SUBJECT FORENSIC SCIENCE

Paper No. and Title PAPER No.14: Forensic Medicine

Module No. and Title MODULE No.28: Asphyxial Death: Strangulation and
Suffocation
Module Tag FSC_P14_M28

FORENSIC SCIENCE PAPER NO.14 : Forensic Medicine

MODULE NO.28: Asphyxial Death: Strangulation and
Suffocation
 TABLE OF CONTENTS
1. Learning Outcomes

2. Introduction

3. Classification of Asphyxia

4. Symptoms

5. Post Mortem Findings

6. Delayed Deaths

7. Summary

FORENSIC SCIENCE PAPER NO.14 : Forensic Medicine

MODULE NO.28: Asphyxial Death: Strangulation and
Suffocation
 1. Learning Outcomes
After studying this module, you shall be able to-

 Know about the definition and mechanism of asphyxial deaths

 Learn the types of asphyxial deaths
 Learn signs of asphyxia
 Learn about the PM findings in asphyxial deaths

2. Introduction

“True wisdom comes to each of us when we realize how little we understand about life,
ourselves, and the world around us”… Socrates.

Asphyxia is a condition caused by interference with respiration, or due to lack of oxygen in

respired air, due to which the organs and tissues are deprived of oxygen (together with failure
to eliminate CO2), causing unconsciousness or death.

Adelson defined asphyxia as, “the physiological and chemical state in a living organism in
which acute lack of oxygen available for cell metabolism is associated with inability to
eliminate excess of carbon dioxide”

Some authors also defined asphyxia as “(State) condition of the body in which the supply of
02 to the blood and tissues has been reduced appreciably below minimum critical level for
maintenance of vital functions of the body by any mechanical interference with respiration”.

The term “Anoxia” means lack of oxygen.

FORENSIC SCIENCE PAPER NO.14 : Forensic Medicine

MODULE NO.28: Asphyxial Death: Strangulation and
Suffocation
 Gordon’s Classification of Anoxia
(a) Anoxic Anoxia: Oxygen from the atmosphere cannot get entry into blood. E.g.
Hanging, Strangulation, breathing in contaminated atmosphere etc.
(b) Anaemic Anoxia: Oxygen carrying capacity of the blood is reduced. e.g., carbon
mono oxide poisoning, acute massive haemorrhage etc.
(c) Stagnant Anoxia: where the circulation of blood is impaired so that there is of
oxygenated blood transport to the tissues.eg. Heart failure, shock.
(d) Histotoxic Anoxia: Oxygen although freely available in the bloodstream, cannot be
utilized by the tissues due to defect in enzymatic process.eg. Acute cyanide poisoning.

The normal levels of oxygen in the arterial blood (pO2) with a 95% saturation of
haemoglobin ranges from 90 to 100 mm Hg in a healthy young adult. The same is 65–80
mmHg in above 60 years of age. Hypoxia occurs when PO2 is less than 60 mmHg even
though the haemoglobin is 90% saturated. Severe hypoxia occurs when PO2 is 40 mmHg.
Death occurs when PO2 is less than 20 mmHg.

Viscious Cycle of Asphyxia

Asphyxia reduction in
O2 tension

Deficient oxygenation in Capillary dilatation

lungs

Capillary stasis

Reduced pulmonary flow

Diminished venous return to heart Capillary engorgement

Stasis of blood in
organs

FORENSIC SCIENCE PAPER NO.14 : Forensic Medicine

MODULE NO.28: Asphyxial Death: Strangulation and
Suffocation
 3. Classification of Asphyxia
A) Mechanical asphyxia: Air passages blocked mechanically.
 Hanging
 Strangulation
 Suffocation
o Entrapment
o Smothering
o Gagging
o Choking
o Burking
o Overlaying
o Traumatic asphyxia
o Environmental
o Postural or positional

 Drowning

B) Pathological: Entry of oxygen in lungs decreased due to disease of upper respiratory

tract or lung. e.g. bronchitis, acute edema of glottis, laryngeal spasm.
C) Toxic: Poisonous substances preventing use of oxygen. Carbon monoxide poisoning,
paralysis of respiratory centre by opium, barbiturates, strychnine etc.
D) Environmental: Insufficient oxygen in inspired air. eg., enclosed spaces, irrespirable
gas in environment as in sewer gas, high altitude etc.
E) Traumatic: Bilateral Pneumothorax, pulmonary fat embolism from fracture of long
bones, pulmonary thrombo-embolism due to injury of lower limb etc.
F) Postural asphyxia: in unconscious or stuporous person, where upper half of body
lower than remainder.
G) Iatrogenic: anesthetic deaths.

