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THANATOLOGY Thantos:- Death Logos = Science Thanatology. It is the scientific study of Phenomena and practices relating to death.

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lecture notes of forensic medicine on Thanatology

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Page 1: Copy of DEATH I .Ppt1

THANATOLOGY

Thantos:- Death Logos = Science

Thanatology. It is the scientific study of Phenomena and practices relating to death.

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DEATH &

Medico-Legal Aspects

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1. Me Rental and Smith defined death

“Complete and permanent cessation”.

2. Mr Shapiro defines death as

“Irreversible loss of properties of living matter”.

DEFINITION

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3. Mr Clane has defined that

When destruction of brain has been established, the individual has died, no matter – whatever is the state of rest of the body, giving four signs for such a diagnosis.

– Deep irreversible coma – (fixed bilateral dilated pupils)(absent cranial nerve reflexes.)

– No spontaneous respiration.

– Absence of electrical brain activity.

– Cessation of circulation through the retina.

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3. United State Law dictionary defined death (in 1951)

“The cessation of life, the ceasing to exist”

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4. Physician’s Definition.

“Death is a total stoppage of circulation,

and cessation of all vital functions,

such as respiration and pulsation.”

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Muller Claims that

5. Death is not a moment

but

a Continuous Process

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CLASSIFICATION OF DEATH

Biologically

Death occurs in bits & pieces

Moment of start of this disintegration,

cannot be ascertained

Declaring------Death - has become more difficult –

Since 1967-Dec

(First human heart transplant was successfully carried

out)

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Thus Death was classified into 2 Groups.• Body• Organs

Body may be dead

Organs may survive

= in the same body

= in another unit of life

Separate entities

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TWO STAGES

I. Somatic Death (Soma-Body)

Irreversible loss of integrating

and co-coordinating functions

of the organism as a whole-

is labeled as Somatic Death.

It is the complete and persistent loss of

coordinated functioning of tripod of life.

i.e stoppage of

Brain

Heart Functioning and failure to return

Lung

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Life

CN

S fu

nctio

ncirculationresp

irat

ion

Tripod of life

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Modes of death

Syncope

Coma

Asphyxia

Tripod of death

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Circulation

CNSfunction

Respiration

LIFE

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Same is also called

Systemic

Clinical

Legal

Death

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II. Molecular Death

It is the death of individual organs and

tissues (which persisted individually

after somatic death)

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In 1967- Single Organ, – Shifted from a dead

unit to another living unit.

During interval – it was kept alive to avoid

molecular death.

Till it was shifted to already prepared

body – Ready to receive – Heart of Dead

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Time – Interval between Somatic &

Molecular stages

Heart Survives For 60 minutes

Liver Survives for 15 minutes

Kidney Survives for 45minutes

Cornea Survives for 6-24 Hours

Blood Survives for 6 Hours

Bone Marrow Survives for 6 Hours

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Brain death is declared – when there is

1. Permanent – fixed bilateral dilatation of pupils.

2. Absent – all nerve reflexes

3. Cessation of of respiration

(without aids.)

4. Cessation of cardiac activity

(COMPLETE FLAT ECG)

DIAGNOSIS OF DEATH

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D/D of Death

1. Suspended animation

2. Barbiturate poisoning

3. Electrocution

4. Drowning

5. Hypothermia

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Natural & Un-Natural

Un- Natural:

1. Homicidal

2. Suicidal

3. Accidental

NATURE OF DEATH

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Manner or nature of death

Natural –

Unnatural _

Suicidal

Homicidal

- accidental

- manipulative/exhibitionist

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Modes of death

Syncope

Coma

Asphyxia

Tripod of death

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Causes of Coma

Compression of brain

- Inj to Brain - Inj to meninges- Disease of brain

Disease of meninges

Name of coma

Fate of coma

Concussion, hemorrhage,inflammation,

abcess,new growth,

thrombosis, embolism.

1. COMA

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Epilepsy

Heat Stroke

Hypothermia

Effect of Poison

Metabolic Disorders

- Diabetes

- Hypoglycemia

- Uremia

- Hepatic Failure

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POST MORTEM FINDINGS

• Compression• Hemorrhages• Inflammation of meninges• Tumor• Foreign body• Vascular Lesions• Minute Hemorrhages (in poisoning)

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2. SYNCOPE

Failure of Heart

Reduced blood supply to brain

Causes: 1. Anemia

2. Weakness

3. Sudden Fright – Reflex vagal inhibition

- Cardiac

- RespiratoryCenter paralysis

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4. Direct blow on

5. Emotional Stress

6. Sudden Exposure to cold

7. Insertion of instruments in orifices – Uterus

- Bladder

- Rectum

- Any body cavity

Head Head

EpigastriumEpigastrium

TestisTestis

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8. Anesthesia

9. Exhaustion

10. Heart Diseases

11. Hemorrhage

12. Idiopathic

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Post Mortem Findings (Non Specific)

• Heart --- Usually Empty• Organs --- Pale• Capillaries--- Congested

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3. ASPHYXIA

A Condition ----- caused by

• Interference with respiration

• Lack of oxygen in respired air.

• Organs and tissues are deprived of O2

• Failure to eliminate CO2

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Resulting in :

• O2 supply to brain.

• Disturbed functioning of nervous tissues.

• O2 supply to blood

• Rapid unconsciousness

• Stoppage of respiration.

