Asphyxiant Poisoning

Dr. M. Mustafa Arif

Lecturer
Department of Forensic Medicine and
Toxicology
Toxic Gases
Toxic gases may be classified as:
1. Simple Asphyxiants: Displace oxygen form
ambient air and reduce Pp O
2.
Co
2,
nitrogen,
noble gases e.t.c

2. Respiratory irritants: These gases damage the
respiratory tract. Ammonia and hydrogen
sulfide.
3. Systemic Asphyxiants: These gases produce
toxicity by specialized mechanisms. CO, Cyanide,
Smoke

Carbon Dioxide
It is a heavy, colorless, odorless gas, with a
slightly acid taste.

It is given off in the process of respiration,
combustion, fermentation and decomposition
of organic mature.

Atmospheric air contains approximately 0.4%
carbon dioxide

Stage %O
2
Saturation Symptoms
Indifferent 90% Night vision is slightly decreased
Compensatory stage 82%-90%
R/R and Pulse increased, Alertness and
performance ability decreases
Disturbance stage 64%-82%
Compensatory mechanisms become
inadequate/. Air hunger, fatigue, Tunnel
vision, Dizziness, Headache, Euphoria,
Hyperventilation, cyanosis, Poor judgment
Critical Stage 60-70%
Deterioration in judgment an co-ordination
may occur in 3-5 mins. Unconsciousness may
follow leading to death.
Fatal dose:
60-80%

Fatal period:
Instant death.


Treatment
Art. Resp. & oxygen.

Maintain body warmth.

Cardio-resp. stimulants e.g. amphetamine.

Postmortem Appearances:
External :
Body remains warm for a longer period.

Face: pale, swollen, cyanosed, congested.

Tongue: protruded & grasped by teeth.

Froth at mouth & nose.

Pupils dlated.

Internal:
Lungs, brain & its membranes & other organs are
congested.

Heart: right side full of dark blood.

Small intestine: ecchymosed.


Medico legal importance:
Accidental :
In deep old wells, grain godowns, damp cellars,
mines, refrigerating plant and lime burning.

Carbon Monoxide
It is a colorless, odorless and non irritating.

CO has 250 times more affinity for
hemoglobin than oxygen, combines with it
very avidly, depriving the tissues of oxygen
supply (tissue anoxia).

About 15% of inhaled CO combines with extra
vascular proteins like myoglobin.

Signs and symptoms:
These depend upon the degree of saturation
of CO in the blood.

The approximate relationship between
carboxyhaemoglobin level and clinical
manifestation is summarized in the following
table.
Signs and Symptoms:

These depend upon the degree of
saturation of CO in the blood
CO Hb level % Symptoms
10 to 20% Exertional dyspnea, mild frontal headache
20 to 30 % Increasing dyspnea, severe headache
30 to 40% Vertigo, blurred vision, confusion, nausea
40 to 50 % Weakness, trismus, muscle spasms,
vomiting,tachypnea
50 to 60% Convulsions, respiratory failure, coma, bullous
lesions commonly develop in the skin
Over 60% Coma
Fatal dose
50-70% saturation of blood.

Fatal period
Not fixed

Diagnosis
A simple test that can be done by the attending physicians is
to dilute 1ml of the patient`s blood with 10ml of water in a
test tube and add to it 1ml of a 5% solution of sodium
hydroxide. If carboxyhemoglobin (COHb) is present, the
solution will turn
Straw yellow (<20% COHb) or
Pink (>20% COHb)

In the case of normal blood , i.e. oxyhemoglobin, the
solution turns brown in colour.
COHb level in the blood measured by spectrophotometry.
Diagnostic tests
Spectroscopic
test
If blood is examined spectroscopically two bands of COHb
between D & E will be found in the yellow green region. A
calibrated instrument is necessary to appreciate this
difference. Spectroscopic examination of blood is negative
unless the amount of carbon monoxide in the blood exceeds
20-25%
Kunkel`s test or
tannic acid test
A sample of suspected blood is diluted with 4 times its
volume of water and a few drops of 3% aqueous tannic acid
solution are added to it. It is then shaken well. If carbon
monoxide is present, it forms a pinkish white precipitate.
Blood saturated even with 10% carbon monoxide responds
to this test.
Hoppe-seyler Test
A sample of suspected blood is diluted with about 20 times its
volume of water and 10 drops of 10% caustic soda is added
to it. Normal blood produces a dirty greenish brown colour
while blood containing carbon monoxide retains its bright
red colour.
Treatment
Immediate removal from the source of exposure

