Module

3. FORENSIC THANATOLOGY
SUBMODULE 3.1. NOTION OF DEATH AND POSTMORTEM CHANGES

Death is cessation of activity in a biological structure that was aimed at its

preservation and reproduction.

The concept of death refers both to the organism as a whole, and to its parts
(necrosis of cells, brain death, etc.).

Medical and biological classification of death is made according to its causes

and mechanisms; while the basis of socio-legal classification of death is the
circumstances of death.

Forensic classification of death:

► violent death (homicide, suicide, accident) resulting from:

• mechanical injury;

• mechanical asphyxia;

• poisoning;

• exposure to physical factors: extreme temperature, electricity, atmospheric

pressure changes and radiation energy;

► non-violent death resulting from:

• cardiovascular diseases;

• respiratory diseases;

• CNS diseases;

• GIT diseases;

• malignant neoplasm;

• infectious diseases;

• pregnancy and delivery;

• diseases of other organs and systems of the body.

Forensic pathology classifies death into non-violent (resulting from disease)
and violent, caused by external effects (mechanical injury, hypoxia, starvation,
etc.).

In case of non-violent death, postmortem is performed by pathologists.

However, death from a disease sometimes occurs suddenly, in unusual
conditions (at home, in office, in sleep, etc.), unexpectedly for others, in
apparently healthy individual. The unexpected nature of death always
necessitates ruling out external violence: mechanical injury, poisoning, etc. At
a forensicexamination this is an indication of a sudden death case.

By type, violent death is classified into death following a homicide, a suicide or an

accident. Establishment of death type is based on social and legal rather than medical
criteria, thus it is the prerogative of the investigation bodies or the court, and is
beyond the competence of a forensicpathologist. The forensic pathologist is to say
about the type of violent death only filling in the death certificate, in accordance with
the data recorded in official legal documents. The medical data about a human body
(clinical and morphological) constitute the foundation for judgement on the death
causes and mechanism, thus it is formulated regardless of the death circumstances.

Поставить закладку
The fact of death should be registered following the regulation of the Ministry of
Health of the Russian Federation On Establishming the Time of Death,
Abstaining from or Discontinuing Resuscitation of April 10, 1997. The
criteria are as follows.

► The moment of human biological death is the state of irreversible death of

the body as a whole with total brain death.

► Biological death can be stated based on:

• cessation of the heart activity and respiration for more than 30 min;

• cessation of the brain functions including brainstem functions.

► Biological death based on brain death. The sign of irreversible cessation of

the brain function, lack of spontaneous heart activity and respiratory function:

• no pulse on large (carotid and femoral) arteries;

• no heart contractions based on auscultation or chest X-ray, cessation of

heart bioelectrical activity or small wave febrile oscillations registered by
electrocardiography;

• respiratory cessation based on the chest X-ray or auscultation especially in

the jugular vein area;
• cessation of all CNS functions and reactions, in particular: unconsciousness,
no spontaneous movement, no corneal reflex, no rection to sound, pain
proprioceptive and other stimuli like ammonia smell, maximum pupil dilation
and rection to light in them, bioelectric brain activity on EEG.

The so called Beloglazov sign (cat's eye syndrome) appears 10-15 min after
death: upon compression of the eyeball the pupil becomes slit-like indicating
that the CNS is not functioning. After blood circulation stops, the body begins
to cool. Cooling of the body and Beloglazov sign can be the basis for death
statement.

The above mentioned signs are not sufficient for establishment ofbiological
death in case of general hypothermia or poisoning with substances
suppressing the CNS and/or decreasing the body temperature (e.g.
neuroleptics).

Поставить закладку
Cessation ofblood circulation is indicated by absence of pink color in the web
of fingers hels against bright light and absence of changes in the color of
peripheral portions of fingers after placing a ligature round the finger base. No
bleeding after arteriotomy is a reliable sign of death, though it cannot be
recommended in practice since it may cause bodily harm to the patient if
he/she is still alive.

Absolute death signs are so called postmortem changes (livor mortis, rigor
mortis, etc).

