2. Asphyxia-Definition
• Asphyxia: A Greek word literal meaning “pulse-less-ness
or absence of pulsation”.
• Condition caused by interference with respiration, or due
to lack of O2 in respired air, due to which the organs &
tissues are deprived of O2 (together with failure to
eliminate CO2) causing unconsciousness or death.
• “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” (Adelson)
• “(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”
3. Normal levels of oxygen in the arterial
blood (pO2) with a 95% saturation of
haemoglobin range from:
• 90 to 100 mmHg(12-13.5 KPa) at age of 30
years
• 65–80 mmHg ( about 10KPa) >60 years
• Hypoxia: <60 mmHg (< 8 Kpa) even though
the haemoglobin is 90% saturated;
• Severe hypoxia: 40 mmHg (8-5Kpa)
• Death: <20 mmHg (5-3Kpa)
4. Gordon’s Classification (1944)
• • ANOXIA- lack of oxygen
• Anoxic Anoxia: 02 from atmosphere cannot get entry
into blood. e.g. Hanging, Strangulation, Smothering, Choking,
traumatic asphyxia etc.
• • Anaemic Anoxia: i.e. inability of blood to carry
sufficient oxygen due to low haemoglobin contents
• • Stagnant Anoxia: i.e. where the circulation of blood is
impaired so that there is lack of oxygenated blood transport
to the tissues
• • Histotoxic Anoxia: O2 although freely available in the
bloodstream—cannot be utilized by the tissues
5. Histotoxic anoxia(sub-division)
• Extracellular, i.e. tissue oxygen enzyme system is poisoned
Eg: cyanide poisoning, in which the cytochrome-oxidase system is
interfered with. The effects of most of hypnotic and anaesthetic
drugs may also be included in this because they depress cellular
enzyme activity. Aluminium phosphide poisoning.
• Pericellular- oxygen cannot gain access to the cell because of the
decrease in the cell membrane permeability that may be seen in lipid
soluble anaesthetic agents like halogenated hydrocarbons, e.g.
chloroform, halothane, etc.
• Substrate: i.e. there is inadequate food for efficient metabolism by
the cell
• Metabolite histotoxic hypoxia- the end products of cellular
respiration cannot be removed thereby preventing further
metabolism as in uraemia or CO2 poisoning
6. Stages of Asphyxia – 3 stages
• (1) Stage of forced respiration:
- It is due to stimulation of the respiratory center.
- Clinical picture: DYSPNEA
• (2) Stage of convulsions: - It is due to cerebral irritation.
- Clinical picture: CONVULSIONS, CYANOSIS,
HYPERTENSION, LOSS OF CONSCIOUSNESS,
CONSTRICTED PUPILS.
• (3) Stage of paralysis:
- 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..
7. Rule of thumb
• The breathing stops within 20
seconds of cardiac arrest and
Heart stops within 20 minutes
of stoppage of Breathing
‘Anoxia begets anoxia’
8. Vicious cycle of asphyxia
reduction in
O2 tension
Capillary dilatation
Capillary stasis
Capillary engorgement
Stasis of blood in
organs
Diminished venous return to heart
Reduced pulmonary flow
Deficient oxygenation in lungs
Asphyxia
10. Asphyxial Triad
1. PETECHIAL HAEMORRHAGES: Due to increase pressure
on thin walled peripheral venules and capillaries..no role of
Hypoxia, also seen in coughing,sneezing , SIDS, H’gic
diathesis….disappears with PM interval..can apppear &
enlarge PM phenomenon, abnormal postures, seen in normal
and ‘congestive’ deaths, not all punctate lesions in pleura are
petechiae, unreliable however in eyelids, conjuctiva n sclera
needs explanation unless body was head/face down
11. 1. 2. CYANOSIS: Due to reduced oxygen supply to
the tissue, more than 5gm% should be in form of
reduced Hb. Greek word meaning ‘dark
blue’…not apparent in anemia….it can be
overshadowed by Hypostasis
3. CONGESTION AND EDEMA: Due to reduced
venous return, Edema is due to rapid transduation
thru capillaries & venule walls
12. Asphyxia
CLINICAL EFFECTS OF ASPHYXIA
Sphincter relaxation Voiding of urine,
stools, semen
Decreased oxygen
tension and
reduced Hb
Cyanosis
Capillary
endothelium
damage
Increased
capillary
permeability
Pulmonary
edema
Unconsciousne
ss
Loss of
muscle power
Capillary stasis
and engorgement
Increased
intracapillary
pressure
Capillary
rupture
Tardieu’s spots
13. Other signs
4. PULMONARY OEDEMA: Attempts to inspire against closed
airway generates a negative pressure which leads to
increased capillary permeability as the alveoli and
capillaries are damaged.