Administration of 100% oxygen or hyperbaric ( oxygen
under greater pressure than normal atmospheric pressure)

Monitor cardiac and respiratory status.

Watch for increased intracranial pressure. If there is
increased ICP treat with corticosteroids, hyperventilation,
head elevation and mannitol. Convulsions can be controlled
with IV diazepam or phenytoin.

Supportive measures.

Postmortem Appearances:
Cherry pink colour (body)

Pulmonary and cerebral edema

Congestion of viscera with petechia, on the
lungs and heart, and sometimes in the white
matter of brain.

Medico legal Importance
Accidental: disused wells, water gas, coal gas,
illuminating gas, explosion in mines,
dynamites, charcoal stoves, oil heaters, oil
lamps, gas heaters, car engines, exhaust gases
and lime burning.

Suicidal: by Sui gas

Homicidal: very rare

Hydrogen sulphide
Heavy, colorless, flammable gas with a strong rotten
egg odor.
Found in areas where sulphur containing organic
material is undergoing decay such as sewers.

It interferences with cellular respiration by inhibiting
the action of cytochrome oxidase by forming a complex
bond with iron and inhibiting cellular respiration.

It also forms methhaemoglobin.


Signs and Symptoms:
Acute poisoning:
CNS: headache, vertigo, nystagmus, vomiting,
weakness, coma.

Eye : lacrimation, photophobia, conjunctivitis.

RS : rhinitis, bronchitis, pneumonia.

CVS: arrhythmia, myocardial depression.

Chronic poisoning:
Headache, weakness, nausea, weight loss, ataxia,
tremor, etc.


Fatal dose:
0.2% in air.

Fatal period:
Within few minutes.


Treatment :
Remove the victim from the source of exposure.

100% oxygen inhalation, assisted ventilation, etc.
hyperbaric oxygen has not been proved conclusively to be
of any benefit.

Antidote: Amyl nitrite and sodium nitrite enhance the
formation of methhaemoglobin which gets converted to
sulfmethemoglobin, which in turn is spontaneously
detoxified in the body.

Supportive measures: correction of electrolyte imbalance,
pulmonary edema, etc.

Postmortem Appearances:
Signs of asphyxia are present.

External :
Putrefaction: begins much rapidly.

Cyanosis and bloating of body due to gas formation.

Post mortem staining is bluish green.


Internal:
Offensive odour of gas on opening the body.

Blood: fluid and dark brown due to
sulphmethemoglobin.

Lungs: oedematous

Medico legal importance:
Accidental:
mostly from sewer gas.

Chronic poisoning :
In artificial silk works, sulphur dye works, gas
works, tar distillation works.




Hydrocyanic Acid
Hydrocyanic Acid is also known as cyanogen or
prussic acid.
At ordinary temp. the acid is a gas having an odour of
bitter almonds.
In low temp and pressure it is a liquid form.

IT IS USED TO FUMIGATE SHIPS,BUILDINGS AND CITRUS TREES
HCN FORMS CYANIDES WITH METALS
POTASSIUM, SODIUM CYANIDE,MERCURIC CYANIDE AND
SILVER CYANIDE ARE USED IN
PHOTOGRAPHY,ELECTROPLATING,HARDENING OF
STEEL,SILVER AND GOLD PROCESSING AND DYEING
CALCIUM CYANIDE IS USED IN MINING INDUSTRY
MAGNESIUM CYANIDE AND CYANOGEN CHLORIDE ARE USED
AS INSECTICIDES
SOURCES
Hydrocyanic acid is a vegetable acid naturally found in many
fruits : plums, peach etc.
It exists in the form of glucoside amygladin which is harmless.