The cause of death is the primary injury (disease) that resulted in death
directly or through its complications. To establish the cause of death is to
indicate the nosological unit corresponding to the morphological changes in
the body which caused death directly or through a consequence of the
resulting functional disorders.

List of immediate death causes:

► destruction of vitally important organs or the whole body (brain destruction

by a shot delivered at pointblank range, heart avulsion or aortal rupture
following fall from a great height, total body destruction following explosion
injury, etc.);

► acute blood loss;

► shock;

► reflex cardiac arrest;

► blood aspiration;
► compression of vitally important organs by blood or air;

► embolism;

► traumatic toxicosis;

► acute kidney failure;

► secondary disorders of blood circulation in an organ;

► infectious complications.

Acute blood loss results from injury of large and medium caliber vessels. Both
the volume and rate of the blood loss are important in the development of
death. A loss of 2-2.5 liters of blood will cause death in an adult, a human may
survive a slow loss of half the blood volume. On the contrary, a quick

and relatively smaller blood loss especially from the brain and heart vessels
can cause death from acute brain anemia or drop in intracardiac pressure. An
injury of large vessels causes profuse bleeding, and a loss of 1liter of blood
may result in death following blood pressure drop. In this case, the body shows
no pronounced signs of exsanguination.

Поставить закладку
Hemodynamic disorders of acute vascular failure type are of primary
importance in death following blood loss. Disrupted blood supply to organs
results in hypoxia with accumulation of underoxidized metabolic products
followed by respiratory center paralysis. The heart stops simultaneously or
some time later.

Signs of acute blood loss are significant blood accumulation in the cavities
and soft tissues, internal organ anemia and dryness, empty veins and arteries,
no or pale livor mortis, focal hemorrhages under the left ventricular
endocardium (Minakov spots). P.A. Minakov associated these spots with a
rapid arterial blood drop followed by negative pressure in the left ventricle
during the diastole resulting in capillary rupture.

Shock is an acute blood circulation failure resulting from failure of

neuroendocrine mechanisms of homeostasis regulation.

Shock is classified according to its origin:

► pain shock (exoand endogenic);

► hypovolemic;

► cardiogenic;
► septic;

► anaphylactic;

► hemolytic;

► rare types: shock related to hemotransfusion, insulin, histamine or

neurogenic causes following anesthesiology complications and spinal cord
injuries.

The typical clinical manifestations of shock are: cool, clammy, pale

cya-notic or marble skin, tachycardia, low blood pressure, dyspnea, oliguria.
The lungs and kidneys are especially sensitive to microcirculation disorders.
The respective lung and kidney injuries manifest as severe respiratory failure
and increasing arterial hypoxia (shock lung), low urinary concentration
capability, decrease and cessation of urine output, increase of blood waste
product level (shock kidney). Shock is diagnosed if there is a severe injury,
typical clinical presentations of a shock and its morphological
manifestations: pathologic blood

Поставить закладку
deposition in the organs, signs of increased permeability of arteriole and
capillary walls, disseminated intravascular coagulation, dystrophic and necrotic
cellular changes in parenchymal organs, lack of glycogen in the liver, hyaline
membrane formation in the lungs, blood flow shunting in the kidneys, depletion
of endocrine function, especially in the adrenal cortex and pituitary.

Reflex cardiac arrest is followed by a quick death resulting from reflex area
injury: blows to the heart or epigastric area, blows or pressure on the carotid
sinus area, upon severe body concussion. In literature there are descriptions
of reflex cardiac arrest following a sudden exposure to low temperature of the
whole body (e.g. after falling into icy water) and the impact of electric current.
No signs characteristic of morphological and clinical presentations of shock
are observed in this case.

Reflex cardiac arrest is difficult and usually presumptive; indications of cardiac

arrest are often imited to insignificant hemorrhages into the
myocardium, paraganglion supracardiale, carotid sinus or solar plexus area as
well as witness statements about death immediately after the injury.

