CYANIDE POISONING
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Cyanide exposure occurs relatively frequently in patients with smoke inhalation from
residential or industrial fires particularly in the metal trades, mining, electroplating, jewelry
manufacturing, radiographic film recovery, tanning,fumigation of ships and agriculture to
prevent plant decay..
Forms:a) Gaseous: hydrogen cyanide/cyanogas  a colourless gas with a penetrating odour
resembling that of bitter almonds; exists in the form of glucoside amyglin that is hydrolysed
by emulsin and liberates the harmful HCN.
b) Water Soluble Cyanide: Salts KCN and NaCN
c) Poorly Water Soluble Cyanide Salts: mercury, copper, gold, and silver
d) Hydrocyanic/prussic acid )  colourless highly volatile fluid ; a vegetable acid found in many
fruits (peach,plum and bitter almonds) and leaves of cherry royal
e) Cyanide Containing Compounds/Cyanogens: cyanogen chloride and cyanogen bromide,
nitriles (R-CN), and sodium nitroprusside, synthesized compounds (polyacrylonitrile,
polyurethane, polyamide, urea-formaldehyde, melamine) and natural (e.g., wool, silk)
f) Foods: such as cassava root or apricot seeds, may lead to cyanide poisoning.
Routes Of Absorption:Parenteral Administration,Inhalation,Ingestion,Dermal absorption
Fatal Dose:
Pure acid50-60 mg
30 dropspharmaceutical preparation
60 dropscrude bitter almond oik
200 mgKCN
Fatal Period:
CyanogasInstant2-10 mins
KCN30 mins
PathogenesisCyanide containing compound when dissolved in water produces cyanide ions (CN−)  The cyanide
ion halts cellular respiration by inhibiting Cytochrome C Oxidase in the mitochondria  Histotoxic
Hypoxia (because the cells of an organism are unable to use oxygen)
1) Acute poisoning
Acute hydrogen cyanide poisoning can result from inhalation of fumes from burning polymer
products such as wool, silk, polyurethane, or vinyl.
?A fatal dose for humans can be as low as 1.5 mg/kg body weight.
 At lower doses, loss of consciousness may be preceded by general weakness, giddiness,
headaches, vertigo, confusion, and perceived difficulty in breathing.
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At the first stages of unconsciousness, breathing is often sufficient or even rapid, that
progresses to a deep coma, sometimes accompanied by pulmonary edema, and finally
cardiac arrest. A cherry red skin color may be present as the result of increased venous
hemoglobin oxygen saturation.
2) Chronic exposure
Pesticides, insecticides, tobacco smoke, smoke from building fires and some foods, like almonds,
apricot kernel, apple seeds, orange seeds, and cassava.
 Chronic consumption of cyanide-containing foods eventually can result in ataxia and optic
neuropathy and sub acute blindness.
 Cyanide also may cause some of the adverse effects associated with chronic smoking, such
as tobacco amblyopia.
 Exposure to lower levels of cyanide over a long period results in increased blood cyanide
levels, which can result in weakness and a variety of symptoms, including permanent
paralysis, nervous lesions, hypothyroidism, and miscarriages.
 Other effects include mild liver and kidney damage.
Treatment of poisoning and antidotes
1-Of Acute Poisoning
1)
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When To Suspect Cyanide
Sudden collapse of laboratory or industrial worker
Fire victim with coma or acidosis
Suicide with unexplained coma or acidosis
Ingestion of artificial nail remover
ICU patient with altered mental status, acidosis and tachyphylaxis to nitroprusside
2)
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Supportive Crae
Control airway, ventilate and give 100 % oxygen
Crystalloids and vasopressors for hypotension
Administer sodium bicarbonate, titrate according to ABGs and serum bicarbonate
3) Antidote
 Amyl nitrite pearls:
Included in the kit for pre-hospital use
 Give sodium nitrite (NaNO2):
Adult dose:- 10ml/300mg
Preferred methaemoglobin inducer for hospital management
3% solution is given intravenously over 2-4 mins
 Caution
Monitor BP frequently.
Treat hypertension by slowing infusion rate, giving crystalloids and vasopressors.
Obtain met-Hb level 30 mins after dose and consider possible excessive met-Hb formation if
patient deteriorates during therapy
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 Give sodium thiosulfate (NaS2O3)
25% solution is given intravenously
Adult Dose:-50ml/12.5g
Paediatric Dose:-1.65ml/kg
4)
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Decontaminatin
Protect healthcare provider from contamination
Cutaneous: Carefully remove all clothing and flush the skin
Ingestion: Gastric levage with 1g/kg activated charcoal
5)
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Laboratory
ABGs
Electrolytes and glucose
Blood lactate
Whole blood cyanide concentration (for later confirmation only)
Consider a central venous blood gas
2-Of Chronic PoisoningVitamin B12 in the form of hydroxycobalamin, or hydroxocobalamin, may reduce the negative effects
of chronic exposure, and a deficiency can lead to negative health effects following exposure.
Post-Mortem Findings:
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a) External:Smell of bitter almons from the body.
Slight Corrosion of mouth.
SkinC yanosed, NailsBlue.
The eyes may be bright, glistening and prominent with dilated pupils.
The jaws are firmly closed and there is froth in the mouth.
The color of post-mortem staining is bright red/pink.
Early rigor mortisIf death preceeded by convulsive seizures
Internal:Bitter almond like smell from body cavities (stomach,brain,serous cavities).
Brain Hyperemic.
Blood stained froth may be found in the trachea and bronchi.
There is congestion of viscera and edema of lungs. Also petechial hemorrhages may be
present in pleura and pericardium.
All the vessels of the body including veins contain arterial blood.
The mucosa of stomach and intestine is often pink (due to the formation of
cyanmethaemoglobin) and congested. The mucosa may be brown due to haematin
formation.