Asphyxiant Poisons | FMT | Subodh Garg | MBBS
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Oct 07, 2025
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About This Presentation
An in-depth review of Asphyxiant Poisons, adequate for both your UG and PG needs. I made this with the utmost sincerity, and I hope the person reading this uses it in the same manner.
Slide Content
Asphyxiant Poisons
Subodh Garg
Subodh Garg
Definition
A
sphyxiant poisons are chemical substances that interfere with the process of
respiration by depriving tissues of oxygen, leading to hypoxia and potentially death.
They may act by:
Displacing oxygen in inspir
ed air (simple
asphyxiants)
Interfering with oxygen tr
ansport in blood
(chemical asphyxiants)
Inhibiting cellular utilization of o
xygen at
the tissue level (histotoxic
asphyxiants)
In forensic medicine, asphyxiant poisons are important because:
They produce rapid
un
consciousness and
death.
Many are industrial or h
ousehold exposures.
They may mimic natur
al deaths if not
suspected.
A
sphyxiant poisons are chemical substances that interfere with the process of
respiration by depriving tissues of oxygen, leading to hypoxia and potentially death.
They may act by:
Displacing oxygen in inspir
ed air (simple
asphyxiants)
Interfering with oxygen tr
ansport in blood
(chemical asphyxiants)
Inhibiting cellular utilization of o
xygen at
the tissue level (histotoxic
asphyxiants)
In forensic medicine, asphyxiant poisons are important because:
They produce rapid
un
consciousness and
death.
Many are industrial or h
ousehold exposures.
They may mimic natur
al deaths if not
suspected.
Classification of Asphyxiant Poisons
Class Mechanism Examples
1
. Simple (Inert) Asphyxiants Displace oxygen from air ³
hypoxic atmosphere
Methane, Ethane, Propane,
Butane, Ethylene, Hydrogen,
Nitrogen, Carbon dioxide
2. Chemical Asphyxiants
(Blood Poisons)
Interfere with oxygen transport
by hemoglobin
Carbon monoxide, Nitrites,
Aniline, Chlorates
3. Histotoxic Asphyxiants
(Tissue Poisons)
Inhibit cellular enzymes needed
for oxygen utilization
(especially cytochrome oxidase)
Cyanide (HCN, KCN), Hydrogen
sulfide, Arsine
4. Mixed-action Poisons Both blood and tissue level
effects
Hydrogen sulfide, Nitrogen
dioxide
Class Mechanism Examples
1
. Simple (Inert) Asphyxiants Displace oxygen from air ³
hypoxic atmosphere
Methane, Ethane, Propane,
Butane, Ethylene, Hydrogen,
Nitrogen, Carbon dioxide
2. Chemical Asphyxiants
(Blood Poisons)
Interfere with oxygen transport
by hemoglobin
Carbon monoxide, Nitrites,
Aniline, Chlorates
3. Histotoxic Asphyxiants
(Tissue Poisons)
Inhibit cellular enzymes needed
for oxygen utilization
(especially cytochrome oxidase)
Cyanide (HCN, KCN), Hydrogen
sulfide, Arsine
4. Mixed-action Poisons Both blood and tissue level
effects
Hydrogen sulfide, Nitrogen
dioxide
Pathophysiology of Asphyxiation
A
sphyxiant poisons disrupt one or more of these steps.
1A
dequate oxygen in inspired air (21% at
sea level)
2 N
ormal ventilation (airway patency and
pulmonary function)
3A
dequate hemoglobin concentration and
binding
4 N
ormal cardiac output for delivery
5I
ntact cellular oxidative enzymes
A
sphyxiant poisons disrupt one or more of these steps.
1A
dequate oxygen in inspired air (21% at
sea level)
2 N
ormal ventilation (airway patency and
pulmonary function)
3A
dequate hemoglobin concentration and
binding
4 N
ormal cardiac output for delivery
5I
ntact cellular oxidative enzymes
Simple (Inert) Asphyxiants
Mec
hanism:
They are physiologically inert gases that displace oxygen in ambient air, leading to
a fall in partial pressure of oxygen (pO¢) in alveoli ³ hypoxemia ³ tissue hypoxia.
There is no direct chemical interaction with hemoglobin or tissues.
Common examples:
Methane (CH¤) 3 mines,
se
wer gas
Ethane, Propane,
But
ane 3 LPG, lighter
fuel
Nitrogen 3 industrial
gas
Carbon dioxide 3 dry ice storage, fermentation vats
Mec
hanism:
They are physiologically inert gases that displace oxygen in ambient air, leading to
a fall in partial pressure of oxygen (pO¢) in alveoli ³ hypoxemia ³ tissue hypoxia.
There is no direct chemical interaction with hemoglobin or tissues.
Common examples:
Methane (CH¤) 3 mines,
se
wer gas
Ethane, Propane,
But
ane 3 LPG, lighter
fuel
Nitrogen 3 industrial
gas
Carbon dioxide 3 dry ice storage, fermentation vats
Simple (Inert) Asphyxiants
T
oxicity depends on:
Percentage of oxygen left in
t
he air
Duration of exposure Enclosed spaces
C
linical features of hypoxic atmosphere:
<17% O¢: tachypnea,
i
mpaired judgment
12315%: dizziness, headache,
n
ausea
8310%: loss of
c
onsciousness, convulsions
<6%: death within minutes
P
ost-mortem findings:
Usually nonspecific signs of asphyxia:
Congested, cyanotic organs Petechial hemorrhages Fluid, dark blood
T
oxicity depends on:
Percentage of oxygen left in
t
he air
Duration of exposure Enclosed spaces
C
linical features of hypoxic atmosphere:
<17% O¢: tachypnea,
i
mpaired judgment
12315%: dizziness, headache,
n
ausea
8310%: loss of
c
onsciousness, convulsions
<6%: death within minutes
P
ost-mortem findings:
Usually nonspecific signs of asphyxia:
Congested, cyanotic organs Petechial hemorrhages Fluid, dark blood
Chemical Asphyxiants (Blood Poisons)
Th
ese substances interfere with the ability of hemoglobin to carry oxygen.
Th
ese substances interfere with the ability of hemoglobin to carry oxygen.
A. Carbon Monoxide (CO)
Colorless, odorless gas produced by
in
complete combustion.
Sources: motor vehicle exhaust, fire
sm
oke, poorly ventilated heating
appliances.
Mechanism:
CO binds to hemoglobin with ~240 times the affinity of oxygen, forming
carboxyhemoglobin (COHb) . This reduces oxygen carrying capacity and also shifts
the oxyhemoglobin dissociation curve to the left (impairs unloading). CO also binds
to myoglobin and mitochondrial cytochromes.
Colorless, odorless gas produced by
in
complete combustion.
Sources: motor vehicle exhaust, fire
sm
oke, poorly ventilated heating
appliances.
Mechanism:
CO binds to hemoglobin with ~240 times the affinity of oxygen, forming
carboxyhemoglobin (COHb) . This reduces oxygen carrying capacity and also shifts
the oxyhemoglobin dissociation curve to the left (impairs unloading). CO also binds
to myoglobin and mitochondrial cytochromes.
A. Carbon Monoxide (CO)
C
linical features:
Headache, dizziness, nausea Cherry-red skin (esp. in light-
s
kinned bodies)
Confusion, collapse, coma
Death at high COHb levels
T
oxic levels:
1
1
0320% COHb: mild headache
2
3
0340%: severe headache, dizziness
3
5
0360%: unconsciousness
4
6
0%: death
Post-mortem findings:
Characteristic bright <cherry-red=
h
ypostasis (but may be pink)
Frothy pulmonary edema Soot in airways if fire involved
C
linical features:
Headache, dizziness, nausea Cherry-red skin (esp. in light-
s
kinned bodies)
Confusion, collapse, coma
Death at high COHb levels
T
oxic levels:
1
1
0320% COHb: mild headache
2
3
0340%: severe headache, dizziness
3
5
0360%: unconsciousness
4
6
0%: death
Post-mortem findings:
Characteristic bright <cherry-red=
h
ypostasis (but may be pink)
Frothy pulmonary edema Soot in airways if fire involved
A. Carbon Monoxide (CO)
D
iagnosis:
Measure COHb by spectrophotometry.
T
reatment:
Immediate removal from
e
xposure
100% oxygen or h
yperbaric oxygen (233
atm)
Supportive care
M
edico-legal aspects:
Common in accidental d
eaths (fires, heaters,
car exhaust)
Sometimes suicidal (car e
xhaust in garage)
Rare homicidal use (CO c
hambers in Nazi
Germany)
D
iagnosis:
Measure COHb by spectrophotometry.