Blood aspiration as an immediate cause of death results from cutting large

vessels on the neck or larynx, skull base fracture, seldom in nasal bleeding.
Morphological diagnosis is simple: in the trachea, large, medium and small
bronchi there are liquid blood and dark-red blood clots (microscopic
examination reveals blood in alveoli), the surface of a dissected lung is motley
due to alternation of dark-red and gray areas of irregular shape.
Organ compression by blood causes death in case of pericardial bleeding
(heart tamponade) as well as in hemorrhages above and under the dura
mater (brain compression by subdural and epidural hematoma). Entrance of
250 ml and 100 ml of blood into the pericardial and cranial cavity, respectively,
is lethal. Intracranial blood accumulation is especially dangerous since it
dislocates and compresses the brain; coat-like blood distribution over the
cerebral hemispheres is less dangerous. There is no death from lung
compression by the blood entering the pleural cavity since the cavities are
large, the lungs are paired organs, and their function is not disrupted. Death
results from acute anemia caused by profuse bleeding into the pleural cavity.

Organ compression by air follows pneumothorax. Unilateral tension

pneu-mothorax can cause death resulting in dislocation of the heart and
mediastinum, bilateral tension pneumothorax is fatal due to compression of
both lungs and difficult external breathing. Pneumothorax combined with
hemothorax aggravates the injured person's condition severely.

Embolism is acute pathological condition resulting from vessel obstruction by

air, gas, fat, pieces of injured tissues, foreign objects and thrombi.

Air embolism most often results from injury of large venous trunks with rigid
walls (cervical, subclavian or uterine) or dura mater sinuses. The air (gas)
which enters these vessels is carried by the blood flow into the right atrium,
right ventricle and pulmonary artery.

The outcome of embolism depends upon the amount and rate of the air
entering the vessels. A quick entry of 15-20 cm3 of air results in an air bubble in
the right ventricle preventing blood supply from the systemic circulation. The
resulting pulmonary circulation block causes quick death. Air embolism can
also cause reflex cardiac arrest. Infusion of 5-10 cm3 may result in air
dissolution in the blood. Slow entry of large amounts of air may also produce a
favorable outcome.

Air embolism of systemic circulation results from lung barotrauma,

intra-operative pulmonary vein injury, etc. The characteristic feature of cerebral
air embolism is multiple merging hemorrhages predominantly in the cortex.
Death results from medullary vital centers.

Fat embolism can result almost from any mechanical injury. The most severe
fat embolism follows fracture of long tubular bones and crushing of
subcutaneous tissue. Fat embolism can be the immediate cause of death in
case of emboli transfer into the brain vessels especially into the medullary
vessels. Fat embolism of lung can only occur upon obstruction of at least two
thirds of pulmonary vessels. Microscopically, fat embolism manifests as
multiple small hemorrhages in the shoulder-girdle skin and conjunctivas, the
white matter and brainstem. Histological study reveals fat emboli in vessels
often accompanied by adjacent tissue necrosis.

Tissue embolism predominantly results in gross lesions of the brain, adrenal

glands, liver, etc. Tissue emboli are usually found in the pulmonary artery and
its branches. Large emboli can be lethal.

In literature there are reports of cases of human body embolism by tri-chinas,

ascarid larvae, single chamber echinococcus alveoli (following vessel
invasion). Embolism may be caused by amniotic fluid during labor. Septic
processes may result from obstruction by bacterial emboli. Death of embolism
with foreign objects is casuistic - there are examples of embolism by bullets in
gunshot injuries of cardiac and large vessels, by needles and catheters
introduced into the vessels for diagnosis or treatment, etc.

Thromboembolism is a life-threatening and relatively not infrequent injury

complication, especially in injuries of lower extremities accompaniying blood
circulation disorders: venous congestion, stasis and thrombi formation.

The detached thrombus moves to the right heart chamber, enters the artery
and obstructs the main trunk or one of the branches.