FORENSIC SCIENCE PAPER NO.14 : Forensic Medicine

MODULE NO.28: Asphyxial Death: Strangulation and
Suffocation
 4. Symptoms
(1) Stage of DYSPNEA: It is due to stimulation of the respiratory center due to excess of
CO2.

 Clinical picture: Slight cyanosis.

(2) Stage of CONVULSIONS: - It is due to cerebral irritation. The patients gives expiratory
effort to breathe.

 Clinical picture: Cyanosis, hypertension, loss of consciousness, constricted pupils.

(3) Stage of EXHAUSTION: Finally the person undergoes stage of exhaustion.

 Clinical picture: Loss of consciousness, flaccid muscles & lost reflexes, deep
cyanosis, dilated pupils, irregular breathing (cheyne-stokes respiration).

Death occurs in about 3-5 minutes.

The triad of symptoms of asphyxia are : Congestion, cyanosis and petechial hemorrhage.

1. Petechial Hemorrhage: Is mainly due to raised venous pressure, leading to impaired

venous return. As a result of which, there is over distension and rupture of venules, leading to
rupture of the venules. It is not due to hypoxia of vessels. 15 to 30 seconds duration of raised
venous pressure is sufficient to cause petechae. Size of petechae varies from 0.1 to 02 mm
and larger size is termed as ecchymosis. It may be seen anywhere including viscera.

But readily common in serous membrane, particularly in visceral pleura, interlobar fissures,
around the hilum and pericardium. Petechae may also be present in the thymus in case of
children and infants. In the brain they are seen in the white matter and also in the sub
arachnoid space where superficial vessels have ruptured due to venous engorgement.
Multiple petechae may also be present as a common autopsy artifact during reflection of the
scalp flaps in all types of deaths and are basically of not much significance.

In cases where the mode of death is congestive heart failure, they are also present in normal
postmortem hypostasis. In cases where the deceased is found in a head lower down position,
marked congestion, cyanosis and petechial hemorrhages are one of the vital and common
findings. Petechae can also develop after death over the dependent parts of the body.
However, they can be seen rarely on parietal pleura and peritoneum in hemorrhagic diatheses
cases.

FORENSIC SCIENCE PAPER NO.14 : Forensic Medicine

MODULE NO.28: Asphyxial Death: Strangulation and
Suffocation
 2. Cyanosis: Is due to reduced oxygen supply to the tissue. Cyanosis is a Greek word
meaning ‘dark blue’. In order to appreciate cyanosis, the haemoglobin percentage should be
more than 5gm% so it is not apparent in anaemia. It is the bluish discoloration of the skin,
mucous membrane and internal organs.

It follows the congestion of the face, as, venous blood containing much reduced haemoglobin
after perfusing the head and neck becomes bluer. In cases where constriction of the neck
occurs, cyanosis follows congestion of the face. If cyanosis was produced during life, then it
may be overshadowed partly or wholly by hypostasis which is deep purple in color and may
be mistaken for true cyanosis. If the airway is blocked, then the impaired oxygenation in the
lungs causes decrease in the oxygen content of the arterial blood, which causes darkening of
all the organs and tissues and will increase the cyanosis of the face.

But after about 24 hours of death, oxygen will be dissociated from the blood and cyanosis
will appear in any dead body. Cyanosis is marked in places where post mortem lividity
develops. The usual more pronounced sites are lips, ears, tip of nose, fingernails, cheeks and
internal organs like lungs, liver, spleen, kidneys and meninges. However, more than 5
gm/100 ml of whole blood should be in the form of reduced haemoglobin to produce
cyanosis, irrespective of the total haemoglobin concentration. Hence, the essential cause of
cyanosis is diminished oxygen tension in the blood with a rise in proportion of the reduced
haemoglobin. When the carotid arteries are obstructed, intensity of the cerebral, facial and
orbital petechae are less prominent than in cases of venous obstruction. In sudden complete
carotid artery occlusion, facial pallor can be one of the striking features. There can be
associated bleeding from the ear and nose due to the rupture of small superficial vessel as a
result of severe back pressure.

3. Congestion and edema: Congestion occurs due to obstructed venous return and
capillo-venous congestion. The face, lips, tongue become swollen and reddened due to
congestion over the neck. Increased capillary permeability results from a combination of
stasis and hypoxia. The increased capillary and venous permeability causes transudation of
fluid into the tissues. Initially, in the early stages, the same is also accompanied by lymph
drainage and hence edema doesn’t occur.

FORENSIC SCIENCE PAPER NO.14 : Forensic Medicine

MODULE NO.28: Asphyxial Death: Strangulation and
Suffocation
 When the hypoxia continues, the edema develops. Edema of the lungs is common and is
usually due to combination of hypoxia and raised pulmonary vessel pressure. This
phenomenon indicates the struggle for survival for a time. As a result of back pressure and
hypoxia, the brain gets edematous. Both the congestion and edema are non-specific signs and
is due to obstructed venous return.