T
reatment:
Immediate removal from
e
xposure
100% oxygen or h
yperbaric oxygen (233
atm)
Supportive care
M
edico-legal aspects:
Common in accidental d
eaths (fires, heaters,
car exhaust)
Sometimes suicidal (car e
xhaust in garage)
Rare homicidal use (CO c
hambers in Nazi
Germany)
B. Methemoglobinemia-producing agents
Th
ese oxidize ferrous iron (Fe²z ) in hemoglobin to ferric (Fe³z ), forming
methemoglobin which cannot carry oxygen.
Agents:
1
Nitrites (amyl, sodium
nitrit
e)
2
Aniline dyes
3
Nitrobenzene
4
Chlorates
5
Certain drugs: dapsone, prilocaine
Th
ese oxidize ferrous iron (Fe²z ) in hemoglobin to ferric (Fe³z ), forming
methemoglobin which cannot carry oxygen.
Agents:
1
Nitrites (amyl, sodium
nitrit
e)
2
Aniline dyes
3
Nitrobenzene
4
Chlorates
5
Certain drugs: dapsone, prilocaine
B. Methemoglobinemia-producing agents
C
linical features:
Cyanosis unresponsive
t
o oxygen
Chocolate-brown blood Headache, dyspnea,
t
achycardia
Severe cases: arrhythmias, seizures, coma
T
reatment:
100% oxygen Methylene blue
132
mg/kg IV over 5 min
(repeat if needed)
Ascorbic acid
a
djunctively
Post-mortem findings:
Chocolate-brown discoloration of blood and tissues.
C
linical features:
Cyanosis unresponsive
t
o oxygen
Chocolate-brown blood Headache, dyspnea,
t
achycardia
Severe cases: arrhythmias, seizures, coma
T
reatment:
100% oxygen Methylene blue
132
mg/kg IV over 5 min
(repeat if needed)
Ascorbic acid
a
djunctively
Post-mortem findings:
Chocolate-brown discoloration of blood and tissues.
Histotoxic Asphyxiants (Tissue Poisons)
Th
ese poisons prevent cells from utilizing oxygen even though adequate oxygen is
delivered to tissues.
Thus, arterial oxygen tension and oxyhemoglobin saturation may be normal, but tissue
hypoxia occurs because cytochrome oxidase or other oxidative enzymes are
inhibited.
Th
ese poisons prevent cells from utilizing oxygen even though adequate oxygen is
delivered to tissues.
Thus, arterial oxygen tension and oxyhemoglobin saturation may be normal, but tissue
hypoxia occurs because cytochrome oxidase or other oxidative enzymes are
inhibited.
A. Cyanide (Hydrogen Cyanide, HCN, or Cyanide Salts)
1
. Nature and Sources
Hydrogen cyanide gas
(
HCN) 4 <Prussic acid,=
colorless, faint almond-
like odor.
Potassium cyanide (KCN)
a
nd Sodium cyanide (NaCN)
4 white, crystalline solids,
highly water-soluble.
Cyanogen chloride (CNCl)
4
volatile, used in chemical
warfare.
Sources / Situations:
Electroplating,
p
hotographic industry
Mining of gold and silver
(
leaching process)
Metal cleaning
Burning of plastics or
s
ynthetic fibers (e.g.
polyurethane)
Suicide with ingestion of
K
CN/NaCN (rare in India,
common in lab workers)
Homicide is rare due to
d
istinct odor and difficulty
in administration.
1
. Nature and Sources
Hydrogen cyanide gas
(
HCN) 4 <Prussic acid,=
colorless, faint almond-
like odor.
Potassium cyanide (KCN)
a
nd Sodium cyanide (NaCN)
4 white, crystalline solids,
highly water-soluble.
Cyanogen chloride (CNCl)
4
volatile, used in chemical
warfare.
Sources / Situations:
Electroplating,
p
hotographic industry
Mining of gold and silver
(
leaching process)
Metal cleaning
Burning of plastics or
s
ynthetic fibers (e.g.
polyurethane)
Suicide with ingestion of
K
CN/NaCN (rare in India,
common in lab workers)
Homicide is rare due to
d
istinct odor and difficulty
in administration.
A. Cyanide (Hydrogen Cyanide, HCN, or Cyanide Salts)
2. Mechanism of
Action
Cyanide acts mainly by blocking the terminal step of cellular respiration.
It binds to the ferric (Fe³z ) form of cytochrome oxidase (a£ component of cytochrome-
a£3a complex) in mitochondria.
³ Oxidative phosphorylation stops, ATP production ceases, and tissues cannot utilize
oxygen.
Hence, <histotoxic hypoxia.=
Blood oxygen remains high since oxygen is not extracted ³ bright red venous blood .
Also, cyanohemoglobin formation and interference with vitamin B¡¢ metabolism
occur.
2. Mechanism of
Action
Cyanide acts mainly by blocking the terminal step of cellular respiration.
It binds to the ferric (Fe³z ) form of cytochrome oxidase (a£ component of cytochrome-
a£3a complex) in mitochondria.
³ Oxidative phosphorylation stops, ATP production ceases, and tissues cannot utilize
oxygen.
Hence, <histotoxic hypoxia.=
Blood oxygen remains high since oxygen is not extracted ³ bright red venous blood .
Also, cyanohemoglobin formation and interference with vitamin B¡¢ metabolism
occur.
A. Cyanide (Hydrogen Cyanide, HCN, or Cyanide Salts)
3. F
atal Dose & Fatal Period
1
HCN gas: 1503200 ppm
inhalation f
or few
minutes can be fatal.
2
NaCN/KCN ingestion:
2
003300 mg may be
fatal.
3
Fatal period: within 2
3
10 minutes (very rapid).
3. F
atal Dose & Fatal Period
1
HCN gas: 1503200 ppm
inhalation f
or few
minutes can be fatal.
2
NaCN/KCN ingestion:
2
003300 mg may be
fatal.
3
Fatal period: within 2
3
10 minutes (very rapid).
A. Cyanide (Hydrogen Cyanide, HCN, or Cyanide Salts)
4. Clinical F
eatures
Acute poisoning:
1
Initial stage
(stimulation): burnin
g in
mouth/throat, bitter-
almond odor, anxiety,
giddiness, hyperpnea.
2
Convulsive stage: loss of
consciousness,
convulsions, frothing,
mydriasis, hypotension.
3
Terminal stage:
p
aralysis, coma,
gasping respiration,
cardiac arrest.
Chronic exposure: headache, vertigo, ataxia, goiter, optic atrophy (in industries).
4. Clinical F
eatures
Acute poisoning:
1
Initial stage
(stimulation): burnin
g in
mouth/throat, bitter-
almond odor, anxiety,
giddiness, hyperpnea.
2
Convulsive stage: loss of
consciousness,
convulsions, frothing,
mydriasis, hypotension.
3
Terminal stage:
p
aralysis, coma,
gasping respiration,
cardiac arrest.
Chronic exposure: headache, vertigo, ataxia, goiter, optic atrophy (in industries).
A. Cyanide (Hydrogen Cyanide, HCN, or Cyanide Salts)
5. P
ost-mortem Findings
Organ Findings
E
xternal Bright pink or brick-red coloration of skin and mucosa; bitter-
almond odor from mouth (only ~50 % of people can smell it).
Internal Congested viscera, fluid blood of bright red color, odor of
cyanide from stomach contents.
Lungs Congested, edematous.
Brain Congestion, edema.
Stomach Mucosa may be soft, pink, with odor if ingestion occurred.
5. P
ost-mortem Findings
Organ Findings
E
xternal Bright pink or brick-red coloration of skin and mucosa; bitter-
almond odor from mouth (only ~50 % of people can smell it).
Internal Congested viscera, fluid blood of bright red color, odor of
cyanide from stomach contents.
Lungs Congested, edematous.
Brain Congestion, edema.
Stomach Mucosa may be soft, pink, with odor if ingestion occurred.
A. Cyanide (Hydrogen Cyanide, HCN, or Cyanide Salts)
5. P
ost-mortem Findings
Chemical detection:
Prussian blue test:
F
erric ions + cyanide ³
ferric ferrocyanide
(blue color).
Guaiacum test an
d
picric acid test are also
used.
Confirmatory:
spec
trophotometry / gas
chromatography.
