PATHOPHYSIOLOGY OF

DEATH
By: dr. Hafsa salame
Forensic Pathology at Jordan University Hospital
 TYPES OF DEATH
• Cellular death : Cellular death means the cessation
of respiration (the Utilization of oxygen) and the normal
metabolic activity In the body tissues and cells.
Cessation of respiration Is soon followed by autolysis
and decay, which, if it Affects the whole body, is an
evidence of true Death. The differences in cellular
metabolism determine The rate with which cells die and
this can be very Variable
Examples on different levels of cellular
death:
Skin and bone will remain metabolically active
and thus ‘alive’ for many hours and these cells
can be successfully cultured days after somatic
death.
White blood cells are capable of movement for
up to 12 hours after cardiac arrest
The cortical neuron, on the other hand, will die
after only 3–7 minutes of complete oxygen
deprivation. A body dies cell by cell and the
complete process may take many hours.
Somatic death
Somatic death means that the individual will never
again communicate or interact with the
environment. The individual is irreversibly
unconscious and unaware of both the world and his
own existence. The key word in this definition is
‘irreversible’, . Even if irreversible unconsciousness
has occurred, if there continues to be spontaneous
respiratory movements and the heart continues to
beat, it is doubtful if this would be accepted as
fulfilling the criteria of ‘true death’.
BRAIN DEATH
• Criteria : The patient must be in deep coma
and treatable causes such as depressant drugs,
metabolic or endocrine disorders (diabetic or
myxedema coma) or hypothermia must be
excluded.
• The patient must be on mechanical ventilation
because of absent or inadequate spontaneous
respiration.
• Neuromuscular blocking agents excluded as a
possible cause of the respiratory failure.
•a firm pathological diagnosis must be there. The
most common causes are head injury and
intracerebral hemorrhage from a ruptured cerebral
aneurysm.

• Diagnostic tests for brainstem death must be

unequivocally positive. These tests should be
determined by two doctors, preferably one of
whom should be the physician in charge of the
patient. This physician should have been registered
for at least 5 years and should have had
experience of such cases. The second, independent
• • A checklist of the diagnostic tests and their results
should be kept in the patient’s notes and the tests
should be repeated at least once, the interval between
the tests depending on the opinion of the doctors
• All brainstem reflexes are absent, with fixed dilated
and unreactive pupils. Corneal reflexes are absent.
It should be noted that persistence of spinal reflexes are
irrelevant in the diagnosis of brainstem death.
• Vestibulo-ocular reflexes are negative when iced water
is introduced into the ears.
• There are no motor responses to painful stimuli in any of
the cranial nerves.
 .

• There is no gag reflex to a catheter placed in the

larynx and trachea.
• There are no respiratory movements when the
patient is disconnected from the ventilator with an
arterial PCO2 level in excess of 50 mmHg as a
stimulus to breathing.
• Testing must be performed with a body
temperature not less then 35°C to avoid
hypothermia simulating brainstem damage.
 INDICATORS OF BRAIN DEATH

Neuromuscular blocking
Deep coma agents excluded

All brainstem reflexes are

absent, with fixed dilated
Mechanical ventilation and unreactive pupils.
Corneal reflexes are absent
 mummificati
Deat on
h
adipocere

cremation

Putrefactio Assis
n
t
Animal predators
Assis
t
Complete
dissolution unless
fossilized
Skeletenization Fate of body
after death
POST-MORTEM SIGNS OF DEATH
Early
• Eye changes
• Skin
changes
• Muscles Late
• Gastric • Algor
mortis
Insect (cooling)
• Livor mortis
activity (hypostasis
)
• Rigor
mortis

Chemical
changes in Very late
body fluids • Decomposi
(electrolyt tion 13

es)
 CHANGES AFTER DEATH
EARLY CHANGES :

EYE SIGNS :

