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POSTMORTEM CHANGES AND TIME OF DEATH

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Offline Michael

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PostPosted: Sat Oct 18, 2008 4:55 pm   Post subject: POSTMORTEM CHANGES AND TIME OF DEATH   

POSTMORTEM CHANGES AND TIME OF DEATH



A professional PDF from Dundee University concerning changes in the human body after death and thereby ascertaining the Time of Death Ref:

DUNDEE UNIVERSITY


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Last edited by Michael on Sat Nov 15, 2008 6:02 am, edited 1 time in total.
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PostPosted: Sat Oct 18, 2008 6:16 pm   Post subject: DEATH   

DEATH



How death is defined. A lecture by Derrick Pounder, lecturer at Dundee University's Forensic Medicine Department. Ref: D, Pounder., Lecture Notes in Forensic Medicine, (p. 21 - 23, c. 6),

DUNDEE UNIVERSITY


Derrick Pounder wrote:
DEATH

Death is the extinction or cessation of life, but since life itself
is difficult to define there is a reciprocal problem in defining
death. The precise definition of death will always be a subject
of controversy because it has social and religious aspects and
is not a solely scientific issue. There are profound social and
legal repercussions to the diagnosis. An added difficulty is that
in nearly all circumstances human death is a process rather
than an event. Within this process of dying there are points of
no return, the identification of which is the medical diagnostic
challenge.

Diagnosis of death

There is no legal definition of death. The diagnosis of clinical
death, or somatic death, is traditionally made using the triad of
Bichat which states that death is ‘the failure of the body as an
integrated system associated with the irreversible loss of
circulation, respiration and innervation’. Thus the diagnosis of
death is made by excluding possible signs of life. The
irreversible cessation of the circulation has been considered
for centuries a point of no return. It still provides a practical
and valid criterion for the irreversible loss of function of the
human organism as a whole.

To ensure that opportunities for resuscitation are not missed,
care must be taken in making this final diagnosis in order to
avoid mistaking apparent death for actual death. In the
overwhelming majority of deaths the diagnosis can be made
by traditional clinical methods. The same criteria are
applicable whether the death was expected or unexpected.
Firstly, there is a need to make a rapid assessment, based upon
a history and clinical observations, as to whether resuscitation
attempts should be initiated. Cessation of the circulation
results in a deathly pallor (pallor mortis) particularly of the
face and lips, and primary muscular flaccidity leads to
drooping of the lower jaw and sometimes open staring eyes. A
complete physical examination should exclude the presence of
a circulation or breathing. The absence of a pulse should be
determined through the palpation of the carotid, radial and
femoral arteries. The absence of heart and lung sounds should
be determined by auscultation continually for one minute and
repeated intermittently over not less than five minutes. Normal
heart sounds may be indistinct in obese individuals or
conditions such as pericardial effusion. At the same time
observation should be made for respiration. Inspection of the
eyes should disclose pupils which are non-reactive to a bright
light. Indisputable signs of death develop later with the
formation of livor mortis and rigor mortis.

Some situations, most notably hypothermia, produce deathlike
states. Other conditions that can induce a death-like coma
include drug overdose (particularly with barbiturates, alcohol,
tricyclic antidepressants and anaesthetic agents), and
metabolic states including myxoedema coma, uraemia,
hypoglycaemia, hyperosmolar coma, and hepatic
encephalopathy. Situations in which vigorous attempts at
resuscitation may be successful include drowning, airways
obstruction, electric shock, and a lightning strike.

Cellular death

Clinical death represents somatic death, that is to say the death
of a person as a whole. However, not all the cells of the body
die at the same time. For some hours after death the pupils will
still respond to pilocarpine drops by contracting, and electrical
stimulation of muscles will cause contraction. The cornea of
the eye may still be suitable for transplant up to 24 hours after
death. Viable skin grafts can be obtained for up to 24 hours,
bone grafts for up to 48 hours and arterial grafts for up to 72
hours after the circulation has stopped.

Post mortem the cells of the body are destroyed by the process
of autolysis (literally ‘self-destruction’), with waves of cell
death following somatic death. Destructive enzymes released
from lysosomes within the cell initiate the process of autolysis.
The process is more rapid in some organs, for example in the
pancreas which also contains a large number of digestive
enzymes normally secreted into the gut. At a microscopic level
autolysis is evidenced by a homogenous staining of the
cytoplasm of the cell and similar loss of characteristic staining
and detail within the nucleus.

This post mortem change occurring in all the cells of the body
is similar to the change which occurs in damaged cells in a
living body. Within a living person individual cells or large
areas of tissue, comprising groups of adjacent cells, may die
without affecting the viability of the whole organism. This
pathological cell death, or necrosis, is an abnormal change
initiated by some insult to the tissues, such as hypoxia or
physical or chemical trauma. Within a few hours of being
irreversibly damaged the cells show the microscopic changes
characteristic of autolysis. However, unlike post mortem
autolysis, this type of cell death, necrosis, incites an
inflammatory reaction from the surrounding living tissue.
It is the presence of this inflammatory reaction, which can be
identified microscopically, which distinguishes tissue necrosis
which has occurred in life from post mortem autolysis.
Unfortunately the inflammatory reaction only develops to a
level at which it can be identified microscopically between ½
hours and 2 hours after injury. Consequently injuries which
are inflicted very shortly before death, like tissue damage
inflicted after death, show no vital inflammatory reaction.
However, the degree of bruising of the tissues associated with
the injury may give an indication as to whether or not there
was a functioning circulation.

In the living body the cells of all tissues turnover with loss of
some cells and their replacement by more cells created by
mitotic division. Apoptosis (meaning dropping out or falling
away) describes the energy dependant process by which
individual cells are lost. The cell contracts and the nucleus
fragments producing an apoptotic body, pieces of which are
removed by scavenger cells, macrophages. Apoptosis is a
normal process and does not stimulate an inflammatory
reaction from the adjacent tissues. It is important in the natural
turnover of many tissues such as the endometrium during the
menstrual cycle. Unlike necrosis and autolysis, it has no
forensic importance.


