Beruflich Dokumente
Kultur Dokumente
Thantos:- Death
Logos = Science
Thanatology. It is the scientific study of
Phenomena and practices relating to
death.
DEATH
&
Medico-Legal Aspects
DEFINITION
1. Me Rental and Smith defined death
Complete and permanent cessation.
2. Mr Shapiro defines death as
Irreversible loss of properties of living matter.
3.
4.
Physicians Definition.
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)
TWO STAGES
I.
Somatic Death (Soma-Body)
Irreversible loss of integrating
and co-coordinating functions
of the organism as a wholeis 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
Tripod of life
Life
tion
respi
r
func
ation
CN S
circulation
Modes of death
Coma
Syncope
Tripod of
death
Asphyxia
CNS
function
Circulation
LIF
E
Respiration
Death
II.
Molecular Death
It is the death of individual organs and
tissues (which persisted individually
after somatic death)
Survives For
Survives for
Survives for
Survives for
Survives for
Survives for
60 minutes
15 minutes
45minutes
6-24 Hours
6 Hours
6 Hours
DIAGNOSIS OF DEATH
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)
D/D of Death
1. Suspended animation
2. Barbiturate poisoning
3. Electrocution
4. Drowning
5. Hypothermia
NATURE OF DEATH
Natural & Un-Natural
Un- Natural:
1. Homicidal
2. Suicidal
3. Accidental
Modes of death
Coma
Syncope
Tripod of
death
Asphyxia
1. COMA
Name of coma
Causes of Coma
Fate of coma
Compression of brain
- Inj to Brain
- Inj to meninges
- Disease of brain
Disease of meninges
Concussion,
hemorrhage,inflammation,
abcess,new growth,
thrombosis, embolism.
Epilepsy
Heat Stroke
Hypothermia
Effect of Poison
Metabolic Disorders
- Diabetes
- Hypoglycemia
- Uremia
- Hepatic Failure
Compression
Hemorrhages
Inflammation of meninges
Tumor
Foreign body
Vascular Lesions
Minute Hemorrhages (in poisoning)
2. SYNCOPE
Failure of Heart
Reduced blood supply to brain
Causes:
1.
2.
3.
Anemia
Weakness
Sudden Fright Reflex vagal inhibition
- Cardiac
Center paralysis
- Respiratory
Head
4. Direct blow on
Epigastrium
Testis
5. Emotional Stress
6. Sudden Exposure to cold
7. Insertion of instruments in orifices Uterus
- Bladder
- Rectum
- Any body
cavity
8.
9.
10.
11.
12.
Anesthesia
Exhaustion
Heart Diseases
Hemorrhage
Idiopathic
-------
Usually Empty
Pale
Congested
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
Resulting in :
O2 supply to brain.
O2 supply to blood
Rapid unconsciousness
Stoppage of respiration.
Fate After ---- 2 3 minutes ----- Death
TYPES OF ASPHYXIA
Mechanical Asphyxia
Pathological
Asphyxia
Toxic Asphyxia
Environmental
Asphyxia
Traumatic Asphyxia
Positional Asphyxia
Iatrogenic Asphyxia
:
:
:
:
Congestion
Cyanosis
Edema
Petecheal Hemorrhages
:
:
:
Ligature Mark
Bruising
Defense wounds
Non-Asphyxial
SIGNS OF DEATH
A. Immediate
B. Early
C. Late
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)
Cooling of body
Eye changes
Skin changes
Post-mortem lividity
Muscles changes Rigor Mortis
C. LATE SIGNS
Putrefaction (Ultimate fate of all living
creatures.)
Arrest of putrefaction.
(Extra ordinary phenomenon)
- Mummification
- Adipocere formation
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
b. LOSS OF EEG
c. Cessation of circulation
- Feeble sounds
- Thick Chest
- Emphysema
Suspended animation
(Apparent Death)
Heart beat & respiratory movements are not
heard ordinarily (as they are at a very low
pitch.)
Drowning cases
New born
Anesthesia
Concussion
Heat Stroke
Prolonged illness
Electrocution
Deep Shock
ii.
EEG - FLAT
iii.
ECG - FLAT
iv.
d. Cessation of Respiration
i.
ii.
iii.
Mirror Test
iv.
Feather Test
v.
B. EARLY SIGNS
Difference
i.
ii.
iii.
iv.
v.