5. P
ost-mortem Findings
Chemical detection:
Prussian blue test:
F
erric ions + cyanide ³
ferric ferrocyanide
(blue color).
Guaiacum test an
d
picric acid test are also
used.
Confirmatory:
spec
trophotometry / gas
chromatography.
A. Cyanide (Hydrogen Cyanide, HCN, or Cyanide Salts)
6. T
reatment (Emergency Management)
Aim: rapidly dissociate cyanide from cytochrome oxidase and convert it into non-
toxic compounds.
Immediate steps:
1Rem
ove from exposure, provide
100 % oxygen.
2 Est
ablish airway, control seizures.
6. T
reatment (Emergency Management)
Aim: rapidly dissociate cyanide from cytochrome oxidase and convert it into non-
toxic compounds.
Immediate steps:
1Rem
ove from exposure, provide
100 % oxygen.
2 Est
ablish airway, control seizures.
A. Cyanide (Hydrogen Cyanide, HCN, or Cyanide Salts)
6
. Treatment (Emergency Management)
Specific Antidotal Therapy:
Step Agent Mechanism Dose
1
. Induce
Methemoglobinemia
Amyl nitrite (inhalation) or
Sodium nitrite (IV)
Converts part of Hb ³ MetHb,
which binds cyanide to form
cyanmethemoglobin, freeing
cytochrome oxidase
Amyl nitrite: crush 0.3 mL
pearl and inhale for 30 s/min
alternately with O¢.
Sodium
nitrite
: 10 mL of 3 % IV over 5
min.
2. Detoxify cyanide Sodium thiosulfate Converts cyanide ³ thiocyanate
(less toxic, excreted in urine)
50 mL of 25 % IV over 10 min.
3. Alternative Hydroxocobalamin (Vitamin B¡¢a) Combines with cyanide to form
cyanocobalamin
5 g IV over 15 min.
Support Oxygen, mechanical ventilation,
vasopressors if needed
4 4
6
. Treatment (Emergency Management)
Specific Antidotal Therapy:
Step Agent Mechanism Dose
1
. Induce
Methemoglobinemia
Amyl nitrite (inhalation) or
Sodium nitrite (IV)
Converts part of Hb ³ MetHb,
which binds cyanide to form
cyanmethemoglobin, freeing
cytochrome oxidase
Amyl nitrite: crush 0.3 mL
pearl and inhale for 30 s/min
alternately with O¢.
Sodium
nitrite
: 10 mL of 3 % IV over 5
min.
2. Detoxify cyanide Sodium thiosulfate Converts cyanide ³ thiocyanate
(less toxic, excreted in urine)
50 mL of 25 % IV over 10 min.
3. Alternative Hydroxocobalamin (Vitamin B¡¢a) Combines with cyanide to form
cyanocobalamin
5 g IV over 15 min.
Support Oxygen, mechanical ventilation,
vasopressors if needed
4 4
A. Cyanide (Hydrogen Cyanide, HCN, or Cyanide Salts)
7. Medic
o-legal Importance
Situation Remarks
A
ccidental Industrial workers in electroplating or photography.
Suicidal Common among chemists, laboratory staff (NaCN/KCN ingestion).
Homicidal Rare, but notable historical use (e.g., political
assassinations).
Execution Cyanide gas in old <gas chambers.=
7. Medic
o-legal Importance
Situation Remarks
A
ccidental Industrial workers in electroplating or photography.
Suicidal Common among chemists, laboratory staff (NaCN/KCN ingestion).
Homicidal Rare, but notable historical use (e.g., political
assassinations).
Execution Cyanide gas in old <gas chambers.=
B. Hydrogen Sulfide (H¢S)
1. Natur
e and Sources
Colorless gas with
char
acteristic rotten-
egg odor.
Highly toxic at high
c
oncentration (g500
ppm).
Produced by
dec
omposition of
organic matter,
sewage, or petroleum
refining.
Found in sewers, oil wells, tanneries, and pulp mills.
1. Natur
e and Sources
Colorless gas with
char
acteristic rotten-
egg odor.
Highly toxic at high
c
oncentration (g500
ppm).
Produced by
dec
omposition of
organic matter,
sewage, or petroleum
refining.
Found in sewers, oil wells, tanneries, and pulp mills.
B. Hydrogen Sulfide (H¢S)
2. Mechanism of
Action
1In lo
w concentration, H¢S acts like
CO 4 combines with hemoglobin
to form sulfhemoglobin, which
cannot transport oxygen.
2 In high c
oncentration, it inhibits
cytochrome oxidase, producing
histotoxic hypoxia (like cyanide).
3A
dditionally, irritates mucous
membranes and paralyzes
respiratory center.
2. Mechanism of
Action
1In lo
w concentration, H¢S acts like
CO 4 combines with hemoglobin
to form sulfhemoglobin, which
cannot transport oxygen.
2 In high c
oncentration, it inhibits
cytochrome oxidase, producing
histotoxic hypoxia (like cyanide).
3A
dditionally, irritates mucous
membranes and paralyzes
respiratory center.
B. Hydrogen Sulfide (H¢S)
3
. Clinical Features
Exposure level Effects
<
10 ppm Eye irritation, cough, lacrimation
503100 ppm Dizziness, headache, nausea, conjunctivitis
2003300 ppm Loss of consciousness, collapse (<knock-down gas=)
>700 ppm Rapid respiratory paralysis, death within minutes
Other features:
Conjunctival irritation, sore
t
hroat, vomiting.
Skin may show g
reenish-gray
discoloration in fatal cases.
Odor fatigue:
at high
concentration, olfactory
nerve is paralyzed ³ person
no longer smells gas
(dangerous!).
3
. Clinical Features
Exposure level Effects
<
10 ppm Eye irritation, cough, lacrimation
503100 ppm Dizziness, headache, nausea, conjunctivitis
2003300 ppm Loss of consciousness, collapse (<knock-down gas=)
>700 ppm Rapid respiratory paralysis, death within minutes
Other features:
Conjunctival irritation, sore
t
hroat, vomiting.
Skin may show g
reenish-gray
discoloration in fatal cases.
Odor fatigue:
at high
concentration, olfactory
nerve is paralyzed ³ person
no longer smells gas
(dangerous!).
B. Hydrogen Sulfide (H¢S)
4
. Post-mortem Findings
Dark-greenish or bluish-
g
ray discoloration of
skin, especially over
dependent parts.
Sulfide odor
from body
cavities.
Lungs: edema,
c
ongestion.
Brain: edema,
c
ongestion.
Blood: dark and may
s
how presence of
sulfhemoglobin.
No specific changes
d
iagnostic without
chemical analysis.
Chemical test:
Lead acetate paper blackens due to
f
ormation of lead sulfide.
Spectroscopic detection of
s
ulfhemoglobin.
4
. Post-mortem Findings
Dark-greenish or bluish-
g
ray discoloration of
skin, especially over
dependent parts.
Sulfide odor
from body
cavities.
Lungs: edema,
c
ongestion.
Brain: edema,
c
ongestion.
Blood: dark and may
s
how presence of
sulfhemoglobin.
No specific changes
d
iagnostic without
chemical analysis.
Chemical test:
Lead acetate paper blackens due to
f
ormation of lead sulfide.
Spectroscopic detection of
s
ulfhemoglobin.
B. Hydrogen Sulfide (H¢S)
5
. Treatment
1R
emove from source immediately, ensure
fresh air.
2 1
00 % oxygen with assisted ventilation.
3N
itrite therapy (amyl/sodium nitrite) may help
by producing methemoglobin ³ binds sulfide.
4 H
yperbaric oxygen therapy is useful in severe
cases.
5S
upportive care: maintain blood pressure,
correct acidosis.
Prognosis: poor in unconscious victims found in confined spaces.
5
. Treatment
1R
emove from source immediately, ensure
fresh air.
2 1
00 % oxygen with assisted ventilation.
3N
itrite therapy (amyl/sodium nitrite) may help
by producing methemoglobin ³ binds sulfide.
4 H
yperbaric oxygen therapy is useful in severe
cases.
5S
upportive care: maintain blood pressure,
correct acidosis.
Prognosis: poor in unconscious victims found in confined spaces.
B. Hydrogen Sulfide (H¢S)
6. Medic
o-legal Importance
Occupational hazard:
sewers, wells, mines
(<sewer gas
poisoning=).
Accidental e
xposure
most common.
Homicidal/Suicidal use
virtually nonexistent.