Last edited by Michael on Sat Nov 15, 2008 5:53 am, edited 1 time in total.
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PostPosted: Sat Oct 18, 2008 6:54 pm   Post subject: CHANGES AFTER DEATH   

CHANGES AFTER DEATH



A lecture by Derrick Pounder, lecturer at Dundee University's Forensic Medicine Department, on the changes to the human body after death. Ref: D, Pounder., Lecture Notes in Forensic Medicine, (p. 23 - 27, c. 7),

DUNDEE UNIVERSITY


Derrick Pounder wrote:
CHANGES AFTER DEATH

The three principal post mortem changes which occur within
the first day after death are body cooling (algor mortis,
literally: ‘the chill of death’), livor mortis (literally: ‘the
darkening of death’), and rigor mortis (literally: ‘the stiffening
of death’). Putrefaction of the body and its variants are later
post mortem changes. These changes which develop in a
corpse well after death has occurred are of interest for several
reasons. They are indisputable signs of death and indicate that
any attempts at resuscitation would be futile. As they evolve
these post mortem changes produce confusing artefacts and
putrefaction destroys evidence of identity, injuries, and natural
disease. However, each has its own specific forensic uses.
Since they all evolve over time they all have been used also to
estimate the time since death. The importance of body cooling
lies solely in its value for the estimation of the time since
death, and therefore it is discussed in that context in the next
chapter.

Rigor mortis

Death is followed immediately by total muscular relaxation,
primary muscular flaccidity, so that the body collapses into a
position dictated by gravity and surrounding objects.
Flaccidity is succeeded in turn by generalised muscular
stiffening, rigor mortis, which fixes the body in that posture. It
follows that rigor cannot freeze a body in a position which
defies gravity, and any such appearance indicates that the body
has been moved after rigor developed. If the body is supine
then the large joints of the limbs become slightly flexed during
the development of rigor. The joints of the fingers and toes are
often markedly flexed due to the shortening of the muscles of
the forearms and legs. After a variable period of time, as a
result of putrefaction, rigor mortis passes off to be followed by
secondary muscular flaccidity. There is great variation in the
rate of onset and the duration of rigor mortis; the two main
influencing factors are the environmental temperature and the
degree of muscular activity before death. Onset of rigor is
accelerated and its duration shortened when the environmental
temperature is high and after prolonged muscular activity, e.g.
following convulsions. Conversely, a late onset of rigor in
many sudden deaths can be explained by the lack of muscular
activity immediately prior to death.

Classically, rigor is said to develop sequentially, but this is not
constant or symmetrical. Typically rigor is apparent first in the
small muscles of the eyelids, lower jaw and neck, followed by
the limbs. It involves first the small distal joints of the hands
and feet, and then the larger proximal joints of the elbows and
knees, and then the shoulders and hips. Ante-mortem exertion
usually causes rigor to develop first in the muscles used in the
activity. Generally rigor passes off in the same order in which
it develops. Gently attempted flexion of the different joints
will indicate the location of rigor and its degree (complete,
partial, or absent joint fixation), providing no artefact has been
introduced by previous manipulation of the body by others,
such as during the removal of clothing. The forcible bending
of a joint against the fixation of rigor results in tearing of the
muscles and the rigor is said to have been ‘broken’. Provided
the rigor had been fully established, it will not reappear once
broken down by force. The intensity or strength of rigor mortis
depends upon the decedent's muscular development, and
should not be confused with its degree of development, that is
the extent of joint fixation.

Rigor involves voluntary and involuntary muscles. Rigor of
the myocardium should not be mistaken for myocardial
hypertrophy. Likewise secondary muscular flaccidity of the
ventricles should not be mistaken for ante-mortem dilatation
or evidence of myocardial dysfunction. Involvement of the iris
muscles means that the state of the pupils after death is not a
reliable indication of their ante-mortem appearance. Different
degrees of rigor can cause irregularity and inequality of the
pupils. Contraction of the arrectores pilorum muscles during
rigor causes ‘goose-flesh’ (cutis anserina), a phenomenon
commonly seen in bodies recovered from water. Involvement
of the walls of the seminal vesicles by rigor may lead to
discharge of seminal fluid at the glans penis.

The biochemical basis of rigor mortis is not fully understood.
Post-mortem loss of integrity of the muscle cell sarcoplasmic
reticulum allows calcium ions to flood the contractile units
(sarcomeres) initiating the binding of actin and myosin
molecules and mimicking the normal contraction process.
Normal relaxation in life is achieved by energy-dependent
(ATP-driven) pumping of calcium back across the membrane
of the sarcoplasmic reticulum but this fails post-mortem
because of membrane disruption and lack of ATP. The actinmyosin
complex is trapped in a state of contraction until it is
physically disrupted by the autolysis which heralds the onset
of putrefaction. This process is characterised by proteolytic
detachment of actin molecules from the ends of the
sarcomeres, and consequent loss of the structural integrity of
the contractile units. Although the biochemical basis of rigor
mimics that of muscle contraction in life, it does not cause any
significant movement of the body in death, a point of forensic
importance.

Cadaveric spasm

Cadaveric spasm (synonyms: instantaneous rigor,
instantaneous rigidity, cataleptic rigidity) is a form of
muscular stiffening which occurs at the moment of death and
which persists into the period of rigor mortis. Its cause is
unknown but it is usually associated with violent deaths in
circumstances of intense emotion. It has medico-legal
significance because it records the last act of life. Cadaveric
spasm involving all the muscles of the body is exceedingly
rare and most often described in battle situations.

Most commonly cadaveric spasm involves groups of muscles
only, such as the muscles of the forearms and hands. Should
an object be held in the hand of a corpse, then cadaveric spasm
should only be diagnosed if the object is firmly held and
considerable force is required to break the grip. This is seen in
a small proportion of suicidal deaths from firearms, incised
wounds, and stab wounds, when the weapon is firmly grasped
in the hand at the moment of death. In such circumstances the
of the injuries. This state cannot be reproduced after death by
placing a weapon in the hands. It is also seen in cases of
drowning when grass, weeds, or other materials are clutched
by the deceased. Similarly, in mountain falls, branches of
shrubs or trees may be seized. In some homicides, hair or
clothing of the assailant can be found gripped in the hands of
the deceased.