Enzyme emulsion can liberate the harmful gas. Also reactions
with acids can also liberate it.
MECHANISM OF ACTION
IT INHIBITS CYTOCHROME OXIDASE-FORMING
CYTOCHROME OXIDASE CYANIDE COMPLEX-
PARALYSIS OF ELECTRON TRANSPORT SYSTEM-
CELLULAR HYPOXIA
PYRUVATE-LACTATE-METABOLIC ACIDOSIS
ASPHYXIA AT TISSUE LEVEL DESPITE OF AMPLE
SUPPLY OF OXYGEN AND BLOOD IS SATURATED WITH
OXYGEN
ABSORPTION,FATE AND EXCRETION
LIQUID HCN CAN BE ABSORBED THROUGH ALL MUCOUS MEMBRANES
AND SKIN
GASEOUS FORM IS READILY ABSORBED THROUGH RESP TRACT
SALTS VARY IN THEIR RATE OF ABSORPTION
RAPIDITY WITH WHICH SALTS CAUSE DEATH UPON INGESTION DEPENDS
UPON AMOUNT OF ACID PRESENT IN STOMACH AND SUBSEQUENT
LIBERATION OF HYDROGEN CYANIDE ON REACTION WITH ACID OF
STOMACH.PRESENCE OF FOOD IN STOMACH DELAYS ABSORPTION
AFTER ABSORPTION GREATER PART CONVERTED BY MITOCHONDRIAL
ENZYME, RHODANASE INTO THIOCYANATE WHICH IS NON TOXIC
SMALL AMOUNT ELIMINATED THROUGH EXPIRED AIR
MAIN ROUTE OF EXCRETION IS KIDNEY


FATAL DOSE:
50-60 MG OF PURE ACID
60 DROPS OF CRUDE OIL OF BITTER ALMONDS
200MG OF POTASSIUM CYANIDE
FATAL DOSE:
DEATH IN SOME CASES IS IMMEDIATE BUT AVERAGE
PERIOD IS TWO TO TEN MINUTES FOR HCN AND
THIRTY MINUTES FOR SODIUM OR POTASSIUM
CYANIDE
SIGNS AND SYMPTOMS
WHEN INHALED AS A GAS SYMPTOMS OCCUR
WITHIN SECONDS.
MASSIVE DOSES PRODUCE SUDDEN LOSS OF
CONCIOUSNESS AND PROMPT DEATH FROM RESP
ARREST
AFTER INGESTION:SYMPTOMS APPEAR WITHIN
MINUTES,DURING WHICH VICTIM MAY PERFORM
CERTAIN VOLUNTARY ACTS AS CORKING OR
THROWNING AWAY A BOTTLE OR WALKING A LITTLE
DISTANCE
FOLLOWING ORGANS ARE INVOLVED:
GIT:
BURNING TASTE,THROAT NUMBNESS,SALIVATION,FROTHING
AT MOUTH,NAUSEA,VOMITING,SUBSTERNAL AND EPIGASTRIC
PAIN

CNS:
DIZZINESS,HEADACHE,SWEATING,ANXIETY,CONFUSION,DROW
SINESS,SEIZURES,COMA,DEATH

RESP SYSTEM:
INITIALLY TACHYPNOEA AND DYSPNEA
IN LATER STAGE IRREGULAR RESPIRATION,PULMONARY
OEDEMA,CYANOSIS AND RESP ARREST.
BITTER ALMOND LIKE ODOUR IN BREATH
CARDIOVASCULAR SYSTEM:
INITIALLY HYPERTENSION ALONG WITH
REFLEX BRADYCARDIA.FOLLOWED BY
HYPOTENSION,TACHYCARDIA ,ARRHYTHMIAS
VENOUS OXYGEN TENSION APPROACHES
THAT OF ARTERIAL OXYGEN TENSION AND
BRIGHT RED IN COLOUR.

