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HYDROCYANIC ACID (HCN)
PRESENTED BY:
MR. ARSLAN JAMEEL
MR. AHSAN ARSHAD
MR. QAMAR RASHID
PESENTED TO:
DEPARTMENT OF FORENSIC MEDICINE & TOXICOLOGY, FMU FAISALABAD
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.
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
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
MODE OF ACTION
 Inhibits succinic dehydrogenase, superoxide dismutase & carbonic
anhydrase
 Stimulate carotid & aortic bodies resulting in hyperpnea and have a
cardio-toxic role.
.
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
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)
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
RESPIATORY SYSTEM:
Initially:
Tachypnea
Dyspnea
In later stages:
Bradypnoea
Hypopnoea
Irregular respiration
Pulmonary edema
Cyanosis
Respiratory arrest
SYSTEMS INVOLVED
Bitter almond almond smell can be detected in breath
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
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
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
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
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
TREATMENT
Other Antidotes:
Dicobal edetate or tetracemate can be used I/V
followed by 20 ml of 50% glucose
Hydroxocobalamin
METHYLENE BLUE is NOT an antidote for cyanide.
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
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
MEDICOLEGAL IMPORTANCE
Suicidal agents
Accidental poisoning (Fumigation or Disinfection)
Accidental cattle poisoning
Judicial execution (Hydrocyanic acid)
Given to Rasputin in a pastry
REFRENCES
 Practical Note Book On Forensic Medicine & Toxicology
 Images from Web & Medicosis Perfectionalis
HYDROCYANIC ACID.pdf

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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
  • 11. RESPIATORY SYSTEM: Initially: Tachypnea Dyspnea In later stages: Bradypnoea Hypopnoea Irregular respiration Pulmonary edema Cyanosis Respiratory arrest SYSTEMS INVOLVED Bitter almond almond smell can be detected in breath
  • 12.
  • 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
  • 19. TREATMENT Other Antidotes: Dicobal edetate or tetracemate can be used I/V followed by 20 ml of 50% glucose Hydroxocobalamin METHYLENE BLUE is NOT an antidote for cyanide.
  • 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
  • 22. MEDICOLEGAL IMPORTANCE Suicidal agents Accidental poisoning (Fumigation or Disinfection) Accidental cattle poisoning Judicial execution (Hydrocyanic acid) Given to Rasputin in a pastry
  • 23. REFRENCES  Practical Note Book On Forensic Medicine & Toxicology  Images from Web & Medicosis Perfectionalis