1. Loss of the corneal and light reflexes leading to insensitive

corneas and fixed unreactive pupils.
2. The light reflex is lost as soon as the brainstem nuclei suffer
ischemic failure.
3. The pupils usually assume a mid dilated position, which is the
relaxed neutral position of the pupillary muscle, though they
may later change as a result of rigor.
4. The pupils may lose their circular shape after death as a result
6. The eyelids usually close, but
this is commonly incomplete
7. discoloration of the sclera
becoming brown and then sometimes
almost
Black, giving rise to the name 'tache
noire'. --
 EARLY CHANGES OF DEATH
• The muscles rapidly become flaccid (primary flaccidity), with
complete loss of tone
• Skin, conjunctivae and mucous membranes pale. The skin of the face
and the lips may remain red or blue in color in hypoxic/congestive
deaths. The hair follicles die at the same time as the rest of the skin
• Loss of muscle tone in the sphincters may result in voiding of urine;
• Emission of semen is also found in Some deaths; the presence of
semen cannot be used as an indicator of sexual activity shortly
before death.
• Regurgitation is a very common feature of terminal Collapse and it is
a common complication of resuscitation.
 POST MORTEM CHANGES
Hypostasis : it occurs when the circulation ceases arterial,
venous and capillary . Gravity then acts upon the now stagnant
blood and pulls it down to the lowest accessible areas. The red
cells are most affected then skin look as a bluish red
discoloration, plasma also drifts downwards to a lesser extent,
causing an eventual post-mortem 'dependent edema', which
contributes to the skin blistering that is part of early post-mortem
decay.
The distribution of hypostasis : the pattern of hypostasis
depends on the posture of the body after death. Most commonly
body is lying on its back, with the shoulders, buttocks and calves
pressed against the supporting surface so that hypostasis is
prevented from forming there, the skin remaining white.
 HYPOSTASIS WILL DISTRIBUTE ITSELF ACCORDING TO
BODY POSITION, AGAIN WITH WHITE PRESSURE AREAS AT
THE ZONES OF SUPPORT.
 HANGING
Hypostasis will be
most marked in
the feet, legs and
to lesser extent in
the hands and
distal part of the
arms
 OTHER SITES OF HYPOSTASIS

Drowning Epilepsy or
drinkers

• OVER CHEST AND UPPER LIMBS • FACE DOWN WITH WHITENING

AROUND LIPS AND NOSE
 THE COLOR OF HYPOSTASIS
 The usual hue is a bluish red, but variation is wide depends on the
oxygenation state at time of death
 Hypoxic state having a darker tint
 When death has been due to hypothermia or exposure to cold such as
drowning the color of hypostasis may be pink
 The best known is the 'cherry pink of carboxyhaemoglobin, which is a
unique color and is often the first indication to the pathologist of carbon
monoxide poisoning.
 Cyanide poisoning: is said to have its own characteristic dark blue-pink
hue,

But this is an unsure indicator of the mode of death,

 TIMING OF HYPOSTASIS
• May not appear at all, especially in infants, old people or those with anemia.
• Hypostasis can appear within half an hour of death or it may be delayed for
many hours.
• Once hypostasis is established if the body moved the primary hypostasis
may be :
• Remain fixed
• Completely moved to new dependent areas
• Or partially stay fixed and partially moved
• So this is useful in crime investigations if hypostasis not related to the
position Of body but this is not always useful because hypostasis was still
mobile for at least 3 days.
 HYPOSTASIS IN OTHER ORGANS
• The importance in forensic autopsy work is the differentiation of
organ hypostasis from ante-mortem lesions.
• In the intestine, dependent loops of jejunum and ileum may be
markedly discolored and mislead the inexperienced pathologist into
suspecting mesenteric infarction or strangulation.
• The lungs almost always show a marked difference in color
from front to back, the anterior margins being pale and the
posterior edges lying in the paravertebral gutters being dark
blue. Also congestion and edema being more marked
posteriorly.

• The myocardium often shows a dark patch in the posterior wall

of the left ventricle that must not be mistaken for early infarction.
 DIFFERENTIATION BETWEEN HYPOSTASIS AND
BRUISING
 This is rarely a problem in fresh bodies, but when decomposition begins the
two
Conditions become blurred.
 Bruises may be anywhere on the body, are often discoid or have an
irregular margin,
But rarely cover a large area with uniform density and do not have a
horizontal margin.
 The classic test is to incise the suspect area to see if the underlying blood
is Intravascular (hypostasis) or infiltrating the tissues outside the vessels
(bruises).
 The bruise will not be affected by pressure mark such as belt
 Hypostasis can be washed away from the incised surface. A
bruise is often deeper in
The skin and fixed histological examination may be
necessary finally to decide.
 If autolysis happened it is almost impossible to
differentiate
 HYPOSTASIS VS. BRUISES

