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Cyanide poisoning

       Hardi Sdiq
    Collage of pharmacy
   University of sulaimani


                             1
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 .
 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 .
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
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 ) .
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.
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
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 .
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
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.
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 .
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 )

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Cyanide poisoning 2012

  • 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 )