Temperature
2. PRESENCE OF CLOTHING
i.
ii.
3. LOCATION OF BODY
i.
ii.
4. HUMIDITY
Rapid Cooling
Dry Air Less Cooling
Cooling Early
Large Body
Cooling Slower
6. FATTY BODY
Cooling slow (as fat is a poor conductor of
heat)
In ladies having more fat slow cooling.
7. MANNER OF DEATH
Heat loss is slower in chronic bacterial diseases.
Heat loss is faster in wasting diseases.
METHODS OF CALCULATION
Hourly calculation.
Newtons Formula.
Required data:
Cause of death.
Temperature of environment.
ii.
Sun stroke
iii.
Pontine Hemorrhage
iv.
Encephalitis
v.
Lobar pneumonia
vi.
Typhoid Fever
ii.
Septicemia.
Flow of fluid:
cooling rapid
b) EYE CHANGES
i.
ii.
c) SKIN CHANGES
i.
Skin
becomes
pale(more
dependent parts
ii. Skin elasticity is lost
iii. Skin luster is lost
on
non
Also called:
P.M. Hypostasis
Livor Mortis
P.M staining
Cadaveric Lividity
Subcutaneou Hypostasis
Suggilations
Vibices
DEVELOPMENT OF LIVIDITY
After 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
FACTORS AFFECTING
POSTMORTEM LIVIDITY
Position of body +
pressure effect on
specific areas
Ante-Mortem state of
body & Mode of death
Reduced Hb
Colour of skin
Fluidity of blood
Effect of gravity
Colour of blood
COLOUR OF LIVIDITY
Initially bluish pink.
Later becomes bluish purple (dark blue)
In fair skin colour better appreciated
In hemorrhage, anaemia
- Faint colour.
In asphyxia
- Dark purple
Phosphorous
Nitrites
Hydrogen Sulphide
Opium
Burning
Septic Abortion
- Dark brown
- Red Brown
- Bluish green
- Black
- Cherry Red
- Grayish Brown
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
EXCLUDING
Back of head
Back of shoulder
Back of Buttocks
(Areas in contact)
Back of heels
Areas under tight clothing
(Contact Flattening)
CAUSE OF ABSENCE
Pressure from below, prevents distension
and filling of capillaries and minute veins
of skin. It is called contact flattening.
a. Trait
PM Lividity
Cyanosis
Time of onset
Post-Mortem
Ante-Mortem
Location
On dependent parts
On terminal tips
Appearance
Normal
Abnormal&
Pathological
Less
Change of
Position
Shifting of lividity
No change
History of
disease
Not required
Positive
Confirmation
Visible as a PostMortem
Phenomenon
Anti-Mortem
Observation/
Evidence
b. Trait
PM Lividity
Bruise
Situation
Cuticle
Uninjured
Site
Occurs on
Occurs at the site of
extensive areas of injury (may appear any
dependent parts
where)
Appearance
Not elevated
Edges
Clearly Defined
May be injured
Colour
Uniform
Variegated in colour
Section
On incision ,blood is
seen in blood vessels,
can be easily washed
away
Effects of
pressure
May be present in
areas under pressure
Blood
Blood elements seen
elements on in blood vessels with
microscopy no evidence of
inflammation
c. Trait
P.M Lividity
Congestion
Involves whole
organ
Appearance Normal
Pathological
change is evident.
Mucous
Membrane
Normal
Exudate
No inflammatory
exudate
Exudate seen
Hollow
viscera
Stomach, intestine
when stretched show
alternate stained &
unstained areas
Stomach and
intestine show
uniform distribution
MUSCLE CHANGES
Period of relaxation
(Primary Flaccidity)
Cadaveric rigidity
(Rigor mortis)
Period of relaxation
(Secondary relaxation)
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.
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
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.
Relaxation
Contraction
ATP is stored in high concentration in
muscles
Balanced production of ATP from glycogen
stores.
AFTER DEATH
Glycogen stores
resynthesize ATP,only for
No glycogen
No ATP production
No relaxation of muscles
ed interdigitation of
actin &myosin
Actomyosin
ed accumulation of
(stiff gel)
salts in muscles
Stiffening and shortening of muscles
(voluntary + involuntary)
Fixation of joints
Persists till the autolysis of actin & myosin.