Hypostasis Bruises
(Ecchymosis)
Dependant areas Any where

Well defined edges Ill defined edges

Blood is retained in intact Blood escapes through

capillaries ruptured capillaries

Same level on surface Raised

Pale over pressure areas Not change

Incision: blood flows from Incision: blood

the cut vessel (washable) coagulates in tissue
27
With a bruise, blood will not
flow from the cut
 RIGOR MORTIS
• DEFINITION : Temperature-dependent Physicochemical change
that occurs within muscle cells As a result of lack of oxygen. The
lack of oxygen means That energy cannot be obtained from
glycogen via glucose Using oxidative phosphorylation and so
adenosine Triphosphate (ATP) production from this process ceases
And the secondary anoxic process takes over for a short Time but,
as lactic acid is a by-product of anoxic respiration, The cell
cytoplasm becomes increasingly acidic. In the face of low ATP and
high acidity, the actin and Myosin fibers bind together and form a
gel. The outward Result of these complex cellular metabolic
changes Is that the muscles become stiff.
 RIGOR MORTIS
 The flaccid period immediately after death is variable, but
commonly extends to between 3 and 6 hours
 Rigor is first apparent in the smaller muscle groups,
 The sequence of spread of rigor is also variable but tends to affect
the jaw, facial muscles and neck before being obvious in the
wrists and ankles, then the knees, elbows and hips. Depending on
environmental temperature
 Usually infants, the cachectic and the aged, may never develop
recognizable Rigor mortis
 Rigor spreads to involve the whole muscle mass, reach a
maximum within 6-1 2 hours. The duration of full rigor may be 18-
FACTORS AFFECTING TIMING OF RIGOR MORTIS
1. Temperature : cold delays rigor mortis and warmth speed it up
2. Physical activity shortly before death : muscular exertion
increases content Of glycogen and ATPs in muscles and
enhances rigor
rough guide of relation rigor to time of
death
• If the body feels warm and is flaccid, it has been dead less
than 3 hours.
• If the body feels warm and is stiff, it has been dead from 3 to
8 hours.
 RIGOR MORTIS IN OTHER TISSUES THAN
SKELETAL MUSCLES
• Iris : rigor maybe unequal in both eyes , that makes the pupils
unequal in both eyes the position of both pupils post mortem is
unreliable indicator of toxic or neurologic condition before death
• Heart : rigor may make the ventricles to contract which maybe
mistaken by hypertrophy, to differentiate :
measure total weight of heart
measure the wall thickness of
ventricle
• Rigor in erector pili muscle attached to hair follicles : elevation to
cutaneous hair
 BIOCHEMISTRY OF RIGOR MORTIS
• After death cellular respiration stopped .ATP is no
longer provided for pumps in RER , so CA++ diffuses
from areas of higher concentration to lower
concentration ( muscle sarcomere ) leading to binding
to troponin and cross bridging occurs between actin
and myosin leading to muscle contraction that stays
till breakdown of muscle tissue by enzymes during
decomposition ..
 CADAVERIC SPASM
• DEFINITION : A rare form of muscular stiffening that occurs at moment of death,
persists into the period of rigor mortis , and can be mistaken with it . usually
associated with violent death happening under extremely physical
circumstances with intense emotions.
• Typically it affects certain groups of muscles such as forearm .
• Cases seen in drowning victims when grass , roots are clutched provides an
evidence that the victim was alive at time of entry to water
• It may points to the last activity one did prior to death . E.g. . Holding a knife
tightly make us think of suicide rather than weapon planting
• Of course the body must be examined before ordinary rigor might be expected
to have developed, or the presence of cadaveric spasm cannot then be
assumed.
 RIGOR MORTIS VS. CADAVERIC SPASM

Rigor Mortis Cadaveric Spasm

Onset delayed after death (2-3 hrs.). Onset is instantaneous.
Duration up to 36 hrs. Duration is a few hours, until it is
replaced by rigor mortis.
Intensity comparatively moderate. Intensity comparatively very strong.
Mechanism of formation: Breakdown of predisposing factors: Excitement, fear,
ATP below critical level. fatigue, exhaustion, nervous tension,
contraction of Muscles at time of death.

