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