5. FLUIDITY OF BLOOD:
Increased permeability and degeneration of cell membrane
leads to release of plasminogen activator, which increase
fibrinolytic activity and prevents clotting of blood.
6. BLEEDING FROM EAR & NOSE
7. DILATATION OF RIGHT CHAMBERS OF HEART
14. Ischemic Brain Damage
• Brain receives 20% of total Oxygen though it is only 1.4%
body wt, has autoregulatory vascular control mechanism
• Neurons are highly vulnerable to hypoxia because of
presence of acidic excitatory neurotransmitters-
EXCITOTOXINS
• Neurons die in 3 to 7 minutes in anoxia
• Factors that determine Brain damage are -severity of
Hypoxic episode, age of Pt., other CNS diseases, body
Temp.
• In all different forms of Anoxia the end result to brain is
ischemic brain damage which may have following patterns:
Hypoxic-ischemic encephalopathy
Cerebral infarction
15. Pulmonary edema
• The cause of the pulmonary edema can either
be due to anoxic injury to the central nervous
system (neurogenic pulmonary edema) or
from the large negative intrathoracic
pressures seen when the victim struggles to
breathe in against an occluded airway
(obstructive pulmonary edema).
16. Post mortem findings:
Classical Signs,
Nonspecific signs & Specific signs
• External: congestion, edema, petechiae (0.1-2
mm), echchymosis(> 2mm), cyanosis, deep
PM staining, protrusion of tongue, bloody and
frothy fluid from mouth and nose, Swelling of
face, Prominence of eye balls, spontaneous
defecation, urine & sperm excretion
• Note: It is never justified to call one died due
to asphyxia, only on general, non specific
pathological features although present in
most cases, they must be supplemented by
specific signs.
17. Post mortem findings(contd..)
• Internal: Tardieu spots, dark & fluidity of blood,
vomitting could be caused by medullary suboxia,
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
• If Heart stops before Respiration the asphyxial
signs will be less.
19. Histology
• 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
20.
21.
22. Violent asphyxial deaths
• Here the process of respiration i.e, the
exchange of air between the atmosphere &
Lung beds is prevented by some violent
mechanical means
• Types: Hanging
Strangulations
Drowning
Suffocations
25. Possible effects of pressure on neck:
• Explanation for Death due to Partial Hanging
• • Carotid sinus reflex leading to cardiac
arrest
• • Jugular veins compression leading to
cyanosis and petechiae: (2Kg. Tension)
• • Carotid artery compression (3-5 Kg.
Tension) leading to unconsciousness
• • Airway obstruction leading to hypoxia. (15
Kg. Tension)
• • Occlusion of vertebral artery.
(20Kg.Tension), leading to unconsciousness
26.
27.
28.
29.
30.
31.
32.
33.
34. Modified Y-shaped incision
at neck showing base of
ligature mark – brownish
black in colour. Usually it is
pale, white and glistening.
48. Transverse tears in intima
of both carotid arteries in
case of hanging.
It is due to combination of
RADIAL FORCE (
ligature material)&
AXIAL TRACTION(
weight of body due to
suspension)
51. Fracture of left cornu of hyoid bone with inward
displacement.
They are common in victims of age above about 40 years
as the cornu gets calcified after that age.
53. Ingredients of Hanging
• Suspension (POS)
• Ligature encircling
the neck
• Constricting force
• Ligature mark –
oblique, incomplete,
located above
thyroid cartilage
• Fracture of hyoid
bone
• Intimal tears of
carotid
• Pallor – underneath,
extravasations in
surrounding
structures
• Dribbling of saliva
• Signs of asphyxia
54. Sr.
No.
Trait Hanging Strangulation
1 Ligature mark Oblique, incomplete,
high in the neck
Transverse,
complete, mid
level or below
thyroid cartilage
2 Base Pale, hard,
parchment like
Contused
3 Abrasion,
contusion &
Echymosis
Less prominent More prominent
4 Hyoid fracture More common Less common
5 Thyroid cartilage Less common More common
55. Sr.
No.
