Pathophysiology of asphyxia & drowning

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

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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.

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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