Important forensic clue: multiple fatalities in confined space due to one victim
r
escuing another (secondary deaths).
6. Medic
o-legal Importance
Occupational hazard:
sewers, wells, mines
(<sewer gas
poisoning=).
Accidental e
xposure
most common.
Homicidal/Suicidal use
virtually nonexistent.
Important forensic clue: multiple fatalities in confined space due to one victim
r
escuing another (secondary deaths).
C. Arsine (AsH£)
1. Natur
e and Sources
Colorless, highly
poison
ous gas with
garlic odor.
Generated when acid
a
cts on arsenic-
containing metals, e.g.,
zinc with arsenic
impurities.
Common in metal
r
efining, galvanizing,
and battery
manufacturing.
1. Natur
e and Sources
Colorless, highly
poison
ous gas with
garlic odor.
Generated when acid
a
cts on arsenic-
containing metals, e.g.,
zinc with arsenic
impurities.
Common in metal
r
efining, galvanizing,
and battery
manufacturing.
C. Arsine (AsH£)
2. Mechanism of
Action
1A
rsine is absorbed through lungs
³ causes massive intravascular
hemolysis.
2 Th
e liberated hemoglobin leads to
anemia, hemoglobinuria, renal
failure.
3H
ypoxia results from reduced
oxygen-carrying capacity, hence
<asphyxiant.=
2. Mechanism of
Action
1A
rsine is absorbed through lungs
³ causes massive intravascular
hemolysis.
2 Th
e liberated hemoglobin leads to
anemia, hemoglobinuria, renal
failure.
3H
ypoxia results from reduced
oxygen-carrying capacity, hence
<asphyxiant.=
C. Arsine (AsH£)
3. Clinical F
eatures
After 2324 h latency:
1
Malaise, headache,
abdominal p
ain.
2
Hemolysis ³ pallor,
j
aundice,
hemoglobinuria (red
urine).
3
Dyspnea, tachycardia.
4
Severe cases: renal shutdown, convulsions, coma, death.
3. Clinical F
eatures
After 2324 h latency:
1
Malaise, headache,
abdominal p
ain.
2
Hemolysis ³ pallor,
j
aundice,
hemoglobinuria (red
urine).
3
Dyspnea, tachycardia.
4
Severe cases: renal shutdown, convulsions, coma, death.
C. Arsine (AsH£)
4. P
ost-mortem Findings
Skin: pallor, sometimes
j
aundice.
Lungs: congestion,
edema.
Liver and kidneys:
n
ecrosis, congestion.
Blood: h
4. P
ost-mortem Findings
Skin: pallor, sometimes
j
aundice.
Lungs: congestion,
edema.
Liver and kidneys:
n
ecrosis, congestion.
Blood: h
C. Arsine (AsH£)
5
. Treatment
1R
emove from exposure.
2 M
aintain hydration, forced diuresis.
3E
xchange transfusion or dialysis if renal
failure develops.
4 N
o specific antidote, but dimercaprol
(BAL) may help bind arsenic residues.
5O
xygen therapy and supportive care
essential.
5
. Treatment
1R
emove from exposure.
2 M
aintain hydration, forced diuresis.
3E
xchange transfusion or dialysis if renal
failure develops.
4 N
o specific antidote, but dimercaprol
(BAL) may help bind arsenic residues.
5O
xygen therapy and supportive care
essential.
C. Arsine (AsH£)
6. Medic
o-legal Aspects
Purely in
exposure, accidental.
Often affects several
w
orkers
simultaneously.
Prevention via
v
entilation and
monitoring arsenic
contamination.
6. Medic
o-legal Aspects
Purely in
exposure, accidental.
Often affects several
w
orkers
simultaneously.
Prevention via
v
entilation and
monitoring arsenic
contamination.
Mixed-Action Asphyxiants
Som
e gases possess dual mechanisms 4 acting both as blood poisons and tissue
poisons.
Som
e gases possess dual mechanisms 4 acting both as blood poisons and tissue
poisons.
Mixed-Action Asphyxiants
Agent Mechanisms Notes
H
ydrogen sulfide Combines with Hb + inhibits
cytochrome oxidase
Dual action
Nitrogen dioxide
(NO¢)
Direct pulmonary irritant +
chemical asphyxiant
Found in silo gas, welding fumes
Phosphine (PH£) Inhibits cytochrome oxidase and
causes circulatory collapse
From aluminum phosphide
(Celphos)
Nitrous oxide (N¢O) Simple asphyxiant + CNS
depressant
<Laughing gas,= abuse can cause
hypoxia
Agent Mechanisms Notes
H
ydrogen sulfide Combines with Hb + inhibits
cytochrome oxidase
Dual action
Nitrogen dioxide
(NO¢)
Direct pulmonary irritant +
chemical asphyxiant
Found in silo gas, welding fumes
Phosphine (PH£) Inhibits cytochrome oxidase and
causes circulatory collapse
From aluminum phosphide
(Celphos)
Nitrous oxide (N¢O) Simple asphyxiant + CNS
depressant
<Laughing gas,= abuse can cause
hypoxia
A. Nitrogen Dioxide (NO¢)
4 <Silo-Filler9s Disease=
Brownish gas with sharp
o
dor, formed in silos by
fermentation of silage
(oxidation of nitric oxide
from nitrates).
Causes p
and bronchiolitis
obliterans.
Victims may appear fine
i
nitially (latent period)
and die hours later of
respiratory failure.
Treatment:
Remove to fresh air, administer oxygen
a
nd corticosteroids.
Long-term follow-up for chronic
o
bstructive lung disease.
Medico-legal:
Accidental in farm workers; rarely industrial.
4 <Silo-Filler9s Disease=
Brownish gas with sharp
o
dor, formed in silos by
fermentation of silage
(oxidation of nitric oxide
from nitrates).
Causes p
and bronchiolitis
obliterans.
Victims may appear fine
i
nitially (latent period)
and die hours later of
respiratory failure.
Treatment:
Remove to fresh air, administer oxygen
a
nd corticosteroids.
Long-term follow-up for chronic
o
bstructive lung disease.
Medico-legal:
Accidental in farm workers; rarely industrial.
B. Phosphine (PH£)
Colorless gas with garlic/fish odor. Released from aluminum phosphide
(
Celphos) used as grain fumigant ³
common suicide agent in India.
Mechanism:
Inhibits cytochrome oxidase ³ cellular
h
ypoxia.
Also causes myocardial depression and
c
apillary leakage ³ refractory shock.
Clinical Features:
Vomiting, abdominal pain, garlic breath, hypotension
, arrhythmias, metabolic
acidosis, death within hours.
Colorless gas with garlic/fish odor. Released from aluminum phosphide
(
Celphos) used as grain fumigant ³
common suicide agent in India.
Mechanism:
Inhibits cytochrome oxidase ³ cellular
h
ypoxia.
Also causes myocardial depression and
c
apillary leakage ³ refractory shock.
Clinical Features:
Vomiting, abdominal pain, garlic breath, hypotension
, arrhythmias, metabolic
acidosis, death within hours.
B. Phosphine (PH£)
T
reatment:
No specific antidote. Supportive: oxygen, gastric lavage
w
ith potassium permanganate
(oxidizes phosphine), vasopressors,
magnesium sulfate (for arrhythmias).
Post-mortem:
Congested viscera, garlic odor, petechiae.
Medic
o-legal:
Common suicidal poison (especially rural India).
T
reatment:
No specific antidote. Supportive: oxygen, gastric lavage
w
ith potassium permanganate
(oxidizes phosphine), vasopressors,
magnesium sulfate (for arrhythmias).
Post-mortem:
Congested viscera, garlic odor, petechiae.
Medic
o-legal:
Common suicidal poison (especially rural India).
Summary Table 4 Mechanism Overview
Category Main Mechanism Key Example Characteristic
F
eatures
Simple Asphyxiant Displace O¢ Methane, N¢ No odor, confined
spaces
Chemical (Blood)
Asphyxiant
Bind Hb CO, Nitrites Cherry-red or
chocolate-brown blood
Histotoxic
Asphyxiant
Inhibit cytochrome
oxidase
Cyanide Bright red venous
blood, almond odor
Mixed Action Combine mechanisms H¢S, NO¢, PH£ Rotten-egg or garlic
odor
Category Main Mechanism Key Example Characteristic
F
eatures
Simple Asphyxiant Displace O¢ Methane, N¢ No odor, confined
spaces
Chemical (Blood)
Asphyxiant
Bind Hb CO, Nitrites Cherry-red or
chocolate-brown blood
Histotoxic
Asphyxiant
Inhibit cytochrome
oxidase
Cyanide Bright red venous
blood, almond odor
Mixed Action Combine mechanisms H¢S, NO¢, PH£ Rotten-egg or garlic
odor
Clinical Diagnosis of Asphyxiant
P
oisoning
Because many asphyxiant gases are colorless, odorless, or act very rapidly,
diagnosis often depends on circumstantial evidence combined with characteristic
clinical and post-mortem features.