All muscles of the body are affected Selected muscles

gradually. 37
 DECOMPOSITION

• Decomposition may differ from body to body, from

environment to environment, and even from one part
of the same corpse to another
• Dead bodies are usually returned, through reduction
into their various components, to the chemical pool
that is the earth
•
 SUBCLASSES OF DECOMPOSITION
• Putrefaction : the commonest rout of decomposition .in
an average temperate climate may be expected to begin at about
3 days in the unrefrigerated corpse.
• Definition : a stage produced mainly by the action of proteolytic
enzymes released from dead body cells and bacterial enzymes,
mostly anaerobic organisms derived from the bowel. Other
enzymes are derived from fungi, such as penicillium and
aspergilla's and sometimes from insects, which may be mature or
in larval stage. The chief destructive bacterial agent is cl. Welchii,
which causes marked hemolysis other bacteria's streptococci,
staphylococci, B. Proteus and others
 Stages of putrefaction
• first : external autolysis
• 1. Discoloration of skin : to reddish – green color mainly on
abdomen started in right iliac fossa
• 2. Body filled with gases from micro-organisms : started in the
abdomen . then facial and neck swelling making visual
identification is difficult and lead to protruding of tongue and
eye globes
•
 purging of feces and urine . sometimes uterine prolapse extrude , and
reported cases of postmortem delivery.
• 3. Marbling of skin : haemolysing the blood that stains the vessel walls
and adjacent tissues. ,
• 4.Skin blisters : at site of hypostatic edema that eventually burst
• 5. Skin slippage at fingers and toes : making fingerprint identification
difficult
• 6. Bloody fluid out of all body orifices : after 2-3 weeks due to
hemolysis and increase pressure
• 7. Heavy maggot infestation : produce enzymes that hasten autolysis
•
Skin marbling
BLOODY FLUID OUT OF
BODY ORIFICES
EXSANGUINATION
MAGGOT INFESTATION
 INTERNAL DECOMPOSITION

• This occurs at much different period

• Adrenal medulla , pancreas , intestine wall autolyse within hours
• Uterus , prostate in well skeleton body may stay for a year
• Brain liquefy within a month
• Heart is moderately resistant , examination of coronary arteries
can be done after months and the atheroma persists
• Later perforation of maggots and larger predators Eventually
body reduced to a skeleton
 CONDITIONS AFFECTING RATE OF
PUTREFACTION
1. Temperature: putrefaction begins above 10oc and is
optimum between 21oc and 38o C. A temperature
increase of 10oc usually doubles the rate of most
chemical processes and reactions. It is arrested below
0oc, and above 48oc.
2. Moisture: for putrefaction moisture is necessary, and
rapid drying of the body practically inhibits it.
3. Air : free access of air hastens putrefaction, partly
because the air conveys organisms to the body.
4. Clothing: clothes prevent the access of airborne
organisms, flies, insects, etc., Which destroy the tissues

5.Manner of burial: if the body is buried soon after death,

putrefaction is less. Putrefaction is delayed if body is
buried in dry, sandy soil, or in a grave deeper than two
meters ,because it is away from water , air and action of
insects and animals.. Putrefaction is more rapid if
changes of decomposition are already present at the time
of burial.
 IMMERSION AND BURIAL
• Immersion in water or burial will slow the process of Decomposition. It is said
that a body in air will decompose Twice as fast as a body in water and four
times as Fast as a body under the ground.
• . Putrefaction is more rapid in warm, fresh water than in cold, salt water. It is
more rapid in stagnant water than in running water. Putrefaction is delayed
when a body is lying in deep water and is well protected by clothing
• As the submerged cadavers float with face down and head lower than trunk
the gas distension and discoloration started from the face spread to neck,
upper extremities , chest . abdomen . lower extremities in order
• After removal from water putrefaction is faster due to water absorbed in body
 BURIAL
• The effects and the time scale of the changes
following Burial are so variable that little specific
can be said Other than buried bodies generally
decay more slowly, Especially if they are buried
deep within the ground.
• The level of moisture in the surrounding soil and
acidity Of the soil will both significantly alter the
speed of Decomposition.
 FORMATION OF ADIPOCERE
• Adipocere is a waxy substance derived from the body
fat In most instances the change of adipocere is partial
and irregular
• It is caused by hydrolysis and hydrogenation of adipose
tissue, leading to the formation of a greasy or waxy
substance if of recent origin. After months or years
have passed, adipocere becomes brittle and chalky.
• The color can vary from dead white, through pinkish, to
a grey or greenish-grey. The substance itself is off-
white, but staining with blood or products of
decomposition can give it the red or greenish.
The smell was accurately described as being 'earthy, cheesy and ammoniacal
moisture is necessary for the process but body water was sufficient for the hydrolysis to
proceed . and temperature above 5-8 early activity by anaerobes such as clostridium
perfingens assist in the reaction
 IMPORTANCE OF ADIPOCERE FORMATION
 Once it is formed it may last for decades