Other non-specific signs of asphyxia

1. Pulmonary Oedema: The victim attempts to inspire against closed airway, generates
a negative pressure which leads to increased capillary permeability as the alveoli and
capillaries are damaged.

2. Fluidity of Blood: Increased permeability and degeneration of cell membrane leads

to release of plasminogen activator, which increases fibrinolytic activity and prevents
clotting of blood. These are considered obsolete, as they can be seen in any type of
congestive deaths due to generalised rise in the venous and intra cardiac pressure.

3. Dilatation of right chambers of heart: Dilatation of the heart chambers on the right
side in asphyxial deaths is considered obsolete finding and is not regarded as
pathognomonic sign. This can also be seen in any type of congestive deaths, including
primary heart failure from many other causes and is mainly due to generalized rise in
venous pressure and intra cardiac pressure. Distension of the atria and ventricles are
common postmortem findings due to secondary muscular flaccidity.

FORENSIC SCIENCE PAPER NO.14 : Forensic Medicine

MODULE NO.28: Asphyxial Death: Strangulation and
Suffocation
 Asphyxia Voiding of urine,
Sphincter relaxation
stools, semen

Capillary
Decreased endothelium
oxygen damage
tension and
reduced Hb

Increased capillary
permeability Tardieu’s spots
Cyanosis

Unconsciousness Pulmonary
edema Capillary
rupture

Loss of Capillary stasis Increased

muscle power and intracapillary
engorgement pressure

Fig: Sum up of all sequence of events

FORENSIC SCIENCE PAPER NO.14 : Forensic Medicine

MODULE NO.28: Asphyxial Death: Strangulation and
Suffocation
 5. Post Mortem Findings

(A) External:
Nonspecific signs are seen which are common in any kind of violent asphyxial deaths.

 These are congestion, edema, petechae (0.1-2 mm), ecchymosis (> 2mm), cyanosis,
deep postmortem staining, protrusion of tongue, bloody and frothy fluid from mouth
and nose, swelling of face, Prominence of eye balls, spontaneous defecation, urine &
sperm excretion.
 The face is either pale in slow asphyxia, or distorted, congested often cyanosed.
 The eyes are congested with dilated pupils.
 Petechial hemorrhages, known as Tardieu Spots are most marked in areas where
capillary congestion is most prominent for mechanical reasons. Their distribution lies
above the level of obstruction and commonly appears as a rash-like shower in the
scalp, eyelids and face in hanging and strangulation and in the zone above the level of
compression in cases of traumatic asphyxia. In case of confusion, a hand lens may be
used to identify the petechial hemorrhages.

These are produced by simple mechanical obstruction to the venous return of blood
from other parts, thereby causing acute rise in the venous pressure and over distension
and rupture of the thin walled peripheral venules, especially in lax and unsupported
tissues like forehead, skin behind the ears, eyelids, conjunctiva, circumoral skin,
sclera, buccal mucosa, neck, epiglottis, pericardium, visceral pleura, thymus and very
rarely in the serosa of the bowel.

(B) Internal:
On dissection, the following findings may be seen depending on the type of violent asphyxia
(they are discussed in more details under specific headings).

 Tardieu spots, dark & fluidity of blood, congestion of organs, middle ear bleed,
emphysematous lungs, pulmonary edema, with froth in trachea and bronchi, bulky,
crepitant and over-distended lungs, Right ventricular dilatation etc.
 If heart stops before respiration the asphyxial signs will be less. The blood is dark in
color and fluid because of increase amount of CO2.
 There may be bursting of small vessels in the ear drums and nose due to increase in
back pressure, leading to bleeding.

FORENSIC SCIENCE PAPER NO.14 : Forensic Medicine

MODULE NO.28: Asphyxial Death: Strangulation and
Suffocation
  The larynx and trachea are usually congested and may contain varying amount of
blood tinged mucus.
 The lungs are dark and purple in color. If the back pressure still exists, then there is
exudation of sero sanguineous fluid in the alveoli, thereby producing edema.
However, accumulation of fluid in the dependant or posterior parts of the lungs after
death should not be confused with pulmonary edema. The lungs may also show
emphysematous changes near its margin.
 The abdominal viscera show marked congestion.
 The brain is congested and cranial sinuses are filled with dark blood.
 Tardieu spots are usually numerous in areas where capillaries are least firmly
supported. e.g., in sub-conjunctival tissues, under the pleural and pericardial
membranes. However, they can be present anywhere depending on the degree of
congestion and cyanosis.