Traumatic toxicosis (prolonged compression syndrome, crush syndrome,

positional necrosis, etc.) occurs in collapsed buildings, industrial facilities,
mines, tunnels, etc. Prolonged compression of many large muscles results in
shock, muscular necrosis and edema. Massive edema intensifies the collapse;
myolysis products, primarily myoglobin, obstruct renal tubules. Renal blood
circulation disorder of shock kidney type causes acute renal failure. Diagnosis
of traumatic toxicosis is based on detection of diffused skeletal muscles
necrosis (macroscopic findings of "motley muscle" resulting from alternating
pale yellow and pinkish color areas, acute tissue edema, intramuscular
hemorrhage; microscopic findings of waxlike muscular coagulation necrosis),
acute pigmented nephrosis and corresponding clinical presentations.

Acute renal failure can be a lethal complication of other diseases besides

traumatic toxicosis. It often follows hemotransfusion conflict, poisoning with
certain toxins and large thermal burns. Diagnosis of acute renal failure is
based on typical clinical manifestations (oliguria, anuria, azotemia, pulmonary
and cerebral edema) and microscopic signs of toxic-hemorrhagic nephrosis.

Secondary disorders of organs and primary cerebral blood

circulation cause death in subacute and late phases of the traumatic process.
Most frequently, they manifest as focal hemorrhages in the brainstem.
Sometimes they are secondary hemorrhages into cavities, recurrent
hemorrhages into parenchymal organs resulting in ruptures (e.g. two-stage
splenic rupture ).
Infectious complications as an immediate cause of death occur after a
trauma in the long term (pneumonia, peritonitis, sepsis, meningitis, tetanus,
gas gangrene, etc.). The most common complication is pneumonia, and
evaluation of its contribution to death is not simple. It is necessary to find
clinical evidence of developing respiratory failure and estimate the degree of
pulmonary parenchyma lesion. This sometimes requires segment-by-segment
histological examination of lungs, postmortem chest and lung X-ray,
bronchography and pulmonary angiography, as well as bacteriological tests.

At infectious complications resulting in death, it is sometimes necessary to

establish the causal relation between the injury, complication and death. This
is not a trivial task in case of chronic inflammatory diseases and immune
deficiency. The method consists in modeling a sequence of events in case
there was no chronic diseases and in case there was no injury and,
consequently, identifying a more significant factor.

Other lethal injury complications include post-traumatic epilepsy, intestinal

obstruction caused by commissure, traumatic heart defect, aneurysm, tumor,
etc.

SUBMODULE 3.2. POSTMORTEM CHANGES AND ESTIMATION OF TIME

SINCE DEATH

Postmortem changes result from cessation of vital body functions.

Postmortem changes are classified into early and late phenomena allowing an
estimation of time elapsed since death.

Early postmortem changes manifest within the first 24 hours and include
algor mortis, cadaveric drying, livor mortis, rigor mortis and autolysis.

Algor mortis (cooling of dead body)

► In estimating the time since death, thermometry gives only approximate

results since the body temperature at the moment of death is unknown.

Production of heat in the dead body stops and it cools to the ambient
temperature. The dead body temperature can be below the ambient
temperature due to liquid evaporation. Cooling is normally over by the end of
the first day. The open parts of the body (face, wrists) cool quicker, their
cooling is apparent in 1-2 hours, the armpit area cools the slowest. The
temperature should be measured in the rectum or in the liver with electric
thermometer with pin sensors.

The cooling of a dead body provides only approximate reference for time since
death estimation since the body temperature at the moment of death can vary
greatly (table. 3.1). The dead body temperature increases temporarily in
tetanus or sepsis. The dead body temperature can increase at a high ambient
temperature. The cooling slows down upon sunstroke or carbon monoxide
poisoning. Heat release depends on the environment: ambient air temperature,
humidity, ventilation, type of clothes. Individual peculiarities also affect the rate
of cooling: subcutaneous fat (it slows down the cooling because of low thermal
conductivity, age (children cool quicker), the cause of death (alcohol, arsenic
poisoning and blood loss increase the rate of cooling) thus thermo-metry is
ofjust relative value.