The usual dissolution of putrefaction is replaced by adipocere

formation ( adipocere inhibit putrefaction )
Injuries especially bullet holes maybe preserved in a remarkable
fashion
Mainly affect the subcutaneous fat but also may extend to
external fat
Time required to be formed from 3-12 months
It is often mixed with other forms of decomposition
Certain areas have more tendency like cheeks , orbits , chest ,
abdominal wall , buttocks
 MUMMIFICATION
• It is drying of the tissues can coexist with other modes of
decomposition in different areas of the same body.
• More likely than the other modes of decomposition to extend over
the whole corpse.
• Mummification can only occur in a dry environment, which is
usually , also a warm place.
• Mummification can occur in freezing conditions, partly because of
the dryness of the air and partly because of the inhibition of
bacterial growth.
• The most widely known forms of mummification are those in hot,
desert zones
DEAD MUMMIFIED BODY
• The essential requirement for mummification is a dry environment,
preferably with a moving air current.
• The skin is discolored (usually being brown)
• The skin and underlying tissues are hard, making autopsy dissection difficult
• The condition of the internal organs is variable, depending partly on the
length of time since death. They may be partly dried, partly putrefied - and
adipocere is not uncommon.
• Facial recognition may be possible in some instances
• Mummification is likely to occur in temperate climates when the body is left
undisturbed in a dry, warm place. These include closed rooms and cupboards
• Number of these bodies are hidden homicides
• Mummified fetus or newborn infant, concealed in domestic circumstances,
such as a house loft. Where complete mummification has taken place.
• The timing of mummification is not well documented, as most mummified
corpses have been concealed so well that discovery does not occur until long
after the process has reached its maximum effect. Certainly takes some weeks
• After complete drying has taken place, the body may remain in that state for
many years
• Eventually, mold formation and physical deterioration progress, the dried
tissues becoming split and powdery and gradually disintegrating. This process
is usually hastened by animal predation
• Mummification allows major injuries to be preserved
• The stiff tissues can be softened for better examination and histology, by
soaking in a 15 per cent solution of glycerin for several days
500 YEARS MUMMIFIED BOY IN
ASIA
BRAIN OF THAT BOY UNDER
CT SCAN
 POST-MORTEM DAMAGE BY
PREDATORS
• Animal predation is part of the natural food chain
• The beasts varying from ants to foxes, and from bluebottles to
lizards. Foxes can drag parts of a body away to a distance of at
least 2 miles.
DEAD BODY FACE EATEN BY
DOGS
• The type of damage from canine and rodent predators is usually
obvious, as the local removal of large amounts of flesh is usually
accompanied by evidence of teeth marks
• The postmortem nature of which is obvious from the lack of
bleeding or an inflamed marginal zone
• Mice rarely attack bodies, but may help to remove the dried,
crumbling tissue of a mummified corpse
• The most active tissue removers are maggots, the larval stage of
bluebottles and flies
In temperate zones their activity is seasonal, . The
adult insects lay eggs on the fresh corpse (or even
on a debilitated live victim), choosing wounds or
moist areas such as the eyelids, lips, nostrils and
genitalia. Once skin decomposition begins, the
eggs can be deposited anywhere. The eggs hatch
in a day or so, and several cycles of maggot
develop, shedding their cases at intervals,
depending on the species.
• The maggots are voracious and energetic, first exploring the
natural passages, such as mouth and nostrils, then burrowing into
the tissues. They secrete digestive fluids with proteolytic enzymes
that help soften the tissues, burrowing beneath the skin, and
sinuses that hasten putrefaction by admitting air and access to
external micro-organisms
• The ant, which can attack the body soon after death before
putrefaction begins. A common place for ant attack is around the
eyelids, lips and on the knuckles. The lesions are superficial ulcers
with scalloped, margins. They can be mistaken for ante-mortem
abrasions, but their position, margins and lack of bleeding or
inflammatory changes usually make them easily recognizable.
 SKELETELIZATION

 12-18 months: soft tissues will be absent.

 Tendons, ligaments, hair and nails will be identifiable for some time after that.

 After 3 yrs: the bones will be bare and disarticulated.

