pathophysiology of asphyxia & drowning
TRANSCRIPT
Patho-physiology of Asphyxia& Drowning
Dr. Chetan Kumar Forensic Medicine-PG Baroda Medical college
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”
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)
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
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
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..
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’
Vicious cycle of asphyxiareduction 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
04/13/2023 9
Asphyxia Triad
Congestion&
EdemaCyanosis
PetechialHemorrhage
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
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
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
Unconsciousness
Loss of muscle power
Capillary stasis and engorgement
Increased intracapillary
pressure
Capillary rupture
Tardieu’s spots
Other signs4. 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
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
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).
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.
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.
04/13/2023 18
Types (causes) of Asphyxia
1. MECHANICAL eg: a) Smothering b)Hanging/Strangulation/throttling c) Choking d) Drowning e) Traumatic Asphyxia
2. PATHOLOGICAL3. TOXIC4. ENVIRONMENTAL5. TRAUMATIC6. POSTURAL7. IATROGENIC
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
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
[DELAYED DEATHS]
• Hypoxic injury to Brain• Hypostatic Pneumonia• Mediastinal emphysema
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
Modified Y-shaped incision at neck showing base of ligature mark –
brownish black in colour. Usually it is
pale, white and glistening.
Carotid sinus Baroreceptors
HANGING
TYPES
Complete Partial
TYPES
Typical Atypical
Oblique, upwards, backwards, above the level of thyroid cartilage
Oblique, upwards, backwards, at or above the level of thyroid cartilage
Inverted V shape mark
Dribbling of saliva
Protrusion of tongue
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)
Carotid intimal tears
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.
Fracture of left cornu of hyoid bone with outward displacement.
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
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
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
Two parallel & transverse ligature mark on front of neck in case of strangulation. Bleeding from nostrils also present.
Extensive bruising
and abrasions in
a case of
throttling
DROWNING
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.
Phases of drowning:
1. Breath holds2. Inhalation of water, coughing, vomiting and loss of
consciousness3. 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)
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
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.
Autopsy signs of drowning (seen in 35% of cases)
1. Froth in nose and mouth2. Pulmonary edema3. Overdistention of lungs4. Dry drowning 5. Middle ear hemorrhage6. Chemical tests (unreliable)7. Non-specific changes of immersion
Appearance of froth in case of typical drowning
[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 -- Lungs1. 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
• Paltauf’s Hemorrhage• Emphysema Aquosum• Edema aquosum
Cutis Anserina
WASHERWOMAN’S SKIN APPEARENCE: Pale , white, wrinkled, softened skin of palm due to prolonged exposure to water.
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;
Emphysema aquosum
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.
Different common varieties of Diatoms:
Thank you