Fate After ---- 2 – 3 minutes ----- Death

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TYPES OF ASPHYXIAMechanical Asphyxia Air passages blocked mechanically

Pathological Asphyxia

Air entry prevented by diseases of lungs

Toxic Asphyxia Air entry is prevented by poisonous substances

Environmental Asphyxia

Lack of O2 in the Environment

Traumatic Asphyxia Trauma, Pulmonary embolism

Positional Asphyxia Forcible flexion of neck on chest

Iatrogenic Asphyxia Associated with anesthesia

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FINDINGS IN ASPHYXIAL DEATH

• On the body : Congestion

: Cyanosis

: Edema

: Petecheal Hemorrhages

• Around the neck : Ligature Mark

: Bruising• Non-Asphyxial : Defense wounds

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SIGNS OF DEATH

A. Immediate

B. Early

C. Late

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A. Immediate Signs:(Somatic,systemic & clinical death)

a. Insensibility and loss of voluntary power to move. b. Cessation of circulation (Flat ECG for 5 minutes) c. Cessation of respiration. d. Cessation of brain activity – absent reflexes.

(Flat EEG for 5 minutes)

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B. EARLY SIGNS (MOLECULAR DEATH)

a. Cooling of body

b. Eye changes

c. Skin changes

d. Post-mortem lividity

e. Muscles changes – Rigor Mortis

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Putrefaction (Ultimate fate of all living creatures.)

• Arrest of putrefaction.

(Extra ordinary phenomenon)

- Mummification

- Adipocere formation

C. LATE SIGNS

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A. IMMEDIATE SIGNS

a. Insensibility and loss of voluntary power to move. (Not a sure sign of death)

It is the foremost sign but also occurs in:- Prolonged fainting- Vagal inhibition- Epilepsy- Electrocution- Drowning- Suspended Animation

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b. LOSS OF EEG

No EEG for a continuous period of 5 minutes.

(a+b are sure signs of death)

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c. Cessation of circulation

• No heart beat for a continuous period of 5 minutes

(with stethoscope - sure sign)

Difficulty in - Feeble sounds

- Thick Chest

- Emphysema

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• ECG: A flat ECG for 5 minutes confirms death

• Magnus’s Test: Tying a thread around the finger

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• Finger Nail Test: Press and see the pale zone

changes

• Diaphanous Test: Finger web test

• Heat Test : No true blister with red line

• Incision Test: No circulation

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• Suspended animation(Apparent Death)

Heart beat & respiratory movements are not heard ordinarily (as they are at a very low pitch.)

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I. Involuntary S.A may occur in:• Drowning cases• New born• Anesthesia• Concussion• Heat Stroke• Prolonged illness• Electrocution• Deep Shock

All may revive by resuscitation methods

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II. Voluntary S.A

• Yogis (Holding of Breath)

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Confirmation of Death by:

i. Rectal Temp - below 75oF

ii. EEG - FLAT

iii. ECG - FLAT

iv. Ophthalmoscope shows segmentation of retinal

blood capillaries.

The blood stream in retinal vessels rapidly

becomes dotted first & then segmented (Cattle

trucking)

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d. Cessation of Respiration

i. No abdominal movement (Ant.wall)

ii. No auscultation sounds with stethoscope for 5

minutes

iii. Mirror Test

iv. Feather Test

v. Glass water Test. (Winslow’s Test)

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B. EARLY SIGNS

a) Cooling of body: (Algor Mortis)

During life: Balance of temperature is

maintained i.e. Heat produced = Heat loss

After death no heat production, so only

heat loss.

The heat loss is gradual.

This remarkable phenomenon was used to

calculate time since death.

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Measurement of Heat Loss in Dead Body

• Heat is lost till the surrounding temperature is

attained.

• Rectal measurement is best.

• Sub-hepatic and vaginal measurement may

also be made.

• Special clinical thermometer marked from

0- 50oc (graduated in degrees. Thanatometer).

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No fall in first few hour Sudden loss in 5th and 6th hour.

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FACTORS INFLUENCING RATE OF COOLING

1. Atmospheric Temperature

Body Temperature

Atmospheric TemperatureDifference

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i. When difference is more - rate of cooling is rapid

ii. When difference is less - rate of cooling is slower.

iii. Initial few hours (4-5) no loss (called P.M.T plateau)

iv. Gradual fall upto 12 hours.

v. Falling rate decreases after 12 hrs till attainment of Atmospheric temperature (20-24 hours)

Time since death

Temperature

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2. PRESENCE OF CLOTHING

i. Presence of Clothing – Cooling rate is slower.

ii. Absence of clothing – Cooling rate is faster.

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3. LOCATION OF BODY

i. In open area-free air flow – rapid cooling.

ii. Inside the room – less or no air – slow

cooling.

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4. HUMIDITY

• Rapid Cooling

• Dry Air – Less Cooling

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5. STATE OF NUTRITION & DEVELOPMENT

• Small Body : Cooling Early

• Large Body : Cooling Slower

(Depends upon mass and surface area)

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6. FATTY BODY

• Cooling slow (as fat is a poor conductor of

heat)

• In ladies – having more fat – slow cooling.

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7. MANNER OF DEATH

Heat loss is slower in chronic bacterial diseases.

Heat loss is faster in wasting diseases.

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METHODS OF CALCULATION

• Hourly calculation.

• Newton’s Formula.

