cyanide poisoning 2012
DESCRIPTION
Cyanide poisoning Source of Cyanide , Mechanism of toxisity , Clinical manifistatin , Diagnosisand treatment prepared by : Hardi S. MuhemmedTRANSCRIPT
1
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 )