2. 

Cyanide ( hydrocyanic acid, prussic
acid) is NOT a common poison.
Most cyanide ingestions occur from
accidental exposure or intentional
ingestion of a cyanide-containing
compound.

3. 

Some fruit seeds
contain TOXIC
LEVELS of cyanide.
Amygdalin, which is
hydrolyzed to
hydrogen cyanide is
present in the seeds
of
apple, peach, plum,
apricot, cherry, and
almond.

4. Usually exposure occurs in industry.
Hydrocyanide and its derivatives are used
in electroplating, metallurgy, and
extraction of gold and silver from
ores, plastic manufacture, and many
other industries.
 It’s very important to know that
intoxication does not happen only through
ingestion, it also happens from inhalation
or absorption through the skin.
 In the presence of cyanide gas, a gas
mask alone does not offer complete
protection from intoxication.



6. Hydrogen cyanide is
readily volatilized to
hydrogen cyanide, with a
characteristic odor of
bitter almonds.
 Cyanide salts are the most
frequently encountered of
all cyanide-containing
compounds.
 LD50 for these salts is 2
mg/kg, and the ingestion
of 50-75 mg of these salts
results in syncope and
respiratory difficulty.


8. 



Cyanide produces histotoxic cellular hypoxia by
binding to ferric ( Fe3+ ) ion in the electron
transport system.
Cyanide binds to the cytochrome oxidase system
inhibiting electron transport , consequently no
ATP can be generated, this results in reduced
cellular utilization of oxygen.
As a summary, cyanide has the same
pathophysiologic effect as a complete lack of
oxygen .
As a result, aerobic respiration ceases resulting in
a decrease in pyruvate conversion in the Krebs
cycle , therefore lactate increases resulting in
metabolic acidosis .

10. cyanide is extremely rapid acting and
capable of producing death within minutes.
 the classic odor of bitter almond is not
detected by everyone (genetically
determined) .
 Hydrogen cyanide vapors are the most
rapidly acting. But when cyanide salts are
ingested toxicity is delayed because they
are slowly absorbed.
 The severity of acute poisoning is
determined by the dose and time since
exposure.


11. Cyanide stimulates chemoreceptors in
aortic and carotid bodies to signal
respiratory center in the brain which results
in increased respiration (hyperpnea, i.e.
increased minute ventilation)
 As cyanide levels increase (severe
poisoning) respiration rate slows and
gasping occurs, but still, with no or minimal
cyanosis.
 Severe CNS oxygen deprivation may cause
hypoxic convulsions and death due to
respiratory arrest.


12. 





Cardiovascular and central nervous
system most affected body systems
Exposure is rapidly fatal unless antidote
quickly administered
Depend on CN Levels in the body which
are measured by the methemoglobin
level:
Normally <1% of our Hb is methemoglobin
Pts remain Asx to a lvl up to 20% ,showing
only skin discoloration
Sx start to appear at lvls >20% ,and
manifest mainly as neurological toxicity
,tachypnea & tachycarida

13. 1-3% - asymptomatic
 3-15% - slight grayish-blue skin
discoloration
 15-20% - asymptomatic, but
cyanotic
 So 25-50% headache, dyspnea, confusion, wea
kness, chest pain
 50-70% - altered mental
status, delirium


14. Weakness
 Dizziness
 Headache
 Nausea and vomiting
 Tachycardia
 Flushing
 Those occur rapidly and non-specific .


15. Stuporous but responsive to stimuli
 Tachycardia
 Tachypnea


16. Comatose
 Unresponsive
 Hypotension
 Bradypnea & gasping
 Dilated pupils
 Cyanosis ( at high levels)
 Death unless treated immediately


17. The aim is to decrease the amount of
cyanide available for cellular binding, and
decrease its binding to cytochrome
oxidase.
 Treatment must be initiated immediately to
be effective.
 But because it acts so rapidly, intentional
ingestion (suicide) almost always leads to
death. In addition, diagnosis can be
delayed, which also may result in death.
 Luckily, specific antidotes are available.


18. Resuscitation :ABC
2. Decontamination :
 If due to Inhalation :(remove clothes ,flush
with water ,removal of the individual from
the source)
 If due to Ingestion : (Administer activated
Charcoal /gastric lavage)
3. Cyanide Antidote Package
4. Other CN Antidote kits :4methylaminophenol ,Hyperbaric oxygen
1.

19. 


Cyanide (even at toxic concentrations)
can dissociate from ferric ion binding
sites and be converted to thiocyanate in
the presence of thiosulfate and sulfur
transferase.
Thiocyanate is relatively nontoxic and is
rapidly excreted by the kidneys.
BUT, when this endogenous detoxification
system becomes saturated, toxicity
occurs, unless specific treat is initiated.

20. 



The main principle of treatment is to produce
methemoglobin because it contains ferric (Fe3+ )
ion, and thus competes with cytochrome
oxidase for binding cyanide.
Cyanide + methemoglobin 
cyanomethemoglobin
Methemoglobin has a greater affinity for cyanide
than does cytochrome oxidase.
Therefore, methemoglobin can bind to free
cyanide and also cause dissociation of the
cyanide-cytochrome oxidase complex, thus
reactivating it.
In summary, to treat cyanide poisoning we have
to produce methemoglobin in the blood!!!

21. 
How to produce methemoglobin?
1. Methylene blue (in large doses)
2. Amyl nitrite (inhalation) produces only 5%
3. Sodium nitrite (IV)


Hemoglobin(Fe+2 ) + amyl nitrite &/or
sodium nitrite  methemoglobin (Fe+3 )
The desired percentage of methemoglobin
is around 40%.

23. BUT, all the above reactions are REVERSIBLE
and may shift in the opposite direction.
 This is the reason that there is a 2nd phase of
treatment.
 The 2nd phase involves the binding of
cyanomethemoglobin with thiosulfate in the
presence of sulfur transferase to produce
thiocyanate (which is excreted by the
kidneys).
 Cyanomethemoglobin + thiosulfate 
thiocyanate + sulfite + methemoglobin


24. 


BE CAREFUL, because too much methemoglobin
can shift the oxygen dissociation curve to the
left, thus decreasing the amount of oxygen
available for the tissues. And because the tissue
ability to utilize oxygen is already diminished by the
presence of cyanide, too much methemoglobin
can worsen tissue hypoxia.
However, this doesn’t happen unless
methemoglobin concentration reaches 40-50%.
ALSO, nitrites can produce profound hypotension
and cardiovascular collapse thus rendering the
treatment completely ineffective.

25. Oxygen is NOT a specific antidote for
cyanide poisoning. BUT, it is a necessary
adjunct.
 Mechanisms:

1. Displace cyanide from cytochrome oxidase
2. Nonenzymatically convert reduced cytochrome
to oxidized cytochrome enabling the electron
transport system to function again

Unlike treating CO poisoning, oxygen
administration does not produce significant
benefits.