They are usually seen as round, dark and well defined, varying size from pin head to 2
mm which may occur as isolated minute hemorrhages or present in large numbers. At
times they fuse together to form patches of red color, especially at the back of heart.
They are numerous in number in the region of auriculo ventricular junction of heart
and lower lobes and interlobar fissures of the lungs and thymus. In the brain, petechae
are present in the white matter of the brain. There also associated sub-arachnoid
hemorrhage may be present because of acute venous engorgement. Profuse petechae
and ecchymosis are also seen under the scalp for the same reason.

Time taken for all the internal changes to occur varies from few seconds to several
minutes depending on the circumstances. Petechae and ecchymosis are common non-
specific findings and may also be seen in non-asphyxial deaths as well (beneath
pericardium, pleura, inter lobar fissures and around hilum). Most of the times,
petechae occur along with cyanosis and is very difficult to appreciate until unless the
blood is drained out during autopsy. Microscopic examination confirms the nature of
the hemorrhage. Cutaneous and visceral petechae can also appear and enlarge as a
postmortem phenomenon and can appear on front or back of corpse died of reasons
other than asphyxia. Thus, petechae are very unreliable indicator of asphyxial deaths.

FORENSIC SCIENCE PAPER NO.14 : Forensic Medicine

MODULE NO.28: Asphyxial Death: Strangulation and
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 The natural diseases which produce hemorrhages in the skin are: bacterial endocarditis, blood
dyscrasias (especially purpura and hemophilia), meningococcal septicemia, coronary
thrombosis, acute heart failure, and acute secondary shock. Also seen in raised intra thoracic
pressure like asthmatic attack, respiratory failure, heart failure and soon after delivery. They
are distributed generally, while Tardieu spots are present above the level of obstruction.

When the asphyxial signs are prolonged and slight, the congestive element will be
diminished, but with intense and short duration, lividity and congestion are marked.
Sometimes, the findings may not be sufficient to use exact terminology of asphyxia and a
broader framework like “consistent with asphyxia” is being used.

Histology: Under microscopic examination, the following non-specific findings will be seen.

 Disruption of alveolar septa with hemorrhage in alveoli and edema.

 Brick red discoloration of nerve cells in cortex.
 Pallor & Vacuolar degeneration of Purkinje cells in the cerebellum.
 Vacuolar degeneration of liver cells.
 Chemical marker- Hypoxanthine in blood & vitreous

6. Delayed Deaths
Delayed deaths in asphyxia are due to the fact that, in asphyxia the higher cortical centres
suffer first from hypoxic injury, followed by basal ganglia and ultimately vegetative centres.
These delayed deaths usually follow periods of unconsciousness, resulting from anoxic
cerebral damage and hypostatic pneumonia. Other life threatening sequelae are massive
subcutaneous and mediastinal emphysema due to laryngeal and tracheal lacerations or
occlusion of airway due to edematous or hemorrhagic swelling of pharyngeal tissues or the
aryepiglottic fold. In such delayed deaths, the proximate cause of death is the principal
traumatic incident.

FORENSIC SCIENCE PAPER NO.14 : Forensic Medicine

MODULE NO.28: Asphyxial Death: Strangulation and
Suffocation
 7. Summary
 Asphyxia is a condition caused by interference with respiration, or due to lack of
oxygen in respired air, due to which the organs and tissues are deprived of oxygen
(together with failure to eliminate CO2), causing unconsciousness or death.
 Hypoxia occurs when PO2 is less than 60 mmHg even though the haemoglobin is 90%
saturated. Severe hypoxia occurs when PO2 is 40 mmHg. Death occurs when PO2 is
less than 20 mmHg.
 Petechial Hemorrhage is mainly due to raised venous pressure, leading to impaired
venous return.
 In cases where the mode of death is congestive heart failure, they are also present in
normal postmortem hypostasis.
 Petechial hemorrhages, known as Tardieu Spots are most marked in areas where
capillary congestion is most prominent for mechanical reasons.
 If heart stops before respiration the asphyxial signs will be less. The blood is dark in
color and fluid because of increase amount of CO2.
 The natural diseases which produce hemorrhages in the skin are: bacterial
endocarditis, blood dyscrasias (especially purpura and hemophilia), meningococcal
septicemia, coronary thrombosis, acute heart failure, and acute secondary shock.
 Delayed deaths in asphyxia are due to the fact that, in asphyxia the higher cortical
centres suffer first from hypoxic injury, followed by basal ganglia and ultimately
vegetative centres

FORENSIC SCIENCE PAPER NO.14 : Forensic Medicine

MODULE NO.28: Asphyxial Death: Strangulation and
Suffocation