Trait Hanging Strangulation
6 Carotid Intimal tear Not seen
7 Signs of asphyxia Less marked More marked
8 Dribbling of saliva Often Rare
9 Bleeding from nose,
mouth & ears
Rare Often
10 Involuntary
discharge
Occasional Frequent
11 Manner Suicidal Homicidal
12 Injuries on other
body parts
Rare Common
56.
57. Two parallel &
transverse ligature
mark on front of neck
in case of
strangulation.
Bleeding from nostrils
also present.
60. Bodies retrieved/ recovered from water may have:
a) Died from sudden natural disease before falling into the
water.
-- A person walking near water falls in due to IHD/ CAD.
b) Died from sudden natural disease while already in the water.
c) Died from injury before being thrown into the water.
d) Died from injuries while in the water.
e) Died from effects of immersion other than drowning.
-- exhaustion, exposure to cold waters( Titanic)
f) Died from drowning.
61. Phases of drowning:
1. Breath holds
2. Inhalation of water, coughing, vomiting and loss of
consciousness
3. Convulsions, respiratory arrest then cardiac arrest
• BROUARDEL’S EXPERIMENT
• Stage of surprise(5-10 seconds)
• First stage of respiratory failure(1 min)
• Stage of deep respiration (1 min)
• Second stage of respiratory arrest(1 min)
• Stage of terminal gasp (30 seconds)
62. Types:
TYPICAL DRWNING
1. Wet drowning: Water is inhaled into the lungs
a-salt water b. fresh water
ATYPICAL DROWNING
2. Dry drowning; Water enters URT but not lungs.
3.Secondary drowning(near drowning)
Delayed death after resuscitation after living victim is taken out of
waters.
4. Immersion syndrome- Hydrocution
Vagal inhibition as result of :
a) water striking epigastrium
b) Cold water entering ear drums, nasal passage, larynx, pharynx
63.
64.
65.
66.
67.
68.
69. POST MORTEM FINDINGS:
[A] FEATURES OF SUBMERSION:
-- Wet clothes and body surface
-- Soiling with mud, grass etc.
-- Cutis Anserina ( ? Molecular death)
-- Washerwoman’s skin appearance: Pale , white,
wrinkled, softened.
70. Autopsy signs of drowning
(seen in 35% of cases)
1. Froth in nose and mouth
2. Pulmonary edema
3. Overdistention of lungs
4. Dry drowning
5. Middle ear hemorrhage
6. Chemical tests (unreliable)
7. Non-specific changes of immersion
76. [B] FEATURES OF ANTE-MORTEM SUBMERSION:
-- Cadaveric spasm with firmly grasped vegetable materials etc.
-- Froth : White = Colour
Fine = small bubbles
Lathery = soft consistency
Tenacious = Adherent / sticky
Copious = abundant, constant
-- Haemorrhage in middle ear.( water through Eustachian tube )
Trait Fresh water Sea water --
Lungs
1. Size & weight Ballooned but light Ballooned & Heavy
2. Colour Pale pink Purplish / bluish
3. Consistency Emphysematous Soft
4. After removal Do not collapse Collapse
5. On cut section Crepitus heard Crepitus absent
Froth , No fluid Froth + Fluid
85. Specific signs
• SIGN OF KRUSHEVSKY: full of small bubbles white
foam in respiratory tracts
• SPOTS OF RASSKAZOV-LUKOMSKY: reddening and
edema of mucous tunic of respiratory tracts, increasing
and emphysema of lungs, pale, dim hemorrhages on
their surface
• SIGN OF МОRO: presence of water in a small intestine
and abdominal cavity,
• SIGN OF SVESHNIKOV: presence of liquid of drowning
environment in the sinus of sphenoid
• increasing of liver in size and presence of plankton in
inner organs;
87. DIATOM TEST:
What are diatoms?
Unicellular algae with outer siliceous wall.
How they enter blood circulation?
Through ruptured alveolar wall, diatoms up to size 60 microns enter
the pulmonary veins & then to left side of heart, with blood
circulation they are transported to bone marrow, brain & other
organs.
Technique of demonstration:
5 gm of marrow is collected from sternum bone and is subjected to
acid digestion with 5 times volume of nitric acid for 1-2 days.
Sediment is examined under phase contrast or dark ground
illumination microscope.
Interpretation of results: Control samples of water from site treated
with Iodine is compared for type of diatoms.