Table 3.1. Correlation between time since death and rectal body temperature

Time since death, Rectal temperature, Time since death, Rectal temperature,
hrs degrees Centigrade hrs degrees Centigrade
2 35.8 16 27.0
3 34.6 17 25.4
4 33.9 18 26.2
End of the table

End of the table

Time since death, Rectal temperature, Time since death, Rectal temperature,
hrs degrees Centigrade hrs degrees Centigrade
5 33.4 19 25.7
6 32.8 20 25.0
7 32.1 21 24.4
8 31.3 22 24.0
9 30.7 23 23.5
10 30.1 24 23.2
11 29.7 25 22.4
12 29.2 26 21.7
13 28.7 27 21.2
14 28.1 28 21.1
15 27.6 29 20.9
Drying

Drying results from liquid evaporation from the surface of the body. After death
the balance between liquid intake and excretion changes, the body starts to
lose liquid via convection and evaporation. In areas most moisturized in a
living body (lips, scleras) the drying is intense and manifests itself as areas of
parchment density. The epidermis protects the skin from drying, therefore the
areas of epidermal lesion (abrasions, scratches) dry faster. Drying depends on
the environment: the ambient temperature and movement, and individual
peculiarities: nutritional status, presence of dehydration, clothing.

Drying begins with corneas of open or half-open eyes, triangular drying is

called Larcher spots, which become visible 2-4 hours after death (fig. 3.1).
Drying of skin and mucosa starts immediately after death, but the drying
becomes visible in several hours. The lack of correlation between drying and
time

Fig. 3.1. Larcher spots

since death, as well as many confounding factors hinder the use of these
features in estimating the postmortem interval.

Livor mortis

Livor mortis is spots of crimson-blue, pink and rarely other color on the dead
body skin resulting from postmortem blood settling in dependent parts of the
body, overfilling of toneless skin vessels and impregnation of adjacent tissues
with plasma hemoglobin.

After cessation of cardiac activity, the blood settles in dependent parts of the
body under the impact of gravity and overfills the toneless vessels (hypostasis).
Then the plasma escapes to the extravascular space (diffusion), and blood
condenses hindering its movement (stasis). In 24 hours, erythrocyte hemolysis
ends resulting in impregnation of adjacent tissue with plasma and erythrocytes
(imbibition).

Medicolegal importance of livor mortis consists in the following.

► Reliable sign of death.

► The time of death can be evaluated by observing the interval of livor mortis
restoration (livor mortis appear 1-3 hours after death; up to 8-15 hours, livor
mortis disappears upon depression and pales upon rolling over the body; in
12-15 hours, liver mortis turns pale upon depression and partially disappears
upon rolling over the body; in 24-35 hours, livor mortis does not turn pale or
disappear upon depression and does not go away upon rolling over the body
(fig. 3.2); too high or too low ambient temperature accelerates and slows down
the livor mortis development, respectively).

Fig. 3.2. Estimating time of death by observation of the livor mortis restoration
time
Fig. 3.3. Establishing objects under the body according to absence of livor
mortis in the areas of pressure since the vessels are compressed

► Establishment of the cause of death (abundant livor mortis spots develop

upon quick death or death by asphyxiation; weak manifestation of livor mortis
results from anemia; light-red livor mortis is typical of carbon monoxide
poisoning and hypothermia; brown livor mortis results from poisoning with
toxins causing methemoglobin formation).

► Establishing whether the body was moved - if the body position has been
changed, the livor mortis can develop in dependent parts of the body only
within 12 hours after death.

► Establishing objects under the body according to absence of livor mortis in

the areas of pressure since the vessels are compressed (fig. 3.3).

Rigor mortis

Rigor mortis is postmortem shrivelling and contraction of muscles resulting in

restriction of passive movements and ankylosis following the muscle
contrac-ture in the parabiotic state.

Поставить закладку
In the dead body muscles, ATP breakup results in muscle contraction. Muscles
do not relax after cessation of ATP resynthesis. In 2-3 days putrefaction and
lysis result in actomyosin breakdown and muscle relaxation. Medico-legal
importance of rigor mortis consists in the following.