• Average fall = 0.5-0.7 C per hour

No fall in temp for few hours

Then Ist two hours – fall of temp is roughly half

the difference between body temp and

environment temp.

Un – reliable Not applicable

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In next two hours – temp fall 1 ½ of above

rate

Next two hours – ¼ of Ist two hours rate

In tropical country like Pak average loss

is about .5 - .7 C per hour

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Required data:

• Temperature of the body at the time of death.

• Cause of death.

• Temperature of environment.

• Temperature of seat of body.

- Under average circumstances fall may be

presumed as 0.5- 0.7o C per hour (keeping in mind,

the cooling curve).

Note: Other criterions are more reliable. It should be

least preferred.

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RAISED BODY TEMPERATURE (AT THE TIME OF DEATH)

i. High grade fever

ii. Sun stroke

iii. Pontine Hemorrhage

iv. Encephalitis

v. Lobar pneumonia

vi. Typhoid Fever

vii. Strychnine poisoning

viii. Tetanus

ix. Many other diseases

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POST – MORTEM CALORICITY (GAINING HEAT)

i. Environmental Temperature is very high.

ii. Septicemia.

• Body Temperature continues to increase

till several hours after death.

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BODY IN A FLUID MEDIUM(LOSS OF TEMPERATURE)

• Temperature of fluid: Cold water - cooling rapid

Hot water - cooling slow

• Nature of fluid: Dirty water – cooling slow

Fresh water – cooling rapid

Sea water – cooling rapid

• Flow of fluid: Running water-cooling rapid

Stagnant water –cooling slow

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b) EYE CHANGES

i. Permanent fixed bilateral dilatation of

pupils.

ii. Cornea becomes hazy & opaque

iii. Corneal & Conjunctival reflexes are lost

iv. Luster of cornea is lost.

v. Eyes become sunken.

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• Taches noires. These are brownish-black discoloration on the exposed sclera between the eyelids, due to formation of cellular debris & dust. They appear on sclera within 3 hours of death, if eyes remain open.

Potassium content of vitreous humour rises steadily.

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c) SKIN CHANGES

i. Skin becomes pale(more on non

dependent parts

ii. Skin elasticity is lost

iii. Skin luster is lost

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POST – MORTEM LIVIDITY

It is the staining or discoloration of skin and

organs of a dead body due to accumulation

of blood because of gravitation and arrest of

circulation resulting in distension of tone

less capillaries and veins of dependent

parts.

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Also called:

P.M. Hypostasis

Livor Mortis

P.M staining

Cadaveric Lividity

Subcutaneou Hypostasis

Suggilations

Vibices

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DEVELOPMENT OF LIVIDITYAfter somatic or clinical death:-• Circulation stops• Blood remains fluid for some hours• O2 in blood (which is carried in loose

combination with Hb) is still being supplied to the tissue(till molecular death).

• No more pumping of blood by heart• O2 is gradually decreased & Hb is reduced

(Blue colour)• Due to gravity blood settles, directly in

dependent areas of skin or viscerae

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FACTORS AFFECTING POSTMORTEM LIVIDITY

Post Mortem Phenomenon

Post Mortem Lividity

Reduced HbFluidity of blood

Effect of gravity

Colour of bloodColour of skinAnte-Mortem state of

body & Mode of death

Position of body + pressure effect on specific areas

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COLOUR OF LIVIDITY

• Initially bluish pink.

• Later becomes bluish purple (dark blue)

• In fair skin – colour better appreciated

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• In carbon monoxide poisoning - Bright cherry red colour.

• In acute cyanide poisoning - Bright pink colour.

- later on it fades.

• In potassium chlorate poisoning - Chocolate brown colour.

- Due to formation of

methemoglobin.

• In death due to cold - Bright pink colour.

• In hemorrhage, anaemia - Faint colour.

• In asphyxia - Dark purple

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• Phosphorous - Dark brown

• Nitrites - Red Brown

• Hydrogen Sulphide - Bluish green

• Opium - Black

• Burning - Cherry Red

• Septic Abortion - Grayish Brown

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TIME OF PML & FIXATION

• Starts – 1-3 hours after death

• Completes – 3-6 hours after death

• Fixed – About 6-8 hours after death

• Test for Fixation – Press with thumb

i. If bleached – Not fixed.

ii. If not bleached – Fixed.

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DISTRIBUTION OF PM LIVIDITY

• External (In supine position)• PML is found on:-

• Dorsal aspect of trunk• Posterior aspect of head & neck• Dependent areas of upper and lower

limbs• More Marked on:-

Lobes of Ear

Tissues under the nails of fingers

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EXCLUDING

• Back of head

• Back of shoulder

• Back of Buttocks (Areas in contact)

• Back of heels

• Areas under tight clothing (Contact Flattening)

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• Posterior portion of cerebrum & cerebellum

• Posterior wall of lungs

• Posterior wall of stomach

• Dorsal portion of liver & spleen

• Lowermost coils of intestine

(Lividity is changed with a change in position of

body) before its fixing

Internal (In supine position)

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CAUSE OF ABSENCE

• Pressure from below, prevents distension

and filling of capillaries and minute veins

of skin. It is called contact flattening.