Livor mortis

Lividity is a dark purple discoloration of the skin resulting
from the gravitational pooling of blood in the veins and
capillary beds of the dependent parts of the corpse. Synonyms
include livor mortis, hypostasis, post-mortem lividity, and, in
the older literature, post-mortem suggillations. Lividity is able
to develop post mortem under the influence of gravity because
the blood remains liquid rather than coagulating throughout
the vascular system as a consequence of stasis. Within about
30 to 60 minutes of death the blood in most corpses becomes
permanently incoagulable. This is due to the release of
fibrinolysins, especially from capillaries and from serous
surfaces, e.g. the pleura. The fluidity and incoagulability of the
blood is a commonplace observation at autopsy and is not
characteristic of any special cause or mechanism of death.
Hypostasis begins to form immediately after death, but it may
not be visible for some time. Ordinarily its earliest appearance,
as dull red patches, is 20 to 30 minutes after death, but this
may be delayed for some hours. Faint lividity may appear
shortly before death in individuals with terminal circulatory
failure. Conversely, the development of lividity may be
delayed in persons with chronic anaemia or massive terminal
haemorrhage. The patches of livor then increase in intensity
and become confluent to reach a maximum extent and
intensity on average within about 12 hours, although there is
very great variation. Pressure of even a mild degree prevents
the formation of lividity in that area of skin, so that a supine
body shows contact flattening associated with contact pallor
(pressure pallor) over the shoulder blades, elbows, buttocks,
thighs and calves. Similarly tight areas of clothing or
jewellery, as well as skin folds, leave marks of contact pallor.
The distribution of lividity with its associated contact pallor
helps distinguish lividity from bruising, and any doubts are
resolved by incising the skin which reveals lividity as
congested vessels and bruising as haemorrhage infiltrating
tissues.

Lividity is present in all corpses, although it may be
inconspicuous in some, such as following death from
exsanguination. Lividity is usually well marked in the earlobes
and in the fingernail beds. In a supine corpse there may be
isolated areas of lividity over the front and sides of the neck
resulting from incomplete emptying of superficial veins. Other
isolated patches of hypostasis may be due to blood in the
deeper veins being squeezed, against gravity, towards the skin
surface by the action of muscles developing rigor mortis.
Lividity is often associated with post-mortem haemorrhagic
spots, punctate haemorrhages, (given the specific name
‘vibices’ in the German literature) which resemble the
petechial haemorrhages associated with asphyxial deaths, and
from which they must be distinguished. Easily recognised,
occurring only in areas of lividity and sparing adjacent areas
of contact pallor, they develop in the hours immediately
following death as lividity intensifies.

Lividity occurs in the viscera as well as the skin and this
provides some confirmation of the external observations. In
the myocardium lividity may be mistaken for an acute
myocardial infarction, and in the lungs may be misdiagnosed
as pneumonia. Livid coils of intestine may falsely suggest
haemorrhagic infarction. Lividity developing in the viscera of
a body lying prone and resulting in a purplish congestion of
organs usually found pale at autopsy can be disconcerting to
those unaccustomed to these changes.

The importance of lividity lies in its distribution, as an
indicator of body position and contact with objects, and in its
colour, as an indicator of cause of death. The usual purple
colour of lividity reflects the presence of deoxyhaemoglobin
but it does not have the same diagnostic significance as
cyanosis produced during life. In the corpse, oxygen
dissociation from oxyhaemoglobin continues after death and
there may be reflux of deoxygenated venous blood into the
capillaries. For these reasons, the blood of a cadaver becomes
purplish-blue, but this is not a reflection of a
pathophysiological change which occurred in life. Bodies
refrigerated very soon after death have a pink lividity due to
retained oxyhaemoglobin. Death from hypothermia or cyanide
poisoning also imparts the pink hue of oxyhaemoglobin,
carbon-monoxide poisoning produces the cherry red of
carboxyhaemoglobin, and poisoning from sodium chlorate,
nitrates and aniline derivatives impart the gray to brown
colour of methaemoglobin. Infection by Clostridium
perfringens causing gas gangrene is said to give a bronze
lividity.

After about 12 hours lividity becomes ‘fixed’ and
repositioning the body, e.g. from the prone to the supine
position, will result in a dual pattern of lividity since the
primary distribution will not fade completely but a secondary
distribution will develop in the newly dependent parts. The
blanching of livor by thumb pressure is a simple indicator that
lividity is not fixed. Fixation of lividity is a relative, not an
absolute, phenomenon. Well-developed lividity fades very
slowly and only incompletely. Fading of the primary pattern
and development of a secondary pattern of lividity will be
quicker and more complete if the body is moved early during
the first day. However, even after a post-mortem interval of 24
hours, moving the body may result in a secondary pattern of
lividity developing. Duality of the distibution of lividity is
important because it shows that the body has been moved after
death. However, it is not possible to estimate with any
precision, from the dual pattern of livor, when it was that the
corpse was moved. If a prone body is moved some hours after
death but before lividity is fixed then the primary lividity will
fade and may leave behind on the face any lividity-associated
punctuate haemorrhages, or ‘vibices’, creating possible
confusion with the petechiae of asphyxia.

Areas of lividity are overtaken early in the putrefactive
process becoming green at first and later black. The red cells
are haemolysed and the haemoglobin stains the intima of large
blood vessels and diffuses into the surrounding tissues,
gripping of the weapon creates a presumption of self-infliction
highlighting the superficial veins of the skin as a purple-brown
network of arborescent markings, an appearance referred to as
‘marbling’.

