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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 37 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.

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
doctor should have similar experience.

A checklist of the diagnostic tests and their results should be


kept in the patients 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 35C to avoid hypothermia simulating brainstem
damage.

INDICATORS OF BRAIN DEATH

Deep coma
All brainstem reflexes are
absent, with fixed dilated and
unreactive pupils. Corneal
reflexes are absent

Neuromuscular
blocking agents
excluded
No motor
responses to
painful stimuli

Mechanical
ventilation

No gag reflex

no respiratory movements when


the patient is disconnected from
the ventilator

mummification

Death

adipocere
cremation

Putrefaction

Assist
Animal predators

Assist

Complete dissolution
unless fossilized

Skeletenization

Fate of body after


death

POST-MORTEM SIGNS OF DEATH


Early

Insect
activity
Chemical
changes in
body fluids
(electrolyte
s)

Eye changes
Skin
changes
Muscles
Gastric

Late
Algor
mortis
(cooling)
Livor mortis
(hypostasis
)
Rigor
mortis

Very late
Decompos
ition

13

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 of uneven
relaxation.

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

OVER CHEST AND UPPER LIMBS

Epilepsy or
drinkers

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


capillaries

Blood escapes through


ruptured capillaries

Same level on surface

Raised

Pale over pressure areas

Not change

Incision: blood flows from the


cut vessel (washable)

Incision: blood coagulates in


tissue
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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 18-36 hours

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.
If the body feels cold and is stiff, it has been dead from 8 to 36 hours.

If t he body feels cold and is flaccid, it has been dead more than 36
hours.
This crude estimate should never be used as a definitive

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
Onset delayed after death (2-3 hrs.).
Duration up to 36 hrs.
Intensity comparatively moderate.
Mechanism of formation: Breakdown of ATP
below critical level.

All muscles of the body are affected


gradually.

Cadaveric Spasm
Onset is instantaneous.
Duration is a few hours, until it is replaced by
rigor mortis.
Intensity comparatively very strong.
predisposing factors: Excitement, fear,
fatigue, exhaustion, nervous tension,
contraction of Muscles at time of death.

Selected muscles
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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

Factors affecting
body cooling

Obesity

environmental
temperature.

the time of death.


Hemorrhage

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

Winds, draughts,
rain, humidity etc.

Site of reading of
body
temperature(s).

Posture of the
body extended or
curled into a fetal
position.

Body temperature at

HENSSGE NOMO GRAM METHOD

Requirements
to use

No strong
fever or
general
hypothermia

No high
thermal
conductivity
of surface
beneath the
body

No strong
radiation

No certain
severe changes
of cooling
conditions
between time of
death and body
examination

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 eggs soon
after death,

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 20c,

12 days

8-14 hours
6 days
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 Postmortem 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 the Circumstances are obscure.

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.

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