 In temperate zones the bones will remain solid & heavy with the
preservation of bone marrow in long bones for a number of years, that
can sometimes be suitable for specialist DNA analysis.
 After 40-50 years:
 Bone surface becomes dry & brittle.
 Marrow cavity will be empty.
67
 TIMING OF DEATH
Body temperature (body cooling )Algor mortis
• Dead body becomes progressively Colder after death
• The center or 'core' of the body cannot begin to cool
Until a 'temperature gradient' is set up by the cooling
at the Skin surface. As the tissues are poor heat
conductors, this Gradient takes a variable time to
become established and Therefore a thermometer
placed near the core (usually in The rectum) will not
register a fall for some time. This is the Well-known
'plateau',
plateau
• Except where the environmental (ambient) temperature
remains at or even above 37"C, the human body will cool
after death. A uniform, homogeneous laboratory 'body' will
cool according to newton's law of cooling, which states
that the rate of cooling is proportional to the difference in
temperature between the body surface and its
surroundings
• A human body does not obey NEWTON'S law, though
the size of the discrepancy varies according to several
factors
• When death occurs, Heat transfer within the body through the
circulation ceases. Metabolic heat production, occurring mainly
in the muscles And liver, does not cease uniformly and some
heat generation Continues for a variable time. As soon as
the supply of Warmed blood ceases with cardiac arrest, the skin
surface Immediately begins to lose heat.
• Ways to take core temp:
• 1. rectal
• 2. liver
 • Body
Factors temperature
affecting at the time of
body cooling death.
Hemorrhage

• Posture of the • Site of

body – extended
or curled into a
reading of body
fetal position. temperature(s).

• Clothing – type
of material, •
position on the
body – or lack of it. Obesity

• Winds, •
draughts, rain, environmental
humidity etc. temperature.
HENSSGE NOMO GRAM METHOD
Requir No
ement strong
s to radiati
use on

No strong
fever or
general
hypother
mia
 GASTRIC EMPTYING
• The following factors frustrate the use of gastric emptying As a
measure of time since death:
• Digestion may continue for some time after death.

• The physical nature of a meal has a profound effect on Emptying time:

the more fluid the consistency, the Faster the emptying.

• The nature of the food modifies emptying time, notably Fatty substances,
which markedly delay the opening of The pylorus. Strong alcohol, such as
spirits and liqueurs, Also irritate the mucosa and tend to delay emptying.
• Importantly, any nervous or systemic shock or stress, Mediated through the
parasympathetic (vagus) system, Can slow or stop gastric motility and
digestive juice Secretion as well as holding the pylorus firmly closed.
 2. THE ENTOMOLOGY OF DEATH AND POST-MORTEM
INTERVAL
• The most common insect found on relatively fresh corpses is the
blowfly, a group of flying insects with almost worldwide
distribution. They mainly comprise the bluebottles, the green
bottles and the housefly. There are numerous species, with
variations in life cycles that are altered by climatic conditions. The
bluebottle is the most common, the most frequent invader of dead
flesh. These are large, flies about 6-14 mm long, with blue
abdomens.
• They do not fly in the dark and thus eggs are laid only in daylight
bluebottles rarely fly in winter, but may do on fine days, though
when the temperature is below 12 c they are unlikely to lay eggs
• Bluebottles prefer fresh rather than decayed corpse and lay their
• Indeed, they may lay eggs on the living, especially when the victim
(man or animal) is debilitated or wounded.
• Single bluebottle may lay up to 300-2000 eggs
• The eggs are laid on moist areas, such as the eyelids, canthi of the
eyes, nostrils, lips, mouth, genitals and anus. If there are any open
wounds or weeping abrasions, these may also be colonized. The eggs
are yellow and banana-shaped, about 1.7 mm in length.
• The common house fly is different in that, unlike the bluebottles, it
prefers to lay its eggs on already decomposed flesh, though it is more
attracted to garbage than to cadavers.
• The eggs are much smaller and white rather than yellow.
• The whole lifecycle is about 14 days at about 20°c,
 only
in
dayli
ght

Te us e 4
m ov
m tb
12

ab

p. e
days

Fou
dea nd un
d
the d bod er
y
und groun in 8-14
er c d
ar p , 6 days hours
et
2-3 days The whole
lifecycle of
bluebottle 18-24
days
 POST MORTEM CHEMISTRY