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D/D OF P.M LIVIDITY

a. Cyanosis

b. Bruise

c. Congestion

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a. Trait PM Lividity Cyanosis

Time of onset Post-Mortem Ante-Mortem

Location On dependent parts On terminal tips

Appearance Normal Abnormal& Pathological

Volume of blood Enough Less

Change of Position

Shifting of lividity No change

History of disease

Not required Positive

Confirmation Visible as a Post- Mortem Phenomenon

Anti-Mortem Observation/

Evidence

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b. Trait PM Lividity Bruise

Situation Epidermal (due to

engorged vessels)

Sub-epidermal.(Due to

ruptured vessels

Cuticle Uninjured May be injured

Site Occurs on

extensive areas of

dependent parts

Occurs at the site of

injury (may appear any

where)

Appearance Not elevated Area is usually swollen

due to accumulation of

blood & edema.

Edges Clearly Defined Merge with surrounding

area

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Colour Uniform Variegated in colour

Section On incision ,blood is

seen in blood vessels,

can be easily washed

away

On incision, extra -

vasated blood is seen

which is not easily

washed

Effects of

pressure

Not present in areas

under pressure

May be present in

areas under pressure

Blood

elements on

microscopy

Blood elements seen

in blood vessels with

no evidence of

inflammation

Blood elements seen

out side blood

vessels with evidence

of inflammation

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c. Trait P.M Lividity Congestion

Distribution Irregular and on dependent parts

Involves whole organ

Appearance Normal Pathological change is evident.

Mucous Membrane

Dull & lusterless Normal

Exudate No inflammatory exudate

Exudate seen

Hollow viscera

Stomach, intestine when stretched show alternate stained & unstained areas

Stomach and intestine show uniform distribution

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MUSCLE CHANGES

• Period of relaxation (Primary Flaccidity)

• Cadaveric rigidity (Rigor mortis)

• Period of relaxation (Secondary relaxation)

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Primary Flaccidity:• Appears immediately after death

• Usual duration 2-3 hours

• All muscles of body get completely relaxed.

• Muscle tone is lost

• Can be moved in any direction.

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• Due to this lower jaw drops, pupils dilate & sphincters relax & may result in incontinence of urine & faeces.

• The muscle still react to mechanical electrical & chemical stimuli.

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RIGOR MORTIS

Rigor – rigidity

Mortis – death

Rigidity after death

It is stiffening of the muscles both voluntary as well as in voluntary

after initial state of primary flaccidity after death

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It is a condition characterized by

• Stiffening

• Shortening

• Opacity of muscles

• Follows primary relaxation

• Is due to chemical changes

• Involving the proteins of muscle fibers

• Marks the end of cellular or molecular life of muscle

fibres

• The presence of rigor mortis can be elicited by

attempting to flex the neck and the limbs at joints.

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PHYSIOLOGY : (IN LIVING)

• Contractile element of muscle consists of protein filaments.– Myosin– Actin

> Less in relaxed state.> More in contracted state.

They interdigitate

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• Relaxation

• Contraction

• ATP is stored in high concentration in muscles

• Balanced production of ATP from glycogen stores.

of muscles controlled by ATP

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AFTER DEATH

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Glycogen stores resynthesize ATP,only for 2-3 hrs. After 2-3 hours

No glycogen No ATP production

No relaxation of muscles

ed interdigitation of

actin &myosin

Break down of ATP into

- lactates

- Phosphates

Actomyosin

(stiff gel)

ed accumulation of

salts in muscles

• Stiffening and shortening of muscles (voluntary + involuntary)

• Fixation of joints

• Persists till the autolysis of actin & myosin.

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TIME PERIOD

• Early in Summer

• Late in winter

• Starts 2-3 hours after death.

• In face: eyes, mouth then neck upper

limb, trunk, lower limbs Within 12hrs

• Stays for 12 hours passes off in 12hrs

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• 2-3 hours after death

• In face, eyes, mouth & neck

STARTS

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• Upper limb• Trunk • Lower limbs

with in 12 hours

SPREADS

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12 hours

STAYS

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Next 12 hours

PASSES OFF

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Rigor Mortis 36.9oc

(98.4OF)

DecompositionPlateau of variable temp

0 6 12 18 24 30 36 42 48 54

Temperature of environment

Chart showing the major changes by which lapse of time after death might be estimated. The first 4-5 hours often show little fall in temperature.

Hours after death

Lividity

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FACTORS INFLUENCING RIGOR MORTIS

Factor Appearance Passing Off

1. Atmospherea. Dry & cool Late Late

b. Moist & Warm Early Early

c. Cold Water Early Late

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Factor Appearance Passing off

2. Age

a. Children Early Early

b. Elderly Early Early

c. Adults Late Late

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3. Manner of Death

a. Chronic disease Early Early

& emaciation

b. Sudden death Late Late

c. Strychnine Immediate Early

Poisoning

d. Drowning Early Late

e. Arsenic Late Late

poisoning

FactorFactor Appearance Passing offAppearance Passing off

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4. Muscular Condition

a. Healthy muscles Late Late

b. Exhausted & wasted Early Early

muscles

FactorFactor Appearance Passing Appearance Passing offoff

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DIFFERENTIAL DIAGNOSIS OF RIGOR MORTIS

(Simulating Conditions)

1. Heat Stiffening

2. Cold Stiffening

3. Putrefaction stiffening

4. Cadaveric Spasm

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1. HEAT STIFFENING

i. When body is exposed to 75oC or high

temperature.

ii. When body is exposed to high voltage current.

