1 Cyanide poisoning

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.

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 104 mg CN/ 100 g plant tissue Wild Cherries mg CN/ 100 g 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.

Example on cyanide poisning Cyanide used in its attack on the Kurdish village of Halabja in Five thousand people died and many were discovered sitting exactly where they were when the gas hit, their systems paralysed from within. On December 5, 2009, a fire in the night club Lame Horse (Khromaya Loshad) in the Russian city of Perm took the lives of 156 people. 111 people died on the spot and 45 later in hospitalsfire in the night club Lame HorseRussianPerm

Properties that make cyanide more dangerous 1-in some case don’t have specific odour 2- may don’t have color 3- large number of sorce in our life 4-may found in many state

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

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 : g IV )