• The analysis of physiological chemical constituents of the Body

Investigating deaths from metabolic and biochemical Disturbances.
• Unfortunately, the concentration of many natural chemical
Substances in the dead body is rapidly distorted by Post-mortem
autolysis.
• Some substances are more stable, however and when results are
carefully interpreted, considerable information can be obtained.
Urea and creatinine are stable post-mortem , with little
variation even up to 100 hours after death, so the diagnosis of
ante-mortem nitrogen retention is quite reliable.
• The normal urea nitrogen range Found in post-mortem serum
is from 4.9 to 5.5 mmol/l, Creatinine being from about 70.7 to
212.2 micro-mol/l.
• The vitreous fluid (humour ) is much to be preferred to blood
for Post-mortem chemical analyses. Vitreous is far less
contaminated By body autolysis and is remote from the large
Organs and blood vessels of the abdominothoracic cavity.
•
• After death, intracellular potassium leaches from the Retina
through the now permeable cell membranes, into the Vitreous
body, naturally with an uneven distribution Depending on the
distance from the wall of eyeball (which Is why all or a
substantial proportion of the fluid should be Withdrawn for
analysis, to obtain a mean level). If fragments Of retina are
aspirated by the syringe, due to excessive Suction, then a falsely
elevated potassium measurement will Be obtained.
• Generally speaking, the vitreous Potassium method is of most
use after the first 24-36 Hours, when other methods have
ceased to have application. Although the errors are great, some
information can Be derived for up to 100 hours post-mortem.
• In relation to other vitreous electrolytes, the
concentration Of sodium and chlorides decrease after
death, while Potassium rises.
• The equation is increase in potassium 0.19 mmol/l/hr
• Chlorides decrease at less than 1 mmol/l/h and sodium
by About 0.9mmol/l/h, so the loss of this sodium is
Insignificant in the first few hours, differing from
potassium, Which rises appreciably.
• In relation to glucose, a common problem is the
autopsy diagnosis of uncontrolled diabetes and of
hypoglycemia. The vitreous glucose usually falls after
death and ,can reach zero within a few hours.
• Vitreous glucose of more than 1 1.1 mmol/l was an
invariable indicator of diabetes mellitus
• In relation to hypoglycemia, a vitreous glucose of less
than 1.4 mmol/l an indication of a low ante-mortem
blood sugar
 POST MORTEM ARTEFACTS