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Coagulation of actin & myosin

Stiffening of muscles

Flexion of all joints of body

Special posture

(pugilistic attitude or boxer’s attitude)

High Temperature High voltage

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SPECIAL FEATURES

i. Burn marks are present

ii. Stiffening persists till putrefaction

iii. Muscles get lacerated when tried to break

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2. COLD STIFFENING

Freezing temp

Solidification of fats and muscular tissues

Rigidity of Muscles

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• Rigidity is lost when body is moved to

higher temperature.

• Again sets in when moved to freezing

temperature.

• Appears quickly : disappears quickly

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3. PUTREFACTION STIFFENING

Putrefaction

Formation of gases

Accumulation of gases

False rigidity

Stiff Limbs

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4. CADAVERIC SPASM(Instantaneous Rigor)

• A rare type of rigidity of a group of muscles.

• May occur instantaneously after death.

• Before the actual signs develop.

• Does not allow primary relaxation.

• Muscles remains stiff till autolysis.

• Represents a state of extreme physical

activity or emotional state before death.

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Examples:

i. In drowning, victim may seize a bunch of

weeds in an attempt to save himself (found

clutched tightly in hand)

ii. A person committing suicide may grip a

pistol in his hand.

iii. A bunch of hair in homicidal scuffle.

Such objects are proof of nature of death

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DIFFERENCES

Traits Rigor Mortis Cadaveric spasm

1. Time of onset 2 – 3 hours after death

Instantaneous

2. Predisposing factors

Nil Sudden death, fear, excitement, exhaustion, nervous tension.

3. Muscles

involved

All voluntary & Involuntary

Usually a single group of voluntary muscles

4. Muscle

stiffening

Not marked, moderate force can break it.

Marked, moderate force cannot break it.

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Traits Rigor Mortis Cadaveric spasm

5. Medicolegal

importance

Helps in determination of time since death

Indicates nature of death : suicide, homicide, accident.

6. Body Heat Cold Warm

7. Molecular

death

Occurs Does not occur

8. Mechanism Known Not known

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MEDICOLEGAL IMPORTANCE

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RIGOR MORTIS HELPS IN

a.Calculation of time since death.

b.Determination of position of body.

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Rigor Mortis 36.9oc

(98.4OF)

DecompositionPlateau of variable temp

0 6 12 18 24 30 36 42 48 54

Temperature of environment

Chart showing the major changes by which lapse of time after death might be estimated. The first 4-5 hours often show little fall in temperature.

Hours after death

Lividity

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PUTREFACTION

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• Decomposition/dissolution of body

tissues into

– Gases

– Liquids

– Salts

• The ultimate fate of body by conversion of

organic to inorganic state.

It is absolute / surest sign of death

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Based on

Autolysis (Self destruction)

After death, enzymes are released. They soften & liquify tissues of the body.

It commences 3-4 hrs after death and continuous for 2-3 day or longer.

Bacterial Action (Micro-organisms)

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MICRO-ORGANISMS

The micro-organisms responsible are

anaerobic & aerobic. They produce variety of enzymes. They are Clostridium welchi, Streptococci, Esc coli & B. Proteus which act on Carbohydrates, Fat and Proteins. C. Welhi produces lecithinase which hydrolyses the lecithin present in cell membrane resulting in haemolysis of blood and initiation of putrefaction.

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MICRO-ORGANISMS

IN LIVING• Present in body in large numbers • Remain under control JUST AFTER – DEATH• Life control fails• Micro-organisms are out of control• Multiply in large numbers• Become virulent • Enter blood vessels • Spread throughout the body

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BASIC RULE

Organs (First to putrefy)

• Receiving rich blood supply

• Near to source of bacteria

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PUTREFACTION

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Autolysis (self – destruction) Bacterial Action

Molecular death More bacterial growth

Death of tissue

Air

warmth

moisture

Enzymes production

Release of enzymes

from tissue cells

(Cl - w)Production of

Lecithinase EnzymeEffects Tissues (Dissolution )

Softening liquefication of tissue cells

Haemolysis of blood Hydrolysis of lecithinase

Gases, Liquid salts

(Putrefaction of body Tissues)

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STEPS OF PUTREFACTION

i. Color changes

ii. Production of gases

iii. Pressure effects of gases

iv. Appearance of maggots

v. Other sequelae

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COLOR CHANGESExternala. Greenish discoloration over caecum and the

flanks (Rt. iliac fossa) 12-24 hrs (earlier in summer)

• 1st sign.• Indicator of entry of body into advance

putrefaction.

b. Greenish discoloration gradually spreads to whole abdomen. The whole body is discoloured within about next 24 hrs.

c. Color gradually changes from greenish to black.

d. Hb + H2S Sulf-met Hb

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Internal

• Under surface of liver (Internal) due to close contact

with fluid and bacterial contents of bowel.

• Blood is hemolyzed & Hb is liberated.

• Bacteria (Clostridium Welchii) produce H2S with Hb.

• Sulf – met Hb spreads to the whole body (48 hours).

• Greenish discoloration spreads to whole body, both

internal and external.

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HaemolysisLiberation of Hb

Hb + H2S gas

Sulph-met Haemoglobin (greenish color)

Diffuses into tissues

Blood

Bacteria H2S

PROCESS

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The veins converging on the

• Root of neck

• Over the shoulder

• Running into the groins

• Become visible as blue or purplish lines

• Due to pigments from decomposing blood

passing through the blood vessels

MARBLING

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• The course of these veins is thus visible as a

bluish network

• This condition owing to its mosaic or

arborescent pattern is known as Marbling

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• Veins are filled with

– Gas bubbles

– Haemolysing blood

• Marbling commences ____ 24 hours

• Seen prominently ____36 - 48 hours

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PRODUCTION OF GASES

• Within 12 – 13 hrs after death.