Putrefaction

Putrefaction is the post-mortem destruction of the soft tissues
of the body by the action of bacteria and endogenous enzymes
and is entirely capable of skeletonising a body. Refrigeration
of a corpse delays the onset of putrefaction, freezing the body
halts putrefaction, and chemical embalming prevents it. The
main changes recognisable in tissues undergoing putrefaction
are the evolution of gases, changes in colour and liquefaction.
These same changes seen on the surface of the body occur
simultaneously in the internal organs. Bacteria are essential to
putrefaction and commensal bacteria, mainly from the large
bowel, soon invade the tissues after death. Typically, the first
visible sign of putrefaction is a greenish discoloration of the
skin of the anterior abdominal wall due to sulph-haemoglobin
formation. This most commonly begins in the right iliac fossa,
i.e. over the area of the caecum. Any ante-mortem bacterial
infection of the body, particularly scepticaemia, will hasten
putrefaction. Injuries to the body surface promote putrefaction
by providing portals of entry for bacteria. Putrefaction is
delayed in deaths from exsanguination because it is blood
which usually provides a channel for the spread of putrefactive
organisms within the body.

Environmental temperature has a very great influence on the
rate of development of putrefaction, so that rapid cooling of
the body following a sudden death will markedly delay its
onset. In a temperate climate the degree of putrefaction
reached after 24 hours in the height of summer may require 10
to 14 days in the depth of winter. Putrefaction is optimal at
temperatures ranging between 21 and 38C (70 and 100F),
and is retarded when the temperature falls below 10C (50F)
or when it exceeds 38C (100F). Heavy clothing and other
coverings, by retaining body heat, will speed up putrefaction.
The rate of putrefaction is influenced by body build because
this affects body cooling. Obese individuals putrefy more
rapidly than those who are lean.

Gases produced by putrefaction include methane, hydrogen,
hydrogen sulphide and carbon dioxide. The sulphur-containing
amino acids, cysteine, cystine and methionine yield hydrogen
sulphide, which combines with haemoglobin and ferrous iron
to produce green sulph-haemoglobin and black ferrous
sulphide respectively. De-carboxylation of the amino acids
ornithine and lysine yields carbon dioxide and the foul
smelling ptomaines, putrescine (1,4-butanediamine) and
cadaverine (1,5-pentanediamine) respectively. These
ptomaines are detectable by the cadaver dogs used to locate
clandestine graves. Deamination of L-phenylanaline yields
ammonia, and phenylpyruvic acid which forms a green
complex with ferric iron. Bacterial and fungal fermentation
yield ethyl alcohol (ethanol), confounding the interpretation of
post-mortem alcohol concentrations.

Early putrefaction is heralded by the waning of rigor, green
abdominal discolouration, a doughy consistency to the tissues
and haemolytic staining of vessels. Localised drying of the
lips, tip of the nose and fingers may be seen. The face swells
and discolours and the swollen lips are everted, making facial
recognition unreliable. The skin, which now has a glistening,
dusky, reddish-green to purple-black appearance, displays
slippage of large sheets of epidermis after any light contact
with the body, e.g. during its removal from the scene of death.
Beneath the shed epidermis is a shiny, moist, pink base which
dries, if environmental conditions permit, to give a yellow
parchmented appearance. This putrefactive skin-slip
superficially resembles ante-mortem abrasions and scalds.
Body hair and nails are loosened and the skin of the hands
comes away like gloves taking with it fingerprint evidence of
identity. The remaining dermis has a much shallower reverse
print which is technically more difficult to document.

Distention of the abdominal cavity by putrefactive gasses
characterises the bloating stage of decomposition. In males gas
is forced from the peritoneal space down the inguinal canals
and into the scrotum, resulting in massive scrotal swelling.
Gaseous pressure expels dark malodorous fluid, purge fluid,
from the nose and mouth, mimicking ante-mortem
haemorrhage or injury. Similar fluid flows from the vagina
and anus, the rectum is emptied of faeces and prolapse of the
rectum and uterus may occur.

The doughy consistency of the tissues of early putrefaction is
replaced by the crepitant effect resulting from gaseous
infiltration beneath the skin and in deeper tissues. Large subepidermal
bullae fill with gas, sanguinous fluid or clear fluid.
Gas bubbles appear within solid organs such as liver and brain
giving a ‘Swiss-cheese’ appearance, and the blood vessels and
heart are filled with gas. These putrefactive changes are
relatively rapid when contrasted with the terminal decay of the
body. The more dense fibro-muscular organs such as the
prostate and uterus remain recognisable until late in the
process, thus aiding in the identification of sex. When the
putrefactive juices have drained away and the soft tissues have
shrunk, the speed of decay is appreciably reduced.

The progression of putrefaction may be modified by vertebrate
or invertebrate animal activity. Wild animals, domestic pets,
livestock, fish and crustaceans may be involved but most
commonly it is insects, particularly fly larvae (maggots). In a
hot humid environment with heavy insect activity a corpse
may be skeletonised in as little as 3 days. All soft tissues are
generally lost before the skeleton becomes disarticulated,
typically from the head downward, with the mandible
separating from the skull and the head from the vertebral
column, and from central to peripheral, i.e. from vertebral
column to limbs.

Mummification

Mummification is a modification of putrefaction characterised
by the dehydration or dessication of the tissues. The body
shrivels and is converted into a leathery or parchment-like
mass of skin and tendons surrounding the bone. Skin
shrinkage may produce large artefactual splits mimicking
injuries, particularly in the groins, neck, and armpits.
Mummification develops in conditions of dry heat, especially
when there are air currents, e.g. in a desert. Mummification of
forced hot-air heating in buildings or other man-made
favourable conditions. The importance of mummification lays
in its preservation of tissues which aids in personal
identification and the recognition of injuries. However,
mummified tissues may be attacked by rodents and insects,
particularly the omnivorous larvae of the brown house moth
(Hofmannophila pseudospretella) which is found in many
countries worldwide.