P
oisoning
Because many asphyxiant gases are colorless, odorless, or act very rapidly,
diagnosis often depends on circumstantial evidence combined with characteristic
clinical and post-mortem features.
(A) Scene Clues
1V
ictims found in confined, poorly ventilated spaces (sewers, mines, cars, silos,
tanks, grain stores).
2Pr
esence of gas cylinders, fire residues, generators, or chemical containers.
3Multiple
victims simultaneously unconscious ³ suggests environmental gas.
1V
ictims found in confined, poorly ventilated spaces (sewers, mines, cars, silos,
tanks, grain stores).
2Pr
esence of gas cylinders, fire residues, generators, or chemical containers.
3Multiple
victims simultaneously unconscious ³ suggests environmental gas.
(B) Clinical Clues
Feature Suggestive of
Cherry-red skin/lips
Carbon monoxide
Bitter-almond odor Cyanide
Rotten-egg odor Hydrogen sulfide
Garlic odor Phosphine or arsine
Chocolate-brown blood unresponsive to O¢ Methemoglobinemia
Bright red venous blood Cyanide or hydrogen cyanide
Rapid collapse on entry to sewer Hydrogen sulfide (<knock-down gas=)
Feature Suggestive of
Cherry-red skin/lips
Carbon monoxide
Bitter-almond odor Cyanide
Rotten-egg odor Hydrogen sulfide
Garlic odor Phosphine or arsine
Chocolate-brown blood unresponsive to O¢ Methemoglobinemia
Bright red venous blood Cyanide or hydrogen cyanide
Rapid collapse on entry to sewer Hydrogen sulfide (<knock-down gas=)
(C) Vital Signs and Neurological Findings
1T
achypnea, tachycardia ³ progressing to bradycardia and hypotension
2A
ltered sensorium ³ coma, seizures
3C
entral cyanosis or pink coloration (depending on poison type)
4Pupillar
y changes: mydriasis in cyanide, variable in CO
1T
achypnea, tachycardia ³ progressing to bradycardia and hypotension
2A
ltered sensorium ³ coma, seizures
3C
entral cyanosis or pink coloration (depending on poison type)
4Pupillar
y changes: mydriasis in cyanide, variable in CO
Laboratory Diagnosis
1.A
rterial Blood Gas (ABG) and Pulse Oximetry
Caution: Pulse oximeter may give false high SpO¢ in CO or MetHb poisoning
because it cannot distinguish abnormal hemoglobins.
1.A
rterial Blood Gas (ABG) and Pulse Oximetry
Caution: Pulse oximeter may give false high SpO¢ in CO or MetHb poisoning
because it cannot distinguish abnormal hemoglobins.
2.S
Poison Test / Specimen Principle / Finding
C
arbon monoxide Blood (spectrophotometry) COHb > 10 % confirms exposure; >50 %
fatal
Methemoglobinemia Blood color + spectrophotometry Chocolate-brown color; MetHb > 15 %
Cyanide Stomach contents, blood, tissues Prussian blue test; spectrophotometry;
smell
Hydrogen sulfide Tissue, blood Lead acetate paper ³ black (lead
sulfide)
Phosphine Gastric lavage, viscera Silver nitrate paper ³ black; garlic
odor
Arsine Urine, blood Elevated arsenic; hemoglobinuria (<port-
wine= urine)
Poison Test / Specimen Principle / Finding
C
arbon monoxide Blood (spectrophotometry) COHb > 10 % confirms exposure; >50 %
fatal
Methemoglobinemia Blood color + spectrophotometry Chocolate-brown color; MetHb > 15 %
Cyanide Stomach contents, blood, tissues Prussian blue test; spectrophotometry;
smell
Hydrogen sulfide Tissue, blood Lead acetate paper ³ black (lead
sulfide)
Phosphine Gastric lavage, viscera Silver nitrate paper ³ black; garlic
odor
Arsine Urine, blood Elevated arsenic; hemoglobinuria (<port-
wine= urine)
3.O
1CBC (h
emolysis in arsine)
2Renal & li
ver function tests
3EC
G (arrhythmias in CO and phosphine)
4Ch
est X-ray (pulmonary edema in NO¢, H¢S)
1CBC (h
emolysis in arsine)
2Renal & li
ver function tests
3EC
G (arrhythmias in CO and phosphine)
4Ch
est X-ray (pulmonary edema in NO¢, H¢S)
General Principles of Management
A
ll asphyxiant poisonings share two fundamental objectives:
1
Restoration of oxygenation and tissue
perfusion
2
Specific detoxification / antidotal
th
erapy
A
ll asphyxiant poisonings share two fundamental objectives:
1
Restoration of oxygenation and tissue
perfusion
2
Specific detoxification / antidotal
th
erapy
A.I
1R
emove from exposure immediately.
Rescuers must wear self-contained breathing
apparatus to prevent secondary poisoning (esp.
H¢S, CO).
2 A
irway, Breathing, Circulation (ABC).
Airway patency, intubation if needed.
100 % humidified oxygen by non-rebreather
mask or endotracheal tube.
Monitor ECG, SpO¢ (interpret cautiously).
3D
econtamination.
Remove contaminated clothing.
Wash exposed skin with water; avoid mouth-to-
mouth without barrier (risk to rescuer).
4 C
orrect metabolic acidosis.
Sodium bicarbonate 1 mEq/kg IV if pH < 7.1.
5M
anage seizures.
Diazepam 0.2 mg/kg IV slowly; may repeat.
6 M
aintain blood pressure.
IV fluids, vasopressors
(dopamine/noradrenaline).
1R
emove from exposure immediately.
Rescuers must wear self-contained breathing
apparatus to prevent secondary poisoning (esp.
H¢S, CO).
2 A
irway, Breathing, Circulation (ABC).
Airway patency, intubation if needed.
100 % humidified oxygen by non-rebreather
mask or endotracheal tube.
Monitor ECG, SpO¢ (interpret cautiously).
3D
econtamination.
Remove contaminated clothing.
Wash exposed skin with water; avoid mouth-to-
mouth without barrier (risk to rescuer).
4 C
orrect metabolic acidosis.
Sodium bicarbonate 1 mEq/kg IV if pH < 7.1.
5M
anage seizures.
Diazepam 0.2 mg/kg IV slowly; may repeat.
6 M
aintain blood pressure.
IV fluids, vasopressors
(dopamine/noradrenaline).
B.S
Poison Primary Antidote(s) Mechanism Dose / Remarks
C
arbon monoxide (CO) 100 % O¢ / Hyperbaric O¢ Displaces CO from Hb &
restores O¢ delivery
100 % O¢ by mask for g4 h
or until COHb < 5 %;
hyperbaric O¢ (233 atm) if
COHb > 25 %, neurological
symptoms, or pregnancy
Methemoglobinemia
(Nitrites, Aniline, etc.)
Methylene blue Reduces MetHb ³ Hb via
NADPH-MetHb reductase
132 mg/kg of 1 % soln IV
over 5 min; repeat after 1
h if needed;
contraindicated in G6PD
deficiency
Cyanide Nitrite + Thiosulfate or
Hydroxocobalamin
Nitrite forms MetHb to trap
CN; thiosulfate converts to
thiocyanate;
hydroxocobalamin binds CN
Amyl nitrite inhalation ³
Sodium nitrite 10 mL (3 %)
IV ³ Sodium thiosulfate 50
mL (25 %) IV; or
Hydroxocobalamin 5 g IV
Poison Primary Antidote(s) Mechanism Dose / Remarks
C
arbon monoxide (CO) 100 % O¢ / Hyperbaric O¢ Displaces CO from Hb &
restores O¢ delivery
100 % O¢ by mask for g4 h
or until COHb < 5 %;
hyperbaric O¢ (233 atm) if
COHb > 25 %, neurological
symptoms, or pregnancy
Methemoglobinemia
(Nitrites, Aniline, etc.)