• Production of foul smelling gases starts:

– In hollow viscera

– In solid viscera

– Below the skin

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• In 18 – 48 hrs

• Gases collect in hollow viscera.

• They cause false rigidity.

• They exert considerable pressure.

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Gases:-

• H2S

• NH3

• Phosphorated hydrogen

• CO2

• CH4

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PRESSURE EFFECTS OF GASESThe gases gradually increase in quantity and due to this, pressure effect on

various tissues occur. The following pressure effects are seen:-

1. Bloating of features

2. Shifting of areas of PM.L

3. Changes in skin, hair and wounds

4. Extrusion of fluid from nose & mouth

5. Emptying of heart

6. Changes in appearance of genitals

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PRESSURE EFFECTS

a. Bloating of Features. (36 – 48 hrs)

i. Face - swollen.

ii. Identification – difficult.

iii. Tongue, Lips, nose, eyelids & cheeks are

distended

iv. Face becomes bluish green mass.

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v. Bulging of Lips.

vi. Tongue is pushed between teeth.

vii. In females breasts are swollen.

viii. Rectum also protrude (48 – 72 hrs)

ix. Condition of body may be confused with violent

death.

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b. SHIFTING OF AREAS OF HYPOSTASIS

Putrefaction liquification of clottedBlood

Pressure of duodenal gas Post Mortem

staining

Shifting in any direction

Haemolysis of blood

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c. FLUID AND FROTH FROM MOUTH

• Abdominal gases push diaphragm up

• Lungs, heart and stomach are also pushed

upwards.

• Resulting in extrusion of fluid and froth from

mouth & nose.

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d. SKIN SLIP (3 - 4 DAYS)

• Outer layer of skin becomes loosened and it

can be rubbed easily with pressure, to leave

a moist, pink base called “skin slip”.

• Skin from hands and feet may peel off in the

form of gloves or stockings.

• Can be helpful for getting finger prints.

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e. BLISTERS ( 2 – 3 DAYS)

• Blisters are found all over the body.

• They can be confused with blisters of

burns.

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DIFFERENCES

Trait True Blister Putrefaction Blister

Time Ante-Mortem 2-3 days Post Mortem

Vital reaction Present Absent

Contents Full of fluids rich in

albumin

Mainly gas, very little

fluid with

no albumin

On rupturing Fluid escapes but

blister remains.

Gas escapes & blister

is no more visible.

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f. HAIR

• Becomes loosened

• Easily pulled out

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g. CONDITION OF GENITALS

• Male: Penis & scrotum become swollen

• Female: Genitals appear pendulous

• In pregnant ladies fetus may be expelled out.

(in 48 – 72 hrs)

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h. EMPTYING OF HEART

• Increased fluidity of blood

• Heart may become empty

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APPEARANCE OF MAGGOTS

• Putrefied material attracts flies.• Flies lay eggs in.

i. Open wounds.ii. Natural orifices

• Nose• Mouth• Vagina• Anus

Flies lay eggs Larva Pupa AdultTime period varies with type of fly & temp

• Knowledge of flies --- Forensic entomology.

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Flies

Eggs

Larvae

Pupae

Adults

Life Cycle

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FORENSIC ENTOMOLOGY

• Study and knowledge of insects and flies,

about their habitat and life cycle.

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5. OTHER SEQUELAE

a. Beetles

b. Vultures

c. Dogs

d. Other animals

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RESULT IN

i. Liquifaction

ii. Cavities burst

iii. Skeltanization (1-3 month)

iv. Decomposition of bones

• Uncoffined – 1 year

• Coffined – 3 years

• Complete destruction - 25 yrs

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PUTREFACTION OF INTERNAL ORGANS

Starts with External putrefaction

Putrefy early

Putrefy later

Organs - Soft

- More blood

Organs - Hard

- less blood

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i. Stomach and intestines

ii. Trachea, Bronchi, lungs, larynx

iii. Liver, Brain, Spinal cord.

iv. Heart, Kidneys, Diaphragm

v. Prostate, Testis, Uterus, Ovaries

SEQUENCE

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FACTORS INFLUENCING PUTREFACTION

External Factors:

i. TEMPa. 70o to 100o F best temperature putrefaction

b. Freezing point death of bacteria No putrefaction

c. 200oF temp fluids are dried up putrefaction.

(mummification may occur)

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ii. AIR Presence of air putrefaction

Absence of air putrefaction

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Casper Dictum states that

• The rate of putrefaction

• The temp. remaining same in each case

• Is almost equal for

One week in air

Two weeks in water

Eight weeks when the body is buried

(However it is subject to great variation.)

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iii. MOISTURE

• Presence of moisture promotes

putrefaction

(More moisture More Bacteria

Multiplication of Bacteria)

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• Initially maintain temperature and help

putrefaction.

