This presentation includes:
Other names of hydrocyanic acid
Physical appearance of cyanides
Commercial uses of cyanides
Sources of cyanides
Mode of action of cyanides
Fatal Dose and fatal period of cyanides
Acute Poisoning of cyanides
Chronic Poisoning of cyanides
Diagnosis of cyanides
Treatment of cyanides
Post-Mortem appearance
Medicolegal importance
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HYDROCYANIC ACID.pdf
1.
2. HYDROCYANIC ACID (HCN)
PRESENTED BY:
MR. ARSLAN JAMEEL
MR. AHSAN ARSHAD
MR. QAMAR RASHID
PESENTED TO:
DEPARTMENT OF FORENSIC MEDICINE & TOXICOLOGY, FMU FAISALABAD
3. GENERAL INFORMATION
OTHER NAMES:
Cyanogen
Prussic acid
PHYSICAL APPEARANCE:
1. GASEOUS STATE: HYDROGEN CYANIDE,
characterized by peculiar odor of BITTER ALMONDS
2. LIQUID: called as HYDROCYANIC ACID or PRUSSIC
ACID
3. SOLID: Salts of cyanide in the white crystalline
powder.
4. COMMERCIAL USES
INDUSTRIAL:
Electroplating,
metal processing,
extraction of ores,
photographic processes,
production of synthetic rubber
manufacture of plastics
AGRICULTURE: insecticide and rodenticide
MEDICINAL:
oLaetrile: Chemotherapeutic agent for cancer
oSCHEELE’S ACID: used in veterinary medicine contains 4% of the acid
oSODIUM NITROPRUSSIDE: Effective antihypertensive (IV)
LABORATORY: Preparation of Acrylonitrile
5. SOURCES
PLANTS:
Cyanogenic glycosides (Amygdalin)
o Kernels of common cherry
o Peach
o Plum
o Apricot
o Bitter Almonds
COMBUSTION:
oBurning of plastic furniture (Polyurethane),
oBurning of silk or wool
oCigarette smoking
Each cigarette liberates 150-200 ug of HCN
6. MODE OF ACTION
Inhibits succinic dehydrogenase, superoxide dismutase & carbonic
anhydrase
Stimulate carotid & aortic bodies resulting in hyperpnea and have a
cardio-toxic role.
.
7.
8. Fatal period
Fatal Dose
Vegetable Acid
Instantaneously
1 part in 2000
Hydrogen cyanide Within few minutes
1 part in 10,000
Within few hours
1 part in 50,000
2-10 min.
50-60 mg
Hydrocyanic acid
30 minutes
100-200 mg
Cyanide Salt
FATAL DOSE & FATAL PERIOD
Potassium Cyanide Hydrogen Cyanide
HCl
Stomach
9. SIGNS AND SYMPTOMS
ACUTE POISONING:
Inhalation:
a) Causes most rapid onset (within seconds),
b) Serious exposure results in comma and death due to
respiratory arrest
Ingestion: Less rapid onset (within minutes)
10. SYSTEMS INVOLVED
GIT:
Burning taste,
Numbness in mouth and
throat,
Salivation,
Frothing,
Nausea,
Vomiting,
Substernal and
epigastric pain
CNS:
Headache,
Dizziness,
Sweating,
Syncope,
Seizures
Comma
Death
Pupils often dilated and
sluggish in reaction
13. CVS:
Initially hypertension with reflex bradycardia followed by
Hypotension
Tachycardia
Arrhythmia
Venous oxygen tension approaches that of arterial blood
because cellular usage of oxygen is blocked
Bright red color of the venous blood is clearly evident on
fundoscopy
Lactic Acidosis:
Blockade of cellular respiration leads to excessive anaerobic
metabolism causes lactic acidosis
SYSTEMS INVOLVED
14.
15. CHRONIC POISONING
Survivors of serious acute poisoning may develop delayed
neurologic sequelae like PARKINSONS DISEASE and TREMORS
TROPICAL ATAXIC NEUROPATHY:
Pheripheral sensory neuropathy
Deafness
Ataxia
Glossitis
Scrotal dermatitis
LEBER’S HEREDITARY OPTIC ATROPY
Sensitivity of optic nerve to cyanide ( congenital deficiency
of Rhodanese)
TOBACCO AMBLYOPIA:
Loss of visual functions, exclusively in heavy smokers
16. DIAGNOSIS
1. Odour of bitter almonds
2. Serum cyanide level (Confirmatory)
Levels >0.2ug/ml are considered toxic
3. Laboratory findings:
Serum Lactate level >10 m mol/L
Arterial blood gas analysis shows normal O2 saturation
and metabolic acidosis
Elevated venous O2 saturation
4. ECG:
Bradycardia followed by Tachycardia
5. LEE JONE’s TEST:
Ferrous Sulphate + 5cc gastric fluid
Boil and Cool
Add 8-10 drops of HCl
Greenish Blue color indicates cyanide
17. TREATMENT
Time is the essence.
Stabilization:
Assisted ventilation and 100% oxygen
cardiac monitoring
IV excess
Treatment of metabolic acidosis
Vasopressors for hypotension
Decontamination:
Cutaneous exposure
Ingestion
Activated charcoal, cathartics
18. TREATMENT
Antidote therapy:
Consists of 3 steps Eli Lilly Cyanide kit approach
STEP 1: Amyl nitrite (crushed and inhale for 30 sec.
Step 2: Sodium nitrate 3% soln. slow IV i.e. over 5-10 min.
Hb + amylnitrite / sodium nitrite Methemoglobin
Cyanide + Methemoglobin Cyanomethemoglobin
Cyanide Cytochrome Oxidase complex Cyano-methemoglobin
+ +
Methemoglobin cytochrome oxidase complex
Nitrite induces methemoglobinaemia which causes the detachment of
cyanide from the haeme group of cytochrome oxidase and binds to it
itself.
STEP 3: Sodium thiosulphate (25% soln.) 3-5 ml/min. IV
Cyanomethemoglobin+ sodium thiosulphate Thiocynate +
Methemoglobin+ sulphate
20. POST MORTEM APPEARNCE
EXTERNAL APPEARNCE:
Features
External Parts
Bitter almonds
Odor
Brick color
Skin & mucous
membrane
Bright, glistening
with dilated pupils
Eyes
Firmly closed
Jaws
21. POST MORTEM APPEARNCE
INTERNAL APPEARNCE:
Feature
Organ or Tissue
odor
Brain Tissue
Blood strained froth
Trachea & Bronchi
Pulmonary edema
Lungs
Congested with hemorrhagic gastritis
Bright red to brown (Potassium
Cyanide)
Stomach & Intestinal Mucosa
Congestion
Minute necrosis & hemorrhage
Degenerative changes as whole
Brain
Lenticular nuclei
Disseminated petechiae
Brain, meninges, pleura,
lungs & Pericardium
Corroded by cyanide salts
Lips, mouth
Presence of RBC’s
Spleen