Methylene blue Reduces MetHb ³ Hb via
NADPH-MetHb reductase
132 mg/kg of 1 % soln IV
over 5 min; repeat after 1
h if needed;
contraindicated in G6PD
deficiency
Cyanide Nitrite + Thiosulfate or
Hydroxocobalamin
Nitrite forms MetHb to trap
CN; thiosulfate converts to
thiocyanate;
hydroxocobalamin binds CN
Amyl nitrite inhalation ³
Sodium nitrite 10 mL (3 %)
IV ³ Sodium thiosulfate 50
mL (25 %) IV; or
Hydroxocobalamin 5 g IV
B.S
Hydrogen sulfide (H¢S) N
itrites (Amyl/Sodium) +
O¢
MetHb binds sulfide Same as cyanide protocol;
hyperbaric O¢ adjunct
Phosphine (from AlP) No specific antidote Supportive + MgSO¤ for
myocardium
Gastric lavage with
1:10,000 KMnO¤ or coconut
oil; MgSO¤ 1 g IM/IV q6h
Arsine Supportive + BAL
(Dimercaprol)
Chelates arsenic 3 mg/kg IM q4h for 2
days; maintain diuresis
Nitrogen dioxide (NO¢) O¢ + Steroids Relieves pulmonary
inflammation
Methylprednisolone 1
mg/kg/day;
bronchodilators
Simple asphyxiants O¢ + Ventilation Replace oxygen Ensure fresh air;
mechanical ventilation if
needed
Hydrogen sulfide (H¢S) N
itrites (Amyl/Sodium) +
O¢
MetHb binds sulfide Same as cyanide protocol;
hyperbaric O¢ adjunct
Phosphine (from AlP) No specific antidote Supportive + MgSO¤ for
myocardium
Gastric lavage with
1:10,000 KMnO¤ or coconut
oil; MgSO¤ 1 g IM/IV q6h
Arsine Supportive + BAL
(Dimercaprol)
Chelates arsenic 3 mg/kg IM q4h for 2
days; maintain diuresis
Nitrogen dioxide (NO¢) O¢ + Steroids Relieves pulmonary
inflammation
Methylprednisolone 1
mg/kg/day;
bronchodilators
Simple asphyxiants O¢ + Ventilation Replace oxygen Ensure fresh air;
mechanical ventilation if
needed
C.H
Especially indicated for:
CO poisoning with
C
OHb > 25 %
Pregnant women (fetal
Hb af
finity for CO high)
Cyanide with delayed
n
euro symptoms
Mechanism: Increases dissolved O¢ in plasma, accelerates dissociation of CO from Hb, and
supports tissue oxygenation.
Typical regimen: 233 atm pressure for 90 min sessions × 233.
Especially indicated for:
CO poisoning with
C
OHb > 25 %
Pregnant women (fetal
Hb af
finity for CO high)
Cyanide with delayed
n
euro symptoms
Mechanism: Increases dissolved O¢ in plasma, accelerates dissociation of CO from Hb, and
supports tissue oxygenation.
Typical regimen: 233 atm pressure for 90 min sessions × 233.
D.A
Complication Management
Met
abolic acidosis IV sodium bicarbonate
Hypotension / Shock Fluids + vasopressors
Seizures Diazepam / midazolam
Pulmonary edema Furosemide + oxygen
Renal failure (arsine) Dialysis / exchange transfusion
Arrhythmia (phosphine) Magnesium sulfate IV
Complication Management
Met
abolic acidosis IV sodium bicarbonate
Hypotension / Shock Fluids + vasopressors
Seizures Diazepam / midazolam
Pulmonary edema Furosemide + oxygen
Renal failure (arsine) Dialysis / exchange transfusion
Arrhythmia (phosphine) Magnesium sulfate IV
Fatal Dose and Fatal Period (Quick Reference)
Poison Approx. Fatal Dose Fatal Period
C
arbon monoxide 0.1 % (1000 ppm) for 1 h 133 h
Cyanide (NaCN/KCN) 2003300 mg 2310 min
Hydrogen cyanide gas 1503200 ppm 135 min
Hydrogen sulfide 5003700 ppm Few minutes
Arsine 250 ppm for few minutes 132 days (delayed)
Phosphine From 0.5 g AlP tablet 1324 h
Nitrogen dioxide >100 ppm Few hours31 day
Methane / N¢ (simple
asphyxiant)
4 (displaces O¢) Minutes if O¢ < 6 %
Poison Approx. Fatal Dose Fatal Period
C
arbon monoxide 0.1 % (1000 ppm) for 1 h 133 h
Cyanide (NaCN/KCN) 2003300 mg 2310 min
Hydrogen cyanide gas 1503200 ppm 135 min
Hydrogen sulfide 5003700 ppm Few minutes
Arsine 250 ppm for few minutes 132 days (delayed)
Phosphine From 0.5 g AlP tablet 1324 h
Nitrogen dioxide >100 ppm Few hours31 day
Methane / N¢ (simple
asphyxiant)
4 (displaces O¢) Minutes if O¢ < 6 %
Pathophysiological Basis of Antidote Use
Step in Respiration Interfering Poison Antidote Logic
O
¢ intake (air) Simple asphyxiants Fresh air / O¢
O¢ transport by Hb CO, NO¢, nitrites O¢ + specific antidote
(displace or reduce abnormal
Hb)
Cellular utilization Cyanide, H¢S, PH£ Nitrites create alternative
binding for poison;
thiosulfate detoxifies
Hemolytic destruction Arsine Chelation + dialysis
Direct pulmonary irritation NO¢ Corticosteroids
Step in Respiration Interfering Poison Antidote Logic
O
¢ intake (air) Simple asphyxiants Fresh air / O¢
O¢ transport by Hb CO, NO¢, nitrites O¢ + specific antidote
(displace or reduce abnormal
Hb)
Cellular utilization Cyanide, H¢S, PH£ Nitrites create alternative
binding for poison;
thiosulfate detoxifies
Hemolytic destruction Arsine Chelation + dialysis
Direct pulmonary irritation NO¢ Corticosteroids
Differential Diagnosis of Asphyxiant Poisonings
Feature CO CN{ H
¢S MetHb PH£
Odor None Bitter-almond Rotten-egg None Garlic/fishy
Blood color Cherry-red Bright red Dark greenish Chocolate-brown Dark fluid
Mechanism Hb binding Cytochrome
inhibition
Dual Fe²z ³ Fe³z Cytochrome
inhibition +
cardiac
Onset Gradual Instantaneous Instantaneous Gradual Rapid
Treatment O¢, HBOT Nitrite +
Thiosulfate
O¢, Nitrite Methylene blue Supportive
Medico-legal Fire, exhaust Lab, industry Sewer Drugs/dyes Grain fumigant
(suicidal)
Feature CO CN{ H
¢S MetHb PH£
Odor None Bitter-almond Rotten-egg None Garlic/fishy
Blood color Cherry-red Bright red Dark greenish Chocolate-brown Dark fluid
Mechanism Hb binding Cytochrome
inhibition
Dual Fe²z ³ Fe³z Cytochrome
inhibition +
cardiac
Onset Gradual Instantaneous Instantaneous Gradual Rapid
Treatment O¢, HBOT Nitrite +
Thiosulfate
O¢, Nitrite Methylene blue Supportive
Medico-legal Fire, exhaust Lab, industry Sewer Drugs/dyes Grain fumigant
(suicidal)
Prognosis and Complications
Prognosis
depends on:
1C
oncentration & duration of exposure
2Tim
e to initiation of oxygen and antidote
3A
ge and comorbidities
depends on:
1C
oncentration & duration of exposure
2Tim
e to initiation of oxygen and antidote
3A
ge and comorbidities
Common complications:
1Neur
ological sequelae (especially post-CO exposure): memory loss,
Parkinsonism, demyelination of white matter.
2Pulm
onary edema (NO¢, H¢S).
3Renal f
ailure (arsine, phosphine).
4M
yocardial injury and arrhythmias (CO, PH£).
1Neur
ological sequelae (especially post-CO exposure): memory loss,
Parkinsonism, demyelination of white matter.
2Pulm
onary edema (NO¢, H¢S).
3Renal f
ailure (arsine, phosphine).
4M
yocardial injury and arrhythmias (CO, PH£).
Delayed neuropsychiatric syndrome (CO poisoning):
1
May appear days to
w
eeks later despite
apparent recovery.
2
Cognitive deficits,
personalit
y change,
urinary incontinence.
