Cyanide poisoning 2012

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

1. 1 Cyanide poisoning Prepared by : Hardi Sdiq Collage of pharmacy University of sulaimani

2. cyanide It is a rapidly acting lethal agent that is limited in its military usefulness by its high LCt 50 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 104 mg CN/ 100 g plant tissue Wild Cherries 140-370 mg CN/ 100 g 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: Sodium nitrite Sodium thiosulfate Amyl nitrite Activated charcoal Supplemental oxygen 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 )