Adipocere

Adipocere formation, or saponification (literally: ‘making
soap’), is a modification of putrefaction characterised by the
transformation of fatty tissues into a yellowish-white, greasy,
wax-like substance which is friable when dry. During the early
stages of its production it has a very persistent ammoniacal
smell but once its formation is complete it has a sweetish
rancid odour. Adipocere, also known as ‘grave wax’ or
‘corpse wax’, develops as the result of hydrolysis of fat with
the release of fatty acids which, being acidic, inhibit
putrefactive bacteria. Fatty acids combine with sodium or
potassium to form hard soap (‘sapo durus’) or soft soap (‘sapo
domesticus’) respectively. Calcium gives an insoluble soap
which contributes a more brittle quality to the adipocere.
However, fat and water alone do not produce adipocere.
Putrefactive organisms, of which Clostridium welchii is most
active, are important, and adipocere formation is facilitated by
post-mortem invasion of the tissues by commensal bacteria. A
warm, moist, anaerobic environment favours adipocere
formation. Adipocere develops first in the subcutaneous
tissues, most commonly involving the cheeks, breasts and
buttocks. Rarely, it may involve the viscera such as the liver.
The adipocere is admixed with the mummified remains of
muscles, fibrous tissues and nerves. Putrefaction, adipocere
and mummification may coexist in the same corpse or in
adjacent corpses within mass graves as a consequence of
differing micro-environments. The importance of adipocere
lies in its preservation of the body, which aids in personal
identification and the recognition of injuries.

Maceration

Maceration is the aseptic autolysis of a foetus, which has died
in-utero and remained enclosed within the amniotic sac.
Bacterial putrefaction plays no role in the process. The
changes of maceration are only seen when a still-born foetus
has been dead for several days before delivery. Examination of
the body needs to be prompt since bacterial putrefaction will
begin following delivery. The body is extremely flaccid with a
flattened head and undue mobility of the skull. The limbs may
be readily separated from the body. There are large moist skin
bullae, which rupture to disclose a reddish-brown surface
denuded of epidermis. Skin slip discloses similar underlying
discoloration. The body has a rancid odour but there is no gas
formation. Establishing maceration of the foetus provides
proof of a post-mortem interval in-utero, and therefore proof
of stillbirth and conclusive evidence against infanticide.


Last edited by Michael on Sat Nov 15, 2008 5:55 am, edited 1 time in total.
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PostPosted: Sat Oct 18, 2008 7:20 pm   Post subject: TIME SINCE DEATH   

TIME SINCE DEATH



A lecture by Derrick Pounder, lecturer at Dundee University's Forensic Medicine Department, on methods for deducting Time Since Death. Ref: D, Pounder., Lecture Notes in Forensic Medicine, (p. 27 - 31, c. 8),

DUNDEE UNIVERSITY


Derrick Pounder wrote:
TIME SINCE DEATH

All death certificates require an estimate of the time of death
as well as a statement of the underlying cause of death. If the
death was witnessed then providing a time of death presents
no difficulty, but in an un-witnessed death it can be
problematic. Establishing the time of death is of assistance in
any police investigation of a death, whether it was from
natural or un-natural causes. Establishing the time of an
assault and the time of death is critical in criminal proceedings
in which there are legal issues of alibi and opportunity to
commit the crime. If an accused can prove that he was at some
other place when the injury and death of the victim occurred
then his innocence is implicit. However, the time of injury, or
indeed the time of onset of an acute illness, may be separated
from the time of death by a significant survival period.

Evidence of the time elapsed since death, the post-mortem
interval, may come from the body of the deceased, from the
environment in the vicinity of the body, and from information
on the deceased’s habits, movements, and day-to-day
activities. All three sources of evidence - corporal,
environmental and anamnestic - should be explored and
assessed before offering an opinion on when death occurred.
The longer the post-mortem interval then the less accurate is
the estimate of it based upon corporal changes. As a
consequence, the longer the post-mortem interval then the
more likely it is that anamnestic or environmental evidence
will provide the most reliable estimates of the time elapsed.

Many physico-chemical changes begin to take place in the
body immediately or shortly after death and progress in a
fairly orderly fashion until the body disintegrates. Each change
progresses at its own rate which, unfortunately, is strongly
influenced by largely unpredictable endogenous and
environmental factors. Consequently, using the evolution of
post-mortem changes to estimate the post-mortem interval is
invariably difficult, and always of limited accuracy.

Body Cooling

Body cooling is the most useful single indicator of the postmortem
interval during the first 24 hours after death. The use
of this method is only possible in cool and temperate climates,
because in tropical regions there may be a minimal fall in
body temperature post-mortem, and in some extreme climates,
such as desert regions, the body temperature may even rise
after death.

Since body heat production ceases soon after death but loss of
heat continues, the body cools. The fall in body temperature
after death is mainly the result of radiation and convection.
Evaporation may be a significant factor if the body or clothing
is wet, and heat loss by conduction may be considerable if the
body is lying on a cold surface. Newton's law of cooling states
that the rate of cooling of an object is determined by the
difference between the temperature of the object and the
temperature of its environment, so that a graphical plot of
temperature against time gives an exponential curve.

However, Newton's law applies to small inorganic objects and
does not accurately describe the cooling of a corpse which has
a large mass, an irregular shape, and is composed of tissues of
different physical properties. The cooling of a human body is
best represented by a sigmoid curve when temperature is
plotted against time. Thus, there is an initial maintenance of
body temperature which may last for some hours - the socalled
‘temperature plateau’ - followed by a relatively linear
rate of cooling, which subsequently slows rapidly as the body
approaches the environmental temperature. The post-mortem
temperature plateau is physically determined and is not a
special feature of the dead human body. Any inert body with a
low thermal conductivity has such a plateau during its early
cooling phase. The post-mortem temperature plateau generally
lasts between a half and one hour, but may persist for as long
as three hours, and some authorities claim that it may persist
for as long as five hours.

It is usually assumed that the body temperature at the time of
death was normal i.e. 37°C. However, in individual cases the
body temperature at death may be subnormal or markedly
raised. As well as in deaths from hypothermia, the body
temperature at death may be sub-normal in cases of congestive
cardiac failure, massive haemorrhage, and shock. The body
temperature may be raised at the time of death following an
intense struggle, in heat stroke, in some infections, and in
cases of haemorrhagic stroke involving the pons. Where there
is a fulminating infection, e.g. septicaemia, the body
temperature may continue to rise for some hours after death.

Thus the two important unknowns in assessing time of death
from body temperature are the actual body temperature at the
time of death, and the actual length of the post-mortem
temperature plateau. For this reason assessment of time of
death from body temperature cannot be accurate in the first
four to five hours after death when these two unknown factors
have a dominant influence. Similarly, body temperature
cannot be a useful guide to time of death when the cadaveric
temperature approaches that of the environment. However, in
the intervening period, over the linear part of the sigmoid
cooling curve, any formula which involves an averaging of the
temperature decline per hour may well give a reasonably
reliable approximation of the time elapsed since death. It is in
this limited way that the cadaveric temperature may assist in
estimating the time of death in the early post mortem period.