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
STARTS
2-3 hours after death
In face, eyes, mouth & neck
SPREADS
Upper limb
Trunk
Lower limbs
with in 12 hours
STAYS
12 hours
PASSES OFF
Next 12 hours
Plateau of variable
temp
Decomposition
36.9oc
Rigor Mortis
(98.4OF)
Temperature of
environment
Lividity
12
18
24 30
36
42
48 54
FACTORS INFLUENCING
RIGOR MORTIS
Factor
Appearance
Passing Off
Late
Early
Early
Late
Early
Late
1. Atmosphere
a.
b.
c.
Factor
Appearance
Passing off
2.
Age
a.
Children
Early
Early
b.
Elderly
Early
Early
c.
Adults
Late
Late
Factor
3.
a.
b.
c.
d.
e.
Manner of Death
Chronic disease
& emaciation
Sudden death
Strychnine
Poisoning
Drowning
Arsenic
poisoning
Appearance
Passing off
Early
Early
Late
Immediate
Late
Early
Early
Late
Late
Late
Factor
Appearance
Passing off
4.
Muscular Condition
a.
Healthy muscles
Late
Late
b.
Early
Early
muscles
DIFFERENTIAL DIAGNOSIS OF
RIGOR MORTIS
(Simulating Conditions)
1.
Heat Stiffening
2.
Cold Stiffening
3.
Putrefaction stiffening
4.
Cadaveric Spasm
1.
HEAT STIFFENING
i.
When body
temperature.
is
exposed
to
75oC
or
high
ii.
High Temperature
High voltage
Stiffening of muscles
Special posture
(pugilistic attitude or boxers attitude)
SPECIAL FEATURES
i.
ii.
2. COLD STIFFENING
Freezing temp
Solidification of fats and muscular tissues
Rigidity of Muscles
3. PUTREFACTION STIFFENING
Putrefaction
Formation of gases
Accumulation of gases
False rigidity
Stiff Limbs
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.
Examples:
i.
ii.
DIFFERENCES
Traits
Rigor Mortis
Cadaveric spasm
1. Time of onset
2 3 hours after
death
Instantaneous
2. Predisposing
factors
Nil
3. Muscles
involved
Usually a single
group of voluntary
muscles
4. Muscle
stiffening
Not marked,
Marked, moderate
moderate force can force cannot break
break it.
it.
Traits
Rigor Mortis
Cadaveric spasm
5. Medicolegal
importance
Helps in
Indicates nature
determination of of death :
time since death suicide,
homicide,
accident.
6. Body Heat
Cold
Warm
7. Molecular
death
Occurs
8. Mechanism
Known
Not known
MEDICOLEGAL IMPORTANCE
Plateau of variable
temp
Decomposition
36.9oc
Rigor Mortis
(98.4OF)
Temperature of
environment
Lividity
12
18
24 30
36
42
48 54
PUTREFACTION
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
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)
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.
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
BASIC RULE
Organs (First to putrefy)
Receiving rich blood supply
Near to source of bacteria
PUTREFACTION
Bacterial Action
warmth
moisture
Molecular death
Death of tissue
Enzymes production
(Cl - w)
Production of
Lecithinase Enzyme
Effects Tissues
(Dissolution )
Release of enzymes
from tissue cells
Softening
liquefication of
tissue cells
Haemolysis of blood
Hydrolysis of
lecithinase
STEPS OF PUTREFACTION
i.
Color changes
ii.
Production of gases
Other sequelae
COLOR CHANGES
External
a. 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
Internal
PROCESS
Blood
Bacteria
Haemolysis
Liberation of Hb
H2S
Hb + H2S gas
MARBLING
The veins converging on the
Root of neck
Seen prominently
____36 - 48 hours
PRODUCTION OF GASES
Within 12 13 hrs after death.
Production of foul smelling gases starts:
In hollow viscera
In solid viscera
Below the skin
In 18 48 hrs
Gases collect in hollow viscera.
They cause false rigidity.
They exert considerable pressure.
Gases: H2S
NH3
Phosphorated hydrogen
CO2
CH4
1. Bloating of features
2.
3.
4.
5.
Emptying of heart
6.
PRESSURE EFFECTS
a. Bloating of Features. (36 48 hrs)
i.
Face - swollen.
v.
Bulging of Lips.
vi.
vii.
viii.
ix.