3
MRI: demyelination of
globus p
allidus.
1
May appear days to
w
eeks later despite
apparent recovery.
2
Cognitive deficits,
personalit
y change,
urinary incontinence.
3
MRI: demyelination of
globus p
allidus.
Preventive Measures (Occupational and Public
H
ealth)
Level Measures
E
ngineering controls Adequate ventilation, gas-detection alarms, confined-
space entry protocols
Personal protection Gas masks with specific filters, self-contained
breathing apparatus
Monitoring Periodic COHb estimation, air sampling, oxygen sensors
Education Worker training on odor fatigue (H¢S), emergency
evacuation
Regulation Permissible exposure limits (e.g., CO f 50 ppm, H¢S f
10 ppm by OSHA)
H
ealth)
Level Measures
E
ngineering controls Adequate ventilation, gas-detection alarms, confined-
space entry protocols
Personal protection Gas masks with specific filters, self-contained
breathing apparatus
Monitoring Periodic COHb estimation, air sampling, oxygen sensors
Education Worker training on odor fatigue (H¢S), emergency
evacuation
Regulation Permissible exposure limits (e.g., CO f 50 ppm, H¢S f
10 ppm by OSHA)
General Post-Mortem Findings in Asphyxiant
P
oisoning
Feature Description
E
xternal appearance Congestion, cyanosis or unusual coloration (cherry-red, pink, brown, greenish
depending on toxin). Petechial hemorrhages on conjunctivae, serous surfaces,
and skin folds.
Lividity (hypostasis) Often
unusual in color (CO = bright pink; CN = brick-red; MetHb = chocolate;
H¢S = greenish). Distribution depends on position of body.
Eyes Congested, petechial hemorrhages under conjunctiva; occasionally dilated
pupils (cyanide).
Mouth / Nostrils Frothy fluid or soot (fire cases = CO). Characteristic odor may be perceived
when body cavity opened.
P
oisoning
Feature Description
E
xternal appearance Congestion, cyanosis or unusual coloration (cherry-red, pink, brown, greenish
depending on toxin). Petechial hemorrhages on conjunctivae, serous surfaces,
and skin folds.
Lividity (hypostasis) Often
unusual in color (CO = bright pink; CN = brick-red; MetHb = chocolate;
H¢S = greenish). Distribution depends on position of body.
Eyes Congested, petechial hemorrhages under conjunctiva; occasionally dilated
pupils (cyanide).
Mouth / Nostrils Frothy fluid or soot (fire cases = CO). Characteristic odor may be perceived
when body cavity opened.
General Post-Mortem Findings in
A
sphyxiant Poisoning
Internal organs Viscera congested and edematous, right heart and large veins full
of dark fluid blood, left heart usually empty.
Blood Color varies: bright cherry-red (CO), bright pink/red (CN),
chocolate-brown (MetHb), greenish (H¢S). Remains fluid because of
inhibited coagulation.
Lungs Congested, edematous, heavy; may exude frothy fluid.
Brain Edematous, congested; may show petechial hemorrhages.
Other viscera Liver, kidneys, spleen 4 intensely congested.
A
sphyxiant Poisoning
Internal organs Viscera congested and edematous, right heart and large veins full
of dark fluid blood, left heart usually empty.
Blood Color varies: bright cherry-red (CO), bright pink/red (CN),
chocolate-brown (MetHb), greenish (H¢S). Remains fluid because of
inhibited coagulation.
Lungs Congested, edematous, heavy; may exude frothy fluid.
Brain Edematous, congested; may show petechial hemorrhages.
Other viscera Liver, kidneys, spleen 4 intensely congested.
Specific Post-Mortem Features of Individual
P
oison Groups
Poison Distinctive Findings
C
arbon Monoxide Cherry-red hypostasis and muscles; carboxyhemoglobin confirmed
spectroscopically; bright-red meninges and viscera; soot particles in
airways if from fire.
Cyanide Pink mucosae, bright-red blood, bitter-almond odor (in ~50 % people),
corrosion of gastric mucosa if ingested; cyanide may be detected
chemically in blood or viscera.
Methemoglobinemia
(Nitrites / Aniline)
Chocolate-brown blood and internal organs; absence of odor.
Hydrogen Sulfide Greenish-gray discoloration of skin, hair darkening (due to sulfide of
metals), dark-green blood, characteristic rotten-egg odor.
P
oison Groups
Poison Distinctive Findings
C
arbon Monoxide Cherry-red hypostasis and muscles; carboxyhemoglobin confirmed
spectroscopically; bright-red meninges and viscera; soot particles in
airways if from fire.
Cyanide Pink mucosae, bright-red blood, bitter-almond odor (in ~50 % people),
corrosion of gastric mucosa if ingested; cyanide may be detected
chemically in blood or viscera.
Methemoglobinemia
(Nitrites / Aniline)
Chocolate-brown blood and internal organs; absence of odor.
Hydrogen Sulfide Greenish-gray discoloration of skin, hair darkening (due to sulfide of
metals), dark-green blood, characteristic rotten-egg odor.
Specific Post-Mortem Features of
I
ndividual Poison Groups
Arsine Pallor ³ jaundice; enlarged spleen and kidneys with
necrosis; port-wine urine in bladder.
Phosphine (Aluminum
phosphide)
Garlic/fishy odor, congested viscera, petechiae,
myocarditis.
Nitrogen Dioxide Marked pulmonary edema; mucosal erosions in airways; orange-
brown discoloration of mucosa.
Simple asphyxiants
(Methane, CO¢, N¢)
Non-specific signs of asphyxia; no odor; all viscera dark
and congested.
I
ndividual Poison Groups
Arsine Pallor ³ jaundice; enlarged spleen and kidneys with
necrosis; port-wine urine in bladder.
Phosphine (Aluminum
phosphide)
Garlic/fishy odor, congested viscera, petechiae,
myocarditis.
Nitrogen Dioxide Marked pulmonary edema; mucosal erosions in airways; orange-
brown discoloration of mucosa.
Simple asphyxiants
(Methane, CO¢, N¢)
Non-specific signs of asphyxia; no odor; all viscera dark
and congested.
Chemical Analysis of Specimens for
F
orensic Confirmation
Proper sealing, chain-of-custody, and labeling (<suspected gaseous poison=) are essential
medico-legal steps.
F
orensic Confirmation
Proper sealing, chain-of-custody, and labeling (<suspected gaseous poison=) are essential
medico-legal steps.
Chemical Analysis of Specimens for Forensic
C
onfirmation
Specimen Preservative / Container Analysis Purpose
B
lood Sodium fluoride (1 %) to prevent
enzymatic loss
COHb %, MetHb %, cyanide ion
concentration
Stomach contents + viscera Sealed glass bottles Cyanide, phosphine, arsine
Air samples from scene Gas-tight sampling tubes Identify industrial gas
composition
Urine Plain Metabolites or arsenic (arsine)
Tissue for microscopy Formalin-fixed Secondary pathology (edema,
necrosis)
C
onfirmation
Specimen Preservative / Container Analysis Purpose
B
lood Sodium fluoride (1 %) to prevent
enzymatic loss
COHb %, MetHb %, cyanide ion
concentration
Stomach contents + viscera Sealed glass bottles Cyanide, phosphine, arsine
Air samples from scene Gas-tight sampling tubes Identify industrial gas
composition
Urine Plain Metabolites or arsenic (arsine)
Tissue for microscopy Formalin-fixed Secondary pathology (edema,
necrosis)
Medico-Legal Aspects
1.Manner of Death
Manner Typical Examples Remarks
A
ccidental CO from fires, heater leaks; H¢S in
sewers; NO¢ in silos; CO¢ in wells
Most common; occupational hazard.
Suicidal CO in car garage; KCN ingestion; AlP
(phosphine) tablets
<Closed-garage deaths= classic example.
Homicidal Rare 3 HCN or CO in confined space
(esp. historical warfare use).
Executional Cyanide gas in gas chambers (USA 1940s3
1990s).
Occupational disease Chronic low-dose exposure (H¢S, CO,
NO¢) ³ neurologic or cardiac effects.
Manner Typical Examples Remarks
A
ccidental CO from fires, heater leaks; H¢S in
sewers; NO¢ in silos; CO¢ in wells
Most common; occupational hazard.
Suicidal CO in car garage; KCN ingestion; AlP
(phosphine) tablets
<Closed-garage deaths= classic example.
Homicidal Rare 3 HCN or CO in confined space
(esp. historical warfare use).