Unfortunately the linear rate of post-mortem cooling is
affected by environmental factors other than the
environmental temperature and by cadaveric factors other than
the body temperature at the time of death. The most important
of these factors are body size, body clothing or coverings, air
movement and humidity, and wetting or immersion in water.
Body size is a factor because the greater the surface area of the
body relative to its mass, the more rapid will be its cooling.
Consequently, the heavier the physique and the greater the
obesity of the body, the slower will be the heat loss. Children
lose heat more quickly because their surface area to mass ratio
is much greater than for adults. The exposed surface area of
the body radiating heat to the environment will vary with the
body position. If the body is supine and extended, only 80% of
the total surface area effectively loses heat, and in the foetal
position the proportion is only 60%. Clothing and coverings
insulate the body from the environment and therefore slow
body cooling. The effect of clothing has a greater impact on
corpses of low body weight. A bedspread covering may at
least halve the rate of cooling. For practical purposes, only the
clothing or covering of the lower trunk is relevant.

Air movement accelerates cooling by promoting convection,
and even the slightest sustained air movement is significant if
the body is naked, thinly clothed or wet. Cooling is more rapid
in a humid rather than a dry atmosphere because moist air is a
better conductor of heat. In addition the humidity of the
atmosphere will affect cooling by evaporation where the body
or its clothing is wet. A cadaver cools more rapidly in water
than in air because water is a far better conductor of heat. For
a given environmental temperature, cooling in still water is
about twice as fast as in air, and in flowing water, about three
times as fast.

Simple formulae for estimating the time of death from body
temperature are now regarded as naive. The best tested and
most sophisticated current method for estimating the postmortem
interval from body temperature is that of the German
researcher Henssge. Even so, it is acknowledged that the
method may produce occasional anomalous results. It uses a
nomogram based upon a complex formula, which
approximates the sigmoid-shaped cooling curve. To make the
estimate of post-mortem interval, using this method requires
(a) the body weight, (b) the average environmental
temperature since death and (c) the core body temperature
measured at a known time, and assumes a normal body
temperature at death of 37.2oC. Empiric corrective factors
allow for the effect of important variables such as clothing,
wetting and air movement. At its most accurate this
sophisticated methodology provides an estimate of the time of
death within a time span of 5.6 hours with 95% probability.
Gathering the data necessary to use this method for estimating
time of death means that the body temperature should be
recorded as early as conveniently possible at the scene of
death. The prevailing environmental temperature should also
be recorded at the same time, and a note made of the
environmental conditions at the time the body was first
discovered, and any subsequent variation in those conditions.
Measuring the body core temperature requires a direct
measurement of the intra-abdominal temperature. Oral and
axillary temperatures of a corpse do not reflect the core
temperature and cannot be used. Either the temperature is
measured rectally, or the intra-hepatic or sub-hepatic
temperature is measured through an abdominal wall stab. An
ordinary clinical thermometer is useless because its range is
too small and the thermometer is too short. A chemical
thermometer 10 to 12 inches (25 to 30 cm) long with a range
from 0 to 50°C is ideal. Alternatively a thermocouple probe
may be used and this has the advantage of a digital readout or
a printed record.

Whether the temperature is measured via an abdominal stab or
per rectum is a matter of professional judgement in each case.
If there is easy access to the rectum without the need to
seriously disturb the position of the body and if there is no
reason to suspect sexual assault, then the temperature can be
measured per rectum. It may be necessary to make small slits
in the clothing to gain access to the rectum, if the body is
clothed and the garments cannot be pushed to one side. The
chemical thermometer must be inserted about 4 inches (10 cm)
into the rectum and read in situ. The alternative is to make an
abdominal stab wound after displacing or slitting any
overlying clothing. The stab is made over the right lower ribs
and the thermometer inserted within the substance of the liver,
or alternatively a right subcostal stab will allow insertion of
the thermometer onto the undersurface of the liver.

These temperature readings from the body represent data,
which if not collected at the scene of death is irretrievably lost.
Therefore the decision not to take such readings is always a
considered one. If sequential measurements of body
temperature are taken then the thermometer should be left in
situ during this time period. Taking sequential readings is
much easier with a thermo-couple and an attached print-out
device.

Supravital reactivity

The fact that cellular death occurs in waves within the body
tissues following somatic death is evidenced not only by the
possibility of organ and tissue transplantation, but also by the
persisting excitability of muscle after death, supravital
reactivity. Skeletal muscle may be induced to contract in a
corpse using mechanical stimulation or electrical stimulation.
Mechanical excitation of a variety of muscles in the limbs and
face can be achieved by striking them in the immediate post
mortem period but the times at which this excitability is lost is
not sufficiently well documented to be of forensic use in the
determination of the time of death. The testing of electrical
excitability of skeletal muscle requires specific electrical
apparatus and the insertion of needles into the muscle. Using
this technique on the facial muscles some reaction may be
obtained up to 22 hours after death.

In practice two tests for the mechanical excitability of skeletal
muscle in a corpse are of forensic value. Striking the lower
third of the quadriceps femoris muscle about 4inches (10cm)
above the patella causes an upward movement of the patella
because of a contraction of the whole muscle. If present this
reaction indicates death within 2½ hours. It is described as
Xsako’s phenomenon after the person who first described it.
Similarly, striking the biceps brachii muscle and producing a
muscular bulge at the point of impact, due to local contraction
of the muscle, indicates that death had occurred within 13
hours. The absence of muscle contraction in either test
provides no useful information.

