Cyanide poisoning Hardi Sdiq Collage of pharmacy University of sulaimani 1
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 .
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 .
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
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 nitrite2) Sodium thiosulfate3) Amyl nitrite4) Activated charcoal5) Supplemental oxygen6) Hydroxocobalamin
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.
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 .
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 )