• Later protect body from flies

iv. CLOTHES

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v. MANNER OF BURIAL

a. In air tight coffin putrefaction delayed

Body with coffin putrefaction early

b. In deep grave putrefaction delayed

In shallow grave putrefaction early

c. Body buried in lime putrefaction delayed

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d. Body buried in water logged area

putrefaction early.

e. Body buried in sandy area

f. Body buried in porous land Mummification

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INTERNAL FACTORS

i. AGE

a. Infants, still born, sterile putrefy late

b. Children putrefy early than adults

c. Old, less fatty putrefy late

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ii. CONDITION OF BODY

a. Fatty body early putrefaction

b. Emaciated body late putrefaction

c. Mutilated body early putrefaction

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iii. SEX

• Very little influence

• Female Fatty early putrefaction.

• Female dying after child birth early

putrefaction.

• Female dying of septicemia early

putrefaction.

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iv. MODE OF DEATH

a. Infection more bacteria early putrefaction

b. Anemia less blood late putrefaction

c. Wasting diseases Atrophy of muscles late putrefaction

d. Poisons may delay putrefaction.

eg. Arsenic, Antimony, Zinc

e. Sudden Death Good Health slow putrefaction

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PUTREFACTION IN WATER

• Much slower

• Once body is out of water rate is

higher (16 times)

• Also depends on water, cond. of

body & water animals

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• Fast in still water ----- slow in running water

• Fast in dirty water ----- slow in clean water

• Fast in deep water ----- slow in shallow water

• Fast in naked body ----- slow in clothed body

• Fast in body effected ----- slow in body not

by water animals effected by water e.g

fish, crocodiles, animals

insects.

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APPEARANCE OF COLOR CHANGES

Putrefaction in water Putrefaction in

air

i. Face & neck i. Abdomen

ii. Thorax ii. Chest

iii. Shoulder iii. Face

iv. Arms iv. Legs

v. Abdomen v. Shoulder

vi. Legs vi. Arms

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FLOATATION OF BODY

In summer 24 hrs

In winter 2-3 days

Position of body : Abdomen – Above (higher due to gases)

Spine – Below (Heavy)

No floatation of body:- If sub merged under water with a

weight tied with it, entrapped by weeds

when sufficient gases are produced

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Depends uponi. Age Adult Early

Children LateElderly Late

ii. Built Strong & Fatty EarlyWeak Late

iii. Sex Female EarlyMale Late

iv. SurroundingWater

Clear water EarlyDirty water Late

iv. WeatherSummer EarlyWinter Late

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MUMMIFICATION

• It is also a modification of putrefaction

process, which becomes arrested and body

tissues undergo mummification.

• It is characterized by dehydration or

desiccation of body tissues and viscerae after

death

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The ideal conditions for mummification are

(1) High atmospheric temp devoid of moisture

(2) Free air circulation round the body (3) Dry porous sandy soil

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Shallow grave Free air High temperature Evaporation

Dry atmosphere

DEAD BODY Loss of moisture

Porous earth

Shriveled & Dry Tissues Dry & Healthy Skin

Dry Soil

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MUMMIFICATION (MEDICO-LEGAL IMPORTANCE)

Time period required 3 Months

Artificial Mummification also possible

Mummification may help in:-

i. Identity

ii. Establishing the cause of death

iii. Time since death

iv. Indicates place of recovery

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ADIPOCERE (SAPONIFICATION)

It is a modification of process of

putrefaction, which may become arrested

and fatty tissue of body may get converted

into fatty acids. It has the properties of fat

and wax, so the name

(Adipo - soft fat) (Cera- Wax)

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It results from conversion of unsaturated fats to saturated fats by bacterial fat splitting enzymes. The fat is hydrolysed to a wax compound.

The ideal condition are

(1) Moisture

(2) Warm temperature (moderate)

(3) Diminution of air

Adipocere is a pale, greasy semifluid material with a rancid smell.

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Dead Body Damp soil

Fatty Areas Less AirMoisture

UN-SATURATED BODY FATS Warm Temperature

Bacteria Lecithinase Firm Fat

Cl-welchii

Release Enzymes

SATURATED FATTY ACIDS

Palmitic, stearic,Ca-Soaps

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Areas involved:• Abdomen• Cheeks• Breasts• Buttocks• Rarely in infants & obese, whole body is

converted

Time: one limb – 3-6 weeks

whole body – one year

If body is immersed in fluid - early

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MEDICOLEGAL IMPORTANCE

i. Identification

ii. Injuries are present – cause of death

iii. Indicates time elapsed since death.

iv. Indicates the place – water or moist

ground from which the body has been

recovered

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Bio Chemical Changes In Body Fluid After Death

• Blood

• C.S.F

• Ocular fluid.

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Changes In Blood• Concentration of all blood components

Changes after death.

Factor which are responsible for his changes are:

1- Function of organ between Somatic and molecular death.

2- Post –mortem action of bacteria and enzymes.

3- Altered permeability of dying cell membrane.

Also at the time of certain natural deaths certain changes take place in blood.

Due to altered body function like agonal acidosis which is associated with marked.

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In Lactic AcidLactic acid 1 meq/ L.• 1 hour P/M 20 meq/L.• 12 hour P/M 50 meq/L .• 24 hour P/M 75 meq/ L.

Urea nitrogen• @12-30 mg/ dl up to 70 mg/ dl.

Amino Acid Nitrogen

@3-5 mg/dl.

12 hour P/M 10-12 mg/dl.

All as result increase tissue break down.

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Ph: of blood and tissue fall (acidic) , due to terminal accumulation of CO2 and lactic Acid after death After about 24 hours due to production of NH3 from enzymatic break down of proteins ,PH starts rising and reaction again become alkaline.