Putrefaction
liquification of clottedBlood
Haemolysis of blood
Pressure of duodenal
gas
Post Mortem
staining
e. BLISTERS ( 2 3 DAYS)
Blisters are found all over the body.
They can be confused with blisters of
burns.
DIFFERENCES
Trait
Time
True Blister
Putrefaction Blister
Ante-Mortem
Absent
fluid with
no albumin
On rupturing
blister remains.
is no more visible.
f.
Becomes loosened
Easily pulled out
HAIR
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)
h. EMPTYING OF HEART
Increased fluidity of blood
Heart may become empty
APPEARANCE OF MAGGOTS
Life Cycle
Flies
Eggs
Larvae
Pupae
Adults
FORENSIC ENTOMOLOGY
Study and knowledge of insects and flies,
about their habitat and life cycle.
5. OTHER SEQUELAE
a. Beetles
b. Vultures
c. Dogs
d. Other animals
RESULT IN
i. Liquifaction
ii. Cavities burst
iii. Skeltanization (1-3 month)
iv. Decomposition of bones
Uncoffined 1 year
Coffined
3 years
- Soft
- More blood
Organs
- Hard
- less blood
Putrefy early
Putrefy later
SEQUENCE
i.
ii.
FACTORS INFLUENCING
PUTREFACTION
External Factors:
i. TEMP
a. 70o to 100o F
b. Freezing point
c. 200oF
temp
best temperature
death of bacteria
fluids are dried up
putrefaction
No putrefaction
putrefaction.
ii. AIR
Presence of air
Absence of air
putrefaction
putrefaction
iii. MOISTURE
Presence
of
moisture
promotes
putrefaction
(More moisture More Bacteria
Multiplication of Bacteria)
iv. CLOTHES
v. MANNER OF BURIAL
a. In air tight coffin
Body with coffin
b. In deep grave
In shallow grave
c. Body buried in lime
putrefaction delayed
putrefaction early
putrefaction delayed
putrefaction early
putrefaction delayed
Mummification
INTERNAL FACTORS
i. AGE
a. Infants, still born, sterile
b. Children
putrefy late
putrefy late
ii.
CONDITION OF BODY
a. Fatty body
early putrefaction
b. Emaciated body
late putrefaction
c. Mutilated body
early putrefaction
iii. SEX
Very little influence
Female
Fatty
early putrefaction.
Female dying
putrefaction.
after
Female dying
putrefaction.
of
child
birth
septicemia
early
early
PUTREFACTION IN WATER
Much slower
rate is
effected by water
animals
insects.
APPEARANCE OF COLOR
CHANGES
Putrefaction in water
Putrefaction in air
i.
i. Abdomen
ii.
Thorax
ii. Chest
iii. Shoulder
iii. Face
iv. Arms
iv. Legs
v.
v. Shoulder
Abdomen
vi. Legs
vi. Arms
FLOATATION OF BODY
In summer 24 hrs
In winter 2-3 days
Depends upon
i.
ii.
iii.
iv.
iv.
Age
Adult
Children
Late
Elderly
Late
Built
Strong & Fatty
Weak
Late
Sex
Female
Male
Late
Surrounding
Water
Clear water
Dirty water
Late
Weather
Summer
Early
Winter
Late
Early
Early
Early
Early
MUMMIFICATION
It is also a modification of putrefaction
process, which becomes arrested and body
tissues undergo mummification.
It
is
characterized
by
dehydration
or
Shallow grave
Free air
Evaporation
High temperature
Dry atmosphere
Dry Soil
DEAD BODY
Loss of moisture
MUMMIFICATION
(MEDICO-LEGAL IMPORTANCE)
Time period required
3 Months
Identity
ii.
ADIPOCERE (SAPONIFICATION)
It
is
modification
of
process
of
soft fat)
(Cera- Wax)
Dead Body
Moisture
Fatty Areas
Bacteria
Lecithinase
Cl-welchii
Release Enzymes
Damp soil
Less Air
Warm Temperature
Firm Fat
Palmitic, stearic,Ca-Soaps
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
MEDICOLEGAL IMPORTANCE
i.
Identification
ii.
moist
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.
In Lactic Acid
Lactic 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.
Plasma Chloride
Enzymes
Post 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.
C.S.F
@Amount in life is 150 ml start disapperaing at 2448 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 %
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.
A: Biodata of deceased
B: Cause of death
I. Disease or condition
---------------------------------------