► Reliable sign of death.

► Estimation of time since death (rigor mortis appears within 3-4 hours, first in
the facial muscles; in 8-14 hours rigor mortis affects all the muscles

and resolves in 2-3 days; rigor mortis development and resolution goes from
top to bottom). A higher ambient temperature accelerates both rigor mortis
development and resolution since the rate of biochemical reactions increases
with temperature. Poisoning with strychnine, hemlock toxin, acids as well as
asphyxia accelerate rigor mortis due to seizures (fig. 3.4).

► The postmortem posture is fixed [in medullar lesion, rigor mortis can
develop instantaneously fixing the posture right before the death (cataleptic
stiffness)].

► Establishing whether the body was moved: rigor mortis disturbed 1012
hours after death does not restore.

Autolysis

Dead body autolysis is an ability acquired via evolution: body's cells are
destroyed through the action of their own digestive enzymes.

Autolysis is hydrolytic decomposition of a biological object resulting from

enzymatic activity without participation of bacteria, it manifests as tissue
softening and liquefaction. Autolysis begins in organs rich in proteolytic
enzymes (pancreas, adrenal glands, stomach, spleen, liver). Autolysis can
develop inside the cells upon formation of lysosomes followed by lysis of
individual cell components (mitochondria, ribosomes, etc.) resulting from
ly-sosome enzymatic activity. The cells disintegrate releasing enzymes
normally isolated from the tissues. Tissue acidosis stimulates the enzymatic
activity. Autolysis has a negative medicolegal importance since it imitates
intravital pathological processes.

Поставить закладку
Late postmortem changes become apparent starting on the second day and
are classified into destroying ones (putrefaction) and preserving ones
(adipo-cere, greenish to black discoloration, mummification).
Fig. 3.4. The sequence of development and resolution of rigor mortis

Putrefaction

Putrefaction is decomposition of biological tissue caused by microflora

(bacterial enzymes).

Putrefaction is decomposition of biological tissue caused by bacterial

enzymes. The degree of decomposition has a medicolegal importance in
establishing the time since death.

► Within 1-2 days the abdominal walls turn dirty-green starting from the iliac
areas (putrid green) (fig. 3.5); this color is caused by sulphmetha-hemoglobin:
a product of reaction between hemoglobin and hydrogen sulfide resulting from
putrefaction in the intestines.

► In 2-4 days, putrid venous pattern becomes visible through the skin whose
crimson and dirty-green color results from iron sulfide and
sulph-methahemoglobin formation in the decomposing blood.

► By the end of the first week, cadaveric emphysema (bloating) develops

resulting from gas formation and accumulation in the subcutaneous tissue and
body cavities (fig. 3.6). The putrefactive gases may include flammable
methane and fluorescent hydrogen phosphate. The gases increase the inner
pressure to 1-2 atmospheres turning the uterus with the fetus inside out
(cadaveric or grave delivery) and making the deadbody float. The dirty-green
color spreads to the entire abdomen and chest from the crotch area.

► On day 10-12 the cadaveric skin becomes dirty-green, the epidermis swells
resulting in blisters filled with ichor (fig. 3.7).

► After the second week, cadaveric putrefaction intensifies. The tissues

become slimy and are easily ruptured, greenish color of the skin turns
brownish and darkens. The putrefaction process involves most of the internal
organs: the brain acquires greenish porridge-like consistency; later
putrefaction involves the uterus, prostate, ligaments and cartilages.

Поставить закладку
► By the end of the third to sixth month, production of putrefactive gases
sharply decreases, tissue emphysema disappears and the volume of tissues
and organs decreases followed by progressive putrid tissue liquefaction (fig.
3.8).