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Plasma Chloride @95- 105 mg/dl.

• Soon after death chlorides in plasma and R.B.C equalize become 74 m.mol/L and then concentration drops due to extra cellular diffusion and become half i.e 37 m.mol /l in 72 hour s.

Mg++: @ 0.07 – 1.2 m.mol/L.• With the onset of putrification it starts rising and

reach eight times in 72 hours.

K+: @ 3.8 -5 m.mol/L.

Start rising after death owing to diffusion from vascular endothelium .

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EnzymesPost –mortem accumulation of enzymes in serum like

:

• Amylases: @23 – 85 I.U/L

• Lactic Phosphataes : @ 90 – 250 MILI units /L.

• Acidic phosphataes : @ up to 0.7 Units /L.

• Alkaline Phosphtates : @ 30- 95 mili units/L.

• Transimanase : @ 5- 35 milil units/L

Rise in first few hour s after death as a result of increased tissue break down and peak activity varies for each enzymes .

Amylase & Phosphates :34 -48 hours.

Transaminase: 48-60 hours.

Lactic Dehydrogenase: 4th day.

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Sugar and Urea • Blood sugar and Blood Urea also rises after death.• Breakdown of liver glycogen result in accumulation of

dextrose in inferior vena cava and hence in right side of heart . Blood sugar rise more than 300 mg /dl. Within first 24 hours.

Diffusion does not extend beyond the heart as lungs provide an effective barrier. So no reliance can be placed on blood dextrose levels if blood is collected from inferior vena cava or right side of the heart .

• Examination of peripheral blood might help if raised more than 200 mg/dl but care should be taken in interpretation as agonal rise in blood dextrose can be produced by Hypoxia, CO poisoning and effect of trauma.

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• Blood urea concentration can rise in agonal period to the level of 150 mg/dl but usually serum level within first 48 hours is never above 100 mg/dl unless there is an increase in urea concentration during life.serum concentration of urea > 300 mg/dl and creatinine more than 10 mg % undoubtly indicate renal failure with uremia.

• @creatiae 0.42 -2.42 mg%( in C.S.F)

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C.S.F

• @Amount in life is 150 ml start disapperaing at 24-48 hours after death.

• Time of death can be estimated with +8to – 8 hour of actual time .

• Sample can be easily obtained by tapping cisterna magna .In first fifteen hours after death:

Lactic Acid rise from 15 %mg to over 200 mg %

N.P.N : from 15 mg % to 40 mg %

A.A.N: from 1 mg % to 12 mg %

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Following conclusion can be drawn

• A.A.N: less than 14 mg % death less than 12 hour PM.

• N.P.N. less than 80 mg %death less than 24 hours PM.

• Creatine less than 5 mg % death less than 12 hours PM.:

• Phosphorus less than 15 mg/dl death less than 10 hour s PM.

Ocular Fluid:

• Vireous and Aqueous fluids are free from contamination in a dead body

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Ocular Fluid:Vireous and Aqueous fluids are free from

contamination in a dead body and up to 2 ml of fluid can be eaisly withdrawn from each eye ball with needle and syringe.

Steady rise in K+ in Viterous after death for over 100 hours . There is a linear relationship between K+ concentration and P/M interval over 100 hours death.

There is a standard error of +4.7 to – 4.7 hours and this did not increase with time.

• @3.4 meq/L.

• Rate of increase is 0.17 meq/l/hour.

Ascrobic Acid, Pyruvic Acid , N.P.N: Studies are also helpful in determining time since death but K+ is more reliable and dependable.

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International Form of Medical Certificate Cause of Death

A: Biodata of deceased

B: Cause of deathI. Disease or condition Approximately interval between

Directly leading to death. 0nset &death.

Antecedent causes morbid a)---------------------------------

Condition, if any, giving rise Due to(or as a consequence of)

to the above causes ,starting the b)---------------------------------

underline condition last. Due to(or as a consequence of)

II. Other significant conditions c)-----------------------------------

Contributing to the death but not

Related to the disease or conditions

cause it. ---------------------------------------

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• This does not mean the mode of dying e.g heart failure ,cardiopulmonary failure , etc It means disease, injury or complication which cause death.

• Filling of death certification:

Content s and design of death certificate . There are two sections. The first headed “I” asks for:

a. Immediate cause .

b.Morbid conditions if any giving rise to the immediate cause.

It would be sufficient for instance to write acute General Peritonitis

Under “Ia” and perforated Gastric Ulcer under “Ib”

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• Second headed “II” asks for other significant conditions (if important ) contributing to death but not related to immediate cause.

• There would be none in the above example but if “Ia” Uraemia, “ I b” supportive pyelonephritis, and then we can place “II” Carcinoma of prostate or Diabetes Mellitus.

• All that is required is that the precise cause of death should be set out starting from the immediate cause and working back to the underlying disease responsible .

• Terms which merely describe mode of dying like heart failure or coma should be avoided.

• If precise cause of death is not known one should not start guessing it. Ambiguities like “Birth injuries” ,”C.V.A” or termination of pregnancy should be avoided \rather qualification must be given to make it clear that they were natural not accidental or of criminal occurrence .

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Under no circumstances should a doctor sign blank or partially blank death certificate.

Under Birth and death Registration Act 1874,it is a statutory duty of a doctor (mandatory) who has been in attendance of the patient during the last illness to issue a certificate .no fee should be charged although there is no regulation.

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