• The pancreas is one of the first organs to undergo Autolysis,

because of he proteolytic enzymes within it The autolysed
tissue is often hemorrhagic and can Easily be mistaken for acute
pancreatitis, though Histology will rapidly resolve the problem.
• Patches of hemorrhage, sometimes quite large and confluent, can
occur in the tissues behind the esophagus in the neck.
These lie on the anterior surface of the cervical vertebrae and are
caused by distension and leakage from the venous plexuses that
lie in this area. Their importance lies in confusion with deep neck
bleeding in strangulation (and sometimes with spurious neck
fractures), which is why the skull should be opened before the
neck in any suspected strangulation or hanging, to release the
pressure in the neck veins before handling the tissues.
• Autolytic rupture of the stomach can occur postmortem In both
child and adult, described by john Hunter in the eighteenth
century. This so-called 'Gastromalacia' appears as a slimy
brownish black Disintegration of the fundus with release of the
Stomach contents into the peritoneal cavity. Sometimes, the left
leaf of the diaphragm is also Perforated through a ragged
fenestration, with escape Of gastric contents into the chest.
• Heat fractures of the bones, either skull plates or long bones,
may be seen in victims of severe fires, but are not evidence of
ante-mortem violence. Also in conflagrations, the 'heat
hematoma' within the burned skull can resemble an extradural
hemorrhage of ante mortem origin. The site is often at the
vertex or occiput; however, unlike the usual parietal
hemorrhage, there is no fracture line crossing the middle
meningeal artery, the usual cause of a true extradural bleed.
The frothy brown appearance of the false
clot, together with heating effects in the
adjacent brain, should indicate the true
diagnosis. Shrinkage of the Dura due to heat
may cause it to split, with herniation of the
brain tissue into the extradural space. Severe
burns of the body surface may lead to heat
contractures of the limbs with tears over
joints such as the elbow. These must not be
confused with ante mortem lacerations or
incised wounds.
• The bloating, discoloration and blistering of a ‘ Putrefying body
must not be misinterpreted as disease On injury. Blisters are
quite unlike those of burns and Dark blackish areas of
discoloration must be Distinguished from bruising.
• Blood or bloody fluid issuing from the mouth may be Due to
putrefaction, even if the body surface is not Overtly
decomposed. If the lungs and air passages are Discolored and
filled with sanguineous liquid, then This must be taken to be
cause of the purging from the Mouth and nostrils.
• Dark red discoloration of the posterior part of the Myocardium is
usually due to post-mortem Gravitational hypostasis, not early
infarction. Segmental patches of dark red or purple discoloration
of The intestine is hypostasis, not infarction.
• Some post-mortem animal injuries also resemble abrasions Such
as insect bites, especially by ants.
• The demonstration of intracranial bleeding from the
Vertebrobasilar system is difficult, as the very process of
Opening the skull at autopsy and removing the brain, These
artefacts cannot be distinguished from original Bleeding points
due to ante-mortem trauma.
• 'Banding' of the esophagus these bands are pale areas in the
mucosa caused by postmortem Hypostasis being prevented
from settling by the External pressure of adjacent anatomical
structures, including Parts of the larynx, trachea and aortic arch
• Air embolism cannot occur in the cerebral veins and it was
Proved many years ago that air bubbles in those veins are
Artefacts caused by removing the tentorium
RESUSCITATION ARTEFACTS
• Bruising of the anterior chest wall, hemorrhage into the
subcutaneous tissues and pectoral muscles, fractures of the
sternum, fractures of the ribs, haemothorax, bruised lung,
lacerated lung, pericardial hemorrhage, and even fractured
dorsal spine, following energetic external cardiopulmonary
resuscitation (CPR). Thoracic cage fractures are rare in children,.
• Internally all types of damage to the heart may occur,
including ruptured atria and even ventricles, septal rupture and
valve damage. The great vessels can suffer severe trauma,
marrow emboli in the pulmonary vessels have also been
reported after cardiac massage
• Petechiae in the eyes and intra-ocular hemorrhages can
occur after CPR, as well as after violent sneezing or coughing;
they are well known to occur during whooping cough.
• Bruising of the face and neck, finger marks and nail
Marks on the face and neck, and damage to the lips
and Inner gums from mouth-to-mouth resuscitation,
when The face and neck have been gripped by hands.
Damage To lips, gums, teeth and pharynx can occur
from the Introduction of an artificial airway or
endotracheal tube, Especially in difficult, hurried
emergency situations. Injuries to the larynx, even
including fracture of the Hyoid and thyroid cornuae,
can occasionally occur From these procedures, which
are difficult to Distinguish from manual strangulation if
• Puncture marks for venipuncture may be Confused with injection
marks in drug dependence. The introduction of intravenous cannulae
into veins In the neck may cause large hematomata and more Diffuse
bleeding into the tissues alongside the larynx.
• The effects of injected
• Noradrenaline and electrical defibrillation on the Histological
appearance of the myocardium are well Recorded, with contraction
bands being the most Obvious artefacts which can be mistaken for
preexisting Myocardial ischemia.
• Damage to the mouth, palate, pharynx and larynx Can
occur from attempts to introduce a laryngoscope Or airway.
Even fracture of the mandible has been Caused in this way.
In infants, even digital clearance Of the pharynx can cause
mucosal damage. Damage To the pharyngeal mucosa may
cause bleeding, Which can seem sinister to police or
relatives; this May be mixed with -the fluid of pulmonary
edema To produce copious pink, bloody froth, seen in a
Number of cases, including sudden infant death Syndrome.
• During the Heimlich maneuver to clear an airway Obstruction,
rupture of the esophagus, stomach and Intestines have been
reported. The esophagus can be Perforated by an incorrectly
inserted airway. In the Abdomen, external cardiac massage may
cause ruptured Stomach, ruptured liver, and damage to spleen
and Pancreas.
• Gastric contents in the air passages may have Reached there by
spontaneous regurgitation or by pumping the chest and upper
abdomen During resuscitation attempts. This makes the Finding of
vomit in the larynx and trachea.
• The administration of oxygen by mask or tube may Cause damage,
as can over energetic mouth-to-mouth Resuscitation. Ruptures of
esophagus and lung have been Occurred, and other types of
barotrauma include Ruptured stomach and intestine. Where a pre-
existing Gut lesion exists, the administered gas may escape into
The abdomen. The diagnosis of a pre-existing Pneumothorax may
be impossible where forced Ventilation has been administered.
• In the central nervous system, subarachnoid Hemorrhage has
been described after external cardiac Massage
• Myocardial and pulmonary bone marrow embolism Has been
reported following cardiac massage
• Retinal hemorrhages, classically a sign of raised Intracranial
pressure and of head injury, have also been Described in
whooping cough and after CPR.
Thank you