Executional Cyanide gas in gas chambers (USA 1940s3
1990s).
Occupational disease Chronic low-dose exposure (H¢S, CO,
NO¢) ³ neurologic or cardiac effects.
2.Legal Points in Investigation
1Sc
ene must be
checked for
ventilation status,
combustion sources,
cylinders, containers.
2C
ollect air samples
before body removal.
3Docum
ent odors,
color of blood/lividity,
and any safety-gear
defects (e.g. broken
respirator).
4Multiple de
aths in
same environment ³
industrial negligence
³ corporate liability
under Indian Penal
Code §304-A (causing
death by negligence).
5Oc
cupational Safety
and Health standards
(Factory Act 1948,
Workmen9s
Compensation Act)
apply for
compensation.
6In suspec
ted suicide
or homicide,
toxicological
confirmation is
mandatory; odor
alone is not proof.
1Sc
ene must be
checked for
ventilation status,
combustion sources,
cylinders, containers.
2C
ollect air samples
before body removal.
3Docum
ent odors,
color of blood/lividity,
and any safety-gear
defects (e.g. broken
respirator).
4Multiple de
aths in
same environment ³
industrial negligence
³ corporate liability
under Indian Penal
Code §304-A (causing
death by negligence).
5Oc
cupational Safety
and Health standards
(Factory Act 1948,
Workmen9s
Compensation Act)
apply for
compensation.
6In suspec
ted suicide
or homicide,
toxicological
confirmation is
mandatory; odor
alone is not proof.
Important Differential Features
Feature CO Cyanide H¢S MetHb
(
Nitrite)
Phosphine
(AlP)
Arsine
Odor None Bitter almond Rotten egg None Garlic / fishy Garlic
Color of blood Bright cherry-
red
Bright red Greenish black Chocolate Dark fluid Hemolyzed dark
Main mechanism CO ³ carboxy-
Hb
Cytochrome
oxidase block
Hb + enzyme
block
Fe²z ³ Fe³z Enzyme block +
shock
Massive
hemolysis
Fatal period 133 h 2310 min Minutes Variable 1324 h 132 days
Antidote 100 % O¢ /
HBOT
Nitrite +
Thiosulfate /
Hydroxocobalam
in
Nitrites + O¢ Methylene blue Supportive +
MgSO¤
BAL + dialysis
Medico-legal
nature
Accident /
suicidal
Suicidal /
accident
Accident Drug-related Suicidal
(rural India)
Industrial
accident
Feature CO Cyanide H¢S MetHb
(
Nitrite)
Phosphine
(AlP)
Arsine
Odor None Bitter almond Rotten egg None Garlic / fishy Garlic
Color of blood Bright cherry-
red
Bright red Greenish black Chocolate Dark fluid Hemolyzed dark
Main mechanism CO ³ carboxy-
Hb
Cytochrome
oxidase block
Hb + enzyme
block
Fe²z ³ Fe³z Enzyme block +
shock
Massive
hemolysis
Fatal period 133 h 2310 min Minutes Variable 1324 h 132 days
Antidote 100 % O¢ /
HBOT
Nitrite +
Thiosulfate /
Hydroxocobalam
in
Nitrites + O¢ Methylene blue Supportive +
MgSO¤
BAL + dialysis
Medico-legal
nature
Accident /
suicidal
Suicidal /
accident
Accident Drug-related Suicidal
(rural India)
Industrial
accident
Chronological Sequence of Death in Rapid
A
sphyxiant Exposure
1Inhalation ³ stimulation:
h
yperpnea, dizziness.
2 L
oss of consciousness ³
convulsions.
3Respir
atory arrest ³ cardiac arrest.
Entire sequence may take < 3 minutes with cyanide or H¢S.
A
sphyxiant Exposure
1Inhalation ³ stimulation:
h
yperpnea, dizziness.
2 L
oss of consciousness ³
convulsions.
3Respir
atory arrest ³ cardiac arrest.
Entire sequence may take < 3 minutes with cyanide or H¢S.
Histopathological Changes
1Br
ain: neuronal necrosis in cerebral cortex & hippocampus (due to hypoxia).
2He
art: sub-endocardial hemorrhages, myocardial degeneration.
3L
ungs: acute edema and alveolar hemorrhages.
4Kidn
eys: tubular necrosis (esp. arsine and phosphine).
Though non-specific, the combination with chemical analysis strengthens
diagnosis.
1Br
ain: neuronal necrosis in cerebral cortex & hippocampus (due to hypoxia).
2He
art: sub-endocardial hemorrhages, myocardial degeneration.
3L
ungs: acute edema and alveolar hemorrhages.
4Kidn
eys: tubular necrosis (esp. arsine and phosphine).
Though non-specific, the combination with chemical analysis strengthens
diagnosis.
Important Medico-Legal Case Illustrations
<Garage Deaths=
(En
gland 1930s
onward): CO poisoning
from car exhaust.
Bhopal Disaster (1984):
Meth
yl isocyanate 4
pulmonary irritant &
chemical asphyxiant.
Mine accidents:
Methan
e explosion ³
simple asphyxiation
by CO¢ & CO.
<Sewer Rescue Deaths=: H¢S
exposure 4 secondary victims
succumb while rescuing first one.
Celphos tablets (India): Ph
osphine 4
common suicidal agent in rural
areas.
<Garage Deaths=
(En
gland 1930s
onward): CO poisoning
from car exhaust.
Bhopal Disaster (1984):
Meth
yl isocyanate 4
pulmonary irritant &
chemical asphyxiant.
Mine accidents:
Methan
e explosion ³
simple asphyxiation
by CO¢ & CO.
<Sewer Rescue Deaths=: H¢S
exposure 4 secondary victims
succumb while rescuing first one.
Celphos tablets (India): Ph
osphine 4
common suicidal agent in rural
areas.
Preventive and Public Health Importance
1Regular maint
enance of gas heaters and chimneys to prevent CO build-up.
2W
arning signs and ventilation in silos, sewers, mines.
3P
ortable gas detectors and oxygen alarms.
4Oc
cupational health surveillance programs including periodic COHb levels and
urine arsenic tests.
5Em
ergency response training for workers (never enter confined space without
breathing apparatus).
1Regular maint
enance of gas heaters and chimneys to prevent CO build-up.
2W
arning signs and ventilation in silos, sewers, mines.
3P
ortable gas detectors and oxygen alarms.
4Oc
cupational health surveillance programs including periodic COHb levels and
urine arsenic tests.
5Em
ergency response training for workers (never enter confined space without
breathing apparatus).
Summary
Asphyxiant poisons
constitute
one of the most important
groups of toxic agents
encountered in forensic
practice, causing death by
depriving tissues of oxygen
through various mechanisms
4 displacement of oxygen,
interference with its transport,
or inhibition of its cellular
utilization.
Clinically they manifest as
s
udden unconsciousness,
convulsions, and respiratory
arrest, often without external
injury.
Diagnosis depends upon
e
nvironmental evidence,
characteristic blood color or
odor, and specific laboratory
tests.
Prompt administration of
o
xygen and the appropriate
antidote (methylene blue for
methemoglobinemia; nitrite-
thiosulfate sequence for
cyanide; hyperbaric oxygen for
CO) can be lifesaving.
Forensic awareness of scene
s
afety, timely toxicological
analysis, and implementation
of occupational preventive
measures remain essential for
saving lives and ensuring
justice.
Medico-legally, most cases are
a
ccidental, but suicidal and
industrial negligence cases
are frequent.
Asphyxiant poisons
constitute
one of the most important
groups of toxic agents
encountered in forensic
practice, causing death by
depriving tissues of oxygen
through various mechanisms
4 displacement of oxygen,
interference with its transport,
or inhibition of its cellular
utilization.
Clinically they manifest as
s
udden unconsciousness,
convulsions, and respiratory
arrest, often without external
injury.
Diagnosis depends upon
e
nvironmental evidence,
characteristic blood color or
odor, and specific laboratory
tests.
Prompt administration of
o
xygen and the appropriate
antidote (methylene blue for
methemoglobinemia; nitrite-
thiosulfate sequence for
cyanide; hyperbaric oxygen for
CO) can be lifesaving.
Forensic awareness of scene
s
afety, timely toxicological
analysis, and implementation
of occupational preventive
measures remain essential for
saving lives and ensuring
justice.
Medico-legally, most cases are
a
ccidental, but suicidal and
industrial negligence cases
are frequent.
THANK YOU
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