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Cyanide

poisoning Prepared by:

Hardi SdiqCollage of pharmacy

University of sulaimani

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 minutesIngestion

Delayed onset: 15 to 30 minutesSkin 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

almond250 mg CN/100g plant tissue

Cassava104 mg CN/ 100 g

plant tissue

Wild Cherries140-370 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 hypoxiaMetabolic 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 toxicityMild Toxicity

NauseaDizzinessDrowsiness

Moderate ToxicityLoss of consciousness for a short periodConvulsionVomitingCyanosis

Severe ToxicityDeep comaDilated non-reactive pupilsDeteriorating cardio-respiratory function

diagnosis

Case historysuspicion of exposure

Clinical presentationmetabolic acidosis, multisystem involvementodor of bitter almonds

Laboratory diagnosisblood cyanide levels can be drawn .high anion gap metabolic acidosisarterial and venous pO2 may be elevated .

treatmentTreatment 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 )