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Cyanide poisoning 2012


Published on

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

Published in: Health & Medicine
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Cyanide poisoning 2012

  1. 1. Cyanide poisoning Hardi Sdiq Collage of pharmacy University of sulaimani 1
  2. 2. cyanideIt 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. 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 minutesDeath occurs in 6 to 8 minutes after inhalation of a high Concentration .2 to 5 mg/kg of it is lethal .
  4. 4. Plant source almond 250 mg CN/100g plant tissue Cassava Wild Cherries104 mg CN/ 100 g plant 140-370 mg CN/ 100 g tissue plant material
  5. 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. 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. 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. 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. 9. treatment Treatment regimen depends on : severity of symptoms, route of exposure ,and what is available Treatment options are:1) Sodium nitrite2) Sodium thiosulfate3) Amyl nitrite4) Activated charcoal5) Supplemental oxygen6) Hydroxocobalamin
  10. 10. Commercial cyanide antidote kits contain Sodium nitrite & sodium thiosulfateFirst 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. 11. Second step :use sodium thiosulfate : which is administered IV.The sodium thiosulfate and cyano-methemoglobinbecome thiocyanate, releasing the hemoglobin, andthe thiocyanate excreted by the kidneys .
  12. 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 )