In the post mortem period the smooth muscle of the iris is
reactive to electrical and chemical stimulation for a longer
time than skeletal muscle. The early death of the cells of the
nervous system effectively denervates the smooth muscle of
the iris, which becomes super-sensitive to chemicals which act
at the neuromuscular junction. A change in the size of the
pupil of the eye of a corpse can be produced by chemical
stimulation of the iris following sub-conjunctival injection of
solutions of acetylcholine, noradrenaline, and atropine. The
strongest and longest surviving post mortem chemical
stimulation is by acetylcholine and noradrenaline, the former
producing miosis (papillary contraction) and the latter
mydriasis (papillary enlargement). Reactivity to these two
chemical neurotransmitters is lost at the earliest 14 hours after
death and persists at the latest until 46 hours after death.
Atropine produces mydriasis; the reactivity is lost by 3 hours
post mortem at the earliest and is present until 10 hours post
mortem at the latest.

Biochemical methods

A wide range of biochemical tests have been explored in an
attempt to find one of use in estimating time of death, but
without any success. This is not surprising since all postmortem
biochemical changes will be temperature dependent
and therefore less reliable than the use of body temperature
itself in time of death estimation.

The biochemical method most frequently referred to is the
measurement of potassium in the vitreous humour of the eye.
There are sampling problems because the potassium
concentration may differ significantly between the left and
right eye at the same moment in time. The confounding effect
of possible ante-mortem electrolyte disturbances can be
excluded by eliminating all cases with a vitreous urea above
an arbitrary level of 100 mg/dl, since high urea values in
vitreous humour always reflect ante-mortem retention and are
not due to post mortem changes. Having eliminated cases with
possible ante-mortem electrolyte imbalance, there is a linear
relationship between potassium concentration and time after
death up to 120 hours, but the 95% confidence limits are ± 22
hours, so the method is too imprecise to have practical value.

Rigor mortis

There is great variation in the rate of onset and the duration of
rigor mortis, so that using the state of rigor mortis to estimate
the post-mortem interval is of very little value. In general, if
the body has cooled to the environmental temperature and
rigor is well developed, then death occurred more than 1 day
previously and less than the time anticipated for the onset of
putrefaction, which is about 3 to 4 days in a temperate climate.
Gently attempting flexion of the different joints will indicate
the degree and location of rigor. Typically slight rigor can be
detected within a minimum of one half hour after death but
may be delayed for up to 7 hours. The average time of first
appearance is 3 hours. It reaches a maximum, i.e. complete
development, after an average 8 hours, but sometimes as early
as 2 hours post-mortem or as late as 20 hours. As a general
rule when the onset of rigor is rapid, then its duration is
relatively short. The two main factors which influence the
onset and duration of rigor are the environmental temperature
and the degree of muscular activity before death. Onset of
rigor is accelerated and its duration shortened when the
environmental temperature is high, so that putrefaction may
completely displace rigor within 9 to 12 hours of death.

The forcible bending of a joint against the fixation of rigor
results in tearing of the muscles and the rigor is said to have
been ‘broken’. Provided the rigor had been fully established, it
will not reappear once broken down by force. Reestablishment
of rigor, albeit of lesser degree, after breaking it
suggests that death occurred less than about 8 hours before
rigor was broken.

Livor Mortis

The development of livor is too variable to serve as a useful
indicator of the post-mortem interval. Lividity begins to form
immediately after death, but it may not be visible for some
time. Ordinarily its earliest appearance, as dull red patches, is
20 to 30 minutes after death, but this may be delayed for up to
2, or rarely 3 hours. The patches of livor then deepen, increase
in intensity, and become confluent within 1 to 4 hours postmortem,
to reach a maximum extent and intensity within about
6 to 10 hours, but sometimes as early as 3 hours or as late as
16 hours. Faint lividity may appear shortly before death in
individuals with terminal circulatory failure. Conversely, the
development of lividity may be delayed in persons with
chronic anaemia or massive terminal haemorrhage.

Putrefaction

There is considerable variation in the time of onset and the
rate of progression of putrefaction. As a result, the time taken
to reach a given state of putrefaction cannot be judged with
accuracy. An observer should not assert too readily that the
decomposed state of a body is inconsistent with a time interval
alleged. As a general rule, when the onset of putrefaction is
rapid then the progress is accelerated. Under average
conditions in a temperate climate the earliest putrefactive
changes involving the anterior abdominal wall occur between
about 36 hours and 3 days after death. Progression to gas
formation, and bloating of the body, occurs after about one
week. The temperature of the body after death is the most
important factor determining the rate of putrefaction. If it is
maintained above 26C (80F) or so then the putrefactive
changes become obvious within 24 hours and gas formation is
seen in about 2 to 3 days.

The progression of putrefaction may be modified by vertebrate
or invertebrate animal activity. Wild animals, domestic pets,
livestock, fish and crustaceans may be involved but most
commonly it is insects, particularly fly larvae (maggots). In a
hot humid environment with heavy insect activity a corpse can
be skeletonised in as little as 3 days. All soft tissues are
generally lost before the skeleton begins to disarticulate,
typically from the head downward, with the mandible
separating from the skull and the head from the vertebral
column, and from central to peripheral, that is from vertebral
column to limbs. Remnants of ligaments and tendons
commonly survive about one year, and an odour of
decomposition for a few years.

Skeletal remains are of forensic interest only if the time since
death is less than a human lifespan, about 75 years, because
any perpetrator of a crime may still be alive. Dating skeletons
is difficult but is aided by associated artefacts, such as
personal effects, and evidence from the grave and its
environment. Usefully the bones of individuals who died after
the 1940s contain high levels of strontium-90 acquired in life
from the atmospheric contamination caused by nuclear
explosions.

The presence of any adipocere indicates that the post-mortem
interval is at least weeks and probably several months. Under
ideal warm, damp conditions, adipocere may be apparent to
the naked eye after 3-4 weeks. Ordinarily, this requires some
months and extensive adipocere is usually not seen before 5 or
6 months after death. Extensive changes may require not less
than a year after submersion, or upwards of three years after
burial. Once formed, adipocere will ordinarily remain
unchanged for years.

Mummification develops in conditions of dry heat, especially
when there are air currents. The time required for complete
mummification of a body cannot be precisely stated, but in
ideal conditions mummification may be well advanced by the
end of a few weeks.

