power point presentation of Clinical evaluation of strabismus
Cyanide poisoning 2012
1. Cyanide poisoning
Hardi Sdiq
Collage of pharmacy
University of sulaimani
1
2. 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 .
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 Wild Cherries
104 mg CN/ 100 g plant 140-370 mg CN/ 100 g
tissue 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:
1) Sodium nitrite
2) Sodium thiosulfate
3) Amyl nitrite
4) Activated charcoal
5) Supplemental oxygen
6) 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 )