DIAGNOSIS
DIAGNOSIS CAN BE DONE BY:
HISTORY
CLINICAL EXAMINATION
MEASUREMENT OF WHOLE BLOOD CYANIDE
LEVEL
CYANIDE ASSAYS NOT ROUTINELY AVAILABLE
SO MAJOR DIAGNOSIS ON HISTORY AND
CLINICAL EXAMINATION
TREATMENT
STABILIZATION:
IT INCLUDES ASSISTED VANTILATION,OXYGEN ADMINISTRATION,CARDIAC
MONITORING,TREATMENT OF METABOLIC ACIDOSIS,VASOPRESSORS FOR
HYPOTENSION

DECONTAMINATION:
IN CASE OF CUTANEOUS EXPOSURE REMOVE CLOTHING AND WASH WITH
SOAP AND WATER.
IN CASE OF INGESTION STOMACH WASH WITH 5%SODIUM THIOSULPHATE
SOLUTION.
INSTILL ACTIVATED CHARCOAL AT BEGINNING AND END OF STOMACH
WASH.LAVAGE SHOULD BE DONE AFTER STABILIZING THE PATIENT AND
INITAITING ANTI DOTAL THERAPY.



ANTIDOTAL THERAPY:
CONSISTS OF THREE STEPS:
1. ADMINISTRATION OF AMYL NITRATE-ONE AMPOULE OF
0.2ML-INHALED OVER 30 SEC OF EACH MINUTE AND USE
FRESH AMPOULE EVERY 3MINUTES

2. 2
ND
STEP:ADMINISTRATION OF SODIUM NITRITE-AS 3%
SOLUTION AT A DOSE OF 300-450 MG/10-15ml SLOW IV
OVER 5-10 MIN

3. 3RD STEP:ADMINISTRATION OF SODIUM THIOSULPHATE(AS
25% SOLUTION AT A DOSE OF 12.5gm/50 ml IV,3-5 ML PER
MINUTE)
POSTMORTEM APPEARANCES
EXTERNAL:

SKIN PRESENT VIOLET APPEARANCE
POST MORTEM STAINING IS BRIGHT RED DUE TO FORMATION
OF CYAN-METHAEMOGLOBIN AND DUE TO BRIGHT RED
BLOOD IN VEINS
FINGERS MAY BE CLENCHED,FINGER NAILS BLUE AND FROTH
AT THE MOUTH AND NOSTRILS
EYES MAY BE BRIGHT,GLISTENING AND PROMINENT WITH
DILATED PUPILS
JAWS FIRMLY CLOSED
RIGOR MORTIS SETS EARLY AND LASTS LONGER

INTERNAL FINDINGS:

CRANIALCAVITY SHOULD BE OPENED FIRST AS ODOUR IS USUALLY WELL
MARKED IN BRAIN TISSUE
BLOOD STAINED FROTH MAY BE PRESENT IN TRACHEA AND BRONCHI
PULMONARY OEDEMA IS EVIDENT
MUCOSA OF STOMACH AND INTESTINE IS CONGESTED
IN CASE OF CYANIDES LIPS AND MOUTH MAY BE CORRODED
MUCOUS MEMBRANE OF STOMACH AND DUODENUM MAY BE BRIGHT
RED TO BROWN IN COLOUR
BRAIN LUNGS AND BLOOD IN ADDITION TO OTHER VISCERA SHOULD BE
SENT FOR TOXICOLOGICAL EXAMINATION
MEDICOLEGAL ASPECTS
HYDROCAYNIC ACID AND ITS SALTS ARE USED FOR SUICIDAL
PURPOSES BECAUSE OF ITS QUICK ACTION
ACCIDENTAL POISONING CAN OCCUR WHEN IT IS USED FOR
DISINFECTING PURPOSES
HCN IS ALSO USED AS CATTLE POISON.
CATTLE POISONING HAS BEEN KNOWN TO HAVE OCCURRED
FROM EATING KADVI JUAR AND PLANT DUE TO NATURAL
DEVELOPMENT OF A CYANOGENIC GYCOSIDE WHICH MAY
LIBERATE HCN
USE AS HOMICIDAL PURPOSE IS RARE
THANK YOU
Any Questions?