Gastric contents

If the last known meal is still present in the stomach of a
corpse and the time of that meal is known, then it can give
some general indication of the interval between the meal and
death. In general if all or almost all of the last meal is present
within the stomach then, in the absence of any unusual factors,
there is a reasonable medical certainty that death occurred
within 3 to 4 hours of eating. Similarly if half of the meal is
present then it is reasonably certain that death occurred not
less than one hour and not more than 10 hours after eating.
However, these are broad generalisations and difficulties arise
in individual cases because the biology of gastric emptying is
complex and influenced by a wide variety of factors including
the size and type of meal, drugs, stress and natural disease.

Remarkably liquids, digestible solids and non-digestible solids
ingested together in the same meal will leave the stomach at
different rates. The emptying of low-calorie liquids is volume-dependant
(monexponential) resulting from the motor activity
of the proximal stomach. By contrast digestible solids empty
more slowly, in an approximately linear pattern after an initial
lag period, primarily as a result of the motor activity of the
distal stomach. Non-digestible solids which cannot be ground
up by the stomach into smaller particles are emptied after the
liquid and digestible solids, during the so called inter-digestive
period, as a result of a specific wave of motor activity in the
stomach. In general meals of a higher osmotic and caloric
content are emptied more slowly.

However, there is a substantial variation in gastric emptying
rates in normal people. Individuals who suffer severe injuries
resulting in coma and survive several days in hospital may still
have their last meal within the stomach at autopsy. These are
extreme examples of delayed gastric emptying but serve to
illustrate the point that the stomach is a poor forensic timekeeper.

There have been several cases of alleged miscarriages of
justice in which medical experts have wrongly used the
stomach contents at autopsy to provide estimates of time of
death to an accuracy of half an hour whereas the degree of
accuracy possible is at best within a range of 3 or 4 hours.

Entomology

Insects will colonise a corpse if given the opportunity. The
most important flies whose larvae (maggots) feed on corpses
belong to the groups Calliphoridae or blow-flies and
Sarcophagidae or flesh-flies. The blow-flies are the bright
metallic blue and green ‘bottle flies’ commonly found around
refuse. Each part of the world has its own indigenous species
of these flies and, as a consequence of the movement of
human populations, some old world species have been
introduced into North America and Australasia. While fly
larvae feed on the corpse, beetles feed on the larvae, although
some beetle groups will feed directly on the corpse. Beetles
appear on the corpse later than flies and are some of the last
insects to colonise fragments of soft tissue remaining on
skeletonised bodies.

Fly eggs are laid on the moist body parts such as the eyes,
nares, mouth, perineum and wounds. Head hair, folds in
clothing and the crevice between the body and the ground are
sites of oviposition also. Early maggot colonisation of parts of
the body not usually colonised suggests that there was a
breach in the skin, a wound, at that site to attract oviposition,
e.g. on the palms of the hands. After the adult female fly has
laid its eggs they hatch within a few hours, depending on
species and the ambient temperature, giving rise to the first of
three stages (instars) of larvae. They are very small, usually
less than 2mm in length, and difficult to see. Flesh-flies,
unlike blow-flies deposit first instar living larvae rather than
eggs on the corpse. First instars moult, shedding their
exoskeleton, to produce second instar larvae which grow to a
length of up to 4-6mm. The second instars moult to yield third
instar larvae, the largest maggot stage, and that most
commonly observed; they are voracious feeders on the corpse.
When present in large masses they generate considerable heat
and a strong odour of ammonia, their main excretory product.

Post feeding larvae, prepupae, migrate from the corpse,
wandering off to find a protected place for pupation. The
exoskeleton of the third stage larvae hardens and browns
forming the puparium. This pupal stage of development is
similar to the chrysalis of butterflies where metamorphosis to
the adult form of the species occurs. In due course an adult fly
will emerge from the pupa.

For each species this life-cycle follows a known temperature-dependant
time course. Consequently, maggots of a known
stage of development and species found on a corpse give an
indication, from the time required for their development, of
the minimum period since death. Even in bodies long dead the
remnants of insects such as pupa cases and the exoskeletons of
beetles may provide useful information.

The pattern of corpse colonisation by successive waves of
insects provides a source of further information. Moving a
body or burying it some days after death interrupts the normal
succession of insects, from which it can be deduced that an
event occurred to disturb the normal chain of entomological
events. Blow-flies of certain species are found in either an
urban or a rural habitat. Finding urban blow-fly larvae on a
corpse in a rural setting would suggest death and blow fly
oviposition in an urban environment followed by dumping of
the body in the rural environment.

The larvae feeding on a corpse may contain any drugs present
in the corpse, and are often easier to analyse than body tissue
because the corpse contains large numbers of masking
chemicals produced by decomposition. Many years after the
death, drugs may still be identified in the remnants of pupal
cases associated with skeletonised remains.

Botany

Plants and parts of plants may provide evidence of time since
death if a plant is in contact with the body or buried with
human remains. Ideally a botanist should attend the scene,
otherwise colour photographs must be taken and the plant
material preserved by drying it between sheets of newspaper.
Perennial plants, such as trees, often have seasonal or annual
growth rings which can provide a minimum age for human
remains where the plant has grown through them or has been
damaged by their deposition. Roots can be useful in a similar
way.

Annual plants give an indication of time because they
complete their life cycles in known time periods in specific
seasons, so that disturbances which can be related to a point in
the life cycle can be dated. Bodies lying over green plants
shade and kill the chlorophyll, and new shoots may develop
from damaged stems, changes upon which a time frame can be
placed.


Last edited by Michael on Sat Nov 15, 2008 5:56 am, edited 1 time in total.
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Offline Michael

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PostPosted: Sat Oct 18, 2008 7:43 pm   Post subject: HENSSGE NOMOGRAM   

HENSSGE NOMOGRAM



The Henssge Nomogram temperature based formula for establishing Time Since Death is the most reliable, although most complicated, available. Ref:

HENSSGE UP TO 23C

HENSSGE ABOVE 23C


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Offline dracs


Joined: Thu May 20, 2010 11:37 am

Posts: 2

PostPosted: Thu May 27, 2010 9:58 pm   Post subject: Re: POSTMORTEM CHANGES AND TIME OF DEATH   

Another great post admin. This is such good info for my research. I will bookmark your post here on Digg.
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