sodium nitrite but
with little systemic distribution: second line
agent used when sodium nitrite is not available .
Activated charcoal :
-For alert, asymptomatic patients
following ingestion .
Oxygen supplement :
-100% for suspected exposure .
Hydroxocobalamin
-Mechanism: direct binding agent,
chelate the cyanide.( dose : 4 - 5 g IV )