The rate of putrefactive changes depends upon the type and conditions of
putrefaction. Dry putrefaction (decay) results from insufficient liquid in the body,
e.g. in cachexia and blood loss. Humid putrefaction results from excessive
liquid in the body, e.g. at edemas. Gas putrefaction takes place in sepsis or
drowning since bacteria enter the body with the water. The body

Fig. 3.5. Green cadaver

Fig. 3.6. Cadaveric emphysema

temperature is optimal for putrefaction; at an ambient temperature above 60 °С

putrefaction stops and autolysis begins. No putrefaction occurs at an ambient
temperature below 0 °С. In summer and in the open air, a cadaver putrefies
especially quickly, an adult cadaver can fully decompose (turn into a skeleton)
within 1-2 months. Casper's law introduced a 1:2:8 ratio, i.e. a cadaver
decomposes twofold and eightfold slower in water and in soil, respectively,
than in the open air.

Fig. 3.7. Putrefactive blisters

Fig. 3.8. Progressive putrid liquefaction of tissues

Burial time. To establish the time of burial one considers the degree of bone
skeletonization, type of soil, where the cadaver was buried, presence of coffin,
fly larvae and insect presence, the possibility of animals preying on the body,
etc. The examination involves emission spectral analysis, ultrasound tests, etc.
In 6 months, putrefactive liquefaction of tissue takes place. The brain, liver,
spleen and gastrointestinal tract putrefy quicker than the kidneys, bladder,
heart and especially large vessels, diaphragm and aseptic uterus. In 12-18
months, soft tissues decompose. In 3-5 years, soft tissues disappear. In 5-10
years, tendons, ligaments and cartilages decompose and disappear. Bones
and hair persist for hundreds and even thousands of years, the time of burial
can be established according to the degree of bone destruction taking into the
account the type of soil where the remains were found.

Поставить закладку
Adipocere

Adiposere or saponification is dense jelly-like consistence of a dead body or

its parts resulting from increased humidity with lack or insufficient access of air,
causing hydrolyzation of fatty tissue followed by fat oxidation and formation of
fatty acid salts. This is a kind of natural preservation of a dead body.
Adipocere (saponification) is a kind of natural preservation of a dead body (fig.
3.9). Adipocere forms in humid environment: in the water, in humid soil. A dead
body acquires whitish (in water) or yellowish (in soil) consistence. Adipocere
has a rancid butter smell; it can be easily cut with a knife, it is light-

Fig. 3.9. Adipocere

er than water, melts if heated, leaves grease spots on paper; dried adipocere
crumbles. Medicolegal importance of adipocere:

► estimating the time since death (minimal time since death can be
established according to adipocere intensity: 3-4 months after death,
adipo-cere is present in muscles and internal organs, a neonate body can fully
turn into adipocere within 4-5 months, an adult body can fully turn into
adipocere within 1 year);

► establishing the type of injury;

► establishing the cause of death;

► possibility of body identification.

Bog body

Bog body is a human cadaver that has been naturally mummified in a peat
bog. The body feathures a decrease in volume and dark staining of the skin,
internal organs and muscles as well as bone demineralization under the
influence of acidic environment of peat bogs.

Bog body is a kind of natural preservation of dead bodies resulting from body
interaction with peat boggy soils containing humus acids. The skin shrivels and
turns grayish-brown, the internal organs and muscles decrease in volume,
mineral salts in the bones are dissolved and the bones became soft and can
be cut with a knife. Medicolegal importance of bog body:

► establishing the type of injury;

► possibility of body identification;

► it is impossible to estimate the time since death for a bog

body. Mummification

Mummification is parchment outlook and brown color of the skin, as well as

tissue shrivelling with significant weight loss resulting from overall drying of the
dead body following the effect of dry warm air and good ventilation.

Mummification is full general cadaver drying resulting from the effect of dry
warm air in good ventilation. The rate of weight loss is over 90%. The tissues
shrivel, wrinkle, the skin acquires brown color and parchment outlook.
Medicolegal importance of mummification:

► estimation of time since death (complete mummification of a newborn takes

3-4 weeks, complete mummification of an adult takes 3-6 months);

► establishment of the type of injury;

► establishment of bone disease;